Histological alterations of the human myocardium during minimally invasive direct coronary artery bypass operation

To study the ischaemia caused to myocardial cells during the Minimally Invasive DirectCoronary Artery Bypass (MIDCAB) procedure,ten patients underwent surgical revascularizationof the anterior descending artery using the MIDCAB technique. During the anastomosis, the left anterior descending (LAD) was snared with two sutures 4-0 prolene.The time of ischaemia was 13-22 min (mean 16.4 min). Three biopsies were taken from the anteroapical part of the left ventricle: a) Prior to the ischaemia b) At the end of theischaemic period c) 25 minutes after bloodflow had been restored. The degree of cellular and perivascular damage was studied by electron microscopy.Simultaneously, an electrocardiogram (ECG)was performed and the biochemical markers of myocardial ischaemia were measured.There were no deaths or myocardial infarctions.Slight ischaemic changes were found in all tissue samples before occlusion of the LAD. A semiquantitative analysis showed that a large percentage of myocytes (83.5-90%) in all phases were normal or only slight changes. A few myocytes (3-6%) were severely or irreversibly damaged. The morphometric analysisof mitochondrial oedema revealed no statisticallysignificant differences. In conclusion, the MIDCAB technique can be applied for the surgical revascularization of the LAD without significant ischaemic changes to the myocardial cells (AU)

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Constrictive pericarditis after coronary artery bypass surgery as a cause of unexplained dyspnea: a report of five cases.

Constrictive pericarditis after coronary artery bypass grafting (CABG) is rare and can present as unexplained dyspnea. We report five consecutive cases of post-CABG constrictive pericarditis seen within a period of 17 months at our institution. All patients presented with heart failure of unknown etiology within a period of 8-84 months after surgery. During the initial post-CABG period, two patients had developed postcardiotomy syndrome that was successfully treated with steroids. They were all assessed noninvasively and invasively. In all patients, the diagnosis of constriction was initially suspected clinically (symptoms, high jugular venous pressure with deep "X" and "Y" descents, pericardial knock). Echocardiography showed transmitral flow typical of constriction in all patients and hepatic venous flow in two. Two patients showed rapid left ventricular relaxation. In all patients, hemodynamic assessment showed diastolic equalization of pressures in all chambers, "W" shape waveform in right atrial pressure, and "dip and plateau" configuration in right and left ventricular pressure waveforms. Diagnosis was confirmed surgically in four patients who were subjected to pericardiectomy-pericardial stripping (three survived, one died). One patient refused surgery. We conclude that constrictive pericarditis, although rare, should be suspected in every case of unexplained dyspnea post CABG. It can appear early or late after surgery, and clinical examination plays an important role in its early recognition. It requires a full noninvasive and invasive assessment in case of clinical suspicion.