12 penyakit jantung didapat
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Penyakit Jantung Didapat
Idrus Alwi
Divisi KardiologiDepartemen Penyakit Dalam FKUI-
RSCM
Content Cardinal Symptoms Epidemiology Spesific Diseases
CAD/Penyakit Jantung Koroner Hypertension and Hypertensive Heart
Disease(Penyakit Jantung Hipertensi) Rheumatic Fever (Demam Rematik),
RHD(dan Penyakit Jantung Rematik (Katup) Penyakit Jantung Tiroid Penyakit Jantung Paru Penyakit Vaskular Perifer Endokarditis, Miokarditis, Perikarditis,
Kardiomiopati Disritmia Aneurisma Aorta
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Cardinal Symptoms in CVD
Sakit dada (chest discomfort) Sesak nafas (breathlessness) Berdebar-debar (palpitasi) Pingsan (dizzy,black out/syncope) Bengkak (edema) Cepat capek (fatique)
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World Health Report 1997.World Health Report 1997.
Cardiovascular Disease: A Worldwide Epidemic
Circulatory diseases are the number 1 cause of death worldwide 15 million deaths, or 30% of annual total
CAD accounted for 7.2 million deaths worldwide in 1996 14% of global total deaths One third of deaths in industrialized countries
Cerebrovascular disease accounted for 4.6 million deaths
Hypertension occurs in 690 million people worldwide
Developing countries: projected 28% increase in cardiovascular deaths
Global Burden of Cardiovascular Global Burden of Cardiovascular DiseaseDisease
In 2002: CVD contributed to approximately a third of
all global deaths (17 million) 80% of burden is in low and middle-income
countries
By 2020: CHD and stroke will become the leading
cause of death and disability worldwide Mortality from CVD will increase to 20 million
Clinical care of CVD is costly and prolonged
International Cardiovascular Disease Statistics 2005; AHA.
PJ di Indonesia 1978
46.6% (IHD)PJI 17.9% RHD(PJR) 14.3% Heart Dis
of Hypertension(PJH)
10.7% Cong HD(PJB) 7.1%Pulm HD( PJP) 18 per 1000
penduduk
Others Endokarditis(Rig
ht HD and Drug Abuse)
Kardiomiopatia
Boedi Darmojo et al,1978Buku Laporan Seminar Kardiologi Sosial,hal 5-6,FKUI,Jakarta,Januari 1987
Violence
Self-inflicted injuries
Stroke
Road traffic accidents
Tuberculosis
Coronary heart disease
HIV/Aids 2279
15–59 years
Coronary heart disease
Stroke
Diabetes
Hypertensive heart disease
Trachea, bronchus, lung cancers
Lowe respiratory infections
Chronic obstructive pulmonary disease
735
754
928
1396
2399
4689
5825
>60 years
No of deaths(thousands)
Deaths from Coronary Heart Deaths from Coronary Heart Disease Compared with Other Disease Compared with Other Causes (2002)Causes (2002)
WHO Cardiovascular Atlas 2002
473
672
783
814
1036
1332
2279
Categories of Risk Factors Major, independent risk factors Life-habit risk factors Emerging risk factors
Major Risk Factors (Exclusive of LDL Cholesterol) That Modify LDL Goals Cigarette smoking Hypertension (BP 140/90 mmHg or on
antihypertensive medication) Low HDL cholesterol (<40 mg/dL)† Family history of premature CHD
CHD in male first degree relative <55 years CHD in female first degree relative <65
years Age (men 45 years; women 55 years)
† HDL cholesterol 60 mg/dL counts as a “negative” risk factor; its presence removes one risk factor from the total count.
Life-Habit Risk Factors
Obesity (BMI 30) Physical inactivity Atherogenic diet
The future…?The future…?
Emerging Risk Factors
Lipoprotein (a) Homocysteine Prothrombotic factors Proinflammatory factors Impaired fasting glucose Subclinical atherosclerosis
Risk Assessment
Count major risk factors
For patients with multiple (2+) risk factors Perform 10-year risk assessment
For patients with 0–1 risk factor 10 year risk assessment not required Most patients have 10-year risk <10%
Odds ratio adj for age, sex, smoke
Yusuf S, et al. Lancet. 2004;364(9438):937–52
INTERHEARTINTERHEART: Risk of AMI : Risk of AMI Associated with Risk Associated with Risk FactorsFactors
Major Manifestations of Vascular Disease and Atherothrombotic
EventsCerebral
Ischemic stroke
Transient ischemic attack (TIA)
Vascular dementia
Cardiac
MI
Angina pectoris (stable, unstable)
Peripheral arterial disease (PAD)
Claudication, critical limb ischemia
CHD-Risk in
Relation to HDL-C and LDL-C
Coronary heart disease (n = 280)
Position in model VariableP value
1st LDL-C <0.0001
2nd HDL-C 0.0001
3rd Hemoglobin A1c0.0022
4th Systolic BP 0.0065
5th Smoking 0.056
HDL-C1002,58
1604,13
2205,68
0,0
1,0
2,0
3,0
2545
6585
CHD-Risk
LDL-C The The Framingham Framingham Heart StudyHeart Study
UKPDSUKPDS
(Adapted from Verschuren et al, 1995)
35
30
25
20
15
10
5
0
Dea
th r
ate
fro
m C
HD
/100
0 m
en
2.60 3.25 3.90 4.50 5.15 5.80 6.45 7.10 7.75 8.40 9.05
Serum total cholesterol (mmol/L)
Northern Europe
United States
Southern Europe, inland
Southern Europe, Mediterranean
Japan
Serbia
Relationship of serum cholesterol to mortality
(Seven Countries Study)
Multiple Studies Showed a Relationship Between LDL-C Reduction & CHD Relative
Risk
MI = myocardial infarction.
