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Biomedical subjects

F Zannad

Publications and source records attributed to F Zannad.

At least 127 records · Page 7Linked to original sources
PubMed1988

Effect of diltiazem on myocardial infarct size estimated by enzyme release, serial thallium-201 single-photon emission computed tomography and radionuclide angiography.

Diltiazem is a calcium antagonist with demonstrated experimental cardioprotective effects. Its effects on myocardial infarct size were studied in 34 patients admitted within 6 hours after the first symptoms of acute myocardial infarction. These patients were randomized, double-blind to placebo or diltiazem (10-mg intravenous bolus followed by 15 mg/hr intravenous infusion during 72 hours, followed by 4 X 60 mg during 21 days). Myocardial infarct size was assessed by plasma creatine kinase and creatine kinase-MB indexes, perfusion defect scores using single-photon emission computed tomography with thallium-201 and left ventricular ejection fraction measured by radionuclide angiography. Tomographic and angiographic scanning was performed serially before randomization, after 48 hours and 21 days later. Groups were comparable in terms of age, sex, inclusion time and baseline infarct location and size. Results showed no difference in creatine kinase and creatine kinase-MB data between controls and treated patients, a significant decrease in the perfusion defect scores in the diltiazem group (+0.1 +/- 3.0 placebo vs -2.2 +/- 1.9 diltiazem, p less than 0.02) and a better ejection fraction recovery in the diltiazem group (-4.2 +/- 7.4 placebo vs +7.7 +/- 11.2 diltiazem, p less than 0.05). Myocardial infarct size estimates from perfusion defect scores and enzyme data were closely correlated. These preliminary results suggest that diltiazem may reduce ischemic injury in acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Enzyme Tests↗
PubMed1988

Hemodynamic and electrophysiologic effects of a new alpha 2-adrenoceptor agonist, rilmenidine, for systemic hypertension.

The hemodynamic and electrophysiologic effects of rilmenidine were examined after single oral administration to hypertensive patients. In 8 untreated hypertensive patients, cardiac output, pulmonary pressure and blood pressure were measured before and for 10 hours after the administration of 25 micrograms/kg of rilmenidine (1.3 to 2.4 mg, mean 1.88). In addition, electrophysiologic investigations were performed before and 2 hours after administration. Hemodynamics were repeated in 8 other hypertensive patients receiving 50 micrograms/kg rilmenidine (3.0 to 4.8 mg, mean 3.85 mg). The electrophysiologic study was repeated in 8 other hypertensive patients receiving 50 micrograms/kg of rilmenidine (3.2 to 4.4 mg, mean 3.90). In contrast to the results obtained at the dose of 50 micrograms/kg, there was no significant variation in pulmonary arterial pressure, cardiac index or stroke index after administration of 25 micrograms/kg. No significant variation was observed in heart rate, sinus function, conduction parameters or atrial, nodal and ventricular refractory periods after administration of 25 and 50 micrograms/kg. Rilmenidine, after single oral administration at the 25 micrograms/kg dose, led to a significant reduction in blood pressure and peripheral resistance without any significant change in cardiac output; the 25- and 50-micrograms/kg doses led to no alteration in heart rate and cardiac electrophysiology.

Adrenergic beta-Agonists↗
PubMed1988

Haemorheological abnormalities in arterial hypertension and their relation to cardiac hypertrophy.

Haemorheological characteristics were measured in a group of 52 patients with essential arterial hypertension (HT), and were compared with those of a group of normotensive subjects. The relationships between the arterial blood pressure (BP), the echocardiographic indices of left ventricular hypertrophy (LVH), and the haemorheological measurements, were studied. The group of hypertensive patients was found to have a hyperviscosity syndrome with significant elevations of blood viscosity at all shear rates (for gamma = 0.20/s, 29.6 +/- 0.6 versus 28.0 +/- 0.3 mPa.s, P less than 0.01: for gamma = 128/s, 4.2 +/- 0.05 versus 4.1 +/- 0.02 mPa.s, P less than 0.02, of plasma viscosity (1.29 +/- 0.01 versus 1.22 +/- 0.06 cSt, P less than 0.001); of erythrocyte aggregation index (17.8 +/- 0.06 versus 14.6 +/- 0.4, P less than 0.001); of erythrocyte filterability index (13.3 +/- 0.5 versus 8.8 +/- 0.2, P less than 0.001) and plasma fibrinogen level (3.4 +/- 0.9 versus 2.8 +/- 0.6 g/l, P less than 0.02). The haematocrit did not differ from that of normotensive subjects (43.3 +/- 0.6 versus 44.7 +/- 0.5%, NS). The left ventricular mass was increased and was positively correlated with the blood viscosity at a high shear rate (r = 0.38, P less than 0.01) and with the erythrocyte aggregation index (r = 0.47, P less than 0.01). Systolic, diastolic, and mean arterial blood pressures were positively correlated with the left ventricular mass (r = 0.34-0.47, P less than 0.05) and with the erythrocyte aggregation index (r = 0.42-0.46, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Multiparameter correlative study of respiratory gas exchange during exercise].

