Effects of platelet transfusion on post cardiopulmonary bypass bleeding.

A common complication of cardiopulmonary bypass (CPB) surgery is post-operative bleeding that may result in re-exploration. Bleeding is often due to the coagulopathy that follows the procedure, rather than the surgical technique. Etiology of this coagulopathy has been attributed to platelet dysfunction. We reviewed the medical records of 592 patients who had undergone CPB surgery between 1992 and 1994. Bleeding times (both pre and post operative) in treated (those who received platelets) and untreated patients were recorded where available. Both groups showed a rise in bleeding time (295 sec versus 192 sec, respectively, p<0.001). However, the treated group had a greater increase in the bleeding time compared to the un-treated (p<0.05). The result was the same when we compared 2 subgroups with similar pre-operative bleeding times. When the treated group was subdivided into those who received >10 units of platelets and those who received <10 units, there was no significant difference in the increase in their bleeding times (p>0.1). Administration of platelets did not improve bleeding time abnormalities induced by CPB. Both treated and untreated groups had a significant rise in their bleeding times, irrespective of the amount of platelets administered. The mean rise in the bleeding time in patients who bled significantly to require surgical re-exploration (but did not receive platelets) was not significantly different from those who received platelets. These observations suggest that the administration of platelets has no clinical benefit in improving bleeding time following CPB.

Scanning electron microscopic changes in the morphology of rabbit pulmonary tissue biopsied following ischemia and reperfusion: a window of opportunity?

Reperfusion is known to cause tissue damage in ischemic pulmonary tissue. We investigated the time frame of this occurrence by examining electron microscopic changes in lung tissue. Isolated, perfused, and ventilated rabbit lungs (and heart) were placed en bloc in a 37 degrees C chamber and perfused through the pulmonary artery at 15 mm Hg pressure with oxygenated Krebs-Henseleit buffer, pH 7.4, 70 ml min(-1), for 20 min and the pulmonary pump and ventilator were stopped. The resultant ischemic state was maintained for 2 h, and reperfusion resumed with the same buffer. The lungs of four groups of rabbits (n = 5 per group) were each subjected to 30 min, 1, 2, and 4 h of reperfusion respectively. Upon completion, lungs were biopsied for scanning electron microscopy. Ischemic damage including the loss of lung architecture, and edema were seen. Reperfusion restored some of the tissue anatomy and the return to normalcy increased up to 1 h of reperfusion after which the damage increased with time. Results suggest that damage due to ischemia alone may be reversible. Initial recovery is due to the re-establishment of circulation. However, with time, the damage seen may be due to free radicals and with 4 h of reperfusion, cell death may have occurred.

Incidence of postinfarction aneurysm within one month of infarct. Experiences with sixteen patients in Hawaii.

BACKGROUND: We report on sixteen patients with a left ventricular aneurysm presenting at less than a month following myocardial infarction. METHODS: All patients had significant left anterior descending coronary artery disease, and in eight cases (50%), this was the only significant pathology. Two patients who were treated conservatively, died within three months of infarction. RESULTS: Of the fourteen surgically treated patients, one died. There have been two late deaths, one at ten months and the other at four years postinfarction. Patients who present early after infarction, usually have a large anterior aneurysm, requiring early surgical repair with ventricular aneurysmectomy and revascularization. This group of patients showed a higher risk for major complications (such as thrombo-embolism, arrhythmias) and/or death. Emergency coronary artery bypass surgery may prove beneficial in the prevention of aneurysm formation by revascularizing the viable but ischemic tissue in that area.

Acute epicardial ECG parameters as quantitative predictors of infarct size at 1 week in the baboon.

We describe an experimental baboon model that allows quantitative prediction of myocardial necrosis measured at 1 week from acute epicardial ECG parameters recorded from a high-resolution matrix of fixed epicardial electrodes. The electrode grid overlies a circumscribed area of ultimate necrosis, produced by the occlusion of a selected diagonal branch of the left anterior descending coronary artery (LAD). This grid allowed examination of the pattern of changes in ST segment elevation (ST increases) throughout their return to control levels, and profiled changes in the distribution of electrodes recording TQ-ST segment deflections. Those points more centrally located within the area of ST increases consistently showed greater absolute values of ST increases and remained elevated longer than the more peripheral electrodes. Areas of the electrode matrix corresponding to those electrode points showing significant ST increases (2 mV above control) at each recording interval through 8 hr were fitted to the area of necrosis underlying this electrode grid. While the maximum area of ST increases (maxAst) uniformly overestimated infarct size between animals on the order of 25%, regression analysis allowed prediction of the extent of infarct from maxAst with an error of only 5%. Correlation of maxAst with the epicardial extent of infarct, total weight, and volume yielded coefficients of 0.95, 0.85, and 0.91 respectively, while mean ST increases (ST increases) showed a poorer correlation with respective coefficients of 0.49, 0.55, and 0.39. MaxAst proved to be the single best predictor of infarct size assessed at 1 week.