Robinson JG et al. J Am Coll Cardiol. 2005;46:1855–1862.
15 20 25 30 35 40
–20
0
20
40
60
80
100
LDL-C reduction, %
No
nfa
tal
MI
and
CH
D d
eath
re
lati
ve r
isk
red
uct
ion
, %
4S CARDSPOSCH ASCOT-LLANHLBI PROSPERLRC ALERTUpjohn HPSLos Angeles AF/TexCAPSMRC LIPIDOslo CARELondon WOSCOPS
Adapted from Pepine CJ. Am J Cardiol. 2001;88(suppl):5K-9K.
Mechanisme and progression of CVD
Risk factors
Oxidative stress
Functional alterations
Atherosclerosis
Clinical sequelae
Age, gender, smoking, inactivity, obesity,cholesterol, BP, glucose
Genetic factors
Endothelial function EPCs
EPCs = endothelial progenitor cells
The Progression from CV Risk Factors The Progression from CV Risk Factors to Endothelial Injury and Clinical to Endothelial Injury and Clinical
EventsEvents
The Progression from CV Risk Factors The Progression from CV Risk Factors to Endothelial Injury and Clinical to Endothelial Injury and Clinical
EventsEventsRisk factors
Oxidative stress
Endothelial dysfunction
NO Local mediators Tissue ACE-Ang II
PAI-1 VCAM
ICAM cytokines
Endothelium Growth factors matrix
Proteolysis
LDL-C BP Heart failureSmokingDiabetes
Vasoconstriction Vascular lesion and remodelling
Plaque ruptureInflammationThrombosis
Clinical endpoints
NO Nitric oxideGibbons GH, Dzau VJ. N Engl J Med 1994;330;1431-1438.
1.Coronary Artery Disease(Synonim)
Ischemic Heart Disease Atherosclerotic Heart Disease Coronary Artery Disease Indonesia = Penyakit Jantung Koroner
Etiology of CAD
Most Common Obstructive Coronary artery
disease(CAD) from AtherosclerosisASHDischemia = IHD
Other causes Coronary Arteritis (SLE,Rh Arthritis..) Sifilisarteritis of Ao Congenital
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Causes of Atherosclerosis : Multi FactorialRisk Factor
of AtherosclerosisA. Un-modified RF Age(P>45;W>55),Sex,Fam
history(Keluarga langsung PJK(P<55,W<65)
B. Modified RF Smoking,DM~CAD,Lipid(HDL,LDL,TG),BMI>30kg/m2,Lack of excercise,BP >140/90 mmHg (On BP treatment)
C.Emerging RF Lp(a),Homosistein,Prothrombotic
Factor,Proinflammatory factor,IFG. MMP
FoamFoamCellsCells
FattyFattyStreakStreak
IntermediateIntermediateLesionLesion AtheromaAtheroma
FibrousFibrousPlaquePlaque
ComplicatedComplicatedLesion/RuptureLesion/Rupture
Endothelial dysfunction
Smooth muscleand collagen
From first decadeFrom first decade From third decadeFrom third decade From fourth decadeFrom fourth decade
Growth mainly by lipid accumulationThrombosis,haematoma
Adapted from Stary HC et al. Circulation 1995;92:1355-1374.
Atherosclerosis Timeline
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Dislipidemia ----- Atherosclerosis ----- CVD A Progressive Disease
CRP=C-reactive protein; LDL-C=low-density lipoprotein cholesterol.
Libby P. Circulation. 2001;104:365-372; Ross R. N Engl J Med. 1999;340:115-126.
Monocyte LDL-C
Adhesion molecule
Macrophage
Foam cell
OxidizedLDL-C
Plaque rupture
Smooth muscle cells
CRP
Plaque instabilityand thrombusOxidationInflammationEndothelial
dysfunction
Libby P. Circulation 1995;91:2844–2850.
The Synthesis and Breakdown of Atheromatous
Plaques
Atherothrombosis: Thrombus Superimposed on Atherosclerotic
Plaque
Adapted from Falk E, et al. Circulation. 1995;92:657-671.