Patients with chronic heart failure were evaluated simultaneously by conventional methods and by heart-lung exploration during exercise with the purpose of validating the latter method. Only 50 patients were evaluated on two occasions and therefore included in the correlative statistical study. In this study such data as NYHA classification, cardiothoracic ratio, ejection fraction, echocardiographic fibre shortening fraction and biochemical values (venous lactate, plasma noradrenaline levels) were compared with data obtained from evaluation during exercise, i.e. VO2 max, VO2 peak, anaerobic threshold, oxygen pulse, VCO2, O2 equivalent and respiratory quotient, alveolar ventilation per minute, duration and load of exercise. Very good correlation was found with the indices obtained from VO2 and in particular with the O2 pulse and the VO2 max percentage. Good correlation was also found with VCO2 and the O2 equivalent as well as with alveolar ventilation per minute. In contrast, the anaerobic threshold and respiratory quotient correlated poorly with the first set of data and therefore were disappointing. It appears from this study that the indices obtained from VO2 are highly representative of the heart-lung unit in patients with heart failure. It seems, however, that the muscular status of the patients plays a considerable role in their exercise capacity. We suggest that these indices should be used in clinical pharmacology studies.

Aged↗
PubMed1987

Placebo-controlled study of oral enoximone in congestive heart failure with initial and final intravenous hemodynamic evaluation.

Seventeen patients with stable congestive heart failure (class II and III New York Heart Association) received intravenous and oral enoximone in a 2-part study. Hemodynamic data were first obtained after intravenous administration of 0.75 mg/kg of enoximone; data were again obtained after 12 weeks of therapy with either oral enoximone (150 mg 3 times daily) or placebo. The efficacy and safety of oral enoximone were also studied in a 12-week, double-blind randomized format. In the intravenous study, enoximone was delivered over 5 minutes and hemodynamic data were measured for up to 12 hours after. Cardiac index increased 2.76 +/- 0.63 to 3.42 +/- 0.72 liters/min/m2), pulmonary wedge pressure decreased (19.5 +/- 8.8 to 14.6 +/- 8.0 mm Hg) as did mean arterial blood pressure (101 +/- 14.8 to 85 +/- 13.7 mm Hg) and systemic vascular resistance (1,880 +/- 573 to 1,254 +/- 383 dynes s cm-5). Heart rate increased slightly (82 +/- 17 to 86 +/- 14 beats/min). All these changes were maximal 1 to 2 hours after infusion and lasted 8 hours at least. Patients were then randomized double-blind to oral treatment. Baseline values showed that the 7 patients who received placebo had more severe CHF. Therefore, comparison might be biased. Patient overall assessment showed a continuous benefit in both groups. Ejection fraction improved from 30.1 +/- 6.8% to 33.9 +/- 9.9% in the enoximone group while it remained unchanged with placebo (23.4 +/- 6.5% to 23.4 +/- 1.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Conversion from intravenous to oral slow-release disopyramide in acute myocardial infarction.

Twelve patients with acute myocardial infarction were given 1.5 mg/kg/5 min bolus +0.4 mg/kg/hr 6 hr IV infusion of disopyramide followed by 250 mg twice daily of a slow-release oral formulation of this drug. Plasma concentrations of total disopyramide rapidly reached steady-state within the therapeutic margins. The plasma steady-state concentrations of the major metabolite mono-N-dealkyl-disopyramide (MND) showed large intra-individual variations. There was no correlation between plasma levels of either disopyramide or MND and the occurrence of anticholinergic side effects. The drug had no significant effect on mean blood pressure, heart rate, or ECG intervals. This therapeutic regimen, including conversion from the IV form to oral slow-release tablets, could be recommended in myocardial infarction.

Adult↗
PubMed1987

[Effects of intravenous nicardipine on blood pressure, hemorheology platelet function in arterial hypertension. Dose-effect relations].

