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West Virginia-ACC

Poster Competition

Abstracts

April 30, 2016

FIT Research

West Virginia-ACC Poster Competition Abstract Do NOT write outside the boxes. Any text or images outside the boxes will be deleted. Do NOT alter this form by deleting parts of it (including this text) or adding new boxes. Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * Conclusion Please structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * Conclusion

Title:

The Appropriateness of Dual Antiplatelet Therapy Choice Post Percutaneous Coronary Intervention at St. Mary Medical Center.

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )

1.Introduction:

Coronary artery stents are used in the majority of patients who undergo percutaneous coronary intervention (PCI), as they significantly reduce the need for repeat target vessel revascularization compared to balloon angioplasty. Stent thrombosis is an uncommon but serious complication that almost always presents as death or a large non-fatal myocardial infarction (MI), usually with ST elevation. 2.Background: Stent thrombosis within the first year appears to occur with similar frequency in patients with bare metal stents (BMS) or drug-eluting stents (DES), as long as patients are treated with dual antiplatelet therapy for the recommended duration. Three P2Y12 receptor inhibitors are approved in the United States for treatment of ischemic myocardial disorders are Clopidogrel, Prasugrel and Ticagrelor. The composite primary endpoint (cardiovascular death, nonfatal MI, and stroke) was reduced in patients treated with prasugrel compared to Clopidorel. This was driven by a risk reduction for MI and stent thrombosis with no difference in mortality. Counterbalancing the salutary effects of prasugrel was a significant increase in spontaneous bleeding, life-threatening bleeding, and fatal bleeding in the patients treated with prasugrel compared with patients treated with clopidogrel. Ticagrelor is an oral, reversibly binding P2Y12 inhibitor with a relatively short plasma half-life (12 hours). Compared with clopidogrel, ticagrelor has a more rapid and consistent onset of action and, because it is reversible, it has a faster recovery of platelet function. In patients with NSTE-ACS treated with ticagrelor compared with clopidogrel, there was a reduction in the composite outcome of death from vascular causes, MI, or stroke. The mortality rate was also lower in those patients treated with ticagrelor. Although overall major bleeding was not increased with ticagrelor, a modest increase in major bleeding and non–procedure-related bleeding occurred in the subgroup of patients who did not undergo CABG. ACC/AHA guidelines of 2014 reported that It is reasonable to use ticagrelor in preference to clopidogrel for P2Y12 treatment in patients with NSTE-ACS who undergo an early invasive or ischemia-guided strategy (Class IIa). Switching antiplatelet therapy from clopidogrel to either prasugrel or ticagrelor was associated in significant reduction of maximal platelet aggregation, and should be considered in patients with high risk of in stent thrombosis or non-responders to clopidogrel. In our research, will study the use of dual antiplatelet therapy for patient patients who underwent elective or emergent PCI at St Mary Medical center between July 2014 and July 2015 and its appropriateness in correlation with the current guidelines (ACC/AHA). 3.Aim of the study:Raise cardiologist awareness of the current guidelines for the appropriate use of dual antiplatelet therapy. This research will discuss the appropriate choice of DAPT used in patients following coronary artery stenting whether post ACS or elective stenting. 4.Study design:Retrospective chart review study of 200 patients who underwent emergent or elective PCI. Data will include type of DAPT used, comorbidities, risk of bleeding and lab workup. 5. Study location:St. Mary Regional Heart Center, Huntington, WV

6. Study population:Patient who unrweemergent or elective PCI with DES and were eligible for dual

antiplatelet therapy.

7. Study procedure and timeline:- Data collection: 4-6 weeks; Data Analysis: 2 weeks; Manuscript proposal: 2

weeks.

West Virginia-ACC Poster Competition Abstract Authors:

PI: Rameez Sayyed, M.D. CO-I: David Francke, M.D.;Aala Gabi, MD, Ebrahim Sabbagh, DO; Ahmed Amro M.D.

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Author to Receive Correspondence - Contact Information

Full Name: Francke David D.J.

Last First M.I.

Address: 2250 Cherry Ave

Street Address Apartment/Unit #

Huntington WV 25701

City State ZIP Code

Work Phone: 304-546-9472 Alternate Phone:

E-mail Address: [email protected]

Training Program: Marshall University

_x__I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC Annual Meeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Detectable subclinical myocardial necrosis is associated with cardiovascular risk in stablepatients with diabetes.


BACKGROUND:Detection of systemic levels of cardiac troponin is associated with the presence of ongoingmyocardial necrosis and fulfills the contemporary definition of myocardial infarction (MI) in thepresence of ischemic symptoms. However, a minimal increase in cardiac troponin levels belowthe diagnostic range often provides clinical challenges, particularly in stable ambulatory patientswithout overt signs and symptoms suggestive of underlying ischemia and normal renal function.As biochemical assays become more and more sensitive, the ability to detect minimal myocardialdamage may allow risk assessment in stable cardiac patients beyond the acute setting.OBJECTIVE:To investigate the relationship between different degrees of subclinical myocardial necrosis,glycemic control, and long-term adverse clinical outcomes within a stable patient population withdiabetes mellitus.METHODS:We examined 1,275 stable patients with diabetes mellitus undergoing elective diagnosticcoronary angiography with cardiac troponin I (cTnI) levels below the diagnostic cut-off for definingmyocardial infarction (MI) (<0.03 ng/mL). The relationship of subclinical myocardial necrosis(cTnI 0.009-0.029 ng/mL) with incident major adverse cardiovascular events (MACE; defined asany death, MI, or stroke) over 3 years of follow-up was examined.RESULTS:Subclinical myocardial necrosis was observed in 22% of patients. A strong association wasobserved between the magnitude of subclinical myocardial necrosis and risk of 3-year incidentMACE (hazard ratio, 1.98; 95% confidence interval, 1.48-2.65; P < 0.001) and remainedstatistically significant even after adjustment for traditional risk factors, high-sensitivity C-reactiveprotein, and creatinine clearance. Only a weak correlation was observed between the presenceof subclinical myocardial necrosis and either glycemic control (r = 0.06; P = 0.044 for hemoglobinA1c versus cTnI) or insulin resistance (r = 0.04; P = 0.094 for glucose-to-insulin ratio versuscTnI).CONCLUSIONS:The presence of detectable subclinical myocardial necrosis in stable patients with diabetesmellitus is associated with heightened long-term risk for MACE, independent of traditional riskfactors and glycemic control.

West Virginia-ACC Poster Competition Abstract

Authors:

Naveed S. Iqbal MD, W.H. Wilson Tang MD, Yuping Wu PhD, Earl Britt Jr. BS, Stanley Hazen MD, PhD.

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Full Name: Iqbal Naveed SLast First M.I.

Address: 223 Riverview DriveStreet Address Apartment/Unit

#Barboursville WV 25504

City State ZIP CodeWork Phone: 312-339-0015 Alternate Phone:


TrainingProgram: Department of Cardiovascular Medicine at Marshall University School of Medicine

__X_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Project to assess proper documentation of I/O’s in patient admitted with heart failure

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this)Background: Heart failure is associated with significant mortality, morbidity, and healthcare expenditures in the US. Theprevalence of HF is > 5.8 million, with >550 000 new cases diagnosed each year. Nearly 1 million hospitalizations for HFoccur each year and the 30 days readmission rate for HF is 25%. West Virginia has among the highest readmission rate in thenation. Currently, hospital readmissions are quality indicators, with downward adjustment of Medicare payment for hospitalswith higher 30-day readmission rates. Strict monitoring of input/output and daily weight monitoring are parts of the standard ofcare of patients admitted to the hospital for decompensated heart failure. These documentations would help doctors to adjustdiuretic dose for patients there by affecting clinical improvement and duration of hospital stay. However, clinicians oftenexpress their frustration when these important parts of patient care are missed/ overlooked or poorly documented.

Objective: The aim of our study is to assess the proper documentation of input/output and daily weight in patients admitted toCabell Huntington hospital with a diagnosis of heart failure

Methods: List of patients admitted to Cabell Huntington hospital with heart failure between Sept – Oct 2015 was obtained fromCabell Huntington hospitals quality and performance improvement office, data collected from each patient’s medical recordson weight measurement and documentation of I/Os. The data was entered in to Excel and analyzed

Results: Our study revealed that daily weight monitoring was not consistently documented in significant proportion of patients,Intake documentation was found to be very poor, and inconsistent irrespective of the level of care.


Authors:Okhumale P, Zeleke G, Wehner P

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Full Name: OKHUMALE PAUL ILast First M.I.

Address: 334 LEDGESTONE DRIVEStreet Address Apartment/Unit

#BARBOURSVILLE WV 25504



TrainingProgram: MARSHALL UNIVERSITY

_IPO__I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:The Practice of Transesophageal Echocardiography In Evaluation of Infective Endocardititis: Can We Keep It Safeand Appropriate?


Introduction: Transesophageal echocardiography (TEE) is a key imaging modality for the diagnosis and in theassessment of the severity and complications of infective endocarditis (IE). It also plays a great role in theprediction of short- and long-term prognosis, and in management planning and future patient follow-up.unlike Transthoracic echocardiographic (TTE) procedures, a Transesophageal echocardiographic (TEE) is a semi-invasive procedure that require insertion of the TEE probe to the esophagus and upper portion of the stomach, andrequires local anesthetics and use of moderate sedation. The overall complication rate from TEE is relatively low,however, rare but potentially serious complication can arise from local anesthetics, moderate sedation as well asTEE probe manipulation.

