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Biomedical subjects

A M Zeiher

Publications and source records attributed to A M Zeiher.

137 records · Page 8Linked to original sources
PubMed1989

Flow-dependent coronary artery dilatation in humans.

To determine the role of endothelium-mediated flow-dependent coronary dilatation in humans, we studied the coronary dilatation exerted by maximal pharmacologic increase of coronary flow in 14 patients with normal coronary arteries. Biplane views of the circumflex (Cx) and left anterior descending (LAD) coronary arteries were obtained before and 80 seconds after inducing a maximal increase in flow selectively in the Cx by injecting 7 mg papaverine through a 2F infusion catheter in the midportion of the Cx (n = 10). The diameter of the proximal Cx segment (exposed to increased flow but not to papaverine directly) increased with papaverine by 11.1 +/- 4% (range, 5.2-16.4%, p less than 0.001 vs. control), whereas the LAD diameter did not change. LAD and Cx diameters increased by 18.3% and 21.2% after nitroglycerin given into the left main artery, which showed the preserved capability of the LAD to dilate. In four patients with normal coronary arteries and six patients with coronary artery disease (CAD, non-flow-limiting stenosis), a similar protocol was applied with the LAD for the assessment of flow-dependent dilatation. Simultaneously, intracoronary blood flow velocity was measured by an intracoronary Doppler catheter. Papaverine-induced coronary flow reserve (peak/resting velocity ratio) in the LAD was 4 +/- 0.7 (range, 3.5-5) in normal arteries and was 3.5 +/- 0.6 (range, 2.7-4.4) in CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Hierarchy of levels of ischemia-induced impairment in regional left ventricular systolic function in man.

We tested the hypothesis that different subsets of ischemia-induced wall motion disorders are characterized by specific patterns of abnormal regional left ventricular systolic function. Regional contraction was quantitatively assessed from two-dimensional echocardiograms by an automated integrative analysis considering the time course of wall motion during the entire contraction sequence in 20 patients with chronic myocardial infarction, in 13 patients with impending myocardial infarction (less than 2 hr after the onset of symptoms), and in nine patients during transient myocardial ischemia. Wall motion abnormalities were detected in all patients by the integrative analysis. In contrast, the sensitivity for detecting wall motion abnormalities was 80% during chronic infarction, 77% during impending infarction, and 56% during transient ischemia if only end-diastolic and end-systolic frames were compared for assessment of overall regional systolic function. There were distinct differences in the time course of abnormal wall excursion between the three groups. Chronic infarction was characterized by a monophasic contraction pattern, with abnormal synergy in regional contractile events occurring predominantly during early systole. In contrast, transient ischemia caused predominantly mid-to-late systolic abnormal synergy followed by late systolic shortening corresponding to a polyphasic contraction pattern. During impending infarction, an intermediate temporal contraction pattern was present with both early and mesosystolic abnormal synergy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Radiological prerequisites for spatial intracoronary orientation and quantitation in interventional cardiology.

The prerequisite for the safe performance of an intracoronary intervention is an optimal angiographic visualization. This includes high resolution film and video equipment and the acquisition of spatial information about anatomic details during the procedure. The geometric properties of modern biplane multidirectional X-ray equipment allow for exact spatial computations. These can be used for optimal portraying of coronary segments by computed triple orthogonal projections. In addition, an improvement in quantitative angiography is possible by calculation of the exact radiological magnification factor of coronary stenosis.

Angiography↗
PubMed1986

Noninvasive evaluation of pulmonary hypertension by quantitative contrast M-mode echocardiography.

Although it has been shown that pulmonary flow velocity can be calculated from contrast M-mode echocardiographic tracings, the clinical value of this noninvasive method has not been established. We used contrast M-mode echocardiography to examine the flow velocity pattern at the pulmonary valve in 30 adults referred for diagnostic cardiac catheterization. In the 15 patients with normal pulmonary artery pressure (PAP) (mean pressure less than or equal to 20 mm Hg), midsystolic pulmonary flow velocity was significantly (p less than 0.001) higher (654 +/- 140 mm/sec) compared to the 15 patients with pulmonary hypertension (342 +/- 85 mm/sec, mean pressure greater than 20 mm Hg). Fourteen of the 15 patients with pulmonary hypertension exhibited an early systolic flow velocity peak, whereas all patients with normal PAP showed a dome-shaped systolic flow velocity profile with maximal flow velocity occurring in midsystole. A significant close correlation was found between the relative early to midsystolic flow velocity change and mean PAP (r = 0.96; p less than 0.001). Thus quantitative contrast M-mode echocardiography reliably differentiates patients with pulmonary hypertension from patients with normal mean PAP. In addition, this technique allows a noninvasive estimation of PAP.