Thick, VSMC-rich fibrous cap
The Stable Atherosclerotic Plaque Stable AP
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ThrombusThrombus
FewFewSMCsSMCs
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Plaque rupture leading to thrombotic occlusion (A)
Manifestation of CAD Asymptomatic—ch1,45—Primary
Prevent Stable Angina Pectoris (Chronic
CAD)ch54 STEMI = total oclusion (ch 50,51) UAP and NSTEMI = partial occlusion (ch53) Sudden Death (ch36) Arrythmias (ch31,32) Heart Failure (Acute or Chronic Congestion)
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Pathology & ECG
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Diagnosis of Acute MI STEMI / NSTEMI
At least 2 of the following
Ischemic symptoms
Diagnostic ECG changes
Serum cardiac marker elevations
Diagnosis of Angina
Typical angina—All three of the following
Substernal chest discomfort Onset with exertion or emotional stress Relief with rest or nitroglycerin
Atypical angina 2 of the above criteria
Noncardiac chest pain 1 of the above
Diagnosis of Unstable Angina Patients with typical angina - An episode
of angina Increased in severity or duration Has onset at rest or at a low level of exertion Unrelieved by the amount of nitroglycerin or
rest that had previously relieved the pain
Patients not known to have typical angina First episode with usual activity or at rest
within the previous two weeks Prolonged pain at rest
Acute Management
Initial evaluation & stabilization
Efficient risk stratification
Focused cardiac care
Evaluation Efficient & direct history Initiate stabilization
interventions
Plan for moving rapidly to indicated cardiac care
Time is muscle
Occurs Occurs simultaneouslysimultaneously
Chest pain suggestive of ischemia
12 lead ECG Obtain initial
cardiac enzymes
electrolytes, cbc lipids, bun/cr, glucose, coags
CXR
Immediate assessment within 10 Minutes
Establish Establish diagnosisdiagnosis
Read ECGRead ECG Identify Identify
complicatiocomplicationsns
Assess for Assess for reperfusionreperfusion
Initial labsInitial labsand testsand tests
Emergent Emergent carecare
History & History & PhysicalPhysical
IV accessIV access Cardiac Cardiac
monitoringmonitoring OxygenOxygen AspirinAspirin NitratesNitrates
Focused History Aid in diagnosis and
rule out other causes
Palliative/Provocative factors
Quality of discomfort Radiation Symptoms associated
with discomfort Cardiac risk factors Past medical history -
especially cardiac
Reperfusion questions
Timing of presentation
ECG c/w STEMI Contraindication to
fibrinolysis Degree of STEMI
risk
Targeted Physical
Recognize factors that increase risk
Hypotension Tachycardia Pulmonary rales, JVD,
pulmonary edema, New murmurs/heart
sounds Diminished peripheral
pulses Signs of stroke
Examination Vitals Cardiovascular
system Respiratory
system Abdomen Neurological
status
ECG assessment
ST Elevation or new LBBBST Elevation or new LBBBSTEMISTEMI
Non-specific ECGNon-specific ECGUnstable AnginaUnstable Angina
ST Depression or dynamicST Depression or dynamicT wave inversionsT wave inversions
NSTEMINSTEMI
Normal or non-diagnostic EKG
ST Depression or Dynamic T wave Inversions
ST-Segment Elevation MI
Definition and atypical features of angina pectoris pain
Referred Pain
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Angina “Equivalent”
Dyspnea Jaw and Neck discomfort Shoulder, elbow/arm discomfort(left) Epigastric discomfort Back (interscapular) discomfort
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Canadian Cardiovascular Society Functional
Class(CCS) I.Ordinary physical activity does not cause angina
II.Slight limitation of ordinary activity III.Marked limitation of ordinary
physical activity IV.Inability to perform any physical
activity without discomfort.Angina may be present at rest.
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Cor Angiography
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Patogenesis AP Stabil
Resistensi
Vaskular
Coronary
Flow
suplai
HR
KontrraktilityWall stress
Demand
iskemiaOxygen carrying capacity
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Treatment
Reduce symptoms (Anti-angina) Prevent death and MI
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Emergency in CAD:Acute Coronary Syndrome
UAP NSTEMI STEMI CV EmergencyInitial
TreatmentRefer Why:UnpredictableSudden Death
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Guidelines
ACC guideline 2008 ESC guideline 2008
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CV Prevention Premordial Prevention
reduction of risk factor levels in a population
Primary Prevention Primary prevention involves reducing the
incidence of disease in those at high risk of developing it, in other words, people with significant risk factors
Secondary Prevention involves preventing recurrent disease in
people who already have the disease
Pais Prem. Preventing ishaemic heart disease in developing countries. Evidence-based Cardiovascular Medicine - Volume 10, Issue 2 (June 2006) - Copyright © 2006 Churchill Livingstone, Inc.
