Coronary Arterial Occlusion.

As discussed above, transmural acute MI results from a dynamic interaction among several or all of the following—coronary atherosclerosis, acute atheromatous plaque change (such as

rupture), superimposed platelet activation, thrombosis, and vasospasm—resulting in an occlusive intracoronary thrombus overlying a disrupted plaque. In addition, either increased

myocardial demand (as with hypertrophy or tachycardia) or hemodynamic compromise (as with a drop in blood pressure) can worsen the situation. Recall also that collateral circulation

may provide perfusion to ischemic zones from a relatively unobstructed branch of the coronary tree, bypassing the point of obstruction and protecting against the effects of an acute

coronary occlusion.

In the typical case of MI, the following sequence of events can be proposed:

• The initial event is a sudden change in the morphology of an atheromatous plaque, that is, disruption—manifest as intraplaque hemorrhage, erosion or ulceration, or rupture or

fissuring.

• Exposed to subendothelial collagen and necrotic plaque contents, platelets undergo adhesion, aggregation, activation, and release of potent aggregators including thromboxane

A2 , serotonin, and platelet factors 3 and 4.

• Vasospasm is stimulated by platelet aggregation and the release of mediators.

• Other mediators activate the extrinsic pathway of coagulation, adding to the bulk of the thrombus.

• Frequently within minutes, the thrombus evolves to completely occlude the lumen of the coronary vessel.

The evidence for this sequence is compelling and derives from (1) autopsy studies of patients dying with acute MI, (2) angiographic studies demonstrating a high frequency of thrombotic

occlusion early after MI, (3) the high success rate of therapeutic thrombolysis and primary angioplasty, and (4) the demonstration of residual disrupted atherosclerotic lesions by

angiography after thrombolysis. Although coronary angiography performed within 4 hours of the onset of apparent MI shows a thrombosed coronary artery in almost 90% of cases, the

observation of occlusion is seen in only about 60% when angiography is delayed until 12 to 24 hours after onset. [54] Thus with the passage of time, at least some occlusions appear to clear

spontaneously owing to lysis of the thrombus or relaxation of spasm or both.

In approximately 10% of cases, transmural acute MI is not associated with atherosclerotic plaque thrombosis stimulated by disruption. In such situations, other mechanisms may be

involved:

• Vasospasm: isolated, intense, and relatively prolonged, with or without coronary atherosclerosis, perhaps in association with platelet aggregation (sometimes related to cocaine

abuse).

• Emboli: from the left atrium in association with atrial fibrillation, a left-sided mural thrombus or vegetative endocarditis; or paradoxical emboli from the right side of the heart or

the peripheral veins which cross to the systemic circulation, through a patent foramen ovale, causing coronary occlusion.

• Unexplained: cases without detectable coronary atherosclerosis and thrombosis may be caused by diseases of small intramural coronary vessels such as vasculitis, hematologic

abnormalities such as hemoglobinopathies, amyloid deposition in vascular walls, or other unusual disorders, such as vascular dissection and inadequate protection during cardiac

surgery.

Date: 2016-04-22; view: 927