Thus, if blood flow is restored before irreversible injury occurs, myocardium can be preserved; this is the goal of early diagnosis and prompt intervention by thrombolysis or angioplasty. However, as discussed later, reperfusion can have deleterious effects. Even if reperfusion is timely, postischemic myocardium can be profoundly dysfunctional for a number of days due to persistent abnormalities in cellular biochemistry that result in a noncontractile state (stunned myocardium). Such stunning can be severe enough to produce transient but reversible cardiac failure.
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PulmonaryarteryAortaLeft circumflex coronary artery Right coronary artery Left anterior descending coronary artery Acute coronary arterial occlusion Zone of perfusion (area at risk) Cross-section of myocardium Obstructed coronary artery Endocardium Zone of perfusion (area at risk) Zone of necrosis Zone of necrosis Completed infarct involving nearly the entire area at risk 0 hr 2 hr 24 hr
Fig. 11.8 Progressionofmyocardialnecrosisaftercoronaryarteryocclusion.Atransmuralsegmentofmyocardiumthatisdependentontheoccludedvesselforperfusionconstitutestheareaatrisk(outlined). Necrosisbeginsinthesubendocardialregioninthecenteroftheischemiczoneandwithtimeexpandstoinvolvetheentirewallthickness.Notethataverynarrowzoneofmyocardiumimmediatelybeneaththeendocardiumissparedfromnecrosisbecauseitcanbeoxygenatedbydiffusionfromtheventricle.
Myocardial ischemia also contributes to arrhythmias, probably by causing electrical instability (irritability) of ischemic regions of the heart. Although massive myocardial damage can cause a fatal mechanical failure, sudden cardiac death in the setting of myocardial ischemia most often (in 80% to 90% of cases) is due to ventricular fibrillation caused by myocardial irritability.
Irreversible injury of ischemic myocytes first occurs in the subendocardial zone (
Fig. 11.8 ). As already mentioned, this region is especially susceptible to ischemia because it is the last area to receive blood delivered by the epicardial vessels, and also because it is exposed to relatively high intramural pressures, which act to impede the inflow of blood. With more prolonged ischemia, a wavefront of cell death moves through other regions of the myocardium, driven by progressive tissue edema and myocardial-derived reactive oxygen species and inflammatory mediators. An infarct usually achieves its full extent within 3 to 6 hours; in the absence of intervention, an infarct caused by occlusion of an epicardial vessel can involve the entire wall thickness (transmural infarct). Clinical intervention within this critical window of time can lessen the size of the infarct within the “territory at risk.”
The location, size, and morphologic features of an acute myocardial infarct depend on multiple factors:
Size and distribution of the involved vessel (
Fig. 11.9
Rate of development and duration of the occlusion
Metabolic demands of the myocardium (affected, for example, by blood pressure and heart rate)
Extent of collateral supply
Acute occlusion of the proximal left anterior descending (LAD) artery is the cause of 40% to 50% of all MIs and http://ebooksmedicine.net