PJK DAN ARITMIA - DR TRIADHY.pdf

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Penyakit Jantung Koroner

Dr. Triad Dr. Triadhy hy Nug Nugrah raha, a, SpJP SpJP (K) (K),, FIHA Kard Ka rdiol iolog ogii da dan n Ke Kedo dokt kter eran an Vas asku kular  lar  FK UNSUNS- RSUD dr dr. Moeward Moewardii Sur Suraka akarta rta

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Epidemiology Epidemiol ogy of ACS in the United States •

•

•

Single largest cause of death  –

515,204 US deaths in 2000

 –

1 in every 5 US deaths

Incidence  –

1,100,000 Americans will have a new or recurrent coronary attack each year and about 45% will die*

 –

550,000 new cases of angina per year 

Prevalence  –

12,900,000 with a history of MI, angina, or both

* Based on data from the ARIC study of the National Heart, Lung, and Blood Institute, 1987-1994. 1987-1994. Includes Americans hospitalized with definite or probable MI or fatal CHD, not including silent MIs. ACS ACS indicates acute coronary syndrome; MI, myocardial infarction; ARIC, Atherosclerotic Atherosclerotic Risk in Communities; and CHD, coronary 2003 Update. heart disease. From American American Heart Association. Heart Disease and Stroke Statistics — 2003

Slide reproduced with permission from Cannon CP Atherothrombosis slide compendium. Available at:

 Atherothrombosis* is the Leading Cause of Death Worldwide1

6. 3

Pulmonary Disease Injuries

9

AIDS

9.7

Cancer 

12.6 19.3

Infectious Disease

22.3

Atherothrombosis* 0

5

10

15

20

Causes of Mortality (%) *Atherothrombosis defined as ischemic heart disease and cerebrovascular disease. *Atherothrombosis 1The World World Health Report 2001 . Geneva: WHO; 2001.

25

30

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THE EVOLUTION OF THE ATHEROSCLEROTIC PLAQUE

The Longitudinal Section Of An Artery Depicts The “Timeline” Of Atherogenesis

(1) A normal artery , to (2) lesion initiation & accumulation of extracellular lipid in the intima, to (3) the evolution to the fibrofatty stage, to (4) lesio lesion n progression progression with procoagulant procoagulant expres expression sion & weakening of the fibrous cap. An ACS develops when the vulnerable or high risk plaque undergoes disruption of the fibrous cap (5) (5);; disruption of the plaque is the stimulus for thrombogenesis. Thrombus resorption resorption may be followed followed by collagen accumulation accumulation & smooth muscle cell growth (6)

 Atherothrombosis: Thrombus Superimposed on Atherosclerotic Plaque

 Adapted with permission from Falk E, et al. Circulation. 1998;92:657-671. Slide reproduced with permission from Cannon CP. CP. Atherothrombosis slide compendium. Available at: www.theheart.org. www.theheart.org.

Characteristics of Unstable and Stable Plaque Unstable

Thin Few fibrous cap SMCs

Stable

Inflammatory cells

Eroded endothelium Activated macrophages

More SMCs

Thick fibrous cap

Lack of  inflammatory cells

Intact endothelium Foam cells

 Adapted with permission from Libby P. P. Circulation Circulation.. 1995;91:2844-2850. Slide reproduced with permission from Cannon CP. CP. Atherothrombosis slide compendium. Available Available at: www www.theheart.org. .theheart.org.

Timeline Acute Acute Coronary Syndrome

Vulnerable Plaque

Modification Yeghiazarians Yeghiazarians Y, Braunstein JB, Askari Askari A, et al. Unstable angina angina

Thrombus Formation and ACS Plaque Disruption/Fissure/Erosion Thrombus Formation

Old Terminology: New Terminology:

UA

NQMI

Non-ST-Segment Elevation Acute Coronary Syndrome (ACS)

STE-MI

ST-Segment Elevation Acute Coronary Syndrome (ACS)

Spec Sp ectrum trum of IH IHD D

Guidelines relevant to the spectrum of IHD are in parentheses

Clinical Classification of Chest Pain

Peny Pe nyeb ebab ab Ny Nyer erii Da Dada da No Non n An Angi gina na

Figure 2. Management of atherosclerosis: matching therapy with pathophysiology. pathophysiology.

