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