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Biomedical subjects

C A Lefkowitz

Publications and source records attributed to C A Lefkowitz.

8 recordsLinked to original sources
PubMed1991

Left ventricular functional response to moderate and intense exercise.

The left ventricular (LV) volume and ejection fraction (EF) response to upright exercise was assessed on 15 normal subjects during cycle ergometry. Measures of cardiac function and gas exchange were made at rest, at 85% of the ventilatory anaerobic threshold (VAT; WL1), and at peak exercise (WL2). EF increased from rest (58 +/- 12%) during WL1 (66 +/- 10%), reaching significantly higher values at WL2 (69 +/- 8%; p less than .05). End-diastolic volume increased from rest during WL1 (136 +/- 36 ml vs. 118 +/- 32 ml; p less than .05), becoming significantly higher than rest during WL2 (141 +/- 41 ml). End-systolic volume was unchanged from rest (51 +/- 25 ml) during submaximal exercise (50 +/- 20 ml), but it decreased significantly during WL2 (44 +/- 21 ml; p less than .05). The systolic pressure/end-systolic volume ratio increased from 3.0 +/- 1.7 (rest) to 5.8 +/- 3.0 at WL2 (p less than .05). These results suggest that the Frank-Starling mechanism is operative throughout exercise, particularly during exercise below the VAT. LV performance after the VAT is further augmented by increased contractility with continued, yet diminished, utilization of the Frank-Starling mechanism.

Adult↗
PubMed1990

Augmentation of regional function in nonischemic myocardium during coronary occlusion measured with two-dimensional echocardiography.

Increased regional left ventricular function frequently occurs in the nonischemic myocardium after acute coronary occlusion. To further define the regional and global effects of this increased remote function in the ischemic left ventricle, 22 dogs were studied with two-dimensional echocardiography before and 1 h after left circumflex coronary artery occlusion. Two groups of dogs were identified with and without compensatory increased regional left ventricular function, defined as regional wall thickening in the nonischemic zone greater than 2 SD above baseline. After coronary occlusion, nonischemic wall thickening was 76 +/- 15% in the hyperfunction group (n = 11) and 45 +/- 14% in the nonhyperfunction group (n = 11) (p less than 0.001). Despite similar left ventricular end-diastolic cavity areas and equivalent degrees of ischemic wall thinning, dogs with increased left ventricular function in the nonischemic myocardium had a smaller extent of circumferential left ventricular dysfunction (136 +/- 33 versus 170 +/- 43 degrees, p less than 0.001) and a higher area ejection fraction (38 +/- 9% versus 27 +/- 6%, p less than 0.001). These functional differences occurred despite similar myocardial areas at risk by autoradiography (41 +/- 6% versus 37 +/- 12%, p = NS). The data suggest that increased left ventricular function in the nonischemic myocardium determines the global functional impact of acute coronary occlusion and, through interaction with adjacent myocardium, modifies the extent of circumferential left ventricular dysfunction.

Animals↗
PubMed1990

Validation of left ventricular function parameters acquired with the non-imaging nuclear probe: comparison with tantalum marker cine-fluoroscopy.

We evaluated the accuracy of the non-imaging nuclear probe for measuring various parameters of left ventricular function by comparing these with simultaneous measurements acquired via tantalum marker cine-fluoroscopy. Eight patients with surgically implanted mid-myocardial tantalum markers were studied during cardiac catheterization. High temporal resolution tantalum marker-derived volume/time curves were generated and calibrated to absolute endocardial volumes by comparison with contrast left ventricular angiography. Left ventricular function parameters were acquired at baseline and during atrial pacing, nitroprusside infusion and volume loading. Simultaneous measurements obtained with the nuclear probe and via tantalum marker cine-fluoroscopy were compared. The following correlation coefficients were obtained: ejection fraction, r = 0.49, P less than 0.001; peak ejection rate, r = 0.41, P less than 0.01; mean ejection rate, r = 0.62, P less than 0.001; time to peak ejection, r = 0.73, P less than 0.001; peak filling rate, r = 0.73, P less than 0.001; time to peak filling, r = 0.58, P less than 0.001. Relative changes in end-diastolic volume were accurately tracked by the nuclear probe in six of seven patients (r values 0.77-0.93). These results suggest that measurements of certain left ventricular volume parameters with the nuclear probe may not accurately reflect true volume changes as measured by tantalum marker cine-fluoroscopy. Although, the probe may be useful in tracking relative changes in end-diastolic volume, we would advise caution in using this instrument for studies requiring accurate measurements of ejection and filling parameters.

Cardiac Catheterization↗
PubMed1990

Effect of intracoronary nifedipine on coronary bloodflow and myocardial metabolism during pacing-induced ischemia.

