Dr.Aruna Chaminda

Registrar - Emergency Medicine

Patient details

Age : 29 yrs

Sex : Male

Address : Aluvihare , Matale

Marital status : Unmarried

P /C : Tightening Chest Pain for 6 hours

History of presenting Complaint :

Patient had L/sore throat for 1 day and taken treatment from GP

Sudden onset ,bilateral tightening continuous chest pain for the 6 hrs

Severe pain, not radiating, not relieved by rest

Associated with nausea and sweating ,No vomiting

Pain not increase by inspiration or changing in position.

No history of shortness of breath, no palpitation, no history of fever

No history of trauma.

Review of systems :

General:

No loss of weight No change in appetite, No malaise or weakness, No

sleep disturbance

GIT:

No abdominal pain No Diarrhea or constipation , No haematamesis or

melena

Respiratory system:

No difficulty in breathing,No cough

Genito urinary:

No burning micturition No haematuria

CNS:

No fits, No weakness

P.Medical History : No history of heart disease

hypertension,Chest pain or diabetes

P.Surgical History : No significant events

Family History : Mother has DM,No cardiac diseases

Allergic History : No food or drug allergies

Social History : Unmarried, Heavy vehicle driver,

Smoking – 3 cigarette per week

Alcohol – ¼ bottle of Arrack per week

No other substance/drug abuse

Summary :

29 years old male presented with history of bilateral tightening

chest pain for the 6 hrs, chest pain was continuous severe pain associated with nausea and sweating.

Examination :

Male with average height and built lying on bed conscious and oriented.

Temperature: 37.0 c , BMI - 19

No pallor or jaundice, mild plethora. No clubbing or splinter hemorrhages JVP not raised

No neck swelling No palpable lymph nodes

Cardiovascular examination :

Pulse: 68 b/ min regular BP: 140/ 90 mmHg

Pulses equally palpable on both sides, normal volume No radio femoral delay No lower limb or sacral edema

Apex beat in 5th intercostal space at mid clavicular line, non sustained. No thrill or heave , No local tenderness, S1 and S2 with normal intensity No gallop or murmur .

Respiratory system :

Respiratory system Chest bilaterally symmetrical moving with respiration. Vesicular breathing No crepits or ronchi

Gastrointestinal system :

Gastrointestinal system No hepatosplenomegaly

Central Nervous System

Normal sensory and motor exam

SUMMARY :

29 years old male smoker presented with history of bilateral

tightening chest pain for the 6 hrs, chest pain was continuous

severe pain associated with nausea and sweating.

On examination – Mild elevation of blood pressure and no

significant exam finding.

Differential diagnosis :

Myocardial infarction

Coronary vasospasm (Printzmetal’s angina)

Aortic dissection

Musculoskeletal pain

Pulmonary Embolism

ECG 1

Patient was diagnosed as having Anterior STEMI

Patient given Aspirin 300mg

Clopidogrel 300mg

Atovastatin 40 mg

STK infusion started

ECG 2 Post STK

Other investigations:

RBS – 280 mg/dl

FBC

FBC repeated

Symptomatically chest pain was relived with thrombolysis and

other initial treatment and he was haemodynamically stable.

Patient was transferred to Tertiary Hospital for further

investigation and managment.

Cath lab was not functioning

Started on Enoxaparin 60mg BD

CXR

SE

Na + - 136 mmol/l

K+ - 4.9 mmol/l

LFT

AST - 200 U/L (13-31)

ALT - 81 U/L (7 -21)

RFT

BU - 6.6 mmol/L (2.1.-7.1)

SC - 1.08 mg/dl (0.9-1.3)

HBA1c - 8.7 %

ESR - 3 mm/hr

Trop I - 8.6 ng/ml (0.4)

Lipid profile

Total cholest. 240.3 mg/dl BL High

Triglyceride 138 mg/dl Normal

HDL 65.7 mg/dl High

LDL 146.9 mg/dl BL High

LDL/ HDL 2.2

Blood picture

RBC - Normochromic normocytic red cells with mild red cell

crowding.

WBC – Total count elevate absolute neutrophil lekocytosis

Plt –Normal

Polycythemia ? Primary or Secondary ?

Haematology and endocrinology referral done.

Isovolemic venesection done

ABG – Sample clotted repeated attempts,

SpO2 – 98% (Room air)

JAK-2 V617F mutation was Negative.

The abdominal ultrasound was normal with no

hepatosplenomegaly.

Echocardiography- EF 50% with anterior,apex and lateral wall hypokinasesia ,no intracardiac thrombus.

POLYCYTHAEMIA

Myocardial infarction in young

Angiographically normal coronary arteries

(coronary artery thrombosis, embolisation, spasm, or a combination)

• Hypercoagulable states

Nephrotic syndrome

Antiphospholipid syndrome

Protein S and factor XII deficiencies

• Coronary artery spasm

Cocaine

• Coronary embolisation

Endocarditis—Embolisation from - aortic and mitral valves, Bacteraemia

Abnormal coronary arteries

• Accelerated atherosclerosis

Familial hypercholesterolaemia

• Spontaneous dissections

• Aneurysms, ectasia, and anomalous origin of coronary arteries

Egred, M., Viswanathan, G., & Davis, G. K. (2005). Myocardial infarction in young adults. Postgraduate medical journal, 81(962), 741-745.

