Relevance of forearm samples for plasma catecholamine determinations.
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Blood Specimen Collection↗
Biomedical subjects
R Bernard
Publications and source records attributed to R Bernard.
[Comparison of the effects of intravenous diltiazem and a placebo on hemodynamics and blood gases in the acute phase of myocardial infarction].
We compared the effects on hemodynamics and blood gases of an intravenous perfusion of diltiazem vs placebo, administered randomly and in a double-blind fashion, to 20 patients with acute myocardial infarction (less than 24 hours). After 130 minutes, we noted a significant reduction of the arterial blood pressure and the systemic vascular resistances; the other hemodynamic variable are not significantly modified. Diltiazem causes a slight but significant decrease of PaO2 after 130 minutes in intravenous perfusion. This effect is secondary to an increase of the arterio-alveolar gradient in O2, reflecting an increase of the pulmonary shunt. This has no clinical consequence since the oxygen transfer remains stable. In conclusion, intravenous diltiazem administered red in the acute phase of myocardial infarction is well tolerated hemodynamically and clinically. It may induce a minimal arterial hypoxemia by increasing the arterio-alveolar gradient in oxygen.
Adult↗
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.
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.
Adult↗
Predictors of early death after acute myocardial infarction: two months follow-up.
Clinical variables and the results of non-invasive tests (exercise test, echocardiogram, gated equilibrium radionuclide ventriculography and 24 h ECG) were recorded in a series of 202 patients who left the hospital alive after an acute myocardial infarction. The short term (two months) predictive value of all these data was prospectively assessed by uni- and multi-variate analysis. The best correlation with early death was observed with the variables related to the extent of infarction and left ventricular dysfunction, namely: early clinical signs of heart failure, high peak CK-MB level, complete bundle branch block, increased cardiothoracic ratio on chest X-Ray, number of Mets reached during the stress test, echocardiographic dyskinesia index, and decreased left ventricular ejection fraction as measured by radionuclide ventriculography. Using multi-variate stepwise discriminant analysis, the following independent prognostic factors appeared by order of entry: early clinical signs of heart failure, peak CK-MB level and cardiothoracic ratio on chest X-Ray. These results highlight the short-term predictive value of the data related to left ventricular dysfunction and especially of simple clinical data for patients surviving an acute myocardial infarction.
Acute Disease↗
Central inhibition of sympathetic overdrive by clonidine in acute myocardial infarction with systolic hypertension. Haemodynamic study.
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 less than 0.01) and diastolic (81 +/- 4 to 60 +/- 3 mm Hg, p less than 0.01) blood pressures as well as the systemic vascular resistance (26 +/- 2 to 20 +/- 1 IU, p less than 0.01). The cardiac index was reduced from 2.8 +/- 0.2 to 2.4 +/- 0.2 l/min X m2, p less than 0.01. This change was related to a reduction of the heart rate (92 +/- 4 to 81 +/- 4 beats/min, p less than 0.01) as the stroke index was unchanged. Pulmonary wedge pressure (15 +/- 3 to 10 +/- 2 mm Hg, p less than 0.01) and rate pressure product (18.034 +/- 1.159 to 11.274 +/- 917 mm Hg, beats/min, p less than 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 less than 0.02) and oxygen transport (433 +/- 41 to 409 +/- 36, p less than 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.
Aged↗
[Choice of a class I intravenous anti-arrhythmic drug in severe ventricular arrhythmias].
In the choice of a Class I intravenous antiarhythmic medication for the treatment of threatening ventricular extrasystoles, one must take into account the speed of action of the product, its effects on hemodynamics and conduction as well as its efficacy. The rapidity of action implies the ability to reach, without delay, a therapeutic plasma level which will depend upon the distribution volume and the dose injected. An effective plasma level may be quickly reached following the intravenous administration of lidocain, disopyramide, lorcainide, tocainide and flecainide. All antiarhythmic medications have an unfavorable effect on hemodynamics; xylocain and ajmaline seem to depress the least the left ventricular function, followed by lorcainide. Unfavorable effects on the atrio-ventricular conduction are observed with substances of type IC; the duration of QRS may be affected as well by antiarhythmic medications IA and IC, with a lengthening of QT being mostly noted type IA medications. Comparison of the efficacy of antiarhythmic medications requires a strict methodology and the current data from the literature do not permit to assert with certainty the superiority of one antiarhythmic medication over the others.