The interest to review and identify TEE related patient safety issues originated after observing,2 cases of methemogloblinemia, a rare but potentially fatal complication of the benzocaine based local anestheticsused during two of our inpatient TEE procedures in the past 1year and after observing an increasing trend to usingTEE in a low-pretest probability conditions, especially when used in evaluation of suspected cases of IE.

Method: A retrospective chart review of patients who had TEE for evaluation of suspected IE at Cabell HuntingtonHospital from Jan 1st - April 30th 2015. Demographics, clinical and bacteriologic evidence IE, TTE findings andoverall pretest probability of IE was documented as outlined in the table. Phase I of these project looked into theappropriateness of each TEE study based on the current guiding principles of the Appropriate Use Criteria (AUC)and to assess our deviation or compliance to this widely accepted national guidelines.

Result: A total of 12 patients, 8 females & 4 males, age range b/n 34 – 76 yrs. identified to have TEE for IEindication during the time indicated. cept 3 were performed for evaluation of native valve IE (1prosthetic valve, 2 ICD and 1 with mediport). All except 3 have low pretest probability of IE.low risk TTE findings for IE. All except 3 were categorized inappropriate based on the AUC. All 12 TEE’s reportedto have no evidence of IE.

Discussion: As reflected in the data 9 out of the 12 patients had low pretest probability for IE and wereinappropriate for TEE per AUC. All 12 patients had a negative result for any TEE evidence of IE further confirmingthe overutilization ofcohort of patients.

Recommendation and Intervention Plan: Based on this retrospective data review, we will develop strategies toensure appropriate utilization of TEE and improve patient care and safety. We will create and post a focused versionof the AUC criteria's (for TEE) and making it available for a quick reference in common teaching and practice areasincluding TEE lab, resident, fellow, and physicians conference rooms. We Implement a thorough pre-TEEquestioner to evaluate appropriateness of indication and to carefully review risk vs. benefit before any TEEprocedures. Identify potential patient safety related concerns in the pre, intra and post- TEE periods (Phase II) and tocreate a tool to timely identify high risk patients and to create a means of alert system among the various staff, inorder to timely coordinate and modify our strategies to avoid any procedure related inconveniences andcomplications. We will monitor implementation of these strategies through periodic evaluation and assessing itsimpact in practice improvement.


Authors:Tekleyes, F. MD, Okhumale, P. MD, Zeleke G. MD, Thompson, E. MD

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Full Name: Tekleyes Fikadu G.Last First M.I.

Address: 5201 Irwin Road # 5Street Address Apartment/Unit

#Huntington WV 25705

City State ZIP CodeWork Phone: (304) 638 3582 Alternate Phone:


TrainingProgram: Marshall University

_FT__I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

FIT Cases

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Takosubo cardiomyopathy presenting as pulmonary edema after breast lumpectomy

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )IntroductionHigh levels of circulating catecholamines associated with stressful conditions have been implicated in the physiopathology of Takosubo cardiomyopathy [1].Case PresentationA 41-year-old woman underwent right breast lumpectomy under general anesthesia with local infiltration of 1% xylocaine, epinephrine and 0.5 bupivacaine.The surgical procedure was uneventful. Nevertheless, she developed sudden respiratory distress during her stay in the recovery area. A chest X ray (fig. 1)and ECG (fig. 2) obtained immediately suggested pulmonary edema and she was treated accordingly demonstrating significant clinical improvement. Serialtroponins were consistently abnormal: 1.480 and 3.380 ng/ml respectively. And thus, she was taken to the catheterization laboratory for coronary angiographythat showed normal coronary arteries (Fig. 3 and 4) and severe anterolateral and mid-inferior hypokinesis with apical and basal hyperkinesis (Fig 5 and 6)compatible with Takosubo cardiomyopathy.Her clinical status followed a recovery course and she was ultimately discharged without further events.DiscussionRecent attention has been drawn toward a possible relationship with surgical procedures and/or exposure to anesthetic agents [2, 3]. While frequentlypresenting as a chest pain syndrome, acute pulmonary edema has been increasingly reported [4, 5].ConclusionsPrompt recognition of this condition could ultimately prevent the use of further invasive diagnostic procedures.References[1] Arora S, Alfayoumi F, Srinivasan V. Transient left ventricular apical ballooning after cocaine use: is catecholamine cardiotoxicity the pathologic link? MayoClin Proc. 2006 Jun;81(6):829-32.[2] Bradbury B, Cohen F. Early postoperative Takotsubo cardiomyopathy: a case report. AANA J. 2011 Jun;79(3):181-8.[3] Dyrud M, Gupta R, Khan R. Acute myocardial depression with inverted (reverse) takotsubo physiology following bupivacaine/lidocaine injection for axillarynerve block. Chest. 2014 Mar 1;145(3 Suppl):62A.[4] Daly MJ, Dixon LJ. Tako-tsubo cardiomyopathy presenting with acute pulmonary edema. Congest Heart Fail. 2009 Jan-Feb;15(1):46-8.[5] Suzuki T, Nemoto C, Ikegami Y, Yokokawa T, Tsukada Y, Abe Y, Shimada J, Takeishi Y, Tase C. Development of takotsubo cardiomyopathy with severepulmonary edema before a cesarean section. J Anesth. 2014 Feb;28(1):121-4.

Figure 1 Figure 3 Figure 5

Figure 2 Figure 4 Figure 6


Authors:Eric Arguelles, MD, Department of Cardiology, Joan C Edwards School of Medicine - Marshall University, Huntington, WV.Naveed S Iqbal, MD, Department of Cardiology, Joan C Edwards School of Medicine - Marshall University, Huntington, WV.Christopher I Jones, MD, Department of Cardiology, Joan C Edwards School of Medicine - Marshall University, Huntington, WV.Frederick G Schnatz, MD, Department of Cardiology, Joan C Edwards School of Medicine - Marshall University, Huntington, WV.Carolina de Elia, MD, Department of Internal Medicine, Joan C Edwards School of Medicine - Marshall University, Huntington, WV.Ellen Thompson, MD, FACC, Professor of Medicine, Division of Cardiology, Joan C Edwards School of Medicine - Marshall University, Huntington, WV.

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Full Name: Arguelles EricLast First M.I.

Address: 6213 Country Club DriveStreet Address Apartment/Unit


City State ZIP CodeWork Phone: 7862736269 Alternate Phone:


TrainingProgram: Marshall University SOM. Adult Cardiovascular Medicine.

_X__I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Two wrongs don’t make a right


Introduction:

Transposition of the great arteries (TGA) is a congenital heart defect that affects about 1 in every 10,000 births in the UnitedStates.

There are two forms of TGA, L-TGA and D-TGA.

D-TGA involves two separate blood circulations and requires either ASD or VSD for oxygenation of the blood and hencesurvival.

L-TGA, also called congenitally corrected TGA, often presents later in life due to corrected circulation. In this anomaly, the rightatrium enters the morphological LV, which gives rise to the pulmonary artery, and the left atrium communicates with the morphological RV,which gives rise to the aorta. These patients can go undiagnosed and present as adults with heart failure due to failure of thesystemic RV.

Case presentation:

37 year old male presented with shortness of breath. He has a self-reported history of dextrocardia and an unrepaired VSD.He reported that he was followed by a pediatric cardiologist but was lost to follow up about 28 years ago. Initial work uprevealed ascites, transaminitis, acute renal failure, pericardial effusion and possible RV thrombus. ECG revealed NSR withfirst degree AV block and extreme right axis.

He was admitted, started on a heparin drip and underwent diuresis. Transthoracic echocardiogram was obtained from theright chest wall. TTE revealed dextrocardia and L-Transposition. The systemic RV was severely dilated and systolic functionwas severely reduced. There was a possible thrombus in the anatomic LV apex. He was transferred to a transplant center forfurther management. He is presently listed on the transplant list.

Discussion:

L-Transposition is an uncommon cause of heart failure in young persons. However, heart failure is the most commonpresentation of L-Transposition in adults. These patients are usually, but not always, diagnosed as children but can be lost tofollow up as adults. In patients with L-TGA and no significant associated lesions, more than one third had congestive heartfailure by the fifth decade. In patients with significant associated defects and prior open heart surgery, two thirds of patientshad congestive heart failure by the age of 45 years.

Conclusion:

Approximately 800,000 adults in the United States have congenital heart disease. L-Transposition accounts for <1% ofcongenital heart disease in the United States. As these patients are often undiagnosed as children or are lost to follow up, itis not uncommon for them to be diagnosed as adults when presenting with acute heart failure. The reading physician needsto be aware of echocardiographic findings related with congenital heart disease so that the appropriate diagnosis can bemade and correct treatment pursued.


Authors:

Kishore Bingi, MD, Samantha Crites, DO, Cornard Failinger, MD, Stanley Schmidt, MD

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Full Name: Bingi Krishna KLast First M.I.

