Left ventricular venting during coronary bypass operation.
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Biomedical subjects
Publications and source records attributed to H N Oldham.
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The incidence of ECG (14 per cent) indication of acute myocardial infarction complicating coronary artery bypass surgery is documented, corroborating the findings of prior series. An additional 32 per cent of patients had appearance of myocardial specific CPK-MB in serum during the immediate postoperative period. All patients surviving to 1 year following surgery (93 of 103) were asked to return for repeat cardiac catheterization to determine the presence and extent of interim ventricular contraction abnormalities. Sixty-five (70 per cent) of the group returned for evaluation. Preoperative and 1 year postoperative left ventriculograms were compared to determine if new contraction abnormalities would confirm the specificity of perioperative QRS and isoenzyme changes, and if the absence of new abnormalities would confirm their sensitivity. The majority of patients (65 per cent) had new areas of asynergy. However, 73 per cent of these were confined to the apex and thus could have been produced by the vent employed during cardiopulmonary bypass. QRS changes were 100 per cent specific and CPK-MB appearance was 78 per cent specific but they were only 20 and 54 per cent sensitive, respectively. Indeed, 46 per cent of those with new asynergy which was non apical had neither QRS change nor CPK-MB appearance. Thus QRS changes were always--and CPK-MB appearance was usually--associated with new asynergy but, in addition, many patients with no perioperative indication of infarction developed new areas of left ventricular contraction abnormality within the first postoperative year.
The clinical course of most patients with pulmonary embolism is one of gradual resolution with re-establishment of flow in the pulmonary arteries. In a small but definite group of patients, the emboli do not resolve and a state of chronic pulmonary embolism ensues. The primary thrombotic process in the systemic venous system may persist, and in some instances may be unrecognized. Such patients experience recurrent showers of emboli which may ultimately occlude a large part of the pulmonary arterial circulation with development of severe respiratory insufficiency. Six patients with this syndrome are described, and in each there was a history of dyspnea, cyanoiss, and exercise intolerance associated with a low arterial PO2, right ventricular hypertrophy, and pulmonary hypertension. Pulmonary scans and arteriograms demonstrated that more than half of the major pulmonary arteries were occluded and, in addition, smaller vessels were also obstructed. Pulmonary embolectomy was performed in each patient. Five of the 6 obtained a highly gratifying response, including relief of the dyspnea and cyanosis, an increase in arterial PO2, and a decrease in pulmonary arterial pressure. In each of the five in whom improvement occurred, the back-bleeding from the pulmonary artery at the time of embolectomy was quite good. In the sixth patient, the back-bleeding was very poor, and despite embolectomy, the vessel thrombosed postoperatively with no improvement in the patient's clinical course. Follow-up studies in these patients range up to 8 years with demonstration of continued patency of the pulmonary arteries as well as continued improvement in clinical symptoms and in the arterial PO2.
Operative mortality for the first 787 patients who underwent aortocoronary bypass at Duke University Medical Center was 9.7%. Within 699 patients who underwent elective bypass only, operative mortality was 8.8% before January 1, 1972, and 5.4% subsequently. This apparent variation in operative mortality over time was largely a consequence of changing patterns of patient selection, i.e., a two- to three-fold decrease in the prevalence of ventricular dysfunction. Since January 1, 1972, operative mortality for 444 patients with mild or no heart failure who underwent elective bypass only was 5.0%. The 55 patients with left main disease had 12.7% operative mortality. In the 192 patients without left main disease who had one- or two-vessel disease, operative mortality was 1.0%, whereas, 197 patients with three-vessel disease had a 6.6% operative mortality. The 103 patients with three-vessel disease less than 50 years of age underwent operation with a 2.9% mortality. Although these results demonstrate that selected patients may undergo operation with a mortality approaching 1%, it is not clear that only such low risk patients should be offered surgery. Accurate estimates of benefits and risks of aortocoronary bypass surgery are necessary in the management of specific patients.
