Penyakit Jantung Koroner (Coronary Heart Disease)

Dr. Refli Hasan, SpPD, SpJP(K) Dept. Cardiology and Vascular Medicine Fac. Medicine USU / Adam Malik Hospital

Sub Pokok Bahasan

Pengertian Ateosklerosis Aliran darah koroner dan Iskemi Miokard Angina Pektoris (Stabil)

Normal Arterial Wall

Tunica adventitia Tunica media Tunica intima Endothelium Subendothelial connective tissue Internal elastic membrane Smooth muscle cell Elastic/collagen fibres External elastic membrane

Adapted from Weissberg PL. Eur Heart J Supplements 1999:1:T1318

Pathogenesis of Atherosclerotic Plaques

Endothelial damage Protective response results in production of cellular adhesion molecules Monocytes and T lymphocytes attach to sticky surface of endothelial cells Migrate through arterial wall to subendothelial space Macrophages take up oxidised LDL-cholesterol Lipid-rich foam cells Fatty streak and plaque

The Activated Endothelium

activated endothelium

cytokines (e.g. IL-1, TNF-) chemokines (e.g.MCP-1, IL-8)

growth factors (e.g. PDGF, FGF)

CELLULAR ADHESION MOLECULES

attracts monocytes and T lymphocytes which adhere to endothelial cells

induces cell proliferation and a prothrombic state

Adapted from Koenig W. Eur Heart J 1999;1(Suppl T);T1926

Endothelial Dysfunction in Atherosclerosis

Upregulation of endothelial adhesion molecules Leukocyte adhesion

Increased endothelial permeability Migration of leukocytes into the artery wall

Adapted from Ross R. N Engl J Med 1999;362:115126

Fatty Streak Formation in Atherosclerosis

Adherence and entry of leukocytes

Migration of smooth muscle cells

Formation of foam cells

Activation of T cells Adherence and aggregation of platelets

Adapted from Ross R. N Engl J Med 1999;362:115126

Formation of the Complicated Atherosclerotic Plaque

Formation of the fibrous cap

Accumulation of macrophages

Formation of necrotic core

Adapted from Ross R. N Engl J Med 1999;362:115126

The Unstable Atherosclerotic Plaque

Thinning of the fibrous cap Rupture of the fibrous cap

Haemorrhage from plaque microvessels

Adapted from Ross R. N Engl J Med 1999;362:115126

Atherosclerotic Plaque Rupture and Thrombus Formation

Intraluminal thrombus Growth of thrombus

Blood Flow

Intraplaque thrombus

Lipid pool

Adapted from Weissberg PL. Eur Heart J Supplements 1999:1:T1318

The Synthesis and Breakdown of Atheromatous Plaques

Adapted from Libby P. Circulation 1995;91:28442850

The Vulnerable Atherosclerotic Plaque

Adapted from Libby P. Circulation 1995;91:28442850

Atherogenesis and Atherothrombosis: A Progressive Process

Normal Fatty Streak Fibrous Plaque Atherosclerotic Plaque Plaque Rupture/ Fissure & Thrombosis

Myocardial Infarction Ischemic Stroke Critical Leg Ischemia

Clinically Silent

Angina Transient Ischemic Attack Claudication/PAD

Cardiovascular Death

Increasing Age
3

Clinical Manifestations of Atherosclerosis

Coronary heart disease

Angina pectoris, myocardial infarction, sudden cardiac death

Cerebrovascular disease
Transient ischaemic attacks, stroke

Peripheral vascular disease

Intermittent claudication, gangrene

Structure of Lipoproteins
Free cholesterol

Phospholipid

Triglyceride

Apolipoprotein

Cholesteryl ester

Classification of Lipoproteins
Based on density: Chylomicrons Very low-density lipoprotein (VLDL) Intermediate-density lipoprotein (IDL) Low-density lipoprotein (LDL) High-density lipoprotein (HDL)