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Risk Factor and Intervention
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Prediction??Total CV Risk
Framingham Risk Score British Hypertension Siciety ESC/ESH WHO/ISH & JNC VII Kriteria Met Syndrome
http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=prof
Age: 58 Gender: male
Total Cholesterol: 220 mg/dL HDL Cholesterol: 42 mg/dL
Smoker: No Systolic Blood Pressure: 120 mm/Hg
On medication for HBP: No Risk Score results* 10%
Framingham Risk Score
Clinical Identification of Met-Synd
NCEP-ATP III,2001(Modified Asia –Pacific 2000) Waist circ >M:90cm;F>80cm
TG>150mg/dl HDL M<40,F<50mg/dl BP>130/85mmHg FBG>110mg/dl ---MS=--->/3RF
ATP III M
>102cm;F>88cm
ADA:FBG 100-125 2HrOGTT 140-200
2.Hypertension
Definition
95% Primary = Essential Hypertension; the cause is not identifible
5% Secondary Hypertension = identifiable
At the organ-system level, hypertension can result from a gain in function of pathways that promote vasoconstriction and renal retention of salt and water and/or a loss in function of pathways that promote vasodilatation and renal excretion of salt and water
Hypertension, coronary heart disease
and strokeR
elat
ive
risk
of
CH
D o
r st
roke
4.00
2.00
1.00
0.50
0.25
76 84 91 98 105
Approximate mean usual diastolic blood pressure (mmHg)
Stroke
CHD
MacMahon S et al. Lancet 1990; 335: 765–774
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GOAL : CARDIOVASCULAR RISK STRATIFICATION
(1) blood pressure level, (2) comorbidity,(Associate Condition)
and (3) target organ damage
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ESH-ESC 2007 & JNC VII
ESH-ESC
BP Classification
BP BP JNC VII
Bp Classification
Optimal <120 / <80 <120/<80 Normal
Normal 120-129 / 80-84 120-129 /80-84 Prehypertension
High normal 130-139 / 85-89 130-139 / 85-89 Prehypertension
Grade 1 Hypertension (mild)
140-159 / 90-99 140-159 / 90-99 Stage 1 Hypertension
Grade 2 Hypertension (moderate)
160-179 /100-109
>160 / >100
Stage 2 Hypertension
Grade 3 Hypertension (severe)
> 180 / >110
Isolated Systolic Hypertension
Isolated Systolic Hypertension
> 140 < 90
GOAL 3: IDENTIFICATION OF SECONDARY
(IDENTIFIABLE) CAUSES OF HYPERTENSION SUSPECTED SUSPECTED DIAGNOSISDIAGNOSIS
CLINICAL FEATURESCLINICAL FEATURES DIAGNOSTIC TESTINGDIAGNOSTIC TESTING
Renal Renal parenchymal parenchymal hypertensionhypertension
Elevated serum creatinine or Elevated serum creatinine or abnormal urinalysisabnormal urinalysis
24-Hour urine creatinine and protein, renal 24-Hour urine creatinine and protein, renal ultrasoundultrasound
Renovascular Renovascular diseasedisease
New elevation in serum creatinine, New elevation in serum creatinine, marked elevation in serum marked elevation in serum creatinine with initiation of ACEI or creatinine with initiation of ACEI or ARB, refractory hypertension, flash ARB, refractory hypertension, flash pulmonary edema, abdominal bruitpulmonary edema, abdominal bruit
Captopril renogram, duplex Doppler renogram, duplex Doppler sonography, magnetic resonance or CT angiogram, sonography, magnetic resonance or CT angiogram, invasive angiograminvasive angiogram
Coarctation Coarctation of the aortaof the aorta
Arm pulses >leg pulses, arm BP Arm pulses >leg pulses, arm BP >leg BP, chest bruits, rib notching >leg BP, chest bruits, rib notching on chest radiographon chest radiograph
MRI, aortogramMRI, aortogram
Primary Primary aldosteronisaldosteronismm
Hypokalemia, refractory Hypokalemia, refractory hypertensionhypertension
Plasma renin and aldosterone, 24-hour urine Plasma renin and aldosterone, 24-hour urine potassium, 24-hour urine aldosterone and potassium, 24-hour urine aldosterone and potassium after salt loading, adrenal CT scanpotassium after salt loading, adrenal CT scan
Cushing's Cushing's syndromesyndrome
Truncal obesity, purple striae, Truncal obesity, purple striae, muscle weaknessmuscle weakness
Plasma cortisol, urine cortisol after Plasma cortisol, urine cortisol after dexamethasone , adrenal CT scan , adrenal CT scan
PheochromocPheochromocytomaytoma
Spells of tachycardia, headache, Spells of tachycardia, headache, diaphoresis, pallor, and anxietydiaphoresis, pallor, and anxiety
Plasma metanephrine and normetanephrine, 24-Plasma metanephrine and normetanephrine, 24-hour urine catechols, adrenal CT scanhour urine catechols, adrenal CT scan
Obstructive Obstructive sleep apneasleep apnea
Loud snoring, daytime somnolence, Loud snoring, daytime somnolence, obesityobesity
Sleep studySleep study
ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; BP = blood pressure; CT = computed tomography.Modified from Kaplan NM: Clinical Hypertension, 8th ed. Philadelphia, Williams & Wilkins, 2002.
Prevention &Treatment of Hypertension
LIFESTYLE MODIFICATIONS PHARMACOLOGIC THERAPY
Hypertensive Emergency
Hypertensive emergencies are acute, severe elevations in blood pressure that are accompanied by progressive target organ dysfunction such as myocardial or cerebral ischemia/infarction, pulmonary edema, or renal failure.
