28 research outputs found
Fatal cerebral embolism following aorto-coronary bypass graft surgery.
In a case of fatal cerebral embolic infarction following aorto-coronary bypass graft (ACBG) surgery, postmortem examination revealed thrombosis of the vein grafts to the left circumflex and left anterior descending coronary arteries. Continguous with the thrombus in the graft to the circumflex artery was thrombotic material adherent to the aortic sutures and extending several millimeters into the lumen of the aorta. A nonadherent thrombus of similar histologic character was found in the right middle cerebral artery, associated with localized brain infarction. In addition to the risks of cerebral complication associated with other types of open-heart surgery, the location of the vein grafts in patients undergoing ACBG operations seems to offer a unique mechansim for the occurrence of systemic and cerebral embolism, which may be operational in other cases.</jats:p
Regional myocardial wall thickening response to nitroglycerin. A predictor of myocardial response to aortocoronary bypass surgery.
The peak rate of systolic wall thickening (p +/- dTw/dt) in regions of the left ventricle (LV) was determined preoperatively by biplane roentgen videometry in 18 patients before and after sublingual administration of nitroglycerin (NTG) and 3-23 months (median 12) after aortocoronary bypass surgery. The regional LV response to NTG was a reliable predictor for postoperative improvement in regional wall dynamics after successful aortocoronary bypass grafting. The ejection fraction response to NTG or surgery will not predict the regional myocardial response to NTG or surgery, nor will the regional response predict the global response. Subendocardial myocardial infarction is another cause of unimproved regional myocardial function after NTG and aortocoronary bypass surgery.</jats:p
Videometric analysis of regional left ventricular function before and after aortocoronary artery bypass surgery: correlation of peak rate of myocardial wall thickening with late postoperative graft flows.
The peak rate of systolic wall thickening (pdTw/dt) in regions of the left ventricle was determined by biplane roentgen videometry in 60 patients before and a median of 14 mo after aorto-coronary bypass graft surgery. The left ventricular ejection fraction, stroke volume, and end-diastolic volume and pressure did not change significantly after surgery in the presence of patent or occluded grafts (P greater than 0.05). Statistically significant increases occurred in the peak rate of systolic wall thickening regions supplied by patent bypass grafts, and significant decreases occurred in regions with occluded grafts (P less than 0.01). Of 42 preoperatively hypokinetic regions (pdTw/dt greater than 0 less than 5.0 cm/s) supplied by a patent graft, 30 improved by an average of 2.6 cm/s after operation; 18 returned to normal. Failure of 24 hypokinetic regions to improve to normal was associated with myocardial infarction in 11 or with late postoperative graft blood flows of less than 60 ml/min measured by videodensitometry, in 10. All seven preoperatively akinetic (pdTw/dt=0) or dyskinetic (pdTw/dt less than 0) regions did not improve after the operation despite the fact that, in five of the seven, coronary bypass flows were over 60 ml/min. All eight preoperatively hypokinetic regions supplied by coronary artery graft flows of less than or equal 40 ml/min failed to improve to normal after operation. All nine preoperatively hypokinetic regions supplied by coronary artery graft flows of over 60 ml/min improved to normal after surgery. Late postoperative coronary artery bypass graft flows, the functional status of the myocardium, the status and distribution of the native coronary circulation, and decreased regional function elsewhere in the ventricle must all be considered when regional left ventricular function is interpreted