Anti-Arrhythmia Agents↗
Blood gas and hemodynamic changes induced by the treatment of pulmonary congestion with vasodilators in the acute phase of myocardial infarction.
The effects of vasodilators on hemodynamics and blood gases was assessed in 31 patients suffering from acute myocardial infarction (AMI) who had clinical signs of left ventricular failure with high pulmonary wedge pressure (PWP greater than 15 mm Hg). Molsidomine (n = 10), phentolamine (n = 12) and sulmazol (n = 9) were administered intravenously to decrease the PWP by 20%. Molsidomine significantly decreased PWP after one hour with a mild increase in cardiac index (CI) inducing a slight decrease in paO2 (64 to 59 mm Hg, P less than 0.1) with no change in p-vO2. Phentolamine and Sulmazol significantly increased the CI and decreased the PWP, with a substantial increase in the pv-O2 (28 to 32 mm Hg, P less than 0.005 and 28 to 31 mm Hg, P less than 0.001) and no significant change in the paO2 (60 to 65 mm Hg, P less than 0.1 and 68 to 69 mm Hg, NS). None of these drugs significantly changes the pulmonary vascular resistance (PVR) which would explain the lack of any significant change in paO2. The treatment of pulmonary congestion in AMI by either pure venous (molsidomine) or arteriolar and venous (phentolamine and sulmazol) vasodilators does not worsen obviously pre-existant hypoxemia.
Adult↗
[Hemodynamic repercussions and clinical tolerance of 6 class I anti-arrhythmia agents in acute myocardial infarction].
Clinical safety and hemodynamic repercussions were studied after administration of six class I antiarrhythmics (xylocaine, ajmaline, mexiletine, lorcainide, indecainide and tocainide) to patients presenting acute myocardial infarction without complications. The hemodynamic parameters monitored generally followed the same trends. A significant decrease of more than 10 per cent of the initial value was seen in systolic blood flow after injection of lorcainide, indecainide and tocainide. Peripheral vascular resistance increased moderately. Pulmonary capillary pressure increased by more than 40 per cent of the starting value after administration of mexiletine, indecainide and tocainide (significant increase in case of mexiletine). These changes in patients presenting infarction without complications are not of clinical importance. There were, however, two very severe cases of hemodynamic reaction after administration of mexiletine. Other signs of intolerance were seen, but they were of minor importance and administration of the drugs was not interrupted. Xylocaine and ajmaline produced the smallest depression of left ventricular functional activity in these patients.
Ajmaline↗
Randomised trial of intravenous recombinant tissue-type plasminogen activator versus intravenous streptokinase in acute myocardial infarction. Report from the European Cooperative Study Group for Recombinant Tissue-type Plasminogen Activator.
In a single-blind randomised trial in patients with acute myocardial infarction of less than 6 h duration, the frequency of coronary patency was found to be higher after intravenous administration of recombinant human tissue-type plasminogen activator (rt-PA) than after intravenous streptokinase. 64 patients were allocated to 0.75 mg rt-PA/kg over 90 min, and the infarct-related coronary artery was patent in 70% of 61 assessable coronary angiograms taken 75-90 min after the start of infusion; 65 patients were allocated to 1 500 000 IU streptokinase over 60 min, and the infarct-related vessel was patent in 55% of 62 assessable angiograms. The 95% confidence interval of the differences ranges from +/- 30 to -2% (p = 0.054). Bleeding episodes and other complications were less common in the rt-PA patients than in the streptokinase group. Hospital mortality was identical in the 2 treatment groups. At the end of the rt-PA infusion the circulating fibrinogen level was 61 +/- 35% of the starting value, as measured by a coagulation-rate assay, and 69 +/- 25% as measured by sodium sulphite precipitation. After streptokinase infusion, corresponding fibrinogen levels were 12 +/- 18% and 20 +/- 11%. In the rt-PA group only 4.5% of the fibrinogen was measured as incoagulable fibrinogen degradation products, compared with 30% in the streptokinase group. Activation of the systemic fibrinolytic system was far less pronounced with rt-PA than with streptokinase.