Hypertensive urgencies are acute, severe elevations in blood pressure without evidence of progressive target organ dysfunction
HTN
SmokingSmokingDyslipidemiaDyslipidemia
ObesityObesityDiabetesDiabetes
Normal LVNormal LVstructurestructure
and functionand functionLVLV
remodelingremodeling
SubclinicalSubclinicalLVLV
dysfunctiondysfunction
ClinicalClinicalHFHF
Years /Years / MonthsMonthsYearsYears
MI
LVH
HF
Systolicdysfunction
Diastolicdysfunction
Adapted from Levy et al. JAMA 1996;275:1557Adapted from Levy et al. JAMA 1996;275:1557
Progression of HTN to HFProgression of HTN to HFProgression of HTN to HF
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The Cardiovascular Continuum
Adapted from Dzau V, Braunwald E. Am Heart J. 1991;121:1244-1263.
Risk factorsDiabetes, hypertension
Atherosclerosisand LVH
Myocardialinfarction
Remodeling Ventriculardilation
Heart failure
End-stageheart disease
Death
Benefit of Lowering BP
Average Percent Reduction
Stroke incidence 35–40%
Myocardial infarction 20–25%
Heart failure 50%
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JNC VII: Management of Hypertension by Blood Pressure
Classification
ACE-I = angiotensin-converting enzyme inhibitor; ARB = angiotensin-receptor blocker; BB = beta blocker; CCB = calcium channel blocker.Chobanian AV et al. Chobanian AV et al. JAMA. JAMA. 2003;289:2560-2572.2003;289:2560-2572.
Drug(s) for the compelling indications; other antihypertensive drugs (diuretics, ACE-I, ARB, BB, CCB) as needed
Drug(s) for the compelling indications; other antihypertensive drugs (diuretics, ACE-I, ARB, BB, CCB) as needed
BP ClassificationLifestyle Modification
Initial Drug Therapy
Without Compelling Indication
With Compelling Indication
Normal<120/80 mm Hg
Prehypertension120-139/80-89 mm Hg
Stage 1 hypertension140-159/90-99 mm Hg
Stage 2 hypertension≥160/100 mm Hg
Encourage
Yes
Yes
Yes
No drug indicated Drug(s) for the compelling indications
Thiazide-type diuretics for most; may consider ACE-I, ARB, BB, CCB, or combination
2-drug combination for most (usually thiazide-type diuretic and ACE-I, ARB, BB, or CCB)
Type 2 Diabetes CHD Equivalent
3.Why Diabetes is so Important?
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Atherosclerosis Is Common in Newly Diagnosed Diabetes
Mellitus Cardiovascular diseases: common causes of morbidity & mortality in diabetics
>50% of newly diagnosed type 2 diabetics show evidence of cardiovascular
disease Atherosclerosis:
major cause of death among diabetics 75% from coronary atherosclerosis 25% from cerebral / peripheral vascular disease
>75% of hospitalizations of diabetics atherosclerotic disease
Adapted from Amos AF et al Diabet Med 1997;14:S7-S85; Hill Golden S Adv Stud Med 2002;2:364-370; Haffner SM et al N Engl J Med 1998;339:229-234; Sprafka JM et al Diabetes Care 1991;14:537-
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Adapted from Alexander CM, Antonello S Pract Diabet 2002;21:21-28.
Two-Thirds of People with Diabetes Die of Cardiovascular
Disease Among diabetics,
macrovascular complications (incl. CHD, stroke and peripheral vascular disease), are the leading causes of morbidity and mortality.-67%
23% Microvascular
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Surv
ival(
%)
Year
Estimates of probability of Death From CHD in 1059 subjects with Type 2 Diabetes and 1378 Nondiabetic Subjects
with and without Prior MI
Haffner,et al, N Engl J Med 1998; 339:229-34MMP
3.RHD
Classic Triad of agent,host & environtment. Start from Acute Rh Fever >100 subtypes antipagocitic M Prot—
2weeks stay in tissue untill antibody are created
M Antibody(N-acetylglucosamine) mimic myosyn,tropomyosin,heart valvels,synovia,skin caudate nuclei in brain-multi organ involvement
Agent:GABHS(Streptoc group A(Throat Infection)--- Autoimmune disorder whole body-Connective tissue heart,,vascular and joint(Arthritis)
Pathogenesis
Tonsillopharyngitis-Antibody respons---Genetic predisposition-Connective tissue disease/Collagen vascular disease-damage to collagen fibril and connective tissue(Endocardium,myocardium,pericardium)--Repeated RHD
Vulvitis,Structure change and Clinical Manifestation
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Decreasing of RF