In arterial hypertension, hyperviscosity with hemorheological disturbances and platelet dysfunction may play a role in the prognosis and complications of the disease. We studied the effects of Nicardipine (NIC) on these blood disturbances in a group of 21 untreated patients with essential hypertension, aged 25 to 70 years (SBP/DBP = 185 +/- 28/105 +/- 17 mmHg). During one hour before and 4 hours after the IV injection of single doses of 5, 7.5 or 10 mg NIC over 5 min, blood pressure was recorded automatically (Dinamap). Hemorheological variables and platelet function were studied before and 30 min, 3 h and 24 hours after the injection. NIC lowered blood pressure and increased heart rate significantly (At 5 min, SBP = -24 mmHg; DBP = -18 mmHg; HR = +22 b/min). These effects were dose-dependent with rapid onset and short duration (less than 2 hrs). NIC decreased plasma viscosity from 1.36 +/- 0.08 to 1.30 +/- 0.07 Cst; p less than 0.01, whole blood viscosity from 22.4 +/- 2.8 to 20.7 +/- 1.5 mPas; p less than 0.05 for gamma = 0.512 s-1, and erythrocyte filterability with the Ca++ ionophore A 23187 from 16.3 +/- 3.8 to 13.5 +/- 3.1; p less than 0.01. Platelet aggregation with ADP was unchanged, but aggregation with A 23187 decreased from 46.9 +/- 21.2 to 31.3 +/- 25.6; p less than 0.05, as well as plasma levels of beta-thromboglobulin (71.2 +/- 29.8 to 55.4 +/- 24.3 ng/ml; p less than 0.02) and platelet generated malonaldehyde (7.2 +/- 1.8 to 6.7 +/- 1.4 nM/10(9) platelets; NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Clinical evaluation of drugs in chronic cardiac failure].

As the acute complications of cardiovascular diseases are better controlled, the number of patients with chronic heart failure will no doubt increase, together with the need for new treatments of this condition. The effectiveness of these new drugs on the heart function and on the patient's functional status, quality of life and survival must be assessed by very strict evaluation methods. Evaluating the cardiac function requires haemodynamic investigations by proven techniques. Even when taken globally, the haemodynamic values do not always provide information on the patient's clinical and functional status which must therefore be assessed separately, using specific methods. The exercise load, duration and oxygen peripheral consumption measured by established techniques are, in fact, the variables best correlated with the patient's functional status. The effects of drugs must be evaluated at rest and during exercise, but also in short and long term, with a systematic search for tachyphylaxis. Improvements in much less than quality of life much greater than and tolerance of treatment can be evaluated by appropriate questionnaires filled in by the patients. Assessing the effect of any treatment on survival of cardiac patients is always difficult. It requires epidemiological studies which are invariably delicate and costly but cannot be avoided for such an important matter.

Clinical Trials as Topic↗
PubMed1986

[Electrophysiologic effects of intravenous carocainide].

The electrophysiological properties of carocainide a new Class I antiarrhythmic agent (Delalande Research Centre) were studied after intravenous injection of 3.5 mg/kg in 5 minutes in 16 patients aged 24 to 66 years. Five minutes after the injection there was a significant increase (p less than 0.01) in the HV (+/- 12.8 +/- 10.5 msec), AH (+ 21.8 +/- 14 msec) and PR intervals (+ 43.8 +/- 24.2 msec) and in the duration of QRS (+ 20.6 +/- 9.9 msec). The anterograde and retrograde Wenckebach points were decreased (-42 +/- 43 bpm and - 52 +/- 36 bpm respectively, p less than 0.05). All these effects reverted progressively 20 minutes after injection and disappeared by the 40th minute, which corresponds to the pharmaco-kinetic profile of the patient. There were no changes in blood pressure, sinus node function or refractory periods except for the retrograde refractory periods which were prolonged (+ 87 +/- 41 msec). Atrial fibrillation was induced in 2 patients and atrial flutter in 2 others by the extrastimulus technique. These arrhythmias could not be reproduced in these 4 patients during the 40 minutes after injection of carocainide. Five other patients with reciprocating nodal tachycardia induced by atrial extrastimuli had their arrhythmia interrupted by the carocainide injection. We conclude that carocainide acts mainly on atrio-ventricular and intra-ventricular conduction. The results obtained in patients with tachycardias suggest that the product is effective in atrial arrhythmias and paroxysmal junctional tachycardia.

Adult↗
PubMed1986

A case of amiodarone-induced hyperthyroidism and hepatitis: results of clinical laboratory and histological tests.

We report a case of amiodarone-induced hepatitis accompanied by hyperthyroidism in which estimations of amiodarone in blood and in the liver and histological examinations were performed at the start and end of a 3-month interval. Our observation demonstrates the persistence in the liver of amiodarone and its principal metabolite for 3 months after the drug was withdrawn. There was no correlation between the persistence of the drug, the elevation of enzyme levels, and the extent of histological damage in the liver.

Amiodarone↗
PubMed1985

Effects of ketanserin on platelet function and red cell filterability in hypertension and peripheral vascular disease.