LDL-Cholesterol

Strongly associated with atherosclerosis and CHD events 10% increase results in a 20% increase in CHD risk Risk associated with LDL-C is increased by other risk factors: low HDL-cholesterol smoking hypertension diabetes

Triglycerides

Associated with increased risk of CHD events Link with increased CHD risk is complex
may be related to:

low HDL levels highly atherogenic forms of LDL-cholesterol hyperinsulinaemia/insulin resistance procoagulation state hypertension abdominal obesity

May have accompanying dyslipidaemias Normal triglyceride levels <150 mg/dL Very high triglycerides (>1000 mg/dL, 11.3 mmol/L) increase pancreatitis risk

HDL-Cholesterol

HDL-cholesterol has a protective effect for risk of atherosclerosis and CHD The lower the HDL-cholesterol level, the higher the risk for atherosclerosis and CHD
low level (<40 mg/dL) increases risk

HDL-cholesterol tends to be low when triglycerides are high HDL-cholesterol is lowered by smoking, obesity and physical inactivity

Apolipoproteins

Main protein content of lipoproteins Functions include:

Facilitation of lipid transport Activation of three enzymes in lipid metabolism
lecithin cholesterol acyltransferase (LCAT) lipoprotein lipase (LPL) hepatic triglyceride lipase (HTGL)

Binding to cell surface receptors

Exogenous Pathway of Lipid Metabolism

Intestine Intestine
Dietary Dietary triglycerides triglycerides and and cholesterol cholesterol

Chylomicron Chylomicron LP LP lipase lipase Skeletal Skeletal muscle muscle FFA Chylomicron Chylomicron remnant remnant Liver Liver

Remnant Remnant receptor receptor

to to atheroma atheroma

Adipose Adipose tissue tissue

Endogenous Pathway of Lipid Metabolism

LPL LPL Lipoprotein Lipoprotein lipase lipase HL HL LDL LDL LDL LDL receptor receptor LPL HL IDL IDL HL LPL Hepatic Hepatic lipase lipase

Small Small VLDL VLDL LPL HL Large Large VLDL VLDL

Liver Liver

Reverse Cholesterol Transport cholesterol transport

Cell membrane Liver

SRB1

CE ABCA1
FC LCAT HDL HDL3

CE CETP TG

LDL receptor
VLDL, IDL, LDL

Peripheral tissues FC TG CE LCAT CETP Free cholesterol Triglycerides Cholesterol esters Lecithin cholesterol acyl transferase Cholesteryl ester transfer protein

Joint European Guidelines: ESC,

EAS, ESH, ISBM, ESGP/FM, EHN
Estimate absolute CV risk using chart and initial TC value

Absolute CHD risk <20% over 10 years, TC 5 mmol/L

Absolute CHD risk 20% over 10 years

Lifestyle advice Aim: TC<5 mmol/L and LDL-C <3.0 mmol/L Follow-up at 5-year intervals

Measure fasting lipids, give lifestyle advice, with repeat lipids after 3 months

TC <5 mmol/L and LDL-C <3.0 mmol/L Maintain lifestyle advice with annual follow-up

TC 5 mmol/L and/or LDL-C 3 mmol/L Maintain lifestyle advice with drug therapy

Adapted from Wood D et al. Atherosclerosis 1998;140:199270

NCEP ATP III: Focus on Multiple Risk factors

Uses Framingham projections of 10-year absolute CHD risk to identify certain patients with 2 risk factors for more intensive treatment Raises persons with diabetes without CHD to the level of CHD risk equivalent Identifies persons with multiple metabolic risk factors (metabolic syndrome) as candidates for intensified TLC*
*TLC: therapeutic lifestyle changes

National Cholesterol Education Program, Adult Treatment Panel III, 2001. JAMA 2001:285;24862497

