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Biomedical subjects

J E Creamer

Publications and source records attributed to J E Creamer.

11 recordsLinked to original sources
PubMed1994

Serum Lp(a) lipoprotein concentration and outcome of thrombolytic treatment for myocardial infarction.

BACKGROUND: Lp(a) lipoprotein has structural homology with plasminogen and has been shown to inhibit plasminogen activation in vitro. OBJECTIVE: To determine whether the serum concentration of Lp(a) lipoprotein present when streptokinase was given in acute myocardial infarction influenced the outcome as judged by electrocardiographic methods. PATIENTS AND DESIGN: Serum Lp(a) lipoprotein concentration was measured in 135 consecutive patients admitted with a diagnosis of acute myocardial infarction who received streptokinase treatment. Recovery from myocardial injury was assessed by the reduction in the sum of ST segment elevation measured from the J point (STJ) in the electrocardiogram immediately before streptokinase was given compared with that three hours later. RESULTS: The serum Lp(a) lipoprotein concentrations were measured within 12 hours of the onset of symptoms of myocardial infarction and were higher than in healthy reference populations. Recovery from myocardial infarction could be assessed from the STJ in 116 patients (86% of the series). Those in whom it could not had bundle branch block, left ventricular hypertrophy, did not survive three hours, or had started intravenous nitrate treatment or some other clinical procedure before or at the time the second electrocardiogram was to be recorded. Patients with reductions in STJ after streptokinase that were > 4 mm (the median decrease) had mean (range) serum Lp(a) lipoprotein concentrations of 41.0 (0.8-220) mg/dl and those with a smaller reduction in STJ had concentrations of 29.1 (1.7-151) mg/dl. The difference was not statistically significant. CONCLUSION: In this study Lp(a) lipoprotein concentration did not significantly influence the outcome of thrombolytic treatment with streptokinase.

Adult↗
PubMed1991

Mechanism of shock associated with right ventricular infarction.

Various mechanisms have been proposed to explain the shock sometimes associated with right ventricular infarction, but only small numbers of patients with clinical shock have been studied. The haemodynamic profiles of seven patients with clinical cardiogenic shock after right ventricular myocardial infarction were studied prospectively. They were selected because all had a stable cardiac rhythm and none had absolute hypovolaemia during the study period. In all of them the mean right atrial pressure exceeded the pulmonary artery occlusion pressure. After treatment with varying combinations of dopamine, dobutamine, and glyceryl trinitrate (titrated to achieve the optimum haemodynamic response) the mean systemic arterial pressure increased, as did the cardiac index. There was an associated increase in the left ventricular stroke work index but the right ventricular stroke work index was unchanged. There was no significant change in heart rate, mean right atrial pressure, or pulmonary artery occlusion pressure. This suggests that the probable mechanism of the shock associated with right ventricular infarction is concomitant severe left ventricular dysfunction.

Aged↗
PubMed1990

Hemodynamic and oxygen transport variables in cardiogenic shock secondary to acute myocardial infarction, and response to treatment.

There are few data on oxygen transport in cardiogenic shock after acute myocardial infarction. This prospective study examined oxygen transport variables in 19 such patients and assessed their responses to treatment. Femoral and pulmonary arterial catheters were inserted before any therapy except correction of hypoxemia by mechanical ventilation in 8 patients, defibrillation (3 patients) or pacing (5 patients). In 3 patients mean arterial pressure was greater than 80 mm Hg and cardiac index greater than 2.1 liters/min/m2 with normal mixed venous oxygen saturation despite simultaneous clinical shock. They recovered with no further treatment. Sixteen patients were treated with varying combinations of intravenous fluids and dobutamine (37 +/- 25 mu/kg/min) and 14 survived long enough for a second set of measurements to be completed. Mean heart rate increased from 83 +/- 22 to 101 +/- 20 beats/min and mean cardiac index from 1.4 +/- 0.5 to 2.5 +/- 0.4 liters/min/m2 (p less than 0.001). Oxygen consumption (VO2) was maintained even when oxygen delivery (DO2) was less than 330 ml/min/m2. After treatment DO2 increased from 230 +/- 69 to 397 +/- 60 ml/min/m2 (p less than 0.001) and VO2 from 103 +/- 31 to 124 +/- 27 ml/min/m2 (p less than 0.05). Mean mixed venous oxygen saturation increased from 54 +/- 16 to 69 +/- 8% (p less than 0.001) and mean oxygen extraction ratio decreased from 48 +/- 16 to 31 +/- 6% (p less than 0.001). There was no correlation between cuff systolic blood pressure and mean arterial pressure before or after resuscitation. Thirteen patients survived to hospital discharge. When cardiogenic shock responds to treatment, large increases in DO2 lead to small increases in VO2 but large increases in mixed venous oxygen saturation, reflecting improved tissue oxygen availability.

Aged↗
PubMed1987

Efficacy of nisoldipine combined with beta-adrenergic-blocking drugs in the treatment of chronic stable angina.

