Acute coronary syndrome : Acute coronary syndrome :

PathophysiologyPathophysiology

ACS – is a continuum disease process. Patients with acute coronary syndromes have some degree of coronary artery occlusion. The degree of occlusion defines whether the acute coronary syndrome is:

-Unstable angina-non-Q-wave /non-ST segment elevation MI -only the inner layer of myocardium is

damaged.

-Q-wave / ST segment elevation MI -all layers of myocardium is damaged.

Angina - is a subjective experience of chest discomfort resulting from an imbalance oxygen supply and demand.

4 Classifications of Angina:

1.) Stable – predictablepan, in frequency and duration, which can be relieved with nitrates and rest.

2.) Unstable – increased pain, which s easily induced. Occurs even at rest, relieved by rest and /or nitroglycerin.

3.) Prinzmetal or variant – pain from unpredictable coronary artery spasm.

4.) Microvascular or x sndrome – angina-like chest pain due to imparement of vasodilator reserve in a patient with normal coronary arteries.

ACS Pathophysiology

Pathophysiology

The development of any acute coronary syndromes begins with a rupture or erosion of plaque – an unstable and lipid rich substance. The rupture results in platelet adhesions, fibrin clot formation, and activation of thrombin.

ACS most commonly results when a thrombus partially occludes the blood flow.

Distal embolisation of a platelet-rich thrombus causing occlusion of intramyocardial arteriole (arrow). Such an event may result in micro-infarction and elevation of markers of myocardial necrosis.

What Causes It:

Family history of heart disease Obesity Smoking High-fat, high-carbohydrate diet Sedentary lifestyle Menopause Stress Diabetes Hypertension Hyperlipoproteinemia

Risk Factors

Most common in men, specially those older than 50 years

Also in postmenoposal women – due to lack of estrogen that made them prone to atherosclerotic disease, whereby the coronary arteries lose their ability to dilate and to increase blood flow.

What to look for:

Burning Squeezing Crushing tightness in the substernal or

precordial chest that may radiate to the left arm neck, jaw, or shoulder blade.

Goal of Treatment in Angina

To reduce myocardial oxygen demand or increase oxygen supply.

MEDS: Nitrates – reduce myocardial oxygen

consumption. Anti Platelet drugs – to minimized platelet

aggregation. Antilipemic drugs – can reduce elevated

serum cholesterol. Obstruction lesions – CABG and PTCA

Electrocardiogram of a 48 year old woman with unstable angina (top). Note the acute ischaemic changes in leads V1 to V5 (arrows). Coronary angiography revealed a severe mid-left anterior descending coronary artery stenosis (arrow, bottom left), which was successfully stented (bottom right)

•Right coronary artery angiogram in patient with non-ST segment elevation myocardial infarction (top left), showing hazy appearance of intraluminal thrombus overlying a severe stenosis (arrow). Abciximab was given before direct stenting (top right), with good angiographic outcome (bottom)

Myocardial Infarction (MI):

Is a sever, persistent chest pain that isn’t relieved by rest or nitroglycerin.

Pain is describe as crushing or squeezing

Usually substernal, but may radiate to the left arm, jaw, neck, or shoulder blade.

Goal of Treatment in MI

To relieve pain, stabilized heart rhythm, revascularized the coronary artery, preserve myocardial tissue, and reduce cardiac workload.

MEDS: Thrombolytic theraphy – which should be given 6

hours or less before the onset of pain otherwise it will be useless. To be able to dissolve clots it should be a new clot not a clot that is already formed. It is contra indicated to if the pain started more than 6 hours ago because there is no benefit at all in giving the medication and it can only increase bleeding.

PTCA – is an option for opening blocked or narrowed arteries. Oxygen – to increase oxygenation of the blood. Nitroglycerin – administered sublingually to relieve chest pain, Morphine – administered as analgesia. Aspirin – administered to inhibit platelet agregation. Lidocaine – may be used if arrhythmias are present. Physical activity is limited for the first 12 hours – to reduce

cardiac work load. A patient with acute MI is permitted to perform activities that require minimal effort such as bathroom privileges and self care routines. Unsupervised ambulation in the hall is not promoted instead, strict supervision is necessary. Not all activities are allowed to be performed by the patient even if it is supervised since they may not be appropriate given the condition of the patient.

Provide a clear liquid diet – anticipate order for low-cholesterol, low sodium diet without caffeine.

Provide stool softener – to prevent straining during defecation.

The TIMI risk scoreUsed in Identifying higher risk patients By: Antman and colleagues

•Rates of death from all causes and non-fatal myocardial infarction at 14 days, by TIMI risk score. Note sharp rate increase when score ≥ 3

Simplified management pathway for patients with unstable angina or non-ST segment elevation myocardial infarction

TIMI risk scoreTIMI risk score1 point each for presence of :

Age > 65 years Documented prior coronary artery stenosis > 50% Three or more conventional cardiac risk factors (e.g. age, sex,

family history, hyperlipidemia, diabetes, smoking, obesity) Use of aspirin in the preceding 7 days Two or more anginal events in the preceding 24h ST-segment deviation (transient elevation or persistent

depression) Increased cardiac biomarkers

Score 5 – 7 :high risk

Score 3 – 4 :intermediate risk

Score 0 – 2 :low risk

(Pollack et al, 2003)

The perfect markerThe perfect marker

Marker for myocardial necrosis, and also for cardiac ischemia

Linear relationship between blood levels and extent of myocardial injury (and prognosis)

100% sensitive 100% specific Immediate increase (+ constant blood level for

hours to days) Test kits : reliable, rapid, universally available and

inexpensive

What about troponin T and What about troponin T and II ? ?

Very high sensitivity for myocardial necrosis Related to prognosis

Not 100% specific for atherosclerotic coronary artery disease myocarditis, cardiomyopathy, myocardial contusion, ... renal failure, auto-immune diseases, ...)

Up to 6 hours before raised blood levelsno early MI diagnosis possible

Raised blood levels for many daystroublesome diagnosis of re-infarction

BUT

Role for myoglobin ?Role for myoglobin ?

Initial elevation : 1 to 4h after onsetbetter early marker than troponins

BUT : early myoglobin is less sensitive and less specific (due to skeletal muscletrauma) than late troponindecisions mainly based on clinical skills, ECG and late troponin (exceptrarely for reperfusion therapy)

Duration of elevation : 24 – 48huseful for re-infarction diagnosis

Role for CK-MB ?Role for CK-MB ?

Initial elevation comparable with troponins

Less sensitive than troponins

High specificity (comparable with troponins)

Rapid rise and fall (instead of gradual fall for troponins) allowing more accurate estimation of MI extent