Adolescent↗
PubMed1985

[Value of contrast echocardiography in the diagnosis of pulmonary valve insufficiency].

The directional analysis of contrast echographic flow lines is routinely used for tricuspid insufficiency diagnosis. The value of this noninvasive technique for the assessment of pulmonic regurgitation is not yet established. Therefore we evaluated the contrast M-mode echocardiograms at the pulmonary valve in 55 patients. Echographic contrast was obtained by injection of 6-8 ml of indocyanin-saline solution into an antecubital vein. In all 5 patients with documented pulmonic insufficiency (3 patients after repair of tetralogy of Fallot, one with pulmonic endocarditis, one posttraumatic) typical diastolic retrograde directed flow lines crossing the pulmonary valve were recorded. In addition, 6 of 18 patients with primary or secondary pulmonary hypertension exhibited early to middiastolic retrograde flow lines at the pulmonary valve. In contrast, none of the normals (N = 13), and none of 19 patients with various cardiac diseases but unaffected pulmonary valve and normal pulmonary artery pressure, had contrast echographic evidence of pulmonary insufficiency. There were distinctive differences between the contrast flow patterns of the patients with organic pulmonary insufficiency and patients with functional pulmonic regurgitation due to pulmonary hypertension. It is concluded that the directional analysis of contrast echographic flow lines at the pulmonary valve allows a sensitive assessment of pulmonary regurgitation using standard echocardiographic equipment.

Adult↗
PubMedDate not supplied

Effects of inhibition of nitric oxide formation on the regulation of coronary blood flow in anesthetized dogs.

In 11 open-chest dogs with a flowmeter on the left circumflex artery, L-NMMA, a selective inhibitor of nitric oxide-formation, was subselectively infused into the left circumflex artery at a rate of 2.5 mg/ml (ml/min) to avoid systemic hemodynamic effects. The coronary blood flow at normal arterial blood pressure was similar prior to and during L-NMMA infusion. However, when the arterial blood pressure was raised by inflating a balloon in the descending aorta, the nitric oxide suppression induced a dramatic increase in coronary vascular resistance by almost 40% compared to control conditions without L-NMMA infusion at identically elevated arterial blood pressure. L-NMMA induced a significant downward shift and flattening of the pressure-flow relation over a pressure range from 60-150 mmHg. Peak hyperemic coronary flow after 20-s transient coronary occlusion was similar prior to and during L-NMMA infusion, but the duration of the hyperemic flow response was significantly shortened during L-NMMA infusion indicating exaggerated constriction after hyperemic stimulus. The EDRF/nitric oxide-system plays an important role for the regulation of coronary blood flow by counteracting autoregulatory constrictor responses to increased driving pressure and shear stress in the intact canine circulation.

Animals↗
PubMedDate not supplied

Correction of endothelial dysfunction in coronary microcirculation of hypercholesterolaemic patients by L-arginine.

Hypercholesterolaemia impairs endothelial function, possibly by interference with the intracellular formation of endothelium-derived relaxing factor from its precursor L-arginine. Whether L-arginine reverses hypercholesterolaemia-induced endothelial dysfunction in the coronary circulation was thus investigated. Epicardial artery cross-sectional area and coronary blood flow velocity were measured in 8 hypercholesterolaemic patients (mean serum cholesterol 7.8 [SE 0.3] mmol/l) and 7 age-matched controls before and after graded intracoronary infusions of the endothelium-dependent agent acetylcholine (0.036, 0.36, 3.6 micrograms/min). The effect of intracoronary infusion of L-arginine (160 mumol/min via the guiding catheter) on these measurements was then examined. In controls, acetylcholine induced a moderate dose-dependent constriction of the epicardial artery segment of the left anterior descending artery and increased coronary blood flow (by 239% [SE 57] at the highest dose). In patients with hypercholesterolaemia, the vasoconstrictive effect of acetylcholine on epicardial segments was similar to that in controls, but the increase in coronary blood flow with acetylcholine was significantly attenuated (highest dose: 61%, p less than 0.02 vs controls). L-arginine restored the acetylcholine-induced increase in blood flow in patients with hypercholesterolaemia (198% [61] vs baseline) but did not affect coronary blood flow in controls. The findings suggest that hypercholesterolaemia impairs endothelium-dependent dilatation of the coronary microcirculation and that this impairment can be restored by short-term administration of L-arginine. The possibility that L-arginine might form the basis of treatment for coronary endothelial abnormalities induced by hypercholesterolaemia could be worth investigating.

Acetylcholine↗