Address: 1 Medical Center DriveStreet Address Apartment/Unit

#Morgantown WV 26506



TrainingProgram: WVU Cardiology

_x__I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Successful Retrieval of Fracture Pressure Wire (FFR wire) Using A Transcatheter Balloon

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )Introduction:Left Heart Catheterization (LHC) is a diagnostic and therapeutic procedure that has an uncommon, but considerable risk. The incidence ofretained objects during angioplasty is reported to be 0.02% in patients undergoing PCI (1). Various treatment options have been used tomanage this rare complication. We present an interesting case of fracture pressure wire that was retained in the LAD and was retrievedusing inflated balloon at the distal guide catheter.Care report:A 62-year-old Caucasian female presented for elective left heart catheterization (LHC). LHC showed 50-60% stenosis in the Mid-LAD and70% stenosis in the Mid and Distal RCA. Decision was made to proceed with FFR of the mid LAD. Patient was given 10,000 units ofHeparin. FFR wire was normalized in the ascending aorta. Guide catheter was engaged and FFR wire was placed in the mid LAD. Wewere not able to advance the FFR wire into the distal LAD and it was felt to be stuck to the mid LAD. Maverick 2.5/20mm balloon wastaken down closer to the FFR wire but was not able to pass the distal tip of the wire. The balloon was then inflated close to the mid LADlesion. It was not successful in freeing the tip of the FFR wire. Then manual traction was applied to the FFR wire. The wire came out butwas noted to have fractured at the mid body. Proximal part of the wire was taken out. Distal part of the wire had been ripped off themain body and was in the distal part of the guide catheter. Then a BMW Universal wire was passed into the LAD and multiple attempts towrap it around the wire were unsuccessful as well (Figure 1). The residual part of the FFR wire was still in the guide catheter in the arch ofthe aorta. The distal tip of the wire was still lodged in the LAD. Finally, we advanced NC Quantum 3.0/30mm balloon to the tip of theguide catheter. Guide was disengaged from the left main. Balloon was inflated at 14 atmospheres to entrap the wire between the tip ofthe guide catheter and the balloon. The guide catheter along with the balloon were pulled back as one assembly and removed as oneunit through the sheath. Another guide catheter was engaged in the ostium of the left main and angiogram was performed whichshowed the native LAD to be free of any dissection (Figure 2).Discussion:The incidence of retained objects during angioplasty is reported to be 0.1-0.2% in patients undergoing PCI (1). Most of the time it iscaused by engagement of the wire to a side branch with spasm in the involved artery. It is assumed that frequent systolic compressioncan put fatigue and strain on the wire and subsequently lead to detachment during withdrawal. Retained coronary objects cansubsequently lead to arterial thrombosis, embolization or perforation. There are, however, a few cases of retained guidewire that had abenign course over extended time follow up with only conservative management (3). The first case reported was in 1980, in that case theguidewire was left in the right PDA for 18 months before surgical removal during coronary bypass surgery (4).Treatment of this type of complications can vary between conservative management, transcatheter approach or surgical intervention.Management depends on the anatomical location and the characteristics of the vessel involved, proximal extent of the retained materialand the clinical status of the patient (1).Various transcatheter methods have been used to retrieve broken wire. Retrieval using a snare loop was first reported in 1988 when aguide wire was modified to form a snare apparatus to retrieve a broken wire from the diagonal branch of the LAD (5). Bioptomes havebeen used to retrieve wires when the proximal end was close to the coronary ostia (1). Double and triple wire technique has been used aswell, two to three guidewires are deployed distal to the fracture wire then rotated to entangle the fracture wire before retrieval (6).Tornus catheter has also been used to release entrapped guidewire in severely calcified coronary arteries (7). Retrieval using ballooninflation at the tip of the guide catheter, as we reported in our case, has also been used with significant success. In cases wheretranscatheter approach failed to retrieve the retained object, Stent deployment against the guidewire was performed (8).Conclusion:Retained fractured wire during angioplasty is a rare complication that warrants operator awareness of its risk and management.


Authors:

Alaa Gabi, MD Ahmed Amro, MD Faisal Hayat MD, Haytham Aljoudi MD, Rameez Sayyed MD.

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Full Name: Gabi Alaa YLast First M.I.

Address: 1600 Medical Center Dr 4000Street Address Apartment/Unit


City State ZIP CodeWork Phone: 304.691.1700 Alternate Phone: 304.638.1755


TrainingProgram: Marshall University

_AG_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:

Spontaneous Coronary Artery Dissection (SCAD) in Post-partum Period.


INTRODUCTION:SCAD is a rare cause of acute coronary syndrome, particularly seen in womenduring pregnancy or past-partum period. Guidelines for optimal managementhave yet to be established. We present a young patient presenting with SCADtreated with various revascularization strategies.

CASE REPORT:36 y/o WF presented to the ER with sub-sternal chest pain 10 days aftercaesarean delivery. Initial lab work showed elevated D-Dimer. CTA of thechest was negative for acute issues. Cardiac TpI trend was 0.258 and then2.513. Initial EKG did not show any ischemic changes. EKG done 24-48 hrslater showed Inferior STE and Anterior ischemic changes. Echocardiogramshowed LVEF 40-45% with distal antero-septal and apical hypokinesia.Coronary angiography was consistent with the appearance of dissection ofdistal left anterior descending artery (LAD). It was not amenable to PCI.

The patient was treated with standard medical therapy for acute coronarysyndrome without any adverse clinical events. Repeated angiography at 6weeks was performed as follow up. There was significant healing of the distalLAD with almost complete normalization of the wall abnormality.

DISCUSSION:SCAD is an infrequent cause of acute coronary syndrome, mainly affectingyoung females. (1,2). Urgent coronary angiography and intravascularultrasound (IVUS) are indicated for the diagnosis and to determine besttherapeutic approach (3,4). Left anterior descending artery is frequentlyinvolved in females whereas right coronary artery is frequently involved in malepatients (5). Medical therapy, PCI and coronary artery-bypass grafting (CABG)have been applied as treatment modalities. The mortality rate reported in theliterature is 38%. (6).

CONCLUSION:SCAD is rare in general population but is a relatively common cause of acutecoronary syndrome in young women. Acute chest pain in a young female inthe post-partum period should raise the clinical suspicion for SCAD.


Authors:

Hayat.F ,MD ; Irviboge.OA, MD ; Sayyed. R, MD.

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Full Name: Hayat FaisalLast First M.I.

Address: 1249, 15th street 4000Street Address Apartment/Unit


City State ZIP CodeWork Phone: 3046918534 Alternate Phone:


TrainingProgram: Marshall University cardiology

_x__I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Very Late Stent Thrombosis Presenting as Acute ST-Elevation Myocardial Infarction

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )IntroductionPercutaneous coronary revascularization using coronary artery stenting has significantly decreased incidence of acute vesselclosure. Stent thrombosis, while not common, can be devastating. Thrombosis occurs in bare metal stents (BMS) in <1% ofcases. The development of drug eluting stents (DES) has decreased incidence of stent thrombosis, however, there has beenan increase of long-term stent thrombosis. Stent thrombosis is defined as time between stent implantation and thrombosis.Early thrombosis occurs 0-30 days post implantation, with acute being <24 hours and subacute 1-30 days. Late stentthrombosis occurs greater than 30 days post implantation. Very Late stent thrombosis occurs >12 months post stentimplantation. Concern must remain high for potential thrombosis years after stent deployment. Risk factors commonlyassociated with very late stent thrombosis include but not limited to; side branch stenting, diabetes mellitus, end stage renaldisease, greater stent length, small vessel calibre, left ventricular dysfunction, emergent stent placement, malignancy,smoking, bifurcation stenting, and subtherapeutic periprocedural anticoagulation. Here we report a case of very late stentthrombosis of a DES in a patient presenting with acute anteriorlateral ST-elevation myocardial infarction 10 years after initialstent deployment.

Case Presentation:TC, a 49-year-old male with past medical history of hypertension, hyperlipidemia, coronary artery disease status post primarycoronary percutaneous intervention to the mid Left anterior descending artery with Taxus 3.0 X 16mm DES in 2006. TCpresented to our emergency department with sudden onset of substernal chest pain and pressure radiating to bilateral jaw,back and down left arm. EKG showed ST-segment elevation in anteriorolateral leads. TC was taken emergently to the cardiaccatheterization laboratory. Angiography showed thrombosis with 100% occlusion of the mid LAD stent. The lesion was treatedwith an Integrity Resolute 2.75 X 18mm and 3.0 X 18mm DES as well as medical therapy with Plavix, aspirin, statin and beta-blocker.

Discussion:Stent thrombosis results in sudden onset occlusion of a stented artery. Extent of ischemia depends on location of thrombosisand is often associated with late complications of myocardial infarction including arrhythmia, heart failure and mechanicalcomplications. We have presented a case of very late stent thrombosis occurring 10 years after stent deployment. Very latestent thrombosis remains a serious complication of coronary artery intervention and is associated with a high rate of morbidityand mortality. The mechanism of very late stent thrombosis is thought to be due to poor endothelialization following stentplacement. Both intravascular ultrasound (IVUS) and Optical coherence topography (OCT) are commonly used to evaluatestent thrombosis. They provide the resolution needed to evaluate mechanisms of stent failure/late stent complications. Whileat least one of the two aforementioned imaging methods are recommended to evaluate a case of stent thrombosis, their usemay not be practical for an acutely ill patient. Common imaging findings associated with very late stent thrombosis, usingIVUS, are large areas of late stent malapposition from positive remodelling or aneurysm formation, vessel wall inflammation,in-stent atherosclerosis with plaque rupture and strut fracture. OCT has been used to show that 12.3% of patients with verylate stent thrombosis of a DES had uncovered struts and at least 1 cross section with >30% of struts without neointima in 72%patients. Preventive measures such as careful attention to implantation details, uninterrupted dual antiplatelet therapy for ≥12months, and alternative revascularization strategies may decrease adverse event. Our patient responded well to quickstabilization, emergent PCI, appropriate medical therapy and risk factor modification.