Patho RHD
ValvulitisMR/AR Structural change: Fibrinoid degclot -edema -Mononucleus inf (Aschof Cells) Clinical Manifestation:-Valvular inflammation,-Endocarditis,destruction---Regurgitation-Hyaline degeneration,valvular stenosis
The Jones Criteria for RF (Revised 1992)
Major Cirteria Minor Citeria
Carditis Clinical
Migratory polyarthritis Fever
Syndenham chorea Arthralgia
Subcutaneous nodule Laboratory
Erythema marginatum Elevated CRP
PR int>>>
PLUS
Evidence of a recent infection of Group A Streptococci(Throat culture or rapid antigen test or elevated Streptococcal antibody test
AHA,JAMA 268:2069,1992
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D/Rheumatic Fever
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Valvular Heart Disease(Look at the Text Book)
Mitral:MS,MR,MVP Aorta:AS,AR Tricuspid:TS,TR Pulmonary:PS,PR
ENDOKARDITIS INFEKTIFENDOKARDITIS INFEKTIF
Penyakit inflamasi pada endokard yang biasanya melibatkan katup dan jaringan sekitarnya
Endokarditis infektif (EI): inflamasi dikaitkan dengan infeksi
Lesi khas : vegetasi (platelet, eritrosit, fibrin, sel inflamasi dan MO) Klasifikasi dan Terminologi: - Baru (ESC 2004): (a) aktivitas penyakit; (b)
status diagnosis; (c) pathogenesis; (d) lokasi
anatomis; (e) mikrobiologi - Lama : (a) subacute bacterial endocarditis (SBE); (b) acute bacterial endocarditis (ABE); (c) kronik
Infective endocarditis risk:Infective endocarditis risk:
• Intravenous drug abusers (IVDA) 12 X non IVDA
• Prosthetic heart valves 5-10 X native heart valve
Mortality : 7-15 %
Incidence:Incidence:
• 5.9-11.6 annual infection per 100, 000 population• 1.5-20 annual case /1000 IVDA• RSCM : 15-20 % hospitalized IVDA
EpidemiologyEpidemiology
Kerusakanendotel
Deposisitrombosit
Endokarditistrombotik nonbakterial
Endokarditismenyembuh
Endokarditisinfektif
KolonisasiNBTE
Patogenesis SBE
Bakterimia
Patogenesis Nonbacterial Thrombotic Endocarditis (NBTE)dan Subacute Bacterial Endocarditis (SBE) (Durack DT)
Manifestasi Klinis Endokarditis Manifestasi Klinis Endokarditis InfektifInfektifSymptomsSymptoms PercentPercent SignsSigns PercentPercent
Fever 80-85 Fever 80-90
Chills 42-75 Murmur 80-85
Sweats 25 Changing/new murmur 10-40
Anorexia 25-55 Neurological abnormalities 30-40
Weight loss 25-35 Embolic event 20-50
Malaise 25-40 Splenomegaly 15-20
Dyspnea 20-40 Clubbing 10-20
Cough 25 Peripheral manifestation -
Stroke 13-20 Osler nodes 7-10
Headache 15-40 Splinter hemorrhage 5-15
Nausea/Vomiting 15-20 Petechiae 10-40
Myalgia/Arthralgia 15-30 Janeway lesion 6-10
Chest pain 8-35 Retinal lesion/Roth spots 4-10
Abdominal pain 5-15
Back pain 7-10
Confusion 10-20
Lesi Iskemik dan Hemoragis pada Lesi Iskemik dan Hemoragis pada Endokarditis Infektif AkutEndokarditis Infektif Akut
Sumber : Color Plate,Hurst’s The Heart 1994
Vegetasi dengan Perforasi pada Katup Vegetasi dengan Perforasi pada Katup MitralMitral
Sumber : Color Plate, Hurst’s The Heart 1994
KULTUR DARAHKULTUR DARAH
Sebagian besar hasil positif Kultur negatif pada 5% pasien Kultur dalam 2 set : aerob dan anaerob Darah vena 5-10 ml Diinkubasi pada suhu 37 C, 5-6 hari Terapi antibiotik dapat ditunda 2-4 hari (kondisi tidak akut)
• Bayer et al. Circulation 1998;98:2936-48• ESC Guideline 2004
Predisposing Conditions and Microbiology of Native Valve Predisposing Conditions and Microbiology of Native Valve EndocarditisEndocarditisConditions and Microbiology Children (%) Adults (%)
Neonates 2 mo-15 yr 15-60 yr >60 yr
Predisposing conditions
RHD 2-10 25-30 8
CHD 75-90 10-20 2
MVP 5-15 10-30 10
DHD Rare 30
Parenteral drug abuse 15-35 10
Other 10-15 10
None 72 2-5 25-45 25-40
Microbiology
Streptococci 15-20 40-50 45-65 30-45
Enterococci 4 5-8 15
S. aureus 40-50 25 30-40 25-30
Coagulase negative staphylococci 10 5 3-5 5-8
GNB 10 5 4-8 5
Fungi 10 1 1 Rare
Polymicrobial 4 1 Rare
Other 1 2
Culture negative 4 0-15 3-10 5Braunwald, 2005
Microbiology of Endocarditis Associated Microbiology of Endocarditis Associated with with
Intravenous Drug AbuseIntravenous Drug AbuseOrganisms
Number of Cases (%) of Endocarditis Drug Addicts
Right Sided N=346
Left Sided N=204
Total
N=675
Spain (1977-1993)
N=1529
Streptococci 17 (5) 31 (15) 80 (12) 131 (8.5)
