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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 469 records · Page 26Linked to original sources
PubMedDate not supplied

Myocardial cell damage during attacks of vasospastic angina in the absence of persistent electrocardiographic changes.

We have investigated whether vasospastic anginal attacks might be associated with myocardial cell damage even when permanent ORS or ST-T changes are absent. We obtained serum time-activity curves of creatine kinase MB, of myoglobin, and of alpha hydroxybutyrate dehydrogenase in 15 patients with vasospastic angina admitted to our Coronary Care Unit (CCU). A slight but consistent rise and fall of both myoglobin and creatine kinase MB was observed in 7 patients (4 presented a definitive myocardial uptake of 99mTc pyrophosphate, and I had a faint deposition). A similar pattern was observed for myoglobin alone in 3 patients (1 presented a negative myocardial scan), while no consistent changes were found in the remaining 5 patients (2 presented a faint deposition of 99mTc pyrophosphate). No significant change of alpha hydroxybutyrate dehydrogenase was observed in any of the patients. The coherent rise and fall of the levels of myocardial cytosolic components after prolonged episodes of vasospastic angina suggests that cell damage may occur even in the absence of persistent QRS and ST-T changes.

Adult↗
PubMedDate not supplied

Effects of vasoactive stimuli on coronary vascular resistance in isolated perfused rabbit hearts: no vasospastic response to ergonovine with or without atherogenic diet.

The mechanism of ergonovine-provoked coronary vasospasm is poorly understood. We tested the effect of ergonovine in perfused hearts from normal and cholesterol-fed (18 weeks, 2% cholesterol diet) rabbits in a constant-flow Langendorff perfusion. Aortic perfusion pressure was monitored to measure coronary vascular resistance, and left ventricular pressure was measured with an isovolumetric balloon in the left ventricle. Control coronary vascular resistance was 1.12 +/- 0.11 mm Hg/ml/min in hearts from normal rabbits and 1.53 +/- 0.16 mm Hg/ml/min in hearts from cholesterol-fed rabbits (n = 9 each, mean +/- SEM, p less than 0.05). The cholesterol content of aortae from cholesterol-fed rabbits was markedly increased (432 +/- 85 mg/g protein vs. 14.9 +/- 8.2 in controls, p less than 0.001; for coronaries: 396 +/- 136 mg/g protein vs. 125 +/- 25, p less than 0.05). In both groups, increases in coronary vascular resistance were observed with vasopressin (40 IU/l) and phenylephrine (30 microM) and decreases with adenosine (10 microM), isoprenaline (0.1 microM) and 30 sec stop-flow (all p less than 0.05). Ergonovine maleate (10 microM) and serotonin (10 microM) did not increase coronary vascular resistance. Although in whole heart perfusion small changes in the caliber of epicardial vessels may not be detectable, changes severe enough to produce measurable changes in total coronary resistance were not found. Therefore the absence in our model of an increase in coronary vascular resistance after ergonovine is not compatible with a local direct mechanism in epicardial arterial wall, even when sensitized by a high cholesterol diet.

Animals↗
PubMedDate not supplied

Dipyridamole-induced increased glucose uptake in patients with single-vessel coronary artery disease assessed with PET.

BACKGROUND: The aim of this study was to determine the relationship between vasodilatation-induced ischemia and poststress glucose uptake. Coronary vasodilators may induce myocardial ischemia due to coronary steal through collateral circulation or transmural blood flow redistribution with diminished subendocardial perfusion. Myocardial ischemia can be demonstrated by increased glucose uptake as previously shown in patients with exercise-induced ischemia. METHODS AND RESULTS: We studied 11 patients with single-vessel disease and no history of myocardial infarction. Five patients had no collateral circulation, and 6 had angiographic evidence of collateral vessels. We measured myocardial blood flow (MBF) and glucose uptake at baseline and after the administration of dipyridamole (0.56 mg/kg) with positron emission tomography, using O-15 water and fluorine 18 deoxyglucose (FDG) as perfusion and glucose tracers. MBF at baseline was 0.82 +/- 0.13 mL/g/min in normal areas and 0.80 +/- 0.15 mL/g/min in areas supplied by stenotic arteries. MBF during dipyridamole was 2.05 +/- 0.66 and 1.19 +/- 0.66 mL/g/min in normal areas and areas with stenotic arteries, respectively (P < or = .001). FDG uptake at baseline was 1.36 +/- 0.55 in normal areas and 1.57 +/- 0.62 in areas supplied by stenotic arteries. FDG uptake after dipyridamole infusion was 1.79 +/- 1.1 and 4.04 +/- 0.84 in normal areas and areas with stenotic arteries, respectively (P < or =.001). MBF and FDG uptake were not different between patients with collateral circulation and those without collateral circulation. CONCLUSIONS: Increased myocardial glucose uptake was consistently observed after dipyridamole administration in those areas with diminished coronary vasodilatory capacity. The similar MBF and FDG findings in patients with and without collateral circulation may indicate that transmural blood flow redistribution appears to be a possible mechanism of dipyridamole-induced myocardial ischemia.

Blood Glucose↗