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S V Rosenthal

Publications and source records attributed to S V Rosenthal.

9 recordsLinked to original sources

Evolutionary changes in left and right ventricular function in acute myocardial infarction.

To determine the evolutionary changes in right and left ventricular function in acute myocardial infarction, 3 serial gated blood pool scans were performed in 76 patients within 24 hours (24 H), at 10 days (10 D) and 3 months (3 M) following the onset of myocardial infarction. The patients were divided into 3 groups: ANT (anterior MI), INF (inferior MI without right ventricular dysfunction) and RVF (inferior MI with right ventricular dysfunction). LVEF in ANT was significantly lower than that of INF and RVF at 24 H, 10 D and 3 M. The ratio of right ventricular volume to LV volume (RVV/LVV) was compared among 3 groups. The mean values of RVV/LVV in RVF were 1.3 through 24 H and 3 M and they were significantly higher than the other two groups. The RVV/LVV in ANT and INF were around 1.0. LVEDVI in RVF was rather smaller than that of ANT and INF. LVESVI in ANT at 24 H was significantly larger than that of INF and RVF and the mean value of LVESVI in ANT were around 60 ml/M2 from 24 H to 3 M. LVEF in ANT, RVF and INF did not increase significantly during peak exercise at 3 M. However, quantitative regional wall motion analysis revealed that regional wall motion of R2 (posterolateral wall motion) in ANT and R5 (septal wall motion) in INF decreased significantly during peak exercise. These impairments in regional wall motion might be due to the exacerbation of ischemia of non-infarcted area.

Adult↗

Global and regional function in the regionally ischaemic left ventricle related to plasma ionised calcium.

To study the response of function in the regionally ischaemic left ventricle to increased and decreased concentrations of plasma ionised calcium, twenty-two anaesthetised dogs were placed on right heart bypass with constant mean aortic pressure and heart rate. Regional (sonomicrometry) and global left ventricular function were assessed before coronary artery ligation. Then, following ligation, function after 45 min stable ionised hypercalcaemia [( Ca2+] = 1.68 +/- 0.01 mmol x litre-1) and hypocalcaemia [( Ca2+] = 0.73 +/- 0.02 mmol x litre-1) were each compared to function during an immediately preceding normocalcaemic period. Control of cardiac output enabled paired comparisons to be made at matched preloads: systolic shortening from common end-diastolic chord lengths (n = 10), and stroke work at common left ventricular end-diastolic pressures (n = 22). With hypercalcaemia, systolic shortening in the ischaemic region (2.11 +/- 0.39 mm preligation) increased from -0.62 +/- 0.17 to -0.04 +/- 0.20 mm (P less than 0.01), whereas in the control region systolic shortening increased from 1.47 +/- 0.12 to 2.00 +/- 0.15 mm (P less than 0.01) reaching its preligation value (1.67 +/- 0.13 mm). Stroke work at a left ventricular end-diastolic pressure of 1.37 kPa increased (0.248 +/- 0.019 to 0.299 +/- 0.021 joules x beat-1, P less than 0.001) but not to preligation levels (0.364 +/- 0.016 joules x beat-1). Hypercalcaemia also increased myocardial oxygen consumption (by 1.0 +/- 0.3 cm3 x min-1 x 100 g-1, P less than 0.005) but not coronary blood flow. With hypocalcaemia, systolic shortening decreased in ischaemic and control regions, global function curves were markedly depressed, and myocardial oxygen consumption did not change but coronary blood flow increased. Thus hypercalcaemia improved function in ischaemic and control regions but improvement in the ischaemic region was small compared with the depression associated with ischaemia itself. Hypercalcaemia also improved global function, but not to preischaemic levels, at an increased oxygen cost.

Animals↗