Ventriculograms made 9-15 months after surgery in 48 patients with normal preoperative apical contraction were reviewed to determine the influence of apical venting on apical wall motion in patients undergoing coronary bypass surgery. After interpretation of postoperative apical wall motion, the patients were subdivided into two groups. One group consisted of 34 patients who were vented by inserting a catheter through the apex of the left ventricle and the second group included 14 patients in whom no transventricular vent was made. The two groups were similar clinically and hemodynamically before surgery, and the surgical procedures were similar with the exception of vent site. Following surgery, incidences of graft patency and antegrade flow to the apex were also similar. Nineteen (56%) patients in the apically vented group had apical dyskinesia or akinesia observed on the postoperative ventriculogram while none of the patients who were not apically vented had these findings. None of the patients with apical dyskinesia or akinesia had congestive heart failure following surgery. The postoperative ventriculograms of 12 patients with mitral stenosis who underwent valvulotomy by inserting a Tubbs dilator through the apex were also analyzed. Only one patient (8.5%) had apical dyskinesia or akinesia. Since the patients with mitral stenosis probably did not have significant coronary artery disease, it is possible that the combination of the apical vent and ischemic heart disease was responsible for the focal contraction abnormalities observed.
Angiographic changes in the coronary circulation were evaluated in 60 patients 1 year after aortocoronary bypass surgery, and their relation to the postoperative clinical status was examined. Of 124 grafts implanted, 26 were closed, 7 stenotic and 91 (74 percent) patent at 1 year. Progression of occlusive disease occurred in 21 of 57 (37 percent) nongrafted and 78 of 123 (63 percent) grafted vessels. On the basis of location and severity of progression, significant lesions bypassed and patency of grafts, postoperative coronary perfusion was considered optimal in 16 patients (Group I), better in 24 (Group III). Complete freedom from chest pain or lessening of pain (improvement by two New York Heart Association functional classes) occurred in 88 and 79 percent of patients in Group III. Positive preoperative treadmill stress tests became negative after surgery in five of six patients in Group I, five of eight in Grojp II and three of eight in Group III. This study demonstrates that when progression of disease, graft patency and extent of revasculariztion are considered in combination, the postoperative angiographic status of the coronary circulation correlates well with clinical improvement at 1 year. These findings support the hypothesis that improved blood supply to ischemic myocardium is a major factor contributing to relief of angina pectoris after saphenous vein bypass surgery.
The ability of coronary collateral vessels to supply an adequate volume of blood to the subendocardium during the resting state and during periods of stress was studied. Regional myocardial blood flow was determined by the radioactive microsphere technique. Ameroid constricting devices were placed around the left circumflex coronary artery in 22 adult mongrel dogs. Three months later, regional myocardial blood flow was measured in a normal area of the left ventricle as well as in the area supplied entirely by coronary collateral vessels. Collateral blood flow was sufficient in the resting state to prevent myocardial ischemia distal to a gradually occluded coronary artery. However, in 10 animals (Group I) without aorta-coronary bypass grafts (ACBG), a selective underperfusion of the collateralized subendocardium occurred during periods of stress. In 12 animals (Group II), this selective underperfusion of the collateralized subendocardium with stress was abolished by placing ACBG's distal to the site of the coronary artery occlusion.
A case of ventricular aneurysm with refractory ventricular tachycardia is presented. Epicardial mapping was used to localize the site of earliest epicardial activity to the margin of the aneurysm, and subsequent resection of this area abolished the rhythm disturbance.
The evolution and transmural distribution of coronary collateral blood flow in acute myocardial infarction was determined in 24 trained, unanesthetized dogs by injection of radioactive microspheres into the coronary circulation. Acute coronary artery occlusion resulted in a greater decrease in subendocardial flow than subepicardial flow in both the central and marginal zones of the infarct. Coronary collateral blood flow was distributed primarily to the marginal zone and to the subepicardium of the central zone of the infarct. The greatest increase in collateral flow occured between 12 and 18 hours after coronary artery occlusion. By 24 hours after coronary occlusion, blood flow to all areas of the infarct except the subendocardium of the central zone had returned to near control levels. This dispropotionate distribution of coronary collateral blood flow during the early stages of myocardial ischemic injury helps to explain the apparent lack of protection of the subendocardium by collateral flow.
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