Consequences of Reduced Blood Flow to the Myocardium

Consequences of Atherosclerosis
1. Calcification, rigidity and increased fragility
2. Rupture of the fibrous cap exposing thrombogenic material to circulating platelets and coagulants leading to thrombosis. This would result in vessel occlusion and distal myocardial infarction (necrosis). Unstable angina and myocardial infarction
3. Plaque hemorrhage further narrowing the vessel lumen and occluding distal flow
4. Distal embolization of fragmented atheromatous plaque
5. Weakening of the vessel wall, wall expansion and dilatation (aneurysm)

Consequences of Reduced Blood Flow to the Myocardium
The duration and severity of ischemia will determine the fate of the compromised myocardium. Diastolic and systolic dysfunction are one of the first consequences of ischemia. This is followed by elevation of filling pressures, electrocardiographic changes and then, pain. Myocardial necrosis (infarction) is the final outcome of prolonged cessation of blood flow. The extent of myocardial necrosis depends upon the size of the territory supplied by the compromised vessel and the duration of antecedent ischemia to that territory. A sudden occlusion of the proximal left anterior descending coronary artery (LAD) has very grave consequences (an occlusion anecdotally termed the “widow maker”) due to the large size of myocardium perfused by the LAD. The damage incurred by a more distal lesion would be less profound. Complete occlusion of a vessel that had a preceding tight occlusion may result in a smaller myocardial infarction than one occurring in the absence of a tight stenosis. This is partly due to the time dependent formation of collateral circulation that circumvents the site of stenosis and leading to a process known as ischemic preconditioning. Recurrent ischemia results in changes that attenuate the impact of the final complete occlusion. The myocardium supplied by a tightly stenosed vessel may display impaired contractility even if it did not suffer irreversible injury. This is called hibernating myocardium and is important to identify. Restoration of blood flow would restore myocardial function and improve the overall ejection fraction. This should be distinguished from stunned myocardium. Stunned myocardium is myocardium with reversibly impaired contractility that lies adjacent to irreversibly damaged myocardium immediately after an infarction despite restoration of coronary blood flow, resolution of pain and ischemic electrocardiographic changes. With time, myocardial contractility to the stunned segment returns to its former function. Shortly after a myocardial infarction, the segment of infracted myocardium undergoes expansion due to dilation and thinning without further loss of myocardium. This may result in aneurysm formation, and a shift in the hemodynamic forces to the healthier myocardial segments. This results in dilatation of the non infracted segments where by increasing stretch, it compensates for the loss in inotropy caused by the loss of myocardial cells. These changes are collectively called remodeling. While short-term, these changes are using the Frank-Sterling laws to enhance cardiac output and compensate for the loss the heart has suffered, long-term these changes are detrimental. Many of the recently introduced interventions are aimed at preventing or minimizing the impact remodeling has on the heart. These include the early use of angiotensin converting enzyme inhibitors and early revascularization to minimize the size of infracted myocardium.