NCEP ATP III: Modifications of Lipid Classification

Identifies LDL-cholesterol <100 mg/dL (2.6 mmol/L) as optimal Raises categorical low HDL-cholesterol from <35 to <40 mg/dL (<0.9 to <1 mmol/L) Lowers TG cutpoints to: normal: <150 mg/dL (<1.7 mmol/L) borderline high: 150199 mg/dL (1.72.2 mmol/L) high: 200499 mg/dL (2.25.6 mmol/L) very high: 500 mg/dL (5.6 mmol/L)

National Cholesterol Education Program, Adult Treatment Panel III, 2001. JAMA 2001:285;24862497

NCEP ATP III Guidelines

Initiate TLC* Drug therapy if LDL-C considered if LDL-C
160 mg/dL
190 mg/dL (160 189 mg/dL: drug optional)
10- year risk 10 20%: 130 mg/dL 10-year risk <10%: 160 mg/dL

Patients with

LDL-C treatment goal <160 mg/dL

0-1 risk factors

2 risk factors (10-year risk 20%)

130 mg/dL

<130 mg/dL

CHD and CHD risk equivalents (10-year risk >20%)

100 mg/dL

130 mg/dL (100129 mg/dL: drug optional)

<100 mg/dL

100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L

* TLC: therapeutic lifestyle changes

National Cholesterol Education Program, Adult Treatment Panel III. JAMA 2001;285:24862497

NCEP ATP III: LDLCholesterol Goals

CHD or CHD risk equivalents
LDL-cholesterol level

2 risk factors

<2 risk factors

Target
mg/dL

190 -

160

160 -

Target mg/dL

130

130 -

Target mg/dL

100

100 100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L

National Cholesterol Education Program, Adult Treatment Panel III, 2001. JAMA 2001:285;24862497

NCEP ATP III Guidelines Increase the Number of Patients Eligible for Treatment
Risk NCEP ATP II
8,612 19,555 1,264

NCEP ATP III

14,713 23,663 1,264

% increase in drug-eligible patients

71 21 0

High Moderat e Low

Total

29,431

Adapted from Davidson MH. Am J Cardiol 2002;89(Suppl 5A):1C2C

39,640

35

Indonesia : Thn 2001 29,7% kematian di Jawa Bali akibat peny.jantung dan p.darah

ANGINA PEKTORIS

INFARK MIOKARD

Dimana Rasa Nyeri Dirasakan??

APA ARTI FAKTOR RISIKO ?

Faktor risiko adalah keadaan yang ada pada seseorang yang membuatnya lebih berisiko menderita penyakit dibandingkan dengan orang lain yang ciri-cirinya sama dengan dia tetapi tidak memiliki keadaan itu

Contoh: seorang pria perokok berusia 40 tahun mempunyai risiko terkena serangan jantung 2 kali dibanding pria seusia dia tetapi tidak merokok. Tetapi bisa saja pria perokok itu meninggal karena kecelakaan sedangkan si pria tidak perokok bisa meninggal karena serangan jantung

ATP III: Major CHD Risk Factors Other Than LDL-C

Cigarette smoking Hypertension: BP 140/90 mm Hg or on antihypertensive medication Low HDL-C: 40 mg/dL* Family history of premature CHD (1st-degree relative):
male relative age 55 years female relative age 65 years

Age
male 45 years female 55 years
*HDL-C 60 mg/dL is a negative risk factor and negates one other risk factor.
2001, Professional Postgraduate Services www.lipidhealth.org

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497.

ATP III: Additional CHD Risk Factors (Minor)

Life-habit risk factors: targets for intervention; not used to set lower LDL-C goal

obesity physical inactivity atherogenic diet Emerging risk factors: can help guide intensity of risk-reduction therapy; do not categorically alter LDL-C goals
lipoprotein(a) impaired fasting glucose subclinical atherosclerotic factors disease
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497.

homocysteine prothrombotic and proinflammatory

2001, Professional Postgraduate Services www.lipidhealth.org

Efek Faktor Risiko Multipel Terhadap Kemungkinan Penyakit Jantung Koroner: Studi Framingham
42 36 30 24 18 12 6 0
10-Year % Probability of Event 40 21 10 4
+ -

14

SBP Cholesterol HDL-C Diabetes Cigarettes ECG-LVH

150-160 240-262 33-35

+ + -

+ + + -

+ + + + -

+ + + + + -

+ + + + + +

Kannel. Am J Hypertens. 2000;13:3S-10S.

