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Biomedical subjects

M A Frais

Publications and source records attributed to M A Frais.

46 records · Page 3Linked to original sources
PubMed1984

Haemodynamic effects of nicardipine in acute myocardial infarction.

The haemodynamic dose-response effects of the slow-calcium channel blocker nicardipine were evaluated in fifteen male patients with uncomplicated acute myocardial infarction. Following a 1 hr control period, during which the stability of base-line control haemodynamic variables was confirmed, four i.v. boluses of 1.25, 1.25, 2.5 and 5.0 mg of the drug (cumulative dosage 1.25, 2.5, 5.0 and 10.0 mg) were administered at 15 min intervals. The plasma concentrations achieved are within the previously described therapeutic range (greater than 20 micrograms/l). Nicardipine resulted in linear reductions in systemic arterial pressure and vascular resistance, and dose-related increases in heart rate, cardiac and stroke output without change in the left heart filling pressure. Intravenous nicardipine did not induce any depression of left ventricular pumping performance in our patients in the early stages of uncomplicated myocardial infarction.

Blood Pressure↗
PubMed1982

Phase image characterization of ventricular contraction in left and right bundle branch block.

The phase image is a computer-derived functional image, based on the analysis of the time versus radioactivity curve in each pixel location of the multiple gated blood pool scintigram. Within the ventricular regions of interest, the phase angle is roughly equivalent to the time of onset of counts reduction or to the time of onset of ventricular contraction and is expressed in degrees from 0 to 360 degrees. A gray scale-coded image of such a regional phase angle, the phase image, can be looked on as a map of sequential contraction. This method was applied in 33 patients without severe contraction abnormality including 16 patients with normal conduction, 9 with right bundle branch block and 8 with left bundle branch block. In patients with normal conduction the pattern of phase angle distribution, representing the pattern of ventricular contraction, was homogeneous and symmetric in both the left and right ventricles. Analysis in this normal group indicated a slight but significant difference between the mean (+/- standard deviation) phase angle of the left ventricle (8.5 +/- 11.8 degrees) and that of the right ventricle (13.6 +/0 12.9 degrees, p = 0.01). There was a slight, but nonsignificant difference between mean intrapatient left and right ventricular phase angle onset (1.9 +/- 6.5 degrees). The mean phase angle of the right ventricle in patients with right bundle branch block (27.6 +/- 14.2 degrees) and of the left ventricle in those with left bundle branch block (21.9 +/- 14.0 degrees) was delayed compared with that in patients with normal conduction (p less than 0.05 for both). The mean intrapatient difference between left and right ventricular mean phase angles in patients with normal conduction (-5.2 +/- 6.8 degrees) was significantly different from that in patients with right (-21.8 +/- 10.3 degrees, p less than 0.001) or left (21.8 +/- 6.8 degrees, p less than 0.001) bundle branch block. The mean intrapatient difference between onset of left and right ventricular phase angles was also significantly different from normal in patients with right (-10.6 +/- 7.5 degrees, p less than 0.005) or left (18.7 +/- 8.3 degrees, p = 0.01) bundle branch block. Although phase imaging is not without artifactual error, this study demonstrates that the phase image can characterize familiar conduction abnormalities. It presents the potential for application as a general noninvasive tool in the investigation of the timing and sequence of ventricular contraction in patients with normal or abnormal ventricular activation.

Adult↗
PubMed1982

An accurate means of detecting and characterizing abnormal patterns of ventricular activation by phase image analysis.