Enterococci 7 (2) 49 (24) 59 (9) 21 (1)
Staphylococcus aureus 267 (77) 47 (23) 396 (57) 1138 (74)
Coagulase negative staphylococci
- - 44 (3)
Gram negative bacilli 17 (5) 26 (13) 45 (7) 23 (1.5)
Fungi (predominantly Candida species)
- 25 (12) 26 (4) 18 (1)
Polymicrobial/miscellaneous 28 (8) 20 (10) 49 (7) 48 (3)
Culture negative 10 (3) 6 (3) 20 (3) 106 (7)
Braunwald, 2005
Pendekatan Diagnosis dengan Pendekatan Diagnosis dengan Ekokardiografi pada Kecurigaan Ekokardiografi pada Kecurigaan
Endokarditis InfektifEndokarditis Infektif
AHA Guideline, Circulation 2005;111:e394-2433
Vegetasi Katup Trikuspid pada Vegetasi Katup Trikuspid pada Penyalahguna NARKOBA IntravenaPenyalahguna NARKOBA Intravena
Idrus Alwi.doc
Vegetasi Katup Aorta pada Vegetasi Katup Aorta pada Penyalahguna NARKOBA intravenaPenyalahguna NARKOBA intravena
Idrus Alwi .doc
DIAGNOSISDIAGNOSIS
Anamnesis cermat Pemeriksaan fisis teliti Pemeriksaan penunjang
(ekokardiografi, kultur darah) Kriteria Duke yang dimodifikasi
- Temuan ekokardiografi- PNIV : dimasukkan sebagai kondisi
premorbid
Definition of Infective Endocarditis Definition of Infective Endocarditis According to the Modified Duke CriteriaAccording to the Modified Duke CriteriaDefinite infective endocarditis
Pathological criteria
Microorganisms demonstrated by culture or histological examination of a vegetation, a vegetation that has embolized, or an intracardiac abscess specimen; orPathological lesions; vegetation or intracardiac abscess confirmed by histological examination showing active endocarditis
Clinical Criteria
2 major criteria; or1 major criterion and 3 minor criteria; or5 minor criteria
Possible IE
1 major criterion and 1 minor criterion; or3 minor criteria
Rejected
Firm alternative diagnosis explaining evidence of IE; orResolution of IE syndrome with antibiotic therapy for <4 days; orNo pathological evidence of IE at surgery or autopsy, with antibiotic therapy for <4 days; orDoes not meet criteria for possible IE as above
Definition of Terms Used in the Modified Duke Definition of Terms Used in the Modified Duke Criteria for the Diagnosis of Infective EndocarditisCriteria for the Diagnosis of Infective Endocarditis Major Criteria
Pathological criteria
Typical microorganisms consistent with IE from 2 separate blood cultures: Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus, or community-acquired enterococci in the absence of a primary focus; orMicroorganisms consistent with IE from persistently positive blood cultures defined as follows: At least 2 positive cultures of blood samples drawn>12 h apart; or all of 3 or a majority of >4 separate cultures of blood (with first and last sample drawn at least 1 h apart) Single positive blood culture for Coxiella burnetii or anti-phase 1 IgG antibody titer >1:800
Evidence of endocardial involvement
Echocardiogram positive for IE (TEE recommended for patients with prosthetic valves, rated at least “possible IE" by clinical criteria, or complicated IE [paravalvular abscess]; TTE as first test in other patients) defined as follows: oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation; or abscess; or new partial dehiscence of prosthetic valve; new valvular regurgitation (worsening or changing or preexisting murmur not sufficient)
Definition of Terms Used in the Definition of Terms Used in the Modified Duke Criteria for the Modified Duke Criteria for the
Diagnosis of Infective EndocarditisDiagnosis of Infective Endocarditis
Minor Criteria
Predisposition: predisposing heart condition, or IDUFever: temperature >380CVascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway's lesionsImmunologic phenomena: glomerulonephritis, Osler's nodes, Roth's spots, and rheumatoid factorMicrobiological evidence: positive blood culture but does not meet a major criterion as noted above" or serological evidence of active infection with organism consistent with IEEchocardiographic minor criteria eliminated
Spektrum Ekokardiografi Spektrum Ekokardiografi Endokarditis Infektif pada Endokarditis Infektif pada Penyalahguna NARKOBA Intravena Penyalahguna NARKOBA Intravena di RSCMdi RSCMUkuran vegetasi : 1,7-6,2 cmLokasi vegetasi : - Hanya pada katup trikuspid : 80,8 % - Hanya pada katup mitral : 7,7 % - Hanya pada katup aorta : 7,7 % - Katup trikuspid dan aorta : 3,8 %Regurgitasi : - Katup trikuspid : 73 % - Katup mitral : 7,7 % - Katup aorta : 7,7 %
