Occlusion Of Left Circumflex Artery Research Articles

Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs.

Cardiac prostaglandin release was studied in closed-chest dogs during acute coronary occlusion. Aortic and coronary sinus blood was obtained before, and at intervals after, balloon occlusion of the left anterior descending artery in seven dogs. Samples were assayed for prostaglandins F, E, and A by randioimmunoassay. All dogs demonstrated prostaglandin F release, Mean +/- SE postocclusion aortic levels were 0.26 +/- 0.01 ng/ml; coronary sinus levels were 0.67 +/- 0.01 ng/ml (P less than 0.001). In six dogs, prostaglandin E also was released. Mean postocclusion aortic levels were 0.24 +/- 0.01 ng/ml; coronary sinus, 0.44 +/- 0.01 ng/ml (P less than 0.001). There was no release of prostaglandin A. To examine the site of prostaglandin release, simultaneous samples from the aorta, the coronary sinus, and the great cardiac vein were obtained before and after left circumflex artery occlusion in six additional studies. The great cardiac vein drained effluent from nonischemic myocardium, whereas the coronary sinus drainage included blood from both ischemic and nonischemic zones. All six dogs demonstrated prostaglandin F release from the ischemic region. Mean postocclusion aortic prostaglandin F was 0.32 +/- 0.01 ng/ml. Coronary sinus prostaglandin F was 1.69 +/- 0.03 ng/ml (P less than 0.001), whereas the great cardiac vein level remained at 0.34 +/- 0.01 ng/ml (P greater than 0.05). Prostaglandin E was released from both ischemic and nonischemic regions. Mean aortic prostaglandin E was 0.21 +/- 0.01 ng/ml; great cardiac vein, 0.55 +/- 0.02 ng/ml (P less than 0.001); and coronary sinus, 1.07 +/- 0.04 ng/ml (P less than 0.001). These results have led us to conclude that the different local availability of prostaglandins E and F may influence the cardiac response to ischemia.

Correlation between segmental early relaxation of the left ventricular wall and coronary occlusive disease

Fifty of 305 patients studied angiographically had segmental early relaxation phenomenon (SERP) of the anterolateral or apical left ventricular wall. Fourteen of the 50 patients had cardiac abnormality other than, or in addition to, coronary occlusive disease. Of the remaining 36 patients, 35 had significant lesions in the left anterior descending artery (LAD) and one had occlusion of the proximal left circumflex artery. SERP was noted in 35 (37.2 per cent) of 94 patients with LAD disease who did not have severe anteroapical contraction abnormality. SERP was found in none of 49 patients who had neither significant coronary occlusive disease nor other cardiac abnormality. Eight patients were restudied after bypass grafting of the LAD. Three patients with patent grafts no longer demonstrated SERP. Five had persistent SERP, but four of these had occluded LAD grafts or nongrafted disease in other vessels supplying the anterolateral wall. Myocardial ischemia appears to be one cause, but probably not the only cause, of SERP.

Oxygen metabolism and oxygen debt repayment after myocardial ischemia.

Coronary blood flow, myocardial oxygen usage, and coronary venous lactate and pyruvate concentrations before and after release of left coronary or left circumflex artery occlusions (10–120 sec) were studied in anesthetized, open-chest dogs. Flow and oxygen theoretical debts were calculated from control blood flow and oxygen usage and compared to the repayments. Flow debts were usually overpaid for all durations of occlusion. Oxygen debts were repaid with an average excess of 1.0 and 3.5 cc after 15 and 30 sec but with a deficit of 0.4 cc for 10-sec left coronary artery occlusions. Excess lactate, as a measure of oxygen debt, was present after 50% of the 30-sec left coronary artery occlusions and after all of the 120-sec circumflex artery clampings. It was demonstrated that ischemia stimulates blood flow and myocardial oxygen consumption and increases oxygen availability. Results indicate that the myocardium can tolerate only brief periods of arterial occlusion but can develop and repay small oxygen debts.