Acute Coronary Syndromes : Pathophysiology, Diagnosis, Treatment

Sunday, November 24th 2013. | Disease

Acute coronary syndromes (ACSs) include all clinical syndromes compatible with acute myocardial ischemia resulting from an imbalance between myocardial oxygen demand and supply.

ACSs are classified according to electrocardiographic (ECG) changes into (1) ST-segment-elevation ACS (ST-elevation myocardial infarction [STEMI]) and (2) non-ST-segment-elevation ACS (non-ST-elevation myocardial infarction [NSTEMI] and unstable angina [UA]).


Pathophysiology of Acute Coronary Syndromes :

The formation of atherosclerotic plaques is the underlying cause of coronary artery disease (CAD) and ACS in most patients. Endothelial dysfunction leads to the formation of fatty streaks in the coronary arteries and eventually to atherosclerotic plaques. Factors responsible for development of atherosclerosis include hypertension, age, male gender, tobacco use, diabetes mellitus, obesity, elevated plasma homocysteine concentrations, and dyslipidemia.

The cause of ACS in more than 90% of patients is rupture of an atheromatous plaque. Plaques most susceptible to rupture have an eccentric shape, thin fibrous cap, large fatty core, high content of inflammatory cells such as macrophages and lymphocytes, and limited amounts of smooth muscle.

Diagnosis of Acute Coronary Syndrome :

Patient symptoms, past medical history, ECG, and troponin or CK-MB determinations are used to stratify patients into low, medium, or high risk of death or MI or likelihood of needing urgent coronary angiography and percutaneous coronary intervention (PCI).

A 12-lead ECG should be obtained within 10 minutes of patient presentation. Key findings indicating myocardial ischemia or MI are ST-segment elevation, ST-segment depression, and T-wave inversion (see Figure 5-1). These changes in certain groupings of leads help to identify the location of the involved coronary artery. The appearance of a new left bundle branch block accompanied by chest discomfort is highly specific for acute MI. Some patients with myocardial ischemia have no ECG changes, so biochemical markers and other risk factors for CAD should be assessed to determine the patient’s risk for experiencing a new MI or other complications.

Treatment of Acute Coronary Syndrome :

General treatment measures include hospital admission, oxygen administration if saturation is less than 90%, continuous multilead ST-segment monitoring for arrhythmias and ischemia, frequent measurement of vital signs, bedrest for 12 hours in hemodynamically stable patients, use of stools softeners to avoid Valsalva maneuver, and pain relief.

For patients with ST-segment-elevation ACS, either fibrinolysis or primary PCI (with either balloon angioplasty or stent placement) is the treatment of choice for reestablishing coronary artery blood flow when the patient presents within 3 hours of symptom onset. Primary PCI may be associated with a lower mortality rate than fibrinolysis, possibly because PCI opens more than 90% of coronary arteries compared with less than 60% opened with fibrinolytics. The risks of intracranial hemorrhage and major bleeding are also lower with PCI than with fibrinolysis. Primary PCI is generally preferred if institutions have skilled interventional cardiologists and other necessary facilities, in patients with cardiogenic shock, in patients with contraindications to fibrinolytics, and in patients presenting with symptom onset more than 3 hours prior. in patients presenting with symptom onset more than 3 hours prior.

In patients with non-ST-segment-elevation ACS, clinical practice guidelines recommend either PCI or coronary artery bypass grafting (CABG) revascularization as an early treatment for high- and moderate-risk patients. An early invasive approach results in fewer MIs, less need for revascularization procedures over the next year after hospitalization, and lower cost than a conservative medical stabilization approach.


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