MONICA JAKARTA
1988 1993 2000 ==================================================== Tot Cholesterol 250mg% pria 12.3% 14.8% 12.2%

wanita
Hipertensi wanita pria

15.8%
16.0% 13.6

17.8%
17.0% 16.5%

17.1%
12.2% 12.1%

Merokok

wanita pria

5.9% 59.0%

6.2% 56.9%
10.3% 3.6%

1.8% 38.5%
12.0% 6.2%

Obesity BMI 30 kg/m2 wanita 8.9% pria 2.5%

FAKTOR RISIKO PADA PENDERITA Infark Miokard Akut RS JANTUNG HARAPAN KITA
FAKTOR RISIKO PERSENTASE 68.0% 50.5% 31.4% 21.4% 63.1% 62.1%
usia 28-72 tahun

MEROKOK HIPERTENSI DISLIPIDEMIA RIWAYAT KELUARGA STRES TIDAK PERNAH atau KURANG OLAHRAGA

Continuum of Patients at Risk for a CHD Event

Post MI/Angina
Secondary Prevention

Other Atherosclerotic Manifestations

Subclinical Atherosclerosis
Primary Prevention

Multiple Risk Factors

Low Risk

Courtesy of CD Furberg.

Aliran darah koroner dan iskemia miokard

Iskemia miokardial : merupakan ketidak seimbangan antara suplai oksigen dan kebutuhan miokardial. Ketidaksembangan akibat :
Reduksi aliran darah koroner Suplai oksigen Sekunder akibat peningkatan tonus vaskuler, agregasi platelet,atau trombus

Patogenesis iskemia miokardial

Kontrol metabolik Gaya kompresi Ekstravaskuler Autoregulasi RESISTENSI VASKULER

Kontrol neural
Faktor humoral

Fase diastolik

ALIRAN DARAH KORONER

Frekuensi jantung

Kapasitas Membawa O2

SUPLAI

DEMAND

Kontraktilitas Tekanan dinding sistolik

Angina

Merupakan rasa tidak nyaman di dada atau daerah sekitarnya disebabkan oleh iskemia miokardial Dicetuskan oleh aktivitas fisik/aktivitas atau emosional dan berkurang atau hilang dengan preparat nitrogliserin

Clinical Classification of Chest Pain

Typical angina (definite) 1) substernal chest discomfort with a characteristic quality and duration that is ... 2) provoked by exertion or emotional stress and 3) relieved by rest or nitroglycerin Atypical angina (probable) meets 2 of the of characteristics Noncardiac chest pain meets 1 of the typical angina characteristics
J Am Coll Cardiol. 1983;1:574, Letter

Alat bantu diagnosa

EKG

ECG merupakan salah satu instrumen pengukuran medik tertua dalam sejarah. Alat ini bermula dari percobaan Waller di tahun 1889 yang merekam sinyal jantung pada anjing peliharaan menggunakan elektrometer kapiler [5]. Secara total, pengukuran ECG terdiri atas pengukuran gelombang depolarisasi dan gelombang repolarisasi. Gelombang radio yang digunakan memiliki intensitas atau energi yang rendah sehingga tidak membahayakan. Tahap evolusi terbesarnya terjadi di saat sistem ECG diintregasikan dengan micro processor yang hasilnya adalah peningkatan efisiensi pengukuran dan digitasi yang membuka cakrawala baru terhadap peralatan analitik dan intrepetasi data medik.