The ability of scintigraphic phase image analysis to characterize patterns of abnormal ventricular activation was investigated. The pattern of phase distribution and sequential phase changes over both right and left ventricular regions of interest were evaluated in 16 patients with normal electrical activation and wall motion and compared with those in 8 patients with an artificial pacemaker and 4 patients with sinus rhythm with the Wolff-Parkinson-White syndrome and delta waves. Normally, the site of earliest phase angle was seen at the base of the interventricular septum, with sequential change affecting the body of the septum and the cardiac apex and then spreading laterally to involve the body of both ventricles. The site of earliest phase angle was located at the apex of the right ventricle in seven patients with a right ventricular endocardial pacemaker and on the lateral left ventricular wall in one patient with a left ventricular epicardial pacemaker. In each case the site corresponded exactly to the position of the pacing electrode as seen on posteroanterior and left lateral chest X-ray films, and sequential phase changes spread from the initial focus to affect both ventricles. In each of the patients with the Wolff-Parkinson-White syndrome, the site of earliest ventricular phase angle was located, and it corresponded exactly to the site of the bypass tract as determined by endocardial mapping. In this way, four bypass pathways, two posterior left paraseptal, one left lateral and one right lateral, were correctly localized scintigraphically. On the basis of the sequence of mechanical contraction, phase image analysis provides an accurate noninvasive method of detecting abnormal foci of ventricular activation.

Adult↗
PubMed1979

Gastric adenocarcinoma due to ataxia-telangiectasia (Louis-Bar syndrome).

A 26-year-old male with ataxia-telangiectasia died with a gastric adenocarcinoma. Malignancy is a recognised complication of this condition, the majority of cases being reticuloendothelial. There have been three reports of gastric adenocarcinoma associated with ataxia-telangiectasia; this, however, is the first in British published reports.

Adenocarcinoma↗
PubMed1979

Left ventricular failure with labetalol.

A patient treated for hypertension with labetalol developed left ventricular failure. When the drug was withdrawn and the BP controlled with 2 other agents, the signs of heart failure regressed. The ill effects in this case could have been because the beta-blocking effects of labetalol are 4 to 6 times greater than the alpha-blocking effects. Caution should be exercised when prescribing this drug for patients with heart failure or with previous symptoms.

Adult↗
PubMed1979

Ocular reaction to timolol maleate.

A patient prescribed timolol maleate for the control of hypertension developed dryness of the eyes. The symptoms improved on withdrawal of the drug. Vigilance for such adverse reactions must be observed in the use of any beta-adrenoreceptor blocking agent.

Adult↗
PubMedDate not supplied

Cardioselective beta-blockade with atenolol and acebutolol following acute myocardial infarction: a multiple-dose haemodynamic comparison.

In patients with acute myocardial infarction the haemodynamic relevance of the ancillary pharmacological properties of cardioselectivity and of intrinsic sympathomimetic activity (ISA) possessed by beta-blocking drugs is unclear. The dose-response effects of atenolol and acebutolol, two cardioselective compounds, the latter also possessing a degree of ISA, were therefore compared in a single-blind, dose-response, crossover study in patients within 18 h of suffering an uncomplicated acute myocardial infarction. The logarithmic cumulative dosage schedule achieved plasma concentrations in the clinical therapeutic ranges for both atenolol (0.05 +/- 0.04-0.19 +/- 0.03 micrograms/ml) and acebutolol (0.22 +/- 0.14-0.8 +/- 0.29 micrograms/ml). Incremental doses of intravenous atenolol (cumulative, 1-8 mg) resulted in significant decreases in systolic blood pressure, heart rate, cardiac output, stroke volume, and stroke work index (p less than 0.01 for each). Pulmonary artery occluded pressure (p less than 0.05) and systemic vascular resistance (p less than 0.01) increased. Incremental doses of intravenous acebutolol (cumulative, 10-80 mg) also resulted in significant decreases in systolic blood pressure, heart rate, cardiac output, stroke volume, and stroke work index (p less than 0.01 for each). Systemic vascular resistance increased (p less than 0.01); there was no consistent change in the pulmonary artery occluded pressure. Within the limits of the experimental protocol, the additional property of ISA possessed by acebutolol resulted in no statistically significant haemodynamic differences from atenolol. This may reflect either an insufficient degree of ISA possessed by acebutolol to confirm the original hypothesis, or its haemodynamic irrelevance in the presence of the increased sympathetic tone that is frequently present following acute myocardial infarction.

Acebutolol↗