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Dive into the research topics where Roland Bernard is active.

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Featured researches published by Roland Bernard.


Journal of Cardiovascular Pharmacology | 1980

Clinical and hemodynamic effects of dobutamine in acute myocardial infarction with left heart failure

Marc Renard; Roland Bernard

We studied the clinical and hemodynamic effects of dobutamine infused for 24 hr into 10 patients with acute myocardial infarction (<4 days) complicated by left heart failure (pulmonary wedge pressure >15 mm Hg, cardiac index <3.0 liters/min/m2). We measured pulmonary arterial pressures, pulmonary wedge pressure, right atrial pressure, and intravascular systemic blood pressures. The thermodilution method was used for determinations of cardiac output, and the electrocardiogram was followed with a computerized arrhythmia monitoring system. After 1 and 3 hr of infusion with the optimal dose (averaging 8 μg/kg/min), there was a very significant increase of cardiac index (29%) and a decrease of pulmonary wedge pressure (37%) with a moderate increase of heart rate (20%) and without significant changes in blood pressure. After 24 hr of dobutamine infusion, much of the improvement in left ventricular function was lost. This may be attributed either to a decrease of drug action or to an unfavorable evolution of the clinical status. We conclude that infusion of dobutamine is an effective, potent, and well-tolerated short-term procedure in the management of left heart failure during the acute stage of myocardial infarction.


Gerontology | 1984

Hemodynamic Effects of Dobutamine in Patients below and over 65 Years, with Left Heart Failure Secondary to an Acute Myocardial Infarction

Marc Renard; Roland Bernard; Christian Melot; Philippe Jacobs; Marc Englert

The cardiac response to sympathomimetic agents has been reported to be reduced in the elderly. We studied the hemodynamic effects of dobutamine in two groups of patients with acute myocardial infarction (AMI) and left heart failure: group A included 10 patients aged 65 years or less and group B 10 others older than 65. After a 1-hour infusion the increase in cardiac index was highly significant in both groups (27%, p less than 0.001 and 25%, p less than 0.001), and the decrease in pulmonary wedge pressure was greater in group A (42%, p less than 0.001 and 17%, p less than 0.02). The increase in double product was similar in both groups (14%, p less than 0.001 and 18%, p less than 0.005); nevertheless the 4 patients developing angina pectoris during dobutamine infusion were over 65 years. We conclude that dobutamine remains effective in the elderly with AMI and left heart failure but is less well tolerated.


Journal of Cardiovascular Pharmacology | 1984

Effect of labetalol on preload in acute myocardial infarction with systemic hypertension

Marc Renard; Philippe Jacobs; Christian Melot; R. Haardt; Harry Vainsel; Roland Bernard

We assessed the effects of labetalol on pulmonary wedge pressure (PWP) and other hemodynamic variables in 18 patients with acute myocardial infarction (AMI) and systemic hypertension (systolic blood pressure > 150 mm Hg). According to the initial value of PWP, the patients were separated into two groups of nine patients each: Group 1 (PWP ≥ 15 mm Hg) and Group 2 (PWP ≤ 12 mm Hg). Labetalol was infused at increasing rates to lower systolic blood pressure below 130 mm Hg; this optimal rate (mean rates for Groups 1 and 2: 1.8 and 2.1 mg/min, respectively) was maintained for 1 h. Hemodynamic variables were measured before and after 1 h of infusion. Labetalol normalized blood pressure in both groups by a significant decrease in total systemic resistance [22% (p < 0.001) and 13% (p < 0.02)] and in cardiac index [17% (p < 0.005) and 12% (p < 0.02)]. While the hemodynamic responses were rather similar in both groups, the PWP decreased significantly (from 22 to 15 mm Hg, p < 0.01) in Group 1, but did not change significantly in Group 2 (from 7 to 10 mm Hg, NS). The possible mechanisms behind these different responses are discussed. We conclude that labetalol is an effective drug for treating systemic hypertension in AMI which acutely decreases total systemic resistance and preload in patients with moderate left ventricular failure.


