In humans, basal myocardial blood flow remains constant regardless of the severity of coronary-artery stenosis. However, during hyperemia, flow progressively decreases when the degree of stenosis is about 40 percent or more and does not differ significantly from basal flow when stenosis is 80 percent or greater.

Background-Microvascular obstruction within an area of myocardial infarction indicates worse functional recovery and a higher risk of postinfarction complications. After prolonged coronary occlusion, contrast-enhanced MRI identifies myocardial infarction as a hyperenhanced region containing a hypoenhanced core. Because the time course of microvascular obstruction after infarction/reperfusion is unknown, we examined whether microvascular obstruction reaches its full extent shortly after reperfusion or shows significant progression over the following 2 days. Methods and Results-Seven dogs underwent 90-minute balloon occlusion of the left anterior descending coronary artery (LAD) followed by reflow. Gadolinium-DTPA-enhanced MRI performed at 2, 6, and 48 hours after reperfusion was compared with radioactive microsphere blood flow (MBF) measurements and myocardial staining to define microvascular obstruction (thioflavin S) and infarct size (triphenyltetrazolium chloride, TTC). The MRI hypoenhanced region increased 3-fold during 48 hours after reperfusion (3.2Ϯ1.8%, 6.7Ϯ4.4%, and 9.9Ϯ3.2% of left ventricular mass at 2, 6, and 48 hours, respectively, PϽ0.03) and correlated well with microvascular obstruction (MBF Ͻ50% of remote region, rϭ0.99 and thioflavin S, rϭ0.93). MRI hyperenhancement also increased (21.7Ϯ4.0%, 24.3Ϯ4.6%, and 28.8Ϯ5.1% at 2, 6, and 48 hours, PϽ0.006) and correlated well with infarct size by TTC (rϭ0.92). The microvascular obstruction/infarct size ratio increased from 13.0Ϯ4.8% to 22.6Ϯ8.9% and to 30.4Ϯ4.2% over 48 hours (Pϭ0.024). Conclusions-The extent of microvascular obstruction and the infarct size increase significantly over the first 48 hours after myocardial infarction. These results are consistent with progressive microvascular and myocardial injury well beyond coronary occlusion and reflow.

In patients with heart failure and reduced LVEF, chronic ACE inhibition with enalapril prevents progressive LV dilatation and systolic dysfunction (increased ESV). These effects probably result from a combination of altered remodeling and sustained reduction in preload and afterload.

In a subgroup of patients with noninfarcted collateral-dependent myocardium, immature or insufficiently developed collaterals do not provide adequate flow reserve. Despite nearly normal resting flow and oxygen consumption, these collateral-dependent segments exhibit chronically depressed wall motion and demonstrate marked ultrastructural alterations on morphological analysis. We propose that these alterations result from repeated episodes of ischemia as opposed to chronic hypoperfusion and represent the flow, metabolic, and morphological correlates of myocardial "hibernation."