EKG

Conduction System

SA Node Internodal branch AV Node Hiss Bundle Purkinje Fiber Contraction

The Electrocardiogram (ECG)

P wave : atrial depolarisation

QRS complex : ventricular depolarisation T wave : ventricular repolarisation Atrial repolarisation hidden by QRS

P Wave

P Pulmonale

P Mitrale

PR Interval

QRS Complex

ST Segment

T Wave

Normal Sinus Rhythm Rhythm : Regular Rate : 60 100 P wave : Normal in configuration; precede each QRS PR : Normal ( 0. 12 0.20 seconds ) QRS : Normal ( less than 0.12 seconds )

First-degree AV block Rhythm : Regular Rate : Usually normal P wave : Sinus P wave present; one P wave to each QRS PR : Prolonged ( greater than 0.20 seconds ) QRS : Normal

Second -degree AV block, Mobitz I Rhythm : Irregular Rate : Usually slow but can be normal P wave : Sinus P wave present; some not followed by QRS complexes PR : Progressively lengthens QRS : Normal

Second-degree AV block, Mobitz II Rhythm : Regular usually; can be irreguler if conduction ratios vary Rate : Usually slow P wave : Two, three, or four P waves before each QRS PR : PR interval of beat with QRS is constant; PR interval may be normal or prolonged QRS : Normal if block in His bundle; wide if block involves bundle branches

Third-degree AV block

Rhythm : Regular Rate : 40 60 if block in His bundle; 30 40 if block involves bundle branches P wave : Sinus P wave present; bear no relationship to QRS; can be found hidden in QRS complexes and T waves PR : Varies greatly QRS : Normal if block in His bundle; wide if block involves bundle branches

Wolff-Parkinson-White syndrome

ST depresi dan perubahan gelombang T

ST depresi dianggap bermakna bila > 1 mm di bawah garis dasar PT di titik J Titik J didefinisikan sebagai akhir kompleks QRS dan permulaan segmen ST

Bentuk segmen ST :
up-sloping ( tidak spesifik ) horizontal ( lebih spesifik untuk iskemia ) down-sloping ( paling terpercaya untuk iskemia )

Perubahan gelombang T pada iskemia kurang begitu spesifik Gelombang T hiperakut kadang2 merupakan satu-satunya perubahan EKG yang terlihat

Treadmill Test

Digunakan untuk menegakkan diagnosa pasien dengan penyakit jantung koroner khususnya dan penyakit jantung pada umumnya sehingga pencegahan dapat dilakukan, kematian dapat dihindari dan harapan kualitas hidup dapat ditingkatkan. Cara noninvasif untuk mengkaji berbagai aspek fungsi jantung, dengan mengevaluasi aksi jantung selama dilakukan stress fisik, respon jantung terhadap peningkatan kebutuhan oksigen dapat ditentukan.

Manfaat Treadmill Test

Membantu mendiagnosa penyebab nyeri dada, Menentukan kapasitas fungsional jantung setelah miokard infak atau pembedahan jantung, Mengkaji efektivitas terapi pengobatan antiangina dan antidisritmia, Mengidentifikasi disritmia yang terjadi selama latihan fisik, dan Membantu mengembangkan latihan fisik selama rehabilitasi.

Holter Monitor

Adalah hasil evolusi dari perkembangan klinis dan teknis yang ditujukan untuk memenuhi kepentingan mobilitas dan pengukuran. Teknologi ini mampu mengerjakan pengukuran secara kontinu dan merekamnya selama 24 jam untuk tujuan analisis terhadap pasien yang denyut jantungnya tidak normal. Dari kemampuan rekaman yang dimilikinya, penggunaan Ambulatory ECG berlanjut untuk kepentingan observasi PVC (Premature Ventricular Complexes) dan pengobatannya. Saat ini terdapat banyak sekali unit Ambulatory ECG sebagai alat diagnosis yang dilengkapi micro processor, RAM, dan disk drive dengan kapasitas sampai 400 Mbytes.