Literature review

Introduction

Diagnosis Myocardial infarction in young is challenging, as the disease is less likely, due to atherosclerosis.STEMI as first presentation of hypercoagulable state is rare.

Case reports

Presentation of Polychythaemia as AMI is very rare. There are some reports documenting PRV/Secondary Polycythaemia presenting as AMI.

Majority of cases were young males with minimal coronary occlusion.

Shah, N. C., Munir, S. M., & Alp, N. J. (2011). Spontaneous aortic thrombosis causing left main coronary occlusion in a man with secondary polycythaemia. JACC: Cardiovascular Interventions, 4(8), 934-935.

25 yrs old male with sec. polycythaemia(smoker) with a history of DVT

presented with anterolateral STEMI

Angiogram -showed a large filling defect in the left coronary

sinus that extended into the left main coronary artery

The coronary arteries were otherwise angiographically normal.

LCA -directly stented.

Bahbahani, H., Aljenaee, K., & Bella, A. (2015). Polycythemia vera presenting as acute

myocardial infarction: An unusual presentation. Journal of the Saudi Heart Association, 27(1), 57-60.

37-year-old Egyptian woman presented to A& E with severe retrosternal compressive chest pain 3 Hrs. - AMI

.

Due to the unavailability of a cardiac catheterization facility thrombolyzed with reteplase 10 units IV bolus, then 10 units given over 30 min, enoxaparin 1 mg/kg, aspirin 81 mg, clopidogrel 75 mg, lisinopril 10 mg, bisoprolol 10 mg and simvastatin 20 mg.

Patient was diagnosed with polycythemia vera (PV) started on

hydroxyurea 15 mg/kg, aspirin 81 mg,

regular phlebotomy to keep hematocrit less than 45%.

Four weeks later, the patient had myocardial perfusion scintigraphy, CT coronary angiography - normal.

Gouri, A., Yakhlef, A., Dekaken, A., & Bentorki, A. A. (2012, July). Acute myocardial infarction revealing a polycythemia vera. In Annales de biologie clinique (Vol. 70, No. 4, pp. 489-491).

Algeria

55-year-old man with ST-segment elevation myocardial infarction;

Treated beta-blocker,aspirin, statin, low- molecular- weight heparin and & ACE.

After stabilization patient was transferred to another hospital for angiography - stenosis and heterogeneous appearance of the anterior descending coronary artery, with apical akinesia.

Goethals P., Evrard S., Dubois C. Recurrent coronary stent thrombosis. Acta Cardiol. 2000;55(6):371–373

Goethals described the difficulty of maintaining a patent coronary artery due to repeated thrombosis

Wei, Z., Yan, Z., Yuguo, L., Rai, G. I., Duoduo, Z., Pai, L., & Jingjing, K. (2014). Acute ST-elevation myocardial infarction in a patient with polycythaemia vera. Chinese medical journal, 127(2)

Periinterventional GP IIb/IIIa antagonist treatment should be considered for patients with PV and AMI, especially for PCI. Reasonable reperfusion methods should be considered carefully including thrombus suction and intracoronary thrombolysis during PCI.

Wu, C. F., Armstrong, G. P., Henderson, R. A., & Ruygrok, P. N. (2005). Polycythaemia vera presenting as ST-elevation myocardial infarction. Heart, Lung and Circulation, 14(1), 51-53.

Wirth, L. (1960). Myocardial infarction as the initial

manifestation of polycthaemia vera. Military medicine, 125, 544.

Vacca J.B., Thoma G.E., Jr. Myocardial infarction as the initial manifestation of polycythaemia vera. AMA Arch Intern Med. 1959;103(6):974–977

Hermanns B., Handt S., Kindler J., Füzesi L. Coronary vasculopathy in polycythaemia vera. Pathol Oncol Res. 1998;4(1):37–39.

Tekin, M., Gökaslan, S., Diker, E., & Aydoğdu, S. (2008). Development of acute coronary syndrome in three patients with essential thrombocythemia or polycythemia vera. Turk Kardiyol Dern Ars, 36(1), 35-8.

Standard pharmacological treatment for myocardial infarction was effective without the need for an emergency coronary intervention

Conclusions

Young patients with myocardial infarction or ischemic stroke always look for FBC and suspect hypercoagulable state.

Early diagnosis of polycythaemia and treatment is important to prevent systemic thrombotic complications

Standard pharmacological treatment,acute coronary intervntion, periinterventional GP IIb/IIIa antagonist treatment and cytoreduction are the main current strategies for the treatment of AMI in Polycythaemia..

Myelo-proliferative disorders require special attention in maintaining the delicate balance between the risk of hemorrhage and thrombosis tendency.

However, sufficient data do not exist as to the most appropriate treatment approach to these patients, requiring further studies with larger patient groups.