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Biomedical subjects

J M Detry

Publications and source records attributed to J M Detry.

At least 73 records · Page 4Linked to original sources
PubMed1984

Acute and long-term effects of nitrendipine on resting and exercise hemodynamics in essential hypertension.

The hemodynamic effects of nitrendipine have been studied at rest and during exercise in eight patients with mild to moderate essential hypertension. Acutely, nitrendipine (20 mg) induced at rest a decrease in arterial blood pressure (from 194/100 to 151/78 mm Hg) and an increase in heart rate (from 81 to 101 beats/min); the cardiac output was unchanged and the systemic vascular resistances fell by 30%. Similar changes were observed during exercise, i.e., a decrease in arterial blood pressure (from 245/106 to 204/87 mm Hg) and in systemic vascular resistances (-25%) with an increase in heart rate (from 133 to 142 beats/min). After chronic treatment during 55 days (average daily dose was 46 mg), the hypotensive effects of nitrendipine were similar, although less marked, both at rest and during exercise; the tachycardia noted after acute intake disappeared after chronic therapy. The addition of atenolol (100 mg) at the end of the chronic study in six patients further reduced arterial blood pressure at rest (138/80 mm Hg) and during exercise (180/91 mm Hg); the heart rate decreased to 60 beats/min at rest and 94 beats/min during exercise. These data show that nitrendipine is a potent antihypertensive agent that induces an important fall in the systemic vascular resistances both at rest and during exercise; during chronic therapy, these antihypertensive effects were maintained while the reflex tachycardia disappeared. The addition of atenolol during chronic therapy contributed to the normalization of the resting and exercise arterial blood pressures in nearly all patients.

Adult↗
PubMed1983

Hemodynamic effects of felodipine at rest and during exercise in exertional angina pectoris.

To examine the antianginal effects of felodipine, a new calcium antagonist, 8 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 30 minutes after oral administration of 0.1 mg/kg of felodipine. Angina pectoris was always prevented after the drug was given and the exercise intensity was increased until recurrence of angina (5 patients) or exhaustion (3 patients). Hemodynamic data were also recorded at this higher exercise capacity. At rest and during submaximal exercise, felodipine increased heart rate and decreased arterial blood pressure and systemic vascular resistance. The prevention of angina pectoris was accompanied by lower mean pulmonary capillary wedge pressure, systemic vascular resistance and ST-segment depression; the pressure-rate product was unchanged. The 20% greater exercise capacity after felodipine was attended by a 20% increase in maximal cardiac output, a 17% increase in maximal heart rate and a 13% increase in maximal pressure-rate product; the maximal arterial blood pressure and ST-segment abnormalities were unchanged and the systemic vascular resistance was lower. The relation between ST-segment depression and the pressure-rate product during exercise was favorably influenced by felodipine. Thus, felodipine is an active antianginal drug; its major mechanism of action is to lower the systemic vascular resistance. The data also suggest that it improves coronary blood flow during exercise.

Aged↗
PubMed1983

Electrocardiographic changes after physical training in patients with myocardial infarction.

Electrocardiographic voltage measurements were performed in 24 men with an inferior myocardial infarction before and after 14 +/- 0.5 weeks of physical training. Oxygen uptake at peak exercise increased 42% and heart rate at rest was significantly decreased after training. Increases were found in the magnitude of the R waves in leads II, aVF and V4 to V6; of the S wave in leads V1 and V3; of the T waves in V5 and V6; and of the Sokolow index of QRS voltage. Also, the magnitude of the mean electrical vector in the frontal plane was significantly higher after training. These data were compared with those derived from two electrocardiographic tracings, separated by an average of 19 +/- 1.5 weeks, of 20 other patients with an inferior myocardial infarction who were comparable in age, weight, risk factor and delay between infarction and first examination, but who were not trained. When the electrocardiographic changes between the two observations were compared for the two groups, the trained patients show significant increases in the magnitude of the R wave in the left precordial leads, and leads II and aVF and the Sokolow voltage criterion; in the magnitude of the T wave in leads V5 and V6; and in the magnitude of the mean electrical vector in the frontal plane. It is concluded that physical training in patients with myocardial infarction can alter cardiac structure, as evaluated by voltage measurements on the electrocardiogram.

Electrocardiography↗
PubMed1983

Reassessment of the relation between QRS forces of the orthogonal electrocardiogram and left ventricular ejection fraction.

Previous studies have demonstrated the existence of a strong positive correlation between the amplitude of QRS forces of the orthogonal electrocardiogram and the angiographically determined left ventricular ejection fraction. In a large group of patients evaluated for chest pain, we examined the relationship between the arithmetic summation of RX + RY + QZ (sigma R), the maximal and mean spatial QRS vectors and the ejection fraction (EF). In a total of 252 patients, there was a statistically significant correlation between sigma R and EF but a low correlation coefficient value (r:0.22, P less than 0.001). This relationship was essentially due to the group of patients with coronary artery disease and myocardial infarction (r:0.24, P less than 0.015) whereas there was no correlation in the group of normal subjects or in patients with coronary artery disease without myocardial infarction. In the group with myocardial infarction, a significant correlation between sigma R and EF existed only in patients with anterior myocardial infarction (r:0.41, P less than 0.025). In conclusion, both ejection fraction and amplitude of QRS forces decrease in coronary artery disease especially when an anterior myocardial infarction is present. However, despite the positive association between these angiographic and electrocardiographic indices, the low value of the correlation coefficient indicates that it is not possible to predict ejection fraction from the value of sigma R in individual patients.

