Stable Angina
| Overview |
|---|
- Stable Angina is a distinct clinical manifestation of Ischemic Heart Disease characterized by chronic, episodic but fairly predictable pattern of anginal chest pain.
| Pathogenesis |
|---|
- The fundamental etiology of Stable Angina is the presence of an atherosclerotic plaque within a coronary artery. Stable Angina results from progressive narrowing of the coronary artery by the atherosclerotic plaque. This prevents sufficient blood flow from reaching the myocardium resulting in a mismatch between cardiac oxygen demand and cardiac blood flow, especially during contexts of physical or emotional exertion when myocardial oxygen demand is elevated. In addition to physical narrowing, the presence of an atherosclerotic plaque may also induce episodes of inappropriate coronary artery vasoconstriction resulting in further narrowing of the artery. Together, these processes result in mild, rapidly reversible myocardial ischemia which yields brief functional derangements of myocardial contraction and relaxation as discussed in Ischemic Heart Disease.
| Clinical Consequences |
|---|
- Chest Pain
- The symptomology of Stable Angina is dominated by fairly predictable episodes of anginal chest pain caused by physical or emotional exertion. Chest Pain is usually described as a diffuse discomfort, lasts only a few minutes, and is relieved with rest and relaxation. When coronary artery narrowing is mostly due to physical stenosis by the atherosclerotic plaque, a fixed exertional threshold is often described beyond which angina is predictably encountered. In some patients, coronary artery narrowing occurs mostly due to inappropriate plaque-induced vasoconstriction and in these situations angina is encountered following an unpredictable exertional threshold.
- Additional Symptoms
- During episodes of myocardial ischemia, brief functional derangements of ventricular function may occur yielding both defects in ventricular contraction and ejection. Defects in ventricular contraction may transiently lower cardiac output and thus cause reductions in systemic arterial pressure which via mechanisms Systemic Arterial Pressure - Short-term Regulation will activate the SNS, yielding tachycardia and diaphoresis. Defects in ventricular relaxation may result in backup of blood into the lung, causing mild pulmonary edema and thus dyspnea.
- Laboratory
- Because myocardial ischemia is brief and transient in stable angina, no ischemic necrosis takes place. Consequently, serum biomarkers of myocardial infarction are not present.