Biomedical subjects

V LiPreti

Publications and source records attributed to V LiPreti.

3 recordsLinked to original sources

PubMed1990

Comparison of proximal left anterior descending and circumflex coronary artery dimensions in aortic valve stenosis and hypertrophic cardiomyopathy.

To examine the "adequacy" of basal coronary flow in ventricular hypertrophy, the relation between proximal coronary artery dimensions and regional ventricular mass in aortic valve stenosis (AS) and hypertrophic cardiomyopathy (HC) was evaluated. Coronary artery size was determined by quantitative coronary arteriography while global/regional ventricular mass was calculated using computer-processed biplane 2-dimensional echocardiography. In comparison to 18 "normal" subjects, left anterior descending coronary dimensions were significantly larger in those with hypertrophy (normal 3.32 +/- 0.54, AS 3.82 +/- 0.71, HC 4.72 +/- 0.81 mm, p less than 0.05), with progressive increases in left anterior descending/circumflex coronary diameter ratios (normal 1.04 +/- 0.14, AS 1.18 +/- 0.19, HC 1.25 +/- 0.31, p less than 0.01). Compared to the AS group, indexed anteroseptal mass was greater in the HC subjects (AS 40.9 +/- 8.9 vs HC 72.1 +/- 21 g/m2, p less than 0.001). Both septal width/left anterior descending coronary diameter ratios (AS 3.61 +/- 1.06 vs HC 4.85 +/- 1.17 mm/mm, p less than 0.05) and indexed anteroseptal mass/left anterior descending coronary diameter ratios (AS 11.2 +/- 3.0 vs HC 15.6 +/- 3.4 g/m2/mm, p less than 0.01) were greater in HC subjects. Increased coronary dimensions were observed in both AS and HC, with the greatest changes noted within the left anterior descending distribution in HC, but when analyzed with respect to regional ventricular mass, these subjects demonstrated relative "inadequate" enlargement in coronary artery diameters. Underdeveloped epicardial coronary arteries may contribute to anteroseptal myocardial ischemia, with resultant angina pectoris, increased ventricular ectopic activity and sudden death in HC.

Aged↗

PubMed1989

Quantitative arteriographic responses to ergonovine provocation in subjects with atypical chest pain.

To evaluate the nonspecific vasoconstrictor response to intravenous ergonovine, and identify patient-related factors that systematically alter changes in coronary dimensions, 33 subjects (22 women, 11 men), mean age 54 years (range 39 to 70) were studied using a standardized ergonovine provocation test (Stanford protocol). Clinical responses, systemic hemodynamics and electrocardiographic changes were determined, with quantitative arteriography used for sequential measurement of proximal right coronary dimensions. A progressive decrease in proximal right coronary diameter was observed, with average control values and final diameters equaling 3.25 +/- 0.49 and 2.56 +/- 0.49 mm, respectively, thus representing an overall -21.2% change from baseline. No significant differences existed in control dimensions when analyzed with respect to gender (3.20 +/- 0.59 vs 3.40 +/- 0.72 mm, women vs men, difference not significant), although women demonstrated a greater decrease from baseline values (0.80 +/- 0.30 vs 0.50 +/- 0.24 mm, women vs men, p less than 0.05). The presence of minor atherosclerotic disease, as determined by the presence of minor (less than 30% diameter) luminal irregularities within the right coronary artery, failed to alter control dimensions (3.30 +/- 0.48 vs 3.20 +/- 0.51 mm, normal vs atherosclerotic persons, difference not significant), but was associated with more ergonovine-induced coronary vasospasm (0.41 +/- 0.27 vs 0.84 +/- 0.21 mm, normal vs atherosclerotic persons, p less than 0.01). Therefore, sequential intravenous ergonovine maleate infusion resulted in progressive, nonspecific reductions in proximal right coronary artery dimensions in subjects without a history compatible with vasospastic angina. This nonspecific vasoconstrictor effect was accentuated in women and subjects with intimal irregularities suggestive of minor atherosclerotic coronary disease.

Adult↗

PubMed1989

Comparative evaluation of coronary stenoses using fluid dynamic equations and standard quantitative coronary arteriography.

Traditional quantitative coronary arteriographic measurements have largely ignored geometric variables, which may be important in determining the obstructive nature of coronary stenoses. To illustrate the relation between standard quantitative coronary arteriography and calculated transstenotic fluid dynamics, 25 patients with 1-vessel disease referred for coronary angioplasty were analyzed. Minimal lumen diameter and percent stenosis were measured and the values compared with calculations of pressure loss that used standard hydraulic formulas encompassing both frictional and separation components within the stenotic segments. Baseline flow velocity was assumed to equal 4 cm/s and normal hyperemic flow response was presumed to equal 5 times that of baseline. Fluid dynamic estimates suggested that initial translesional pressure gradients would develop at a minimal diameter of 0.6 mm (80% diameter), with an exponentially severe pressure differential beyond a minimal coronary diameter of 0.3 mm (92% diameter). Maximal velocities were calculated based upon an assumed normal hyperemic flow response of 5 times that of baseline, with the demonstration of early impairment of hyperemic flow reserve at minimal diameters of 1.2 mm (46% diameter). Furthermore, hyperemic flow reserve was completely abolished at a minimal diameter of 0.3 to 0.5 mm (89 to 92% diameter). Beyond a minimal diameter of 0.2 mm (93% diameter), resting hypoperfusion was anticipated with flow velocities below the initially assumed value (4 cm/s). Thus, it is feasible to estimate transstenotic pressure losses and maximal coronary flow velocity by applying Newtonian fluid dynamic equations to actual angiographic stenoses in man. These calculations generally correlate with traditional quantitative arteriographic estimates of stenosis severity, although other geometric parameters such as lesion length, "exit angle" and blood viscosity may alter transstenotic hemodynamics.

Blood Flow Velocity↗