Authors:

Christopher Jones MD, Anthony Irivbogbe MD, Melissa Lester DO

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Full Name: Jones Christopher ILast First M.I.

Address: 1249 15th Street, Suite 4000Street Address Apartment/Unit


City State ZIP CodeWork Phone: 304.691.8500 Alternate Phone:


TrainingProgram: Marshall Cardiology

__X_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Beneficence, Patient autonomy, and the Moral Imperative

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )Introduction

In ideal clinical scenarios, beneficence and patient autonomy align to create a therapeutic alliance. However, in theevent that these two pillars of ethics are at odds, the barriers to reconciliation must be identified and addressed.

Case Report:The patient is a 62 year old Caucasian male with a past medical history of diabetes, hypertension, hyperlipidemia, and

a strong family history who had initially presented complaining of chest pain. He described an 8-9/10 mid-sternal ache thatstarted while he was walking - it radiated to his back between his shoulder blades and was unassociated with diaphoresis orshortness of breath, and was unlike anything he had ever felt, though it had nearly completely resolved with 1 sublingualnitroglycerin tablet. The first troponin was negative (<0.045), there were no EKG changes, and he was admitted to thehospitalist service, with plans to discharge following a stress test if he ruled out for ACS. The next two troponins increasedslightly, 0.064 and 0.079 respectively, and cardiology was consulted. Given his pre-test probability, left heart catheterizationwas suggested, though he declined – he was completely chest pain free and wanted to get back to work; he reasoned that hehad been healthy up to that point. The physician stressed to him his likelihood of having coronary artery disease, but heremained steadfast, however, he agreed to echocardiography. While undergoing this study, the physician again tried toascertain the reasons for his reluctance, and it was revealed that he was uncomfortable making any decisions without talkingto his family. It was also revealed that, while his EF was preserved and his valvular function was normal, there was mildhypokinesis of his basal inferior, inferolateral, and anterolateral walls. This new information, though confirmation for theclinician, was overshadowed by a phone conversation the patient had with his wife and the urging of his son in convincing himto undergo catheterization. Once the telemetry leads had been connected, he was found to have ST elevation in lead III, andhis case became an emergent one – still he remained chest pain free. He was found to have a totally occluded RCA, 80-90%stenosis of the mid LAD, 99% stenosis of the distal LAD, and received a total of 3 drug eluting stents. Subsequent ECGrevealed inferior Q waves. He did well post-cath and when seen in clinic 1 month after discharge, had returned to his job as aconstruction worker.

Discussion:Most cardiology patient visits deal with chronic problems, and so the building of a therapeutic bond – the foundation

upon which long-term compliance can be built – is a process with the luxury of time. Less frequently patients present withacute coronary syndromes, and generally agree to the interventions suggested to alleviate their pain. In both situations, patientautonomy and beneficence are aligned to deliver high-quality, evidence based care to a patient who is fully informed. In theabove vignette, however, the patient’s decision was at odds with the medical reality. As a competent patient, he was within hisrights to refuse any treatment, however were he to have done so, he would most likely have faced certain morbidity, if notmortality. In such a situation, how is it best to overcome the gulf between patient autonomy and beneficence? Bothmeasurable and immeasurable barriers stand in the way, and all must be dealt with accordingly.

References1. http://medical-dictionary.thefreedictionary.com2. 2012 West Virginia State Health Profile:

http://www.dhhr.wv.gov/publichealthquality/statepublichealthassessment/Documents/2012%20State%20Health%20Profile%20Final%20May%202013.pdf

3. Self Control, Fatalism, and Health in Appalachia. Wendy Welch, Journal of Appalachian Studies Vol. 17, No. 1/2Spring/Fall 2011), pp. 108-122

4. Behringer B, Friedell GH. Appalachia: where place matters in health. Prev Chronic Dis [serial online] 2006 Oct [datecited]. Available from: http://www.cdc.gov/pcd/issues/2006/oct/06_0067.htm.


Authors:

Farley Neasman III M.D.

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Full Name: NEASMAN III M.D. FARLEY B.G.Last First M.I.

Address: 1208 11th St. 2Street Address Apartment/Unit


City State ZIP CodeWork Phone: 956-343-0084 Alternate Phone: same


TrainingProgram: Marshall University Cardiology Fellowship Program

_x_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:SPONTANEOUS CORONARY ARTERY DISSECTION IN THE POST-PARTUM PERIOD

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )Introduction/Objective:Spontaneous coronary artery dissection (SCAD) is a rare but important cause of acute coronarysyndromes and has an incidence of 0.07-1.1 percent. SCAD can be defined as a non-traumatic and non-iatrogenic separationof the coronary arterial walls, creating a false lumen. This disease entity has been documented more commonly in youngerfemales. It appears to be underdiagnosed but with the advent of intracoronary imaging, the incidence in ACS has beenreported to be as high as 3-4%. Common associations including fibromuscular dysplasia, systemic inflammatory diseasestates, connective tissue diseases, and stressors such as trauma, extreme exercise, labor, drug and hormonal use, have beenreported. While the history of the patient plays an important role in this rare diagnosis, retrospectively, after coronaryangiogram is performed, it is important to be aware of this rare cause of ACS in order to initiate appropriate therapies.We present a case of SCAD in the postpartum period, where the high index of clinical suspicion was essential to the patient’soverall management.

Case Presentation: 36 year old G3P2012 female who was 7 days postpartum presented to our hospital for resting chest painassociated with nausea, emesis, and diaphoresis lasting for less than an hour. Her first episode of chest pain began 3 dayspostpartum and resolved spontaneously. Upon arrival to the ED, initial EKG showed NSR with non-specific ST changes andtroponins were elevated 0.258 at 00:18, 2.513 at 03:53, and 2.096 at 07:27, respectively. Transthoracic echocardiogram wasordered which revealed LVEF 40-45% and severe hypokinesis of the apex, apical septal and apical inferior walls. A cardiologyconsultation was placed due to concern of NSTEMI. Subsequent EKG revealed dynamic changes with diffuse T waveinversions. The patient underwent a diagnostic cardiac catheterization, which revealed a long segment of spontaneousdissection in the mid-distal region of the left anterior descending artery. Due to the nature of the lesion (long segment), TIMI3flow, and hemodynamic stability, a conservative approach with medical therapy was adopted. Medical management with dualantiplatelet therapy (aspirin and brilinta), beta blocker (toprol), and statin (lipitor) was commenced. The next day, the patienthad episodes of recurrent chest pain, which was relieved by sublingual nitroglycerin. Repeat EKG showed inferior injury withSTE and deeper diffuse T wave inversions, suggestive of possible extension of the dissection involving a wrap-around leftanterior descending artery. She was cautiously restarted on anticoagulation and long acting nitrates (imdur) were added to hermedical regimen. Due to worsening angina and ongoing dynamic EKG changes, the patient was transferred to a higher levelof care where the possible need for intervention was considered if ischemia persisted. However, her symptoms improved withresolution of EKG changes and therefore, repeat angiogram was not done. She was discharged with the medical therapy asmentioned above and she remained asymptomatic at her post discharge visit 6 weeks later. A repeat diagnostic heartcatheterization revealed near resolution of spontaneous dissection of the left anterior descending artery.

Discussion: Hormonal changes especially in multiparous females, and the development of periarteritis caused by eosinophilicinfiltrates has been the proposed mechanism of coronary artery dissection in the postpartum female. This may result in a tearleading to two lumens or rupture of the vasa vasorum, located within the walls of the coronary arteries. These two hypothesesboth result in the creation of a false lumen, where a hematoma can form, enlarge, lead to myocardial ischemia and finally,present as an acute coronary syndrome, most commonly affecting the left anterior descending artery. Furthermore,spontaneous coronary artery dissections have been described in three types. Although intravascular ultrasound sonography oroptical coherence tomography were not available at the time of angiogram to confirm our diagnosis, due to the long segmentinvolved and absence of atherosclerosis in other coronary arteries, we believe that her anatomy most correlates with a type 2dissection. To date, guidelines dedicated on the management of spontaneous coronary artery dissection do not exist.Management of these rare cases has been based solely on case reports and suggests medical management, percutaneouscoronary intervention, or surgical bypass grafting. While there are not any studies to compare each strategy, a generalconsensus exists against the use of fibrinolytics due to possibility of further propagation of coronary dissection.

Conclusion: The differential diagnosis of chest pain in a postpartum female should include spontaneous coronary arterydissection as this can progress to an acute coronary syndrome. Review of literature supports prompt left heart catheterizationfollowed by initiation of appropriate noninvasive or invasive therapies. Although this patient was not a candidate forpercutaneous coronary intervention or coronary artery bypass grafting due to the nature and location of her dissection (therewas no proximal or ostial involvement), she improved with medical therapies. Therefore, we believe that medical managementwith dual antiplatelet agents, beta blockers, long acting nitrates, and statins should be considered in patients with spontaneouscoronary dissection. The near resolution of her dissection with medicines only supports this conservative approach. Overall,recognizing this patient’s clinical condition and initiating appropriate treatment strategies can lead to a symptom-free lifestyle.


Authors:

Rani Shah, DO; Osareme Anthony Irivbgobe, MD; Rameez Sayyed, MD

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Full Name: Shah Rani ALast First M.I.