Adult↗
Effects of molsidomine on hemodynamics and blood gases in acute myocardial infarction with left heart failure.
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.
Aged↗
Criteria for intraventricular conduction disturbances and pre-excitation. World Health Organizational/International Society and Federation for Cardiology Task Force Ad Hoc.
In an effort to standardize terminology and criteria for clinical electrocardiography, and as a follow-up of its work on definitions of terms related to cardiac rhythm, an Ad Hoc Working Group established by the World Health Organization and the International Society and Federation of Cardiology reviewed criteria for the diagnosis of conduction disturbances and pre-excitation. Recommendations resulting from these discussions are summarized for the diagnosis of complete and incomplete right and left bundle branch block, left anterior and left posterior fascicular block, nonspecific intraventricular block, Wolff-Parkinson-White syndrome and related pre-excitation patterns. Criteria for intraatrial conduction disturbances are also briefly reviewed. The criteria are described in clinical terms. A concise description of the criteria using formal Boolean logic is given in the Appendix. For the incorporation into computer electrocardiographic analysis programs, the limits of some interval measurements may need to be adjusted.
Bundle-Branch Block↗
[Aspects of the physiopathology of left cardiac insufficiency in the acute stage of myocardial infarct: therapeutic implications].
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Heart Failure↗
High-dose intravenous thrombolytic therapy in acute myocardial infarction: efficiency, tolerance, complications and influence on left ventricular performance.
Ten patients with acute myocardial infarction (AMI) underwent coronarographic studies before, immediately after and ten days after an intravenous infusion of 1 500 000 I.U. streptokinase (STK). Mean time between onset of symptoms to initiation of STK infusion was 03 hours 34 minutes. Occlusion of the infarct-related vessel was present in all of them and successful thrombolysis was obtained in 8 of the patients. Systemic fibrinolytic activity was present in 9 patients, one of whom required a transfusion of blood because of severe bleeding. At ventriculography, the global left ventricular ejection fraction and the regional ventricular ejection fraction, whatever the area involved, showed no significant improvement 10 days after the procedure. This suggests that high-dose intravenous STK in AMI, although causing an effective thrombolysis, does not seem to improve early myocardial function.
Adult↗
[Hemodynamic effects of phentolamine in acute and chronic mitral insufficiency after myocardial infarction].
The haemodynamic effects of phentolamine, a selective alpha blocker, were studied in patients with severe mitral regurgitation and cardiac failure in the acute (Group I, 7 cases) or chronic (Group II, 7 cases) phase of myocardial infarction. After 1 hour's treatment a rise in cardiac index (+29 p. 100, p less than 0.001 and +36 p. 100, p less than 0.01), and systolic index (+19 p. 100, p less than 0.001 and +19 p. 100, p less than 0.05) were observed; the V wave of the pulmonary capillary pressure recording decreased (-32 p. 100, p less than 0.005; -26 p. 100, p less than 0.01). Oxygen transport also increased by an average of 36 p. 100, p less than 0.001, without a significant change in arterial pp O2. These results show that phentolamine improves the haemodynamics and decreases mitral regurgitation in the acute and in the chronic phases of myocardial infarction.
Acute Disease↗
[Intracavitary thrombi in the acute phase of myocardial infarction].
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Acute Disease↗
[Systemic embolisms in the acute phase of myocardial infarction].
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Acute Disease↗
[Anticoagulants in myocardial infarction].
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Acute Disease↗
Hemodynamic effects of dobutamine in patients below and over 65 years, with left heart failure secondary to an acute myocardial infarction.
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.
Age Factors↗