Serotonin is a vasoactive substance that acts on blood vessels and platelets but whose primary action lies in its role as an amplifier for other agents. The aim of this work was to study the effects on blood platelets and erythrocytes of the S2-serotonergic receptor antagonist ketanserin. Twenty-seven patients with untreated hypertension and/or intermittent claudication received a bolus intravenous (i.v.) injection of 10 mg ketanserin followed by 2 mg/h during 3 h i.v. infusion. Platelet function and erythrocyte filterability were studied before and 30 min, 3 h, and 24 h after the bolus injection. The results showed decreases of plasma beta-thromboglobulin and platelet factor 4 levels (p less than 0.001) and platelet aggregation induced by epinephrine plus serotonin (p less than 0.001), whereas ADP-induced aggregation remained unchanged 30 min and 3 h after ketanserin administration. Red cell filterability was decreased (p less than 0.01). There was a tendency toward lower mean arterial blood pressure but heart rate remained unchanged. The dual effect of ketanserin on platelet function and erythrocyte filterability might be of great clinical value in hypertension and peripheral vascular disease in which microcirculatory flow is altered.

Adult↗
PubMed1985

[Acute effects of ethanol on the performance and metabolism of the isolated working heart, both normal and failing].

The direct effects of ethanol on cardiac contractility are controversial, probably because of methodological reasons in relation to the choice of appropriate experimental models. We studied the direct effects of 1, 2, 5 and 10 g/l ethanol on myocardial performance and metabolism in the isolated perfused working guinea-pig heart. In the normal heart ethanol induced a dose-dependent, fully reversible depression of cardiac contractility without significant changes of heart rate or cardiac metabolism. In the post-anoxic failing heart this effect was more pronounced. Ethanol had no arrhythmogenic effect even at high concentrations. Finally, it had no measurable effect on anoxic-induced alterations or post-anoxic recovery after a period of 20 minutes of anoxic perfusion. However anoxic-induced lactate production was decreased in hearts pretreated with 10 g/l ethanol. These results demonstrate the direct negative inotropic effect and the lack of chronotropic effect of ethanol. They suggest the lack of effect on excitability. The mechanism of the negative inotropic effect does not seem to be metabolically related since cardiac oxygen consumption and lactate production remained unaltered.

Animals↗
PubMed1985

[Phase imaging of isotopic ventriculographies: contribution to the study of the Wolff-Parkinson-White syndrome].

This study compared the phase images of 12 normal subjects and 14 patients with right ventricular and 5 patients with left ventricular preexcitation. The phase images obtained from equilibrium radionuclide ventriculographies in the left anterior oblique portion with an ECG trigger: Fourier analysis was used to measure the phase and amplitude of the variations. In normal subjects the mean difference in phase was nearly zero: in 12 of the 14 patients with right ventricular preexcitation, right ventricular preceded left ventricular contraction (LV phase - RV phase = + 23 degrees); injection of Ajmaline normalised the ECG and suppressed the premature right ventricular contraction during right ventricular preexcitation (LV phase - RV phase = nearly zero), demonstrating a direct relationship between the abnormal depolarisation and abnormal contraction. In left sided Kent bundles, phase imaging did not seem to show significant premature ventricular contraction under basal conditions. Atrial pacing, which accentuated both left and right electrical preexcitation, increased the difference in ventricular phase. Finally, a satisfactory correlation was observed between the presumed locations of the accessory pathways and the zones of premature right and left ventricular contraction.

Adult↗
PubMed1985

[Hemorheologic disorders in the threatened myocardial infarct syndrome].

Haemorrheological disturbances have already been described in ischaemic heart disease. However, it has not been established whether these changes are secondary to the ischaemia and/or myocardial infarction or whether they play a role in initiating or sustaining the haemodynamic abnormalities which cause infarction. We report our results observed in 14 patients aged 48 to 75 years admitted to the coronary care unit with a diagnosis of acute coronary insufficiency defined as typical persistent anginal pain resistant to glyceryl trinitrate associated with specific ECG changes (without pathological Q waves or increased serum CPK concentrations). Blood samples were obtained on admission for determination of: haematocrit, total blood viscosities at different levels of shear with the patients hematocrit and with corrected hematocrits, total blood filtrability, plasma viscosity and plasma albumin fraction. All patients received 800 mg lidocaine, 40 mg chlorezepate, adequate anticoagulant doses of heparin and a specific antianginal drug: amiodarone, nifedipine or diltiazem. Six patients had a favourable outcome and were discharged from the Coronary Care Unit without myocardial infarction (Group I); the remaining 8 patients (Group II) developed documented changes of myocardial infarction between the 12th and 4th day after admission (see the Table in the text). The haemorrheological parameters on admission of the two patients groups were compared. The abnormalities observed were significantly more severe in the group developing myocardial infarction. This suggests that these changes may play a major role in initiating conditions leading to myocardial necrosis. These observations confirm the results of other workers who have also shown a relationship between the severity of infarction and the incidence of haemodynamic complications and changes in blood viscosity and filtrability.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