Address: 432 Stoneheath DriveStreet Address Apartment/Unit


City State ZIP CodeWork Phone: 4405034555 Alternate Phone: N/A


TrainingProgram: Marshall University Cardiology Fellowship


West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Paradoxical left sided endocarditis complicated by extensive multiple septic emboliAbstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this)

Introduction: Right Sided Infective Endocarditis (RSIE) is frequently complicated by pulmonary septic emboli.Extensive systemic embolization is a rare complication of RSIE. Patent Foramen Ovale (PFO) is the proposedmechanism of this complication in the present case report.

Case presentation: A 36-year-old Caucasian female with a history IVDU presented with chest pain, shortness ofbreath and generalized body aches. On examination, heart rate 115, blood pressure 99/54, temperature 98.2, andrespiratory rate 15. Left lower sternal border grade III systolic murmur. A transthoracic Echocardiogram (TTE)revealed (Figure 1) large mobile vegetation on the tricuspid valve measuring 14x17 mm with moderate tricuspidregurgitation (TR). Computed tomography (CT) of the chest demonstrated innumerable bilateral septic emboli.Additionally, blood cultures grew Methicillin Resistant Staph Aureus (MRSA). The patient responded to intravenous(IV) Vancomycin. Eight weeks later, the patient readmitted with similar symptoms. The patient reported relapsingto IVDU. On examination, scattered tender erythematous nodules on bilateral hands and feet were noted.Transesophageal echocardiogram (TEE) (Figures 2 and 3) revealed tricuspid valve vegetation, severe TR withdirected jet toward atrial septum, left atrial mass measuring 18mm x10 mm attached to atrial septum, PatentForamen Ovale (PFO), severely dilated right atrium and prominent Chiari’s network. Left iliacus muscle abscessmeasuring 35mm x 22mm was detected after patient complained of persistent left hip pain. Concurrently, brainMRI showed bilateral enhancing lesions consistent with septic emboli and brain abscess. TTE and TEE repeatedfive weeks later were free from the valvular vegetation and left atrial mass.

Discussion: Direct extension of tricuspid valve vegetation through the PFO was previously described by Johri et al(1). This possibility is not completely excluded in our case being timing of the echocardiogram is a factor. Differentmechanisms by which PFO opens in the presence of tricuspid valve endocarditis have been reported (1)(2)(3).Mechanisms include high right atrial pressure secondary to pulmonary hypertension (1), right atrial dilatation withventriculisation of right atrial pressure (2) and severe tricuspid regurgitation with jet direction toward atrial septum(4)(5). Hence, severity of tricuspid regurgitation along with jet’s direction toward atrial septum, and the degree ofright atrial dilation are possible co-factors for reopening of the PFO in our case. Additionally, in our case prominentChiari’s network was present. It is a congenital remnant of the right valve of the sinus venosus (6). There isassociation between Chiari’s network and PFO (7). Moreover, significant right to left shunt and unexplainedsystemic embolization were noted in Chiari’s network group favoring paradoxical embolization by directing bloodfrom inferior vena cava toward interatrial septum. Interestingly, our case is the first describing Chiari’s network andRSIE complicated systemic septic embolization. Suero et al (8) reported a case of solitary brain abscess withunderlying isolated tricuspid endocarditis. Paradoxical embolism through a PFO was the underlying mechanism.

Conclusion: Our case demonstrates a rare presentation of tricuspid valve endocarditis complicated by septicpulmonary emboli and extensive systemic embolization through PFO. Chiari’s network illustrated in our case is anadditional finding and serves as and additional possible explanation for paradoxical septic systemic embolization inRSIE. Physicians should be aware of the correlation between the right and left endocarditis in the presence ofPFO. Thorough echocardiograms should be performed in RSIE.1. Johri AM, Kovacs KA, Kafka H . An unusual case of infective endocarditis: Extension of a tricuspid valve vegetation into the left atrium through a patent foramen ovale. Can J Cardiol 2009;25(7):429-431.2. Bru P, Iacono C, Collet F, Vaillant A, Malméjac C, Belhadj M, Houël J. Tricuspid endocarditis with right-left shunt in the atrium. Arch Mal Coeur Vaiss. 1986 Apr;79(4):511-3.3. Morelon P, Eicher JC, Chavanet P, Diebold H, Coudert B, Portier H, David M, Louis P. Tricuspid endocarditis with right-left auricular shunt through a patent foramen ovale]. Ann CardiolAngeiol (Paris). 1987 Jan;36(1):23-6.4. Turek MA, Karovitch A, Aaron SD, Brais M. Persistent hypoxemia occurring as a complication of tricuspid valve endocarditis. J Am Soc Echocardiogr. 2000 May;13(5):412-4.5. Gans CP, Kao JA. Tricuspid regurgitation causing a right to left interatrial shunt with normal pulmonary pressures. Cardiology. 2007;107(4):429-32.6. Chiari H. Über Netzbildungcn im rechten Vorhof des Herzens. Beitr Pathol Anat 1897;22:1-10.7. Schneider B, Hofmann T, Justen MH, Meinertz T. Chiari's network: Normal anatomic variant or risk factor for arterial embolic events?. J Am Coll Cardiol. 1995;26(1):203-210.8. Gregory Sueroa, b, Rekhi Varghesea, Moneal Shaha, David Lasordaa. Embolic Brain Abscess in a Patient With Tricuspid Valve Endocarditis and a Patent Foramen Ovale. J Neurol Res.2012;2(3):123-126


Authors:

Yousef, GM, Okumale P, Aljoudi H, Cansino S.

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Full Name: Yousef George MLast First M.I.

Address: 1249 15th streetStreet Address Apartment/Unit


City State ZIP CodeWork Phone: 3046918534 Alternate Phone: 3049424688


TrainingProgram: Marshall university cardiology program.

__x_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Fibromuscular Dysplasia Coexisting with Atherosclerotic Renal artery Stenosis as a cause of Resistant Hypertension.


Introduction

Renal artery stenosis a common cause of secondary hypertension. In 90 % of cases, renal artery stenosis is due toatherosclerotic disease; It mainly involves the proximal renal artery, and often seen in elderly male patients. In about 10% ofthe patients, fibromuscular dysplasia is responsible for renal artery stenosis, and it affects the middle portion of the renalarteries, usually seen among young females. Finding of fibromuscular dysplasia and atherosclerotic renal artery stenosis in thesame patient, affecting the same renal artery is a very rare occurrence. There were 2 cases reported in the literature to this dayto the best of our knowledge. We are reporting unusual case of an elderly male patient, who was found to have renal arterystenosis caused by both atherosclerosis and fibromuscular dysplasia.

Case Report.

A 62 y/o Caucasian male patient was referred for evaluation and management of renovascular hypertension. He wasdiagnosed with hypertension for more than 2 years, and his blood pressure remained poorly controlled despite a combinationof multiple antihypertensive medications. He is a life time non-smoker, has no diabetes mellitus, and no history of heartdisease or stroke. CT angiogram done at the referring facility showed right renal artery stenosis with beaded appearancesuggestive of Fibromuscular dysplasia. Renal Scintigraphy demonstrated absent of flow to the left kidney and decreased flowto the right kidney. The patient subsequently underwent renal angiography which revealed, complete occlusion of the left renalartery at its origin; The right renal artery showed 80% ostial stenosis and significant “string – of –beads” appearance on theproximal and mid portion consistent with Fibromuscular dysplasia. The proximal and mild portion was treated with balloonangioplasty, and then the ostial disease was treated by putting a 6mm/12 mm Herculink stent. There was 0% residual stenosisat the end of the procedure. The patient tolerated the procedure very well and was discharged home after overnightobservation. On subsequent follow up, the patient’s blood pressure was better controlled.

DiscussionFibromuscular dysplasia is common in younger females and tends to involve the middle and distal parts of the renal artery. Incontrast, renal artery stenosis due to atherosclerotic disease usually affects the ostium or the proximal segment of the renalarteries. In addition is a disease of middle-aged men with atherosclerotic disease elsewhere in the vascular bed. Due to thisdifference in the demographic profiles of the two disease processes, they are very rarely present in the ipsilateral renal artery inthe same patient. Our patient had this very unusual coexisting causes of renal artery stenosis.

Currently both atherosclerotic renal artery stenosis and fibromuscular dysplasia can be successfully treated with percutaneousrenal angioplasty and stent deployment. Several reports have showed good success rates with long-term improvement incontrol of refractory hypertension and renal function. This case highlights concomitant existence of atherosclerotic andfibromuscular dysplasia as a cause of renal artery stenosis in the same renal artery.


Authors:

Getachew Zeleke MD, Cardiology Fellow Marshall UniversityZeid Khitan, MD Assistant Professor, Nephrologist, marshall UniversityDaniel Snavely, MD, Intervention Cardiologist, HIMG

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Full Name: Zeleke Getachew TLast First M.I.

Address: 102 Stoneheath DrStreet Address Apartment/Unit


City State ZIP CodeWork Phone: 304-691-8500 Alternate Phone: 304-973-5594


TrainingProgram: Department of Cardiovascular diseases, Marshall University


Resident Cases

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:First Successful Percutaneous Bi-VAD in the state of WV

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )INTRODUCTION: Heart diseases are the leading cause of death in the United States. Acute coronary syndrome and specifically STEMIcarries significant mortality and morbidity when compared to other forms of ACS. Inferior MI are complicated by RV infarction in a thirdof the cases and when that translates into RV failure significant mortality rates are seen despite conventional treatment modalities,including maintaining preload, reduction of RV afterload, and the use of inotropes. The advent of percutaneous ventricular assist devicesmay be of utility in decreasing the significant mortality seen in such case.