Journal of Cardiovascular Pharmacology | 1983

Hemodynamic effects of concurrent administration of metoprolol and tocainide in acute myocardial infarction

Marc Renard; Roland Bernard; M. Ewalenko; Marc Englert

Summary We evaluated the hemodynamic effects of combined administration of metoprolol and tocainide in nine patients with uncomplicated acute myocardial infarction. After 24 h of treatment with oral metoprolol (50 mg q.8 h), intravenous tocainide was given (750 mg over 15 min), followed by oral administration of both drugs (50 mg metoprolol q.8 h; 800 mg tocainide, then 400 mg q.8 h). Hemodynamic variables were measured before and after 25 h of oral metoprolol treatment, immediately after intravenous tocainide (at 15 and 30 min), and then during continued oral treatment with both drugs (at 2 h 15 min and 25 h 45 min). Following injection of tocainide, cardiac index changed significantly (2.7–2.3 L/min·m2; p < 0.01), but the increases in pulmonary wedge pressure (9–13 mm Hg) and total systemic resistance (15.9–18.1 IU) were not significant. During the continued oral treatment with both metoprolol and tocainide no significant hemodynamic interaction was observed. We conclude that the injection of tocainide can slightly and transiently depress left ventricular function in patients treated with metoprolol.


International Journal of Cardiology | 1986

A comparison of the effects of combined or separate alpha- and beta-blockade in the treatment of hypertension in the acute stage of myocardial infarction

Marc Renard; Paul Jacobs; Isabelle Liebens; B. Abou Hamdam; Roland Bernard

We have assessed the benefit of separate or combined alpha- and beta-receptor blockade in the treatment of 33 patients suffering from acute (less than 48 hr) myocardial infarction complicated by sustained (greater than 6 hr) systolic hypertension (systolic blood pressure greater than 150 mm Hg). Eight patients have been treated with metoprolol, 7 with phentolamine and 18 with labetalol. We evaluated the effects of these drugs on hemodynamics and arterial and mixed venous blood gases. The patients were divided into two groups on the basis of the pulmonary wedge pressure. The first group had a pressure greater than 15 mm Hg. It included 9 patients treated with labetalol (1.8 mg/min for 1 hr) and 7 others with phentolamine (0.6 mg/min for 1 hr). The wedge pressure in the second group was less than 13 mm Hg. Nine patients in this group had been treated with labetalol (2.1 mg/min for 1 hr) and 8 others with metoprolol (0.2 mg/kg in 15 min). Labetalol normalized the blood pressure in both groups within 1 hr as did phentolamine. Metoprolol did not significantly reduce either the systolic or the diastolic pressures. The high wedge pressures in the first group were reduced by both labetalol and phentolamine. The cardiac index was increased following phentolamine administration while it was reduced by labetalol. In the group with low wedge pressure, labetalol and metoprolol induced a slight but significant reduction in cardiac index but the pulmonary wedge pressures were significantly increased for metoprolol only. The rate-pressure product was very significantly decreased by labetalol and metoprolol but not by phentolamine. The emergency treatment of systemic hypertension occurring in the setting of acute myocardial infarction would thus appear to be best achieved by combined alpha- and beta-blockade rather than with either pure alpha- or pure beta-blockade. Phentolamine, however, would be a good drug in the presence of a reduced cardiac index.


Angiology | 1986

Central Inhibition of Sympathetic Overdrive by Clonidine in Acute Myocardial Infarction with Systolic Hypertension. Haemodynamic Study