Kardiologi Nuklir (1)

Merupakan pemeriksaan yang menggunakan alat radioaktif. Melalui pemeriksaan Kardiologi Nuklir para dokter dapat mengkaji aliran darah pada miokard jantung, mengevaluasi fungsi pompa jantung dan melihat ukuran jantung serta lokasi jantung yang mengalami gangguan.

Kardiologi Nuklir (2)

Jenis pemeriksaan yang dilakukan:

Untuk mengetahui perfusi miokar

Utk evaluasi fungsi jantung dengan radionuklir angiografi dan ekuilibrium radionuklid ventrikulografi

Exercise stress test Dypiridamol/adenosin Stress test Dobutamin Stress Test

Gated blood pool study First pass study at rest Exercise first pass study

Coronary Angiography

Coronary Angiography of Stenotic Coronary Artery

Arrow indicates atherosclerosis (stenosis) of the coronary artery

Invasive Vascular Investigations

Conventional arteriography.
Digital angiography.

Arteriography : stenosis at the origin of the two common iliac arteries

Non-Invasive Vascular Examinations

Duplex Scanning

Color-coded Doppler ultrasound of the popliteal cavity: the red flow towards the probe codes the artery, the blue flow away from the probe codes the vein

Doppler Ultrasound

The Ankle-Brachial Index

Lower extremity systolic pressure
Brachial artery systolic pressure Normal ABI IC CLI 0.9 - 1.3 <0.90 <0.50

ABI =

Oscillography
Above knee Below knee

Oscillations
Normal

Abnormal

Oscillography
Oscillations at the ankle

Normal
before After exercise

Abnormal

Grading of Angina of Effort

by the Canadian Cardiovascular Society

Ordinary physical activity does not cause angina, such as walking and climbing stairs. Angina with strenuous or rapid or prolonged exertion at work or recreation. II. Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, or in cold, or in wind, or under emotional stress, or only during the few hours after awakening. Walking more than 2 blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions. III. Marked limitation of ordinary physical activity. Walking one to two blocks on the level and climbing one flight of stairs in normal conditions and at normal pace. IV. Inability to carry on any physical activity without discomfort -anginal syndrome may be present at rest.
Circulation 1976; 54:522-523

I.

Angina Stabil Angina Tidak stabil Infark Miokard Akut Gagal Jantung

Kematian

MANAJEMEN ANGINA PEKTORIS STABIL

Tujuan manajemen : mengurangi simtom /gejala/keluhan angina dan iskemia berulang (kualitatif) mencegah infark miokard akut dan kematian (mengurangi morbiditas dan mortalitas )

Manajemen farmakologis

Antiplatelet (Aspirin, Klopidogrel, Glikoprotein IIb/IIIa, Adenosine Diphosphate Inhibitors) Antiangina (Beta bloker, Ca antagonis, Nitrat) ACE Inhibitor Penurun Kolesterol (statin)

Antiplatelet Agents to Prevent MI and Death

aspirin - Class I

Aspirin 75 to 325 mg daily should be used routinely in all patients with acute and chronic ischemic heart disease with or without manifest symptoms in the absence of contraindications aspirin exerts an antithrombotic effect by inhibiting cyclooxygenase and synthesis of platelet thromboxane A2 in >3,000 patients with stable angina, aspirin reduced the risk of adverse cardiovascular events by 33% in patients with unstable angina, aspirin decreases the short and long-term risk of fatal and nonfatal MI in the Physicians' Health Study, aspirin (325 mg), given on alternate days to asymptomatic persons, was associated with a decreased incidence of MI
ACC/AHA Guideline of Chronic Stable Angina 2001

Clopidogrel

Diberikan bila ada riwayat intoleransi terhadap aspirin

Clopidogrel Blocks the ADP Receptor

Platelet

ADP
Fibrinogen Binding Site

Fibrinogen
Fibrinogen Binding Reduced Acts by selective inhibition of ADP binding to its platelet receptor and prevents subsequent platelet aggregation

Herbert. Exp Opin Invest Drugs 1994;3:449-455.

