Pathophysiological Difference between Stable Angina and Unstable Angina

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Pathophysiological Difference between Stable Angina and Unstable Angina

Angina is the clinical indicator of imbalance between oxygen demand and myocardial blood supply.  Stable angina is caused by atherosclerosis and can be precipitated by cold, emotion, stress, eating, or exercise. It progresses to pre-infarction, also known as unstable angina. Crawfold (1997) notes that unstable angina is a clinical syndrome characterized by increased severity and rate of angina pectoris attacks but not always complemented with ECG changes. It occurs when there is superficial erosion or fissuring of plaque leading to temporary episodes of vasoconstriction and thrombotic vessel occlusion of the plaque damaged site. 

Often, the atherosclerotic develops to surface disruption of small fissures that initiate the thrombosis process. Its symptoms occur when the lumen is transiently occluded by thrombus and improve when thrombus lysis spontaneously re-establishes partial blood flow. In additional to thrombosis it leads to occurrence of vasoconstriction which is produced by the platelet-mediated discharge of TXA2 (Kusumoto, 1999). The exact mechanism causing initial plaque instability is not known with some studies suggesting that disrupted atherosclerotic plaque is associated with an increased number of monocytes and macrophages. There is a possibility of collagen macrophage degradation causing plaque disruption.

In stable angina, the association between demand or workload and ischemia is relatively predictable. Conversely atherosclerotic arterial constricting is not entirely fixed. It differs with the normal variations in arterial tone that occur in all people (Kusumoto, 1999). Many people have angina in the morning while arterial tone is moderately high. Similarly, abnormal endothelial function contributes to arterial tone variation, for example, in endothelium impaired by atheroma. Catecholamine surge stresses cause vasoconstriction rather than dilation. As the myocardium grow into the ischemic, the blood PH of the coronary sinus falls, lactase accumulates, cellular K is lost, the appearance of ECG changes, and ventricular function deteriorates. During angina, the left ventricular (LV) diastolic pressure increases, occasionally inducing dyspnea and pulmonary congestion.

References

Crawford, M. (1997). Unstable angina. New York: Chapman & Hall. 

Kusumoto, F. M. (1999). Cardiovascular pathophysiology. Raleigh, N.C: Hayes Barton Press.