CASE REPORT: A 48-year-old man with no previous medical history transferred to ruby memorial hospital after being found to have anacute inferior myocardial infarction, complicated by VT cardiac arrest and cardiogenic shock, with complete occlusion of the RCA, andmulti-vessel CAD. The patient went through a failed PTCA to the RCA prior to transfer, followed by placement of IABP. Percutaneousplacement of Impella CP LV assist device and Impella RP RV assist device was completed following presentation as he was in profoundcardigenic shock despite being on pressor support. The patient’s initial TTE showed dilated right ventricular size with reduced function.His initial TTE also showed a preserved EF, though subsequent TTE showed a reduced function of 30 – 35% with hypokinesis, the patientremained on the percutaneous Bi-VAD for 8 days, and on the seventh day after showing hemodynamic improvement, the patient was takento the catheterization lab and he underwent PCI to critical lesions in the left system namely in the mid LAD, Diagonal and Mid LCx. Hisventricular assist devices were weaned the second day and removed successfully without complication. The patient’s hospital course wascomplicated by thrombocytopenia that resolved following removal of the devices, aspiration pneumonia, and volume overload followinginitial aggressive fluid resuscitation that resolved with aggressive diuresis afterwards. He also was found to have a small frontal lobe infarctand seizures. The patient recovered over his stay and was discharged following an uneventful period on the floor, and he completed hisrehabilitation as an outpatient. The patient’s repeat TTE showed an improved EF to 35 – 45 %, though his RV EF showed 20 – 25%. Thepatient continues to have close follow up as an outpatient and he reported fair exercise tolerance.

DISCUSSION: The patient presented with profound right ventricular failure and cardiogenic shock despite being on pressors and theplacement of IABP, placement of right ventricular assist device along with fluid resuscitation and augmenting the left ventricular functionshowed to be beneficial to this patient, especially in light of the reported resilience of the right ventricle and the high chance of recoveryfollowing the initial hemodynamic insult. Bridging the patient to recovery was the main target of the device placement with fruitfuloutcome in this case. It is reported that IABP might be beneficial in patient with RV failure following an RV infarct through augmentationof the coronary blood flow, however, in our patient his right system was completely occluded which might explain why his cardiogenicshock was refractory to IABP.

Complications in our patient included hemolysis and thrombocytopenia requiring multiple blood product transfusion, though not classifiedas major bleeding by criteria, there was minimal bleeding at the site of insertion with no significant retroperitoneal hematoma. The patient’ssmall area of infarct is related to hypotension rather than a thromboembolic event most likely, there was no report of valvular injury byechocardiography. The patient’s rate of thrombocytopenia and hemolysis improved minimally following repositioning of the devices.There are no randomized controlled trials to compare outcomes of conventional therapy versus percutaneous mechanical circulatorysupport, though the data available showed significant hemodynamic improvement following devices placement, though complicationsvaried between different devices and points of access.

COINCLUSION: Percutaneous mechanical circulatory support serves as an easier, safer option for patient with refractory to conventionaltherapy right ventricular failure as a bridge for recovery. Further studies needed to compare the outcomes and long-term mortality benefitfor patient’s where this treatment modality is utilized compared to others.


Authors:

Sami Aljohani, MD, Ali Hama Amin, MD, Jason Moreland, MD.

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Full Name: Aljohani SamiLast First M.I.

Address: 1 Medical Center DriveStreet Address Apartment/Unit


City State ZIP CodeWork Phone: 3045984850 Alternate Phone: 2023619980


TrainingProgram: WVU Internal Medicine Residency, Morgantown, WV 26505

I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Brugada syndrome unmasked/triggered by viral pharyngitis.


Introduction:Brugada syndrome has been described in the literature to triggered and unmasked by fever. We are reporting a case of brugada syndromethat was triggered by viral pharyngitis in the absence of objective fever.

Case Presentation:A 61 years old male patient with PMH of HTN, HLP, DM, COPD, smoking and recent history of syncope with a normal work up at thattime, presented to the ER complaining of sore throat and general weakness since 1 week. He denied chest pain, palpitation, and SOB. Hisv/s showed HR of 110, Temperature of 98. Physical exam showed diffusely reddened pharynx. Initial work up showed elevated WBCsother wise normal labs. ECG was done due to tachycardia and general weakness, which showed ST elevation in V1 and V2, leadscharacteristic for Brugada pattern type 1. He was sent for LHC that showed mild non-obstructive CAD with preserved EF. Other thanhistory of syncopal attack with normal work up he denied history of VFib/VTAK, denied family history of sudden cardiac death. RepeatECG showed no ST elevation. The patient was diagnosed with Brugada syndrome that was likely triggered by viral pharyngitis as he hascharacteristic Brugada type 1 pattern on ECG along with history of unexplained syncope, and discharged with life vest.

Discussion:Brugada syndrome (BrS) is a genetic disorder inherited as autosomal dominant with incomplete penetrance and variable expressivity.Genetic had shown >100 SCN5A mutations which encode for sodium channels. The prevalence of asymptomatic Brugada syndrome in thegeneral population is 0.05%. Occur typically in the age group of 30 to 60 years. Patients with Brugada syndrome are at risk for suddencardiac death (SCD) due to ventricular fibrillation (VF), which can be the first manifestation. Some patients present with syncope or can beasymptomatic for life. It is characterized by persistent or transient ST elevation with successive negative T wave in the right precordialleads (V1, V2) with or without right bundle branch block in the absence of structural heart abnormalities. These ECG changes are dynamic,often hidden, and may reveal themselves in the presence of triggers like Fever, intoxication (alcohol, cocaine, or cannabis), anesthetics(propofol, bupivacaine), vagal stimulation, psychotropic agents (amitriptyline, lithium), sodium channel blockers and electrolyteimbalance. In our case the trigger was the viral pharyngitis in the absence of documented fever. Which suggest another triggeringmechanism. The criteria for the diagnosis of Brugada syndrome (BrS) include the presence one of the typical ECG patterns in conjunctionwith the presence of one the following criteria: a history of documented VF/VT, family history of SCD at less than 45 years of age, afamily history of type 1 Brugada pattern ECG changes, nocturnal agonal respiration during sleep, unexplained syncope suggestive oftachyarrhythmia or inducible VT/VF during electrophysiological study. ECG patterns described in Brugada syndrome: Type 1 (coved typeST segment elevation) defined as ST-segment elevation of ≥2 mm (0.2 mV), followed by a negative T wave with little or no isoelectricseparation in the right precordial leads. Type 2 (saddle-back type ST segment elevation) defined as a J wave amplitude of ≥2 mm (0.2 mV),gives rise to a gradually descending ST segment elevation (remaining ≥1 mm above the base line) followed by a positive or biphasic Twave that results in a saddle-back configuration. Type 3 is a right precordial ST segment elevation (saddle-back type, coved type, or both)without meeting the typical criteria for type 1 or 2.

Conclusion:

There are several triggering factors for ECG changes in patients with brugada syndrome that have been described in the literature as Fever,sodium channel blockers and others. In this case our patient had a viral pharyngitis without fever, which suggest the association betweenBrugada syndrome and viral infection.

Figure 1..Figure 2..


Authors:

Authors:Ahmed Amro1,MD; Alaa Gabi2,MD; Rameez Sayyed2,MD; FACC, FSCAI.

1- Department of Internal Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, WV, USA.2- Department of Cardiovascular Services. Marshall University Joan C. Edwards School of Medicine, Huntington, WV, USA.

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Full Name: Amro AhmedLast First M.I.

Address: 6421 country club drive 6421Street Address Apartment/Unit




TrainingProgram: Marshall University School of Medicine.

__AA_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Chronic Pericardial effusions status post mitral valve replacement


IntroductionPericardial effusions are a common finding after open heart surgery as a consequence of pericardial irritation andinflammation, many of which occur days to weeks after surgery. These effusions rarely progress to a large (>1000mL) size and rarely, require intervention. The patients that do progress to have large pericardial effusions and/ortamponade often present with symptoms of dyspnea and may have physical exam findings of jugular venousdistention, hypotension, pericardial rub, and muffled heart sounds. Many authors suggest that the history andphysical are up to 90 percent of information needed to make the diagnosis. I present a case in which thedevelopment of a large pericardial effusion after valve replacement surgery was an incidental finding, suggesting aneed of periodic routine echocardiography.Case Descriptions31 year old male with a history of hepatitis C and intravenous drug use presented to the hospital for stroke in 2012.At that time, routine transthoracic echocardiogram revealed possible mitral and aortic valve endocarditis andtherefore, transesophageal echocardiogram was pursued. This revealed a perforated mitral valve with moderate tosevere insufficiency and an aortic valve streptococcal vegetation with normal valve. He underwent an open heartprocedure for valve repair/replacement with a number 29 porcine mitral valve prosthesis and an excision ofvegetation in the noncoronary cusp of the aortic valve. The patient tolerated the procedure well and there were nopost-operative complications. Follow up echocardiogram one year later revealed only a trivial pericardial effusion.The patient returned to the office two years after his post operatively visit and was asymptomatic with stable vitalsigns. Due to irregular cardiac auscultation, EKG was performed which revealed atrial flutter with rapid ventricularresponse. Rhythm control strategy was pursued in this young male and he was scheduled for elective DCCV. Hewas scheduled for a repeat transthoracic echocardiogram which revealed an incidental large pericardial effusionwithout signs of tamponade. Therefore, the cardioversion was postponed and a bedside ultrasound-guidedpericardiocentesis was performed and 2200 cc of yellow clear serous fluid was removed. The patient tolerated theprocedure well.Discussion/ConclusionPericardial effusions are a relatively common finding after cardiac surgeries. The effusions are usually seen acutelywithin five to seven days after and are rarely of a large size. This case presents a unique circumstance; a largeasymptomatic effusion was found as an incidental finding on echocardiogram. The 2200cc of fluid removed fromthe pericardium over 72 hours illustrated the cardiac hemodynamic elasticity in a very slow developing pericardialeffusion. In contrast, an acute accumulation of no greater than 50cc of fluid will result in life threatening cardiactamponade and severe hemodynamic compromise for the patient. Effusions have been associated withtachyarrhythmias and may have contributed to the atrial flutter with RVR found on our patient. However our patientdid not present with textbook clinical exam findings. Therefore, the question remains: Should the physician’s clinicalsuspicions and knowledge of past medical history dictate the use of echo or should routine yearly echo’s beperformed? And if so, for how long after the cardiac procedure should this be done, to prevent hemodynamic andelectrophysiological strains on the heart and other vital organs? Further prospective studies are needed to answerthis clinical question.

