Unstable angina – definition and pathogenesis

Unstable angina – definition and pathogenesis

Unstable angina – definition and pathogenesis:

Definition of unstable angina

Following categories come under the group of unstable angina: Angina at rest, new-onset (less than 2 months) exertional angina and recent (less than 2 months) acceleration of angina in the form of lowering of threshold, increase in severity or new sites of radiation.

Likelihood of significant CAD in those presenting with symptoms suggestive of unstable angina

Likelihood of coronary artery disease (CAD) in those presenting with symptoms suggestive of unstable angina is higher in those with previous history of CAD, presence of risk factors for CAD, older age and
ST-T wave changes in ECG suggestive of ischemia.

Unstable angina – Precipitating factors

Following situations can precipitate unstable angina: Inappropriate tachycardia as in anemia, fever, hypoxia, tachyarrhythmias, thyrotoxicosis; High afterload as in aortic stenosis, hypertension and left ventricular hypertrophy; High preload as in high cardiac output and chamber dilatation; Inotropic states like use of sympathomimetic drugs.

Unstable angina – Prognostic indicators

Important prognostic indicators predicting poor prognosis in unstable angina are the presence of ST-T changes with pain; hemodynamic deterioration in the form of pulmonary edema, new onset mitral regurgitation, S3 and hypotension; left ventricular dysfunction, extensive CAD, age and comorbidities like diabetes mellitus, chronic obstructive pulmonary disease, renal failure and malignancy.

Unstable angina – Pathogenesis

The important pathogenic factors leading to unstable angina are plaque disruption, acute thrombosis and vasoconstriction in the coronary arteries. Plaque disruption can be active or passive.

Passive plaque disruption occurs in the soft plaque with high concentration of cholesteryl esters and a thin fibrous cap. Active plaque disruption occurs in macrophage-rich area with enzymes that may degrade and weaken the fibrous cap; predisposing it to rupture.

Acute thrombosis can occur in the vulnerable plaque and in systemic hypercoagulable states. The vulnerable plaque is disrupted plaque with ulceration. It occurs in 2/3 of unstable patients. The exposed lipid-rich core abundant in cholesteryl ester is highly thrombogenic. In systemic hypercoagulable states the plaque is disrupted plaque with erosion. This occurs in 1/3 of unstable patients.

Vasoconstriction of the culprit lesion occurs in response to deep arterial damage or plaque disruption in the area of dysfunctional endothelium near the culprit lesion. Platelet-dependent and thrombin-dependent vasoconstriction are mediated by serotonin and thromboxane A2.