Alwi I dkk, KOPAPDI XI,Surabaya 2000
Komplikasi dan Penyakit Penyerta Komplikasi dan Penyakit Penyerta Endokarditis Infektif pada Endokarditis Infektif pada Penyalahguna NARKOBA Intravena di Penyalahguna NARKOBA Intravena di RSCMRSCM
Pneumonia : 82,9 % Gagal jantung : 14,6
% Efusi pleura : 14,6 % Emboli paru : 7,3 % Strok : 7,3 % DIC : 12,2 %
HIV positif : 63,6 % (n : 22)HCV positif : 86,4 % ( n : 22)HBsAg positif : 21,4 % (n : 14)
Alwi I dkk, not publish
PenatalaksanaanPenatalaksanaan
American Heart Association ( AHA ) guideline
European Society of Cardiology guideline 2004
Therapy of native valve endocarditis caused Therapy of native valve endocarditis caused by by highly penicillin-susceptible highly penicillin-susceptible viridans group streptococci and viridans group streptococci and Streptococcus bovisStreptococcus bovis
Regimen Dosage and Route Duration, wk
Strength of Recommendation
Comments
Aqueous crystalline penicillin G sodium
or
12-18 million U/24 h IV either continuously or
in 4 or 6 equally divided doses
4 IA Preferred in most patients >65 y or patients with impairment of 8th cranial nerve function or renal function
Ceftriaxone sodium 2 g/24 h IV/IM in 1 dose
Pediatric dose: penicillin 200 000 U/kg per 24 h IV in H equally divided doses; ceftriaxone 100 mg/kg per 24 h IV/IM in 1 dose
4 IA
AHA Guideline, 2005
Terapi Terapi SurgikalSurgikal Bakterimia menetap setelah terapi medis
adekuat Regurgitasi aorta atau mitral akut dengan
gagal ventrikel Gagal jantung kongestif yang tak respon
terhadap terapi medis Perforasi atau ruptur katup Vegetasi menetap setelah emboli sistemik Ekstensi perivalvular
Bayer et al, AHA Scientific Statement. Circulation 1998;98:2936-48
KesimpulanKesimpulan
Endokarditis infektif merupakan komplikasi klasik PNIV
Streptococcus viridans merupakan kuman penyebab tersering
Diagnosis ditegakkan berdasarkan kriteria klinis Duke yang dimodifikasi
Penatalaksanaan ideal berdasarkan jenis kuman dan pola resistensi yang sesuai
Teicoplanin efektif pada EI gram positif khususnya Streptoccus viridans sesuai guideline
Look at the Text Book
Clinical Presentation
Pericarditis =Inflammation of Pericardium par/visc
acute pericarditis pericardial effusion and cardiac
tamponade constrictive pericarditis.
5.Disease of MyocardiumLook at the Text Book Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Restrictive Cardiomyopathy
7.Peripheral Arteri/Vena Disease(Look at the Text Book)
Varises Thrombophlebitis Arteritis Arterial Emboli
8.Pulmonary Heart Disease(Look at the text beook) Pulmonary Hipertension Pulmonary Emboli Cor Pulmonale
Contoh:Sakit DadaCV(Potensial Fatal)CV(Potensial Fatal) Respiratory(Pot Respiratory(Pot
Fatal)Fatal)Angina Pektoris,Myo Angina Pektoris,Myo Infarct ,Ao Infarct ,Ao Diseksi ,MioperikarditisDiseksi ,Mioperikarditis
Pulm Emboli Pleuro-Pulm Emboli Pleuro-pneumonia/lobar,pneumothorpneumonia/lobar,pneumothoraks,pneumomediastinumaks,pneumomediastinum
GIGI OtherOther
Esophagitis,Spasm Esophagitis,Spasm esophagus,Hiatus esophagus,Hiatus hernia,ulkus hernia,ulkus peptikum,Kolik peptikum,Kolik bilier,Pankreatitisbilier,Pankreatitis
Muskuloskeletal Muskuloskeletal pain,psikogenik,costochpain,psikogenik,costochondritis,cervical ondritis,cervical sponylosissponylosis
References
Braunwald E.Approach to the patients with CV Disease. In: Harrison TR, Fauci AS. Harrison’s Principles of Intrenal Medicine. 16th Edition. McGraw Hill, New York, 2004
Cannon P C, Lee TH. Approach to the Pts with Chest Pain. In Libby, Bonow, Mann, Zipes. Braunwald’s Heart Disease. A Textbook of CV Medicine,8th ed, vol2, Saunders, 2008,Ch 1,45,49,50,51,53,54,63,83
Kumar P and Clark M,Clinical Medicine,6 ed,Elsevier Saunders,2006.www.studentconsult.com
EHS/ESC Guidelines for the Management of Artrial Hypertension,2007.Eur Heart Journa 2007. http://www.escardio.org/knowledge/guidelines/
JNC VII: Management of Hypertension by Blood Classification, Chobanian AV et al. JAMA. 2003;289:2560-2572
http://www.nhlbi.gov/about/framingham
MMP