ReferencesWeitzman, L. B., Tinker, W. P., Kronzon, I., Cohen, M. L., Glassman, E., & Spencer, F. C. (1984). The incidence and natural history of pericardial effusion aftercardiac surgery--an echocardiographic study. Circulation, 69(3), 506-511.Sagristà-Sauleda, J., Mercé, A. S., & Soler-Soler, J. (2011). Diagnosis and management of pericardial effusion. World Journal of Cardiology, 3(5), 135–143.http://doi.org/10.4330/wjc.v3.i5.135Pepi, M., Muratori, M., Barbier, P., Doria, E., Arena, V., Berti, M., … Tamborini, G. (1994). Pericardial effusion after cardiac surgery: incidence, site, size, andhaemodynamic consequences. British Heart Journal, 72(4), 327–331.M.J Eisenberg, L Munoz de Romeral, P.A Heidenreich, N.B Schiller, G.T Evansn The diagnosis of pericardial effusion and cardiac tamponade by 12-lead ECG:a technology assessment Chest, 110 (1996), pp. 318–324


Authors:

Amir Eslami MS-III, Sarah M. Nease MD, FACC

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Full Name: Eslami AmirLast First M.I.

Address: 1935 Oakridge DrStreet Address Apartment/Unit

#Charleston WV 25311



TrainingProgram: West Virginia School of Osteopathic Medicine - CAMC Memorial

_X_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.

West Virginia-ACC Poster Competition Abstract Do NOT write outside the boxes. Any text or images outside the boxes will be deleted. Do NOT alter this form by deleting parts of it (including this text) or adding new boxes. Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * Conclusion Please structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * Conclusion

Title:

Endocarditis in an Intravenous Drug User with a Ventricular Septal Aneurysm


An aneurysm of the membranous portion of the ventricular septum (AMS) has been shown to promote bacterial

endocarditis among other cardiac consequences. Because an AMS is a common result of spontaneous ventricular

septal defect closure it is an important anomaly to assess, especially in high risk patients.

A 45-year-old woman with history of intravenous drug use and hepatitis C presented from an outside facility in

septic shock with multisystem organ failure including acute respiratory failure, acute kidney injury,

thrombocytopenia, and disseminated intravascular coagulation. Her initial complaint was a one week history of

fever, shortness of breath, malaise, and cough. According to outside records, a chest x-ray showed evidence of

septic emboli and an echocardiogram revealed tricuspid valve endocarditis with a large vegetation. Upon admission

to our facility, she was intubated, started on broad spectrum antibiotics, and required vasopressors for blood

pressure support. Physical examination displayed a 2/6 systolic ejection murmur heard loudest at the left lower

sternal border and wheezing in both lung bases. A transthoracic echocardiogram showed tricuspid valve

regurgitation and an aneurysmal deformity of the basilar ventricular septum with associated ventricular septal defect

(VSD) and a vegetation seen at the VSD site on the right ventricular aspect. During her initial history the patient

stated that her VSD had been diagnosed in childhood. A transesophageal echocardiogram then revealed severe

tricuspid valve regurgitation with a large, pedunculated, mobile vegetation on the atrial aspect of the tricuspid valve

traversing the annulus. The next day a cardiac catheterization showed a membranous ventricular septal aneurysm

protruding from the left ventricle into the right ventricle with no evidence of ventricular septal defect. This

aneurysm likely gave the appearance of a VSD seen on echocardiography. With these cardiac abnormalities,

tricuspid valve replacement was indicated, but she remained high risk for complication due to her comorbidities.

Her condition did not improve and she remained intubated over the next two weeks. Eventually she was transferred

to another facility that had extracorporeal membrane oxygenation ability for a potential valve replacement surgery.

After transfer she was lost to follow up.

This case exemplifies a patient predisposed to endocarditis who was at higher risk due to her actions. The objective

contribution of the AMS to the resultant endocarditis is unknown at this point. This sentiment raises the question if

AMS detection would change intervention for associated pathologies.

West Virginia-ACC Poster Competition Abstract Authors:

Peter Farjo, MD; Abnash Jain, MD

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Full Name: Farjo Peter D

Last First M.I.

Address: 968 Northwestern Ave. 5

Street Address Apartment/Unit #

Morgantown WV 26505

City State ZIP Code

Work Phone: 717-586-4557 Alternate Phone: NA


Training Program: WVU Internal Medicine Residency

_X_I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC Annual Meeting. I understand that if I cannot be present that my poster will be withdrawn.

mailto:[email protected]

West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Spontaneous Coronary Artery Dissection (SCAD) as initial presentation of Fibromuscular Dysplasia (FMD) - A Rare Beast.

Abstract: (Your abstract must use Normal style and must fit into the box. You may not alter the size of this )Introduction/Objective: Spontaneous Coronary Artery Dissection is an uncommon but very serious complication of FMD.Potential initial presenting clinical manifestations of FMD usually include involvement of Renal, Cerebral carotid and vertebralarteries. Coronary arteries involvement in FMD arises less frequently as compared to other arteries, and Acute CoronarySyndrome (ACS) as presentation of FMD is believed to be rare. A string of beads appearance of FMD in renal, carotid andvertebral rarely occurs in coronaries arteries. Most common coronary artery manifestations of FMD include SACD or smoothnarrowing of the coronary artery. The infrequency with which ACS present as initial manifestation of FMD makes promptdiagnosis and treatment of this condition a formidable diagnostic challenge.

Case Presentation: A 40 year old female with no cardiac history presented with typical chest pain and STEMI. She wasimmediately taken to the cath lab and catheterization showed patent LAD and diagonal arteries with minimal plaquing. Thepatient was initially treated as possible Takotsubo cardiomyopathy. On the next day of initial catheterization patient hadrecurrence of severe chest pain with ST elevation and was emergently taken to the cath lab. At that time catheterizationshowed local dissection of the mid to distal left main coronary artery ,a totally occluded diagonal branch and 70-80% lesion inthe mid LAD that was not present in the previous cath. Because of patient scoliosis and tortuous aorta it was difficult tocannulate the left main artery. At that time it was was decided that since she had local dissection of the left main coronaryartery it is not safe to proceed with any further intervention. Intraaortic ballon pump was placed and it was planned to bringpatient after 48 hours to do cath. On 3rd diagonal artery was found to have long linear dissection plane which suggests aspontaneous coronary artery dissection which was the likely culprit etiology for the patient’s initial occlusion of the diagonalbranch on the previous angiogram. On the basis of angiographic findings patient was diagnosed as FMD and was referred tothe Cleveland Clinic and further work up confirmed the diagnosis.

Conclusion: In young patients presenting with SCAD, FMD should be suspected. A pooled analysis of Medline publishedcases from 1931 to 2008 reported 440 cases of SCAD. These cases can have underlying undiagnosed FMD. Diagnosis ofSCAD in FMD patient can be challenging. Initial catheterization can be normal in FMD patient but any recurrence of chest painwith ST segment elevation in the setting of FMD should be taken seriously and immediate cardiac catheterization should beconsidered.


Authors:

Farooq A, MD1. Ali R, MD1. Pervaiz, M MD2

1 Internal Medicine Department CAMC/WVU2 Interventional Cardiology, CAMC/WVU

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Full Name: Farooq Ali ULast First M.I.

Address: 3000 Staunton AV, SE 45Street Address Apartment/Unit

#Charleston WV 25304

City State ZIP CodeWork Phone: 304-533-1597 Alternate Phone: 304-533-1597


TrainingProgram: Internal Medicine, CAMC/WVU


West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Early onset of Lyme carditis with concurrent disseminated Erythema Migran Lesions.


Introduction: Lyme disease is a tick transmitted disease most commonly caused by the Borrelia burgdorferi bacterium inthe United States. The skin manifestation known as Erythema migrans occurs in 90% of infected individuals and represents anearly sign of disease, occurring as early as 24-48 hours following the tick bite. Lyme carditis is a rare clinical presentation ofLyme disease and third degree AV block due to Lyme carditis is even rarer. Lyme carditis is an early-late to late representationof Lyme disease with a mean interval of 21 days after the initial tick bite. This case demonstrates a rare early presentation ofLyme carditis in combination with disseminated Erythema migrans on the patient’s trunk and arms.