Peter Libby, and Pierre Theroux Circulation. 2005;111:34813488

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Acute Coronary Syndrome  The

spectrum of clinical conditions ranging from:  unstable angina  non-Q wave MI  Q-wave MI  characterized by the common pathophysiology pathophysiolog y of a disrupted atheroslerotic plaque

Spectrum of Acute Coronary Syndromes Presentation

Emergency Department

Ischemic Discomfort at Rest

No STST-Segment Elevation

ST-Segment Elevation      +

+ In--Hospital In

Unstable Angina

Non-Q-wave MI

+

Q-wave MI

( : positive cardiac biomarker) ST elevation  injury miocard

Nyer Ny erii da dada da pa pada da an angi gina na pe pect ctor oris is ti tida dak k st stab abil il

General Guidelines to Differentiate Chest Pain of Myocardial Infarction, Unstable and Chronic Stable Angina Chest Pain

Myocardial infarction

Unstable Angina

Chronic Stable Angina

Severity

Very severe

Moderate severe

Mild

Duration

> 30 minutes

15 - 30 30 minutes

< 15 minutes

Frequency

Persistent pain

Increasing frequency

Stable, less frequent

Timing

At rest

At rest or with exertion With exertion

Relief With No Nitroglycerine

Usually no

yes

Other symptoms

Less than MI

Less than MI

anxiety, diaphoresis, dyspnea, na nausea

Criteria for Diagnosis Modified WHO Criteria : Two Out of 3 of the th e Following Establishes the Diagnosis 1. Pr Prol olon onge ged d che chest st di disc scom omfo fort rt or ch ches estt pai pain n 2. ECG ECG evi evide denc nce e of of my myoc ocar ardi dial al in infa farc rcti tion on or ischemia 3. At le leas astt a 2 fo fold ld ri rise se in CK CK-M -MB, B, Tr Trop opon onin in

A. Normal

I

II

III

aVR

aVL

aVF

V1-2 V3-4

V5-6

B. Acute ( 6 weeks)

Cardiac Cardi ac Marke Markerr - Relea Release se Kinet Kinetics ics Cardiac Marker

Spesificity Specificity

Myoglobin CK-MB Troponin I

 Non-specific Moderately Specific

Returns to Duration of action  Normal

Peak Peaks At

1- 3 hours hours 4 - 6 hou hours rs 4 - 6 hou hours rs

24 hours 72 hours 5- 10 day dayss

6 - 9 hou ourrs 12 - 24 hou hours rs 12 - 24 hou hours rs



6

Blood level of Marker above upper limit of normal

Increase Appears At



5   

Myoglobin CK-MB Troponin I



4 

3

2



 





 

1



0

4

8

12 16 20 24

48



72

Time After Postpost AMIMCI ( Hours ) TimeOnset of onset (hours)



96

120

Complications of MI : • Cardiac arrhythmias and sudden death (usually • • • • • • • • •

within 24 hours of MI) Congestive heart failure or ventricular dysfunction Cardiogenic shock Deep venous thrombosis and pulmonary embolism Pericarditis (Dressler’s syndrome) Rupture of papillary muscle Rupture of ventricular septum Rupture of cardiac wall Systemic Systemi c arterial embolism Ventricular aneurysm

Langkah Awal tata laksana sindrom koroner akut 1. Tirah baring (Kelas I-C) 2. Suplemen oksigen harus diberikan segera bagi merek mereka a dengan dengan saturasi saturasi O2 arteri arteri