Cardiac Catheterization↗
PubMed1983

Hemodynamic effects of Corwin (ICI 118,587), a new cardioselective beta-adenoceptor partial agonist.

To describe the mechanisms of action of Corwin (ICI 118,587), a new cardioselective beta-adrenoceptor partial agonist, ten cardiac patients with mild to moderate functional cardiac impairment were studied. Hemodynamic measurements were made at rest and during three consecutive levels of submaximal exercise, before and 10 min after intravenous administration of 0.2 mg/kg of the drug. At rest, Corwin increased heart rate (HR) from 75 to 88 bpm and mean systemic blood pressure (BP) and decreased mean pulmonary capillary wedge pressure (PCWP); the resting cardiac output (CO) tended to increase in patients with a slow control HR. During exercise of low intensity (control HR: 103 bpm), the drug had no significant effect, except for a slight decrease in BP. During exercise of moderate and heavy intensity (control HR: 121 and 149 bpm), Corwin decreased HR (-10 and -24 bpm), BP and PCWP; at the heaviest exercise level, CO also decreased after Corwin. Thus, at rest, when the sympathetic tone is low, Corwin acts mainly as a beta-adrenoceptor agonist. As the sympathetic tone progressively increases with the intensity of the exercise, the beta-adrenoceptor antagonist action of Corwin becomes apparent and is most evident at the highest exercise level. In contrast to a full antagonist, these effects of Corwin appear to be less marked and they are accompanied by an unchanged or decreased PCWP. Corwin has thus interesting hemodynamic properties which deserve further investigation.

Adrenergic beta-Agonists↗
PubMed1983

Bayesian analysis of stress thallium scintigraphy for the detection of multivessel coronary disease.

This study was performed in 224 men to determine the respective contribution of history and thallium-201 stress myocardial scintigraphic imaging in the non-invasive prediction of the severity of coronary disease. Myocardial scintigraphic imaging had the better diagnostic accuracy (80%) for the detection of multivessel disease but the results emphasize the importance of the history in predicting the extent of coronary artery disease. In patients with myocardial infarction, the diagnostic accuracy of the history (80%) was similar to the diagnostic accuracy of myocardial scintigraphic imaging (79%); in the subgroup of patients with residual angina pectoris after infarction, the accuracy of the history was even greater (87%) than that of myocardial scintigraphic imaging (78%). Thus, after myocardial infarction, scintigraphy was useful only in the small subgroup of patients without residual angina pectoris when it had a diagnostic accuracy of 79%, slightly but insignificantly superior to that of the history (62%). In patients without previous myocardial infarction, but with typical angina, myocardial scintigraphy was clearly superior to the simple history (diagnostic accuracy of 78% versus 53%; P less than 0.001). In patients without myocardial infarction and with atypical angina the prevalence of multivessel disease was low (17%) and the diagnostic accuracy of history (83%) was barely different from the diagnostic accuracy of myocardial scintigraphic imaging (90%). Thus, when the likelihood of multivessel disease is very high (angina pectoris post myocardial infarction), or very low (atypical angina), the contribution of exercise testing is very limited. Important additional information is provided by maximal exercise testing and myocardial scintigraphic imaging only in the groups with an intermediate prevalence of multivessel disease, namely in the asymptomatic patients after myocardial infarction and in the patients with typical angina but no previous myocardial infarction.

Angiography↗
PubMed1981

Hemodynamic effects of molsidomine at rest and during submaximal and maximal exercise in patients with coronary artery disease limited by exertional angina pectoris.

To analyze the mechanisms of action of molsidomine, a new antianginal drug, 10 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 1 hour after intravenous administration of 2 mg of molsidomine. When angina pectoris was prevented after the drug was given (6 of 10 patients), the exercise intensity was increased until the recurrence of angina (3 patients) or until exhaustion (3 patients), and hemodynamic data were recorded at this higher exercise capacity. At rest and during submaximal exercise, molsidomine increased heart rate and decreased cardiac output and mean systemic and pulmonary arterial pressures. The prevention of angina pectoris was attended by lower mean systemic and pulmonary arterial pressures and pressure-rate product; cardiac output and heart rate were unchanged. The greater exercise capacity (+26 percent) after molsidomine was attended by increases in maximal cardiac output (+19 percent) and in arteriovenous oxygen difference (+6 percent); the maximal pressure-rate product was unchanged and systemic vascular resistance was lower. The mechanisms of action of molsidomine are very similar to those of nitrates and imply a decrease in venous and arterial tone. Molsidomine deserves further study in patients with angina or congestive heart failure.

