In an angiographically defined study sample, ACE I/D gene polymorphism was not associated with an increased risk for coronary artery disease or myocardial infarction, despite its effects on plasma ACE activity.

Increased synthesis of endothelin, (a powerful physiological vasoconstrictor), is a uniform response to endothelial injury and has been associated with myocardial ischemia and reperfusion. This study tests the hypothesis that coronary artery bypass grafting (CABG) affects endothelin plasma concentrations in various vascular beds. Twenty-four CABG patients were included in this study. Endothelin was determined in multiple plasma specimens obtained from superior vena cava, aortic root and coronary sinus (CS). Venous endothelin plasma concentrations collected in CABG patients before surgery were 1.16 +/- 0.18 pg/ml. They increased after sternotomy (1.71 +/- 0.12 pg/ml) and during (2.97 +/- 0.27 pg/ml) and after cardiopulmonary bypass (CPB, 2.72 +/- 0.21 pg/ml). There is no net release of endothelin from the coronary circulation before (aorta 2.26 +/- 0.13 pg/ml vs CS 2.44 +/- 0.17 pg/ml, not significant (n.s.), during (cardioplegia 2.55 +/- 0.17 pg/ml vs CS 2.45 +/- 0.15 pg/ml, n.s.), and after aortic cross-clamping (aorta 2.95 +/- 0.23 pg/ml vs coronary sinus 2.71 +/- 0.18 pg/ml, n.s.). Pulmonary endothelin clearance is preserved on partial bypass (aorta 2.26 +/- 0.13 pg/ml vs vena cava 2.86 +/- 0.18 pg/ml, P < 0.003), but remains inhibited even 10-30 min after release of the aortic cross-clamp (aorta 2.95 +/- 0.23 pg/ml vs vena cava 2.97 +/- 0.27 pg/ml, n.s.). Two out of 24 patients had severe myocardial ischemia. These patients showed particularly high endothelin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Biochemical markers demonstrate significant postoperative cerebral injury during and immediately after CPB. However, CPB for CABG does not lead to marked impairment of neuropsychological scores, and clinically relevant neurological findings were observed in one patient only.

Severe local and systemic complications may occur after revascularization of extremities exposed to prolonged complete or incomplete ischaemia. These complications may be reduced by controlling the reperfusate and the circumstances of the reperfusion period. Ten adult German domestic pigs were exposed to 6 h of incomplete limb ischaemia by occlusion of the left iliac artery. To simulate the clinical situation of embolectomy, the occlusive snares were released after the ischaemic period in five pigs and normal blood flow developed with systemic pressure (uncontrolled reperfusion). In the other five pigs, a controlled reperfusate was delivered at controlled pressure before establishing normal blood reperfusion (controlled reperfusion). At the end of the observation period (90 min after start of reperfusion), the group with controlled reperfusion had a lower mean(s.e.m.) tissue water content (81.8(0.7) versus 84.3(0.7) per cent, P < 0.05, a greater increase in tissue adenosine 5'-triphosphate compared with values at the end of ischaemia (6.2(1.5) versus -2.5(1.8) mumol per g protein, P < 0.03), a higher tissue pH (7.2(0.1) versus 6.8(0.1), P < 0.03), a smaller temperature decrease (0.3(0.2) versus 1.2(0.3) degrees C, P < 0.05), lower concentrations of creatine kinase (355.0(87.5) versus 624.4(73.4) units/l, P < 0.05) and lactate dehydrogenase (LDH) (369.5(42.5) versus 538.4(39.2 units/l, P < 0.03) in the femoral vein blood and lower LDH concentrations (356.5(48.9) versus 546.0(37.8 units/l, P < 0.03) in central venous blood. These data indicate that severe local and systemic damage occurs with uncontrolled (normal blood) reperfusion even after incomplete limb ischaemia, and that these changes can be reduced by delivering a controlled reperfusate under controlled conditions.

Comparison was made in a cross-sectional study between 658 patients in whom coronary arteriography had shown (n = 304) or excluded coronary artery disease (CHD) (n = 354) and a clinically healthy group as controls (n = 1658), to assess possible risk factors. Patients aged 31-40 years with CHD had the highest total cholesterol levels (286 +/- 43 mg/dl) and the highest number of risk factors (3.6 +/- 0.9) compared to patients without CHD of the same age (204 +/- 30 mg/dl; 2.0 +/- 0.5) and healthy controls (216 +/- 45 mg/dl; 1.7 +/- 0.5) (P less than 0.001). In older patients with CHD, total cholesterol levels were lower (age group 61-70 years: 231 +/- 49 mg/dl), reaching about the same level as that of patients without CHD (232 +/- 54 mg/dl) or healthy controls of the same age (228 +/- 55 mg/dl). Furthermore, it was demonstrated that increased total cholesterol concentration can indicate the presence of other risk factors. It would thus appear that the level of total cholesterol in patients with CHD is decisively influenced by age and the presence of other risk factors.