Marc Renard; Isabelle Liebens; Patrick Waterschoot; Roland Bernard

Intravenous clonidine was used to treat systolic hypertension (systolic blood pressure greater than 160 mm Hg) in 15 patients with acute myocardial infarction and documented sympathetic overactivity (high plasma norepinephrine). Its effects on haemodynamics and blood gases were studied. After one hour, clonidine significantly reduced the systolic (195±7 to 137±7 mm Hg, p < 0.01) and diastolic (81±4 to 60±3 mm Hg, p < 0.01) blood pressures as well as the systemic vascular resistance (26±2 to 20±1 IU, p < 0.01). The cardiac index was reduced from 2.8±0.2 to 2.4±0.2 l/min.m2, p<0.01. This change was related to a reduction of the heart rate (92±4 to 81±4 beats/ min, p < 0.01) as the stroke index was unchanged. Pulmonary wedge pressure (15±3 to 10±2 mm Hg, p < 0.01) and rate pressure product (18.034±1.159 to 11.274±917 mm Hg, beats/min, p < 0.01) were also significantly decreased. The arterial oxygen tension did not change significantly but there was a significant drop in the mixed venous oxygen saturation (63±2 to 61±2%, p<0.02) and oxygen transport (433±41 to 409±36, p < 0.01). Clonidine is thus able to normalize blood pressure in acute myocardial infarction ; this is accompanied by a reduction in myocardial oxygen requirements and pulmonary wedge pressure. Oxygen transport to the tissues, however, may be decreased.


American Heart Journal | 1985

Effects of molsidomine on hemodynamics and blood gases in acute myocardial infarction with left heart failure

Marc Renard; Philippe Jacobs; Isabelle Liebens; Alain Friart; Roland Bernard

We studied the effects of molsidomine on hemodynamic properties and blood gas levels in eight patients with acute myocardial infarction and left heart failure. One hour after an 8 mg intravenous bolus injection, pulmonary wedge pressure and right atrial pressure decreased, respectively, from 30 +/- 9 to 23 +/- 12 mm Hg (p less than 0.01) and from 10.4 +/- 3.6 to 7.8 +/- 4.0 mm Hg (p less than 0.05) without significant changes in heart rate, cardiac index, or systemic blood pressure. There was a mild decrease in arterial oxygen tension (from 61 +/- 15 to 56 +/- 6 mm Hg), but it was not significant. The drug induced no adverse effects. Intravenous bolus injection of molsidomine rapidly relieves pulmonary congestion in patients with acute myocardial infarction.


Acta Clinica Belgica | 1978

Myocardite Au Cours D’Une Pneumonie A Mycoplasma Pneumoniae

Ali Shita; Roland Bernard; Georges Zissis

SummaryThe authors report a case of myocarditis associated with mycoplasma pneumoniae in a 43 year old man. A rise in complement-fixation antibody titers between acute and convalescent phase sera indicated infection by mycoplasma pneumoniae. The clinical symptoms mimicked a myocardial infarction or a pulmonary embolisml The electrocardiogram showed important changes, with right bundle branch block, signs of myocardial infarction and sub-epicardial ischemia in the antero-septal region. Recovery was complete after 10 days of erythromycin treatment.


Acta Clinica Belgica | 1977

INTERET DE LA DOPAMINE DANS LE TRAITEMENT DE L'INSUFFISANCE CARDIAQUE REFRACTAIRE. A PROPOS D'UNE OBSERVATION CLINIQUE

Marc Renard; E. Van Thiel; Georges Primo; Roland Bernard

SummaryThe Dopamine is a natural catecholamine which has mighty positive inotropic properties together with a strong diuretic action.Its use must be reserved to those cases of heart failure unaffected by te classical treatment (Digitaline-diuretics-sodium restriction).The «clinical case which is presented here underlines the remarkable elficacity of the dopamine in a case of untractable heart failure secondary of a mitral and aortic valvulopathy.


British Journal of Clinical Pharmacology | 1988

Pimobendane (UD-CG 115 BS) in the treatment of severe congestive heart failure. An acute haemodynamic cross-over and double-blind study with two different doses

Mary Walter; Isabelle Liebens; Hubert Goethals; Marc Renard; Alb Dresse; Roland Bernard

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Marc Renard

Free University of Brussels

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Marc Englert

Free University of Brussels

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Christian Melot

Université libre de Bruxelles

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Hubert Dereppe

Catholic University of Leuven

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Albert Leduc

Université libre de Bruxelles

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