Adenosine Diphosphate Inhibitors

ADP secreted by platelets (activates/aggregates platelets) P2T cell surface receptors Ticlid (ticlodipine) versus ASA Plavix (clopidogrel) CAPRIE trial Neutropenia, thrombocytopenia

Glycoprotein IIb/IIIa Inhibitors

50,000 receptors per platelet Aggregation final common pathway Passivation; stops deposition Abciximab (Reopro); tirofiban (Aggrastat); eptifibatide (Integrilin) and lamifiban (Canada) Pre-PCI/ Procedural Coronary Intervention

BETA-BLOCKERS

Mechanism of Action
reduction in inotropic state and sinus rate

slowing of AV conduction
decreased myocardial oxygen demand, increased diastolic perfusion time

Clinical Effectiveness
improve the survival rate of patients with recent MI improve the survival rate and prevent stroke and CHF in patients with hypertension adjust the dose of -blockers to reduce heart rate at rest to 55 to 60 bpm increase in heart rate during exercise should not exceed 75% of the heart rate response associated with onset of ischemia

ACC/AHA Guideline of Chronic Stable Angina 2001

Calcium Antagonists
Mechanisms of Action

reduce the transmembrane calcium transport (L-, T-, or N-type channels) alter myocardial oxygen supply and demand
dilate epicardial coronary arteries reduce cardiac contractility

nifedipine >> amlodipine and felodipine verapamil and diltiazem (heart rate-modulating calcium antagonists) can slow the sinus node and reduce AV conduction

decrease heart rate

reduce systemic vascular resistance and arterial pressure

ACC/AHA Guideline of Chronic Stable Angina 2001

PREPARAT NITRAT

Nitrat sublingual atau spray diberikan untuk mengurangi keluhan angina dengan cepat Nitrat jangka panjang dan Ca antagonis diberikan sbg terapi awal apabila terdapat kontraindikasi Beta bloker Nitrat jangka panjang dan Ca antagonis diberikan bila terapi dng Beta bloker tidak berhasil Nitrat jangka panjang dan Ca antagonis bila Beta bloker memberikan efek samping yang tidak diinginkan
ACC/AHA Guideline of Chronic Stable Angina 2001

ACE INHIBITOR

Kelas I : pasien CAD yang juga menderita DM dan atau penurunan fungsi ventrikel kiri

ACC/AHA Guideline of Chronic Stable Angina 2001

MANAJEMEN FAKTOR RISIKO

Tangani Hipertensi Stop merokok Atasi diabetes Program rehabilitasi yang komprehensif Penurunan kadar LDL pada suspect CAD atau penderita CAD dengan kadar LDL > 130 mg/dl ,dng target <100mg/dl Penurunan berat badan pada penderita obesitas

Intervensi Non Bedah

Indication for Cardiac Catheterization

Acute Myocardial infarction

ACS

Primary PCI, refractory post infarct symptom, treatment complication (VSD ruptured). refractory symptom, high risk clinical features high risk clinical symptoms

Stable angina

Severe Asymptomatic ischemia Valvular heart diseases Congenital heart diseases Unexplained heart failure, Malignant Arhythmias or resuscitated cardiac arrest Cardiomyopathy

Risk Cardiac Cathetherization

Mortality Myocardial Infarction SCAI Registry (%) .11 .05

Cerebrovascular accident Arrhythmias Vasclar complication Contrast reaction Hemodynamic complication Perforation of heart chamber Other complication

.07 .38 .43 .37 .26 .03 .28

Equipment

X-ray tube Radiation Exposure Catheters Pressure Recording Oxygen Analysis

Equipment

Catheters

Pressure recording & Oxygen Analysis

VCSH

AVG
VCSL

VCI

Hemodynamic & EKG data of Pt with AS as seen on the TV monitor in Oxygen Saturation measurement In Patients with VSD, RV O2 step up

Percutaneous techniques of catheterization

Right Heart Catheterization

Modified Seldingers technique for percutaneous catheter sheath introduction Left heart Cathetherization