The effects of intracoronary nifedipine on coronary bloodflow, its regional distribution, myocardial oxygen consumption and lactate metabolism during pacing-induced angina were evaluated in 15 subjects. These responses were directly compared to 10 subjects who received an alcohol-based control solvent. Myocardial bloodflow was measured by thermodilution, with changes in regional coronary flow assessed using a dual radiolabelled (technetium-99m and indium-111) intracoronary microsphere technique and single photon emission tomography. Neither intracoronary nifedipine (100 micrograms) or the control solvent produced changes in systemic arterial pressure (nifedipine -2 mmHg and control +2 mmHg, both not significant). Intracoronary nifedipine markedly increased left ventricular end diastolic pressure (pre-nifedipine 13.0 mmHg versus post nifedipine 20.1, P less than 0.05), while increasing total coronary sinus bloodflow (pre-nifedipine 134 mL/min versus post nifedipine 189, P less than 0.05): Regional coronary bloodflow increased in all myocardial segments, regardless of the severity of coronary stenosis (64 to 132% baseline, all P less than 0.05). In addition, intracoronary nifedipine increased myocardial oxygen consumption (pre-nifedipine 12.3 mL/min versus post nifedipine 15.7, P less than 0.05), with a trend towards improved lactate extraction (pre-nifedipine 0.24 mg/mL versus post nifedipine 0.12, not significant). Although decreased ventricular afterload (left ventricular systolic wall stress) may contribute to nifedipine's antianginal properties, a primary increase in regional coronary bloodflow also appears to be an important factor in the alleviation of myocardial ischemia.

Adult↗
PubMed1988

The effects of a critical stenosis on myocardial blood flow, ventricular function, and infarct size after coronary reperfusion.

Immediate percutaneous transluminal coronary angioplasty has been advocated for patients with a residual stenosis after coronary thrombolysis because of the possibility that the residual stenosis may restrict reflow and thereby increase infarct size. Because there are few experimental data bearing on this issue, we measured left ventricular function, myocardial blood flow, and infarct size in 20 anesthetized open-chest dogs during 2 hr of left circumflex occlusion and 4 hr of reperfusion. Ten animals were reperfused through a critical stenosis of the left circumflex artery (critical stenosis group) and the remaining 10 animals underwent full reperfusion without stenosis (control group). In both groups, a comparable degree of echocardiographic systolic wall thinning was present during occlusion and partial recovery of global and regional left ventricular function in the two groups. Subendocardial blood flow was decreased in the critical stenosis group relative to the control group at 5 min after reperfusion (0.52 +/- 0.16 ml/min/g in the critical stenosis group vs 1.55 +/- 0.32 ml/min/g in the control group, p less than .05) but not at 4 hr after reperfusion, when a reduced reflow response was seen in both groups. No differences in subepicardial blood flow were seen in the two groups of animals. Infarct size was slightly greater in the critical stenosis group than the control group, but this difference was not statistically significant (infarct/risk area ratio: 55.5 +/- 7.8% in the critical stenosis group vs 39.4 +/- 9.7% in the control group, p = .21). A close inverse exponential relationship was seen between infarct size/risk area ratio and subendocardial blood flow during occlusion (r = .89, p = .001). Two control animals had high levels of subendocardial collateral flow (greater than 0.2 ml/min/g); when these animals were excluded from analysis, differences in the infarct size/risk area ratio in the control and critical stenosis groups were less striking: (55.5 +/- 7.8% in the critical stenosis group vs 48.4 +/- 9.6% in the control group). Thus, the presence of a critical stenosis results in restriction of hyperemic blood flow to the subendocardium after reperfusion but does not influence infarct size or early left ventricular functional recovery.

Animals↗
PubMed1987

A comparative evaluation of hemodynamic and neurohumoral effects of nitroglycerin and nifedipine in congestive heart failure.

Nitroglycerin and nifedipine have been suggested as useful agents in the therapy of congestive heart failure. Because of the rapid action and feasability for sublingual administration of both drugs, their comparative hemodynamic and neurohumoral effects were studied in 12 patients with congestive heart failure. After sublingual nitroglycerin, there was a significant decrease in mean arterial pressure (96 +/- 17 to 90 +/- 15 mm Hg, p less than 0.01), left ventricular (LV) filling pressure (30 +/- 12 to 22 +/- 10 mm Hg, p less than 0.01), right atrial pressure (15 +/- 6 to 10 +/- 5 mm Hg, p less than 0.01) and systemic vascular resistance (21.5 +/- 7.7 to 19.3 +/- 6.2 units, p less than 0.05) and an increase in cardiac index (2.2 +/- 0.6 to 2.4 +/- 0.7 liters/min/m2, p less than 0.05) and LV stroke work index (20.4 +/- 7.0 to 24.5 +/- 8.6 gm-m/m2, p less than 0.01). After sublingual nifedipine, there was also a significant decrease in mean arterial pressure (96 +/- 16 to 89 +/- 14 mm Hg, p less than 0.01) and systemic vascular resistance (22.1 +/- 7.1 to 18.0 +/- 6.1 units, p less than 0.01) and an increase in cardiac index (2.1 +/- 0.6 to 2.4 +/- 0.6 liters/min/m2, p less than 0.01); in contrast to nitroglycerin, this was unaccompanied by significant changes in right- or left-sided filling pressures or LV stroke work index.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