A double-blind, placebo-controlled study was performed to assess whether a new calcium antagonist, nisoldipine, in doses of either 5 mg or 10 mg daily, in combination with beta-adrenergic-blocking drugs (combination therapy) was more effective than beta-adrenergic-blocking drugs alone (single therapy) in the treatment of chronic stable angina. Treatments were assessed at two-week intervals, using exercise electrocardiography and patients' anginal diaries. A significant improvement in exercise capacity and reduction in anginal attacks occurred only during nisoldipine (10 mg daily) combination therapy compared with single therapy. Mean exercise time increased from 419 +/- 146 s (single) to 454 +/- 158 s (p less than 0.02) after combination therapy. Exercise time to onset of 1 mm ST-segment depression improved from 326 +/- 145 s (single) to 331 +/- 139 s after combination therapy, although the change was not significant. Mean number of anginal attacks decreased from 21 +/- 22 (single to 15 +/- 19 (p less than 0.01) during combination treatment, with an associated significant reduction in glyceryl trinitrate consumption. Adverse effects during combined therapy were minor and tolerable. Thus patients limited by exertional angina despite beta-adrenergic-blocking drugs may obtain supplemental relief of angina and myocardial ischemia with the addition of nisoldipine in a dose of 10 mg daily.

Adrenergic beta-Antagonists↗
PubMed1987

The proarrhythmic effects of antiarrhythmic drugs.

Although antiarrhythmic drugs are effective for controlling cardiac arrhythmias, they may also induce or exacerbate them. Case reports have appeared implicating all classes of antiarrhythmic drugs. It is difficult to assess the size of the problem in practice, as it varies with different subgroups of patients, but rates of up to 13% have been found where proarrhythmic effects were actively sought. Their occurrence is affected both by the electrophysiologic characteristics of the drugs and by the arrhythmia substrate. Mechanisms of proarrhythmic effects may be classified according to the electrophysiologic and hemodynamic effects of the drugs. Detection of drug-induced arrhythmias depends on appreciation of the problem by physicians and, although there are few clear predictors, some form of monitoring of antiarrhythmic drug treatment is recommended. Management of such arrhythmias when they occur involves withdrawal of the offending agent, correcting contributory factors, and reassessing the initial arrhythmia and the strategy for its management.

Anti-Arrhythmia Agents↗
PubMed1986

Acute and chronic effects of sotalol and propranolol on ventricular repolarization using constant-rate pacing.

Sotalol and propranolol were administered both intravenously and orally in conventional equipotent beta-blocking doses to 8 patients with permanent programmable ventricular pacemakers to study their effects on ventricular repolarization. Sotalol prolonged the QT interval by 6.5% (430 to 455 ms) after intravenous administration (p less than 0.01) and by up to 11.5% (430 to 483 ms) after 4 weeks of oral treatment (p less than 0.001). This was entirely due to prolongation of the JT interval, since there was no effect on QRS duration. The magnitude of QT and JT prolongation related to the serum level but the correlation was not statistically significant. QT prolongation was exaggerated after chronic treatment despite lower serum levels of sotalol (2.0 micrograms/ml) compared with levels after acute administration (3.5 micrograms/ml). After propranolol was given, there was no consistent change in QT or JT intervals, and although there was a tendency to slight prolongation of QT interval, by 2.5% after chronic oral administration, this was not statistically significant. This suggests that the prolongation of ventricular repolarization by sotalol is not caused by beta-blockade, but by its class III activity, and that chronic treatment increases the effect. There was no significant effect on chronic ventricular pacing threshold after intravenous or oral administration of either drug.

Adult↗
PubMed1986

The effects of oral nitrendipine and propranolol, alone and in combination, on hypertensive patients with special reference to AV conduction.

The effects of oral nitrendipine and oral propranolol, alone and in combination, on AV conduction have been examined in 11 patients with essential hypertension in whom arterial pressure was not adequately controlled despite treatment with thiazide diuretics. The study was performed double-blind. After a drug free period of 1 week, the patients received two 7 day courses of drug therapy after initial control measurements. Five of the eleven patients were randomised to receive nitrendipine 20 mg daily, the other six patients received propranolol (Inderal LA 160 mg daily) for the first week of therapy. During week 2, 10 patients received combined therapy. In the 10 patients who completed the study, oral nitrendipine, given either alone or in combination with oral propranolol, had no significant effect on resting PR, QRS, QT intervals nor on AV conduction as assessed by ambulatory electrocardiography. Propranolol did not affect the resting PR interval but significantly increased PR intervals on the ambulatory ECG recordings during single and combined therapy. However the maximum PR intervals remained within normal limits.

Administration, Oral↗
PubMed1986

Clinical experience with a software based tachycardia reversion pacemaker.

Current generation antitachycardia pacemakers suffer from limitations concerning detection and distinction of pathological tachycardia and also from the termination modes available. To overcome many of these limitations, a new device (Intermedics Intertach 262-12) has been developed, and has now been implanted in nine patients, all of whom had failed drug treatment. Since implantation, all patients have complete control of their arrhythmias, and only one now requires drug therapy.

Adult↗
PubMed1985

Successful treatment of atrial tachycardias with flecainide acetate.

Intravenous flecainide successfully terminated atrial tachycardia in three patients. Maintenance treatment with oral flecainide prevented the recurrence of tachycardia for up to three years. These results suggest an additional use for flecainide which should be further explored.

Adult↗