Adult↗
PubMed1981

Incidence and prognostic implications of severe ventricular arrhythmias during maximal exercise testing.

Among 7,500 consecutive maximal exercise tests (MET), we have observed 6 cases of ventricular fibrillation (VF) and 40 cases of ventricular tachycardia (VT); 13 patients had a sustained VT and 27 patients had a single short run of VT. No patient died immediately but 11 patients died during the follow-up. The prognosis was determined by the underlying disease (most often coronary artery disease) and the type of arrhythmia. The 5-year survival rate was 84% in patients with a short run of VT and only 43% in patients with VF or sustained VT.

Arrhythmias, Cardiac↗
PubMed1981

Relationship between changes in left ventricular inotropic state and relaxation in normal subjects and in patients with coronary artery disease.

The aim of the study was to examine the changes in left ventricular (LV) relaxation rate induced by variations in inotropic state. Eight normal subjects and 29 patients with coronary artery disease (CAD) were studied. First, we used interventions that increase myocardial calcium influx (atrial pacing or postpacing beat) or decrease it (intracoronary injection of nifedipine). Relaxation rate was estimated from the time constant (T1) of isovolumic LV pressure fall during the fist 40 msec after peak negative dP/dt. Under basal conditions, T1 was impaired in CAD patients (58 vs 43 msec; p less than 0.01), despite similar heart rate, LV pressures and peak positive dP/dt (1620 vs 1787 mm Hg/sec; NS). During atrial pacing at 135 +/- 7 beats/min, peak positive dP/dt increased to 2220 mm Hg/sec in 11 CAD patients and to 2256 mm Hg/sec in eight normal subjects. T1 decreased more in CAD patients than in normal subjects (17 vs 7 msec; p less than 0.01). T1 changes also differed in the postpacing beat between CAD patients and normal subjects (-6 vs 5 msec; p less than 0.01) or when nifedipine was injected during the pacing (4 vs 20 msec; p less than 0.01). Intravenous calcium injection during atrial pacing in another group of 18 CAD patients further improved peak positive dP/dt and T1 (-3 msec; p less than 0.05) and normalized the changes in relaxation during the postpacing heart. Our data indicate that a variable coupling between LV inotropic state and relaxation rate exists in man during changes in calcium influx and that this coupling is abnormal in CAD patients.

Adolescent↗
PubMed1980

Impaired early left ventricular relaxation in coronary artery disease: effects of intracornary nifedipine.

It has been shown that the maximal rate of left ventricular (LV) relaxation is impaired in patients with coronary artery disease (CAD) under basal conditions. To test the hypothesis that this impaired LV relaxation could be related to viable but metabolically abnormal myocardium, we studied the time course of isovolumic LV pressure fall in 21 patients with CAD and in 13 control subjects under basal conditions. This study was repeated after intracoronary injection of the calcium antagonist nifedipine (N) in 11 patients with CAD and in eight controls. Our data showed that isovolumic pressure fall was biexponential in 20 of 21 CAD patients and in six of 13 controls. Moreover, the time constant of isovolumic pressure fall during the first 40 msec after peak (negative) dP/dt (T1) was significantly greater in CAD patients than in controls (62 +/- 3 vs 44 +/- 1 msec, p < 0.002); the time constant of pressure fall during the 40-80 msec after peak (negative) dP/dt (T2) was similar in both groups ( 42 +/- 2 vs 39 +/- 2 msec, NS). Thirty seconds after injection of nifedipine, T1 and T2, were significantly prolonged in patients with CAD (14 msec and 16 msec, respectively, p < 0.005) and in controls 12 msec and 14 msec, respectively, p < 0.05), and a negative inotropic effect was observed in both groups (peak (positive) dP/dt - 16% in controls and -23% in CAD patients, p < 0.01). At rest, impairment of isovolumic relaxation in CAD patients is mainly limited to the first 40 msec after peak (negative) dP/dt, suggesting a dyssynchronous wall motion. This impairment of LV relaxation is better identified by T1 than by peak (negative) dP/dt in individual patients, and cannot be improved by administration of a calcium antagonist.

Adult↗
PubMed1980

Hemodynamic effects of physical training in established arterial hypertension.

Six patients with established arterial hypertension have been studied before and after a three months period of regular intense physical training. After training the maximal oxygen uptake was 9.6% higher (P < 0.02) and the heart rate was lower at rest (-8 beats/min; NS) and during submaximal exercise (-12 beats/min; P < 0.001). This bradycardia was attended by a slight decrease in cardiac output and an increase in the arterio-mixed venous oxygen difference; the blood pressure was unchanged and, accordingly, the peripheral resistance were slightly increased after training (+ 17%, P < 0.005 at rest and + 6.5% NS during exercise). We concluded that physical training has no specific hypotensive effect in patients with established arterial hypertension; in these patients the changes induced by training are very similar to those observed in normal subjects or in patients with coronary artery disease.

Adult↗