Transseptal

Anatomy relevant to puncture A & V Femoralis

Measurement during Cardiac Catheterization

Flow Shunt Calculations Resistance Valve Area calculation

Flow Shunt Calculation (Flow ratio)

Oxymetric method
Flow Ratio =

Qp
Qs

( Sat O2 Ao Sat O2 Mixed Vein)

(Sat O2 PV Sat O2 PA)

Sat O2 Mixed Vein

[ [(VCSH + VCSL) / 2] x 3] + VCI

4

Pulmonary Arterial Resistance (PAR)

PAR = Mean PA pressure Mean Ao pressure

QP

Qp = Flow pulmonal; Qs = Flow Systemic

Cardiac Output =

O2 comsumption (ml/min)
AVO2 differences (ml O2/100ml blood) x 10

AVO2 = O2 content =

[Arterial O2 - Mixed Vein O2]content Saturation x 1.36 x Hb

Valve area Calculation

Gorlin & Gorlin Hydraulic formula
Area(cm2) = Valve Flow (ml/sec)

K (4.33) x C x MVG
CO (ml/min) Diastolic filling period (sec/min)

Mitral Valve Flow

Diastolic Filling Period (sec/min)

Aortic Valve Flow Systolic Ejection Period (sec/min)

= Diastolic period (sec/beat) x HR CO (ml/min) Systolic ejection period (sec/min) Systolic ejection period (sec/beat) x HR

= =

C = Emperical Constant (1=semilunar valve), (0.85=mitral valve) MVG = Mitral valve gradient

Assesment Regurgitant Volume (Sellers)

Minimal regurgitant jet seen. Clears rapidly from proksimal chamber with each beat Moderate opacification of proximal chamber, clearing with subsequent beats.

++

Aortic regurgitation

+++

Intense opacification of proximal chamber, becoming equal to that of distal chamber

Intense opacification of proximal chamber, becoming more dense than that of distal chamber. Opacification often persist over the entire series of image

+++ +

Mitral regurgitation

Coronary Angiography

Anterior View

LAO View

RAO view

Right Coroner View

Percutaneous Coronary Intervention

Percutaneous Coronary Intervention

Pre-Dilatation

Dilatation

Post-Dilatation

Post- Stenting

Early indications Angina Pectoris, myocardial ischemia In : Relatively stable Patients Good LV function Simple Stenotic Lesion 1 VD, proximal Dicrete, Concentric, nonCalsified

Advance in Techical, equipment & medications : enable to performed PCI in more complicated setting

APTS Acute Coronary Syndrome Poor LV function Elderly Post CABG Complicated Lesion ; bifurcatio, calcified

Lower Rate of Restenosis with Stenting (6 month follow-up)

Treatment
External elastic lamina Tunica media Internal elastic lamina

Restenosis

External elastic lamina

PTCA

Internal elastic lamina Intimal area

Treatment

Coronary stenting
Intimal area Lumen

Stent

Angioplasti /PCI

Keberhasilan Primer : 85 - 95 % Kematian : 0.3 - 1.3 % Infark Miokard : 1.6 - 6.3 % Operasi By-pass darurat :1 - 7 % Stenosis lebih lanjut
sblm era stent: 30 - 40 % era stent : 15-20% Drug eluting stent : almost 0%

PTCA

Benefits: ICH 0%, Complications: experience counts >100 cases/yr/ea provider; >600/yr/hospital Mortality: reinfarction 5 vs 12% for TPA; 30 day same as TPA; but in AWMI; age>70 pulse >100 rates 2% vs 10% for TPA Trials: RITA, PAMI (93); MITI (96)

Evolution of PCI for STEMI

AngioJet

Platelet

GP IIb/IIIa inhibitor

Embolization Protection Device

Balloon

Antiplatelet Rx

Stent

DES

Antman. Circulation 2001;103:2310.

Thrombus Removal and Distal Embolization Protection Devices

Thank you