Case Description: A 21 year old man presented from an outside facility with third degree heart bock. The patient initiallypresented at the outside facility with light headedness going on for four days without any syncopal episodes. He endorsedepisodic fever, chills, loss of appetite, fatigue and hip pain with first Erythema migrans rash appearance on the right side of hisneck. Fever was refractory to acetaminophen so, he went to the emergency department at an outside facility. He was startedon fluids, CT scan of head was ordered which did not show any acute process and he was discharged with Tylenol but withoutany antibiotics treatment. Four days after, he noted more rashes on his trunk and arm area. He also started feeling pressureand tightness in his chest area with some associated light headedness. He was found to have third degree AV block on EKGmonitor and was transferred to WVU Medicine Hospital for higher level of care and possible pacemaker placement. Patientpresented with Erythema migrans on his trunk, neck and arms. EKG and telemetry demonstrated third degree AV block withbradycardia. He was diagnosed clinically with Lyme carditis and started on IV ceftriaxone. In house infectious disease andelectrophysiology specialists were consulted. They recommended at least 48 hours of antibiotics therapy prior to pacemakerplacement as most of the time third degree AV block is reversible with antibiotic treatment. During his hospital stay, his heartwent down to the 30s during the night, associated with episodes of fever. Transthoracic echocardiogram demonstrated normalejection fraction with no evidence of dilated cardiomyopathy. Within 48 hours, his third degree heart block evolved into asecond degree AV block and then into a first degree AV block. During this time his heart rate improved to 60s. Lyme disease,Babesia and Ehrlichia workups were initiated as per infectious disease team and Lyme disease serology came back positive.The patient was discharged with a 21 days course of PO doxycyclin due to insurance issue. He was also sent home with a 30days cardiac event monitor with outpatient infectious disease and cardiology follow-up. The patient did not follow-up toscheduled appointments and 2 weeks later presented to the emergency department with another syncopal episode. He wasdischarged with scheduled cardiology follow-up. During this follow-up, he was diagnosed with vasovagal type syncope. Hisevent monitor strip demonstrated first degree AV block and he was sent home with another 30 days cardiac event monitor andpossible need for loop recorder in the future. He followed up with infectious disease clinic and as per them his skinmanifestations had already resolved. He required no future follow-up with them. Patient will be evaluated in cardiology clinic infuture.

Discussion: Lyme carditis related AV block is due to an inflammatory response of cardiac tissue to Borrelia burgdorferiinfection and can lead to pancarditis if left untreated. This case demonstrated that although Lyme carditis is considered a latemanifestation of Lyme disease, early presentation is also common. Erythema migrans is generally considered an early findingof Lyme disease but the disseminated form can be seen the later part of the disease. In this case, if the patient was treatedwith doxycyclin on his first visit to the emergency department, Lyme carditis related third degree AV block could have beenavoided. Early recognition and treatment play an important role in avoiding the later manifestations of Lyme carditis. Also, it isimportant to recognize Lyme carditis as one of the diagnosis in young patients who present with any AV block in the setting ofno cardiac history. To avoid future treatment with a pacemaker, it is important to remember that Lyme carditis AV block can beresolved with Ceftriaxone treatment within 48 hours.

Conclusion: Lyme carditis is one of the rare causes of third degree AV block and it can present with disseminated Erythemamigrans. Erythema migrans and third degree AV block respond to therapy well within the first 48 hours of IV ceftriaxonetreatment. Also, in a young patient with no cardiac history, consider Lyme carditis in the differential of any degree AV block.


Authors:

Kinjan P Patel M.D.1, Ali Hama Amin M.D.2, James Mills M.D.

KFull Name: Patel Kinjan P

Last First M.I.Address: 5203 Chestnut Hill Apartment 5203

Street Address Apartment/Unit#

Morgantown WV 26505City State ZIP Code

Work Phone: 224 572 4242 Alternate Phone: 847 338 8534


TrainingProgram: WVU Internal Medicine Program


West Virginia-ACC Poster Competition AbstractDo NOT write outside the boxes. Any text or images outside the boxes will be deleted.Do NOT alter this form by deleting parts of it (including this text) or adding new boxes.Please structure your clinical research abstract using the following headings: * Background * Objective * Methods * Results (if relevant) * ConclusionPlease structure your case study abstract using the following headings: * Introduction/objective * Case presentation * Discussion * ConclusionTitle:Holt-Oram Syndrome presenting with new-onset CHF, Ischemic Cardiomyopathy, and Arrhythmia


Introduction/ObjectiveHolt-Oram Syndrome is a rare genetic disorder that is estimated to affect 1 in 100,000 individuals. It is characterized byabnormalities in the skeleton, especially in the hands and arms. Cardiac abnormalities are present in about 75% of patients with Holt-Oram Syndrome. The majority of patients with cardiac abnormalities have congenital heart defects, such as atrial septal defects orventricular septal defects. A minority of patients can have cardiac conduction abnormalities, such as atrial fibrillation or bradycardia.In this case report, a patient with no known history of CHF presents with an acute onset of CHF, in addition to a cardiac conductiondefect. Considering that Holt-Oram Syndrome is a rare disorder, and that a minority of patients present with cardiac conductionabnormalities, a patient with no known history of CHF that presents with both is a very rare presentation.

Case PresentationA 59 y.o., male with a PMH of Holt Oram syndrome, LBBB, hypertension, and no known CHF history presented to the ED withdyspnea, abdominal/lower extremity edema, and probable A-Flutter. These symptoms had been getting worse since April 2015. Healso reported having abdominal pain and diarrhea over the last week. The patient’s brother called EMS due to the patient’s legsbecoming more swollen. The patient did not take any medications and did not regularly follow up with a physician. He was seen inthe past for chest pain, but work-up was negative. At that time, it was thought the patient had a LBBB, and he was prescribedmetoprolol but did not take it.

On admission, the patient was found to have a wide complex tachycardia with atrial flutter. It was rate controlled using metoprololand Digoxin. The patient was successfully cardioverted shortly after admission, and returned to sinus rhythm. He was started onAmiodarone after cardioversion, and Eliquis for anticoagulation after a Heparin bridge. Patient had no previous history of atrialflutter. Patient’s BNP on admission was 1460. CXR on admission showed ‘Cardiac enlargement and vascular congestion with rightlung base opacity likely representing fluid and atelectasis.’ Chest x-ray from 2010 was normal, thus this patient’s CHF was acute inonset. Patient’s CHF was treated with Metoprolol, Lisinopril, Spirinolactone and Lasix. Echo was performed, which showed an EFof 15-20%. The patient’s symptoms were consistent with CCS class III progressive to unstable angina. He was subsequently referredfor right and left heart catheterization. Heart catheterization was completed, and showed ‘Severe disease in the proximal to mid leftanterior descending coronary, and moderate disease in the ostial left circumflex.’ The patient underwent successful PCI to theproximal to mid left anterior descending coronary artery with a 3.5 x 24-mm Promus Premier stent. Thus the patient’scardiomyopathy was ischemic in nature. The patient was put on Plavix and Aspirin post-cath. The patient also had abdominal painduring the admission; colonoscopy was performed, and he was found to have internal hemorrhoids and a 2.5 cm pedunculated polyp.The patient’s net I/O was negative 18 liters during the admission. The patient was started on Lipitor at discharge, and also put on aLife-Vest. The patient was doing well and was asymptomatic at time of discharge.

DiscussionHolt Oram syndrome is an autosomal dominant syndrome caused by a mutation in the TBX5 gene. The TBX 5 gene is one of thegenes responsible for the development of the upper limbs and the heart. It also assists in the development of the heart into 4chambers, and thus abnormalities in this gene can lead to issues that cause the cardiac abnormalities reported. Holt-Oram Syndromeis characterized mainly by bone abnormalities. The bony abnormalities are typically in the wrist or carpal bones. Other abnormalitiesinclude polydactyly, a missing thumb, absence of bones in the arm, or abnormalities in the shoulder blades. The cardiacabnormalities mostly consist of cardiac structural issues, such as ASD and VSD. There are very few reported cases of patients withHolt-Oram Syndrome with acute-onset CHF, and patients with Holt-Oram syndrome do not classically present with this finding. Inaddition, this patient only had a clear history of LBBB and hypertension, and yet was found to have ischemic cardiomyopathy withan EF of 15-20%. This was a very rare presentation in the setting of Holt-Oram Syndrome.

ConclusionIn a patient with no known history of CHF, a patient with Holt-Oram syndrome presenting with acute onset CHF and ischemiccardiomyopathy is a rare finding. The majority of patients with Holt-Oram syndrome with cardiac abnormalities have structural orconduction abnormalities. In the future, it is worth researching whether patients with Holt-Oram syndrome are at greater risk ofhaving CHF or ischemic cardiomyopathy than the regular population.


Authors:

By Sardar Musa Shah-Khan, MD; Fahad Al-Qahtani, MD; Sami Aljohani, MD; and Anthony Roda-Renzelli, MD

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Full Name: Shah-Khan Sardar MusaLast First M.I.

Address: 2328 Suncrest VillageStreet Address Apartment/Unit




TrainingProgram: WVU Department of Internal Medicine (Morgantown) /Ruby Memorial Hospital

SMS I understand that submission of an abstract constitutes a commitment to be present at the West Virginia-ACC AnnualMeeting. I understand that if I cannot be present that my poster will be withdrawn.