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Biomedical subjects

C M Pratt

Publications and source records attributed to C M Pratt.

126 records · Page 7Linked to original sources
PubMed1984

Investigational antiarrhythmic drugs for the treatment of ventricular rhythm disturbances.

Currently available antiarrhythmic drugs possess very poor therapeutic-to-toxic ratios, and therefore, there is a great deal of interest in the development of new investigational agents to suppress ventricular rhythm disturbances. This article includes most of the investigational ventricular antiarrhythmic drugs in which there has been a great deal of recent active investigation and interest. It stresses the different patient populations that have been tested with each of these antiarrhythmic drugs, pointing out those drugs that have been documented to be effective in nonsustained ventricular tachycardia or sustained ventricular tachycardia and sudden cardiac death.

Amiodarone↗
PubMed1984

Popliteal vein pseudoaneurysm: a case report.

This is a case report of an athletic, middle-aged man with a remote history of penetrating right leg trauma who developed a pulmonary embolism, thrombosis of the popliteal vein, a mass in the popliteal fossa, and acute ischemia of the right lower leg. At operation a thrombosed pseudoaneurysm was found arising from a defect in the popliteal vein with extrinsic compression of the popliteal artery. The defect was patched with autogenous vein and the long-term result was excellent. Pseudoaneurysm of the popliteal vein is a previously unreported entity. Popliteal venous aneurysms usually begin with phlebitic or pulmonary thromboembolic manifestations and present a diagnostic challenge. Venous aneurysms in general are uncommon pathologic entities with a diverse etiology; the current etiologic concepts and classification are briefly discussed in the text. A new differential diagnosis for masses in the popliteal fossa is introduced by this report.

Aneurysm↗
PubMed1983

Chronic beta blockade therapy in patients after myocardial infarction.

This report is a review of greater than 18 years of experience with clinical trials that have examined the effect of beta blockers on mortality after acute myocardial infarction (MI). Despite inadequate sample size, a substantial number of the early randomized trials demonstrated a trend toward reduction in mortality after MI using a number of beta blockers. This review highlights the larger prospective randomized trials, especially the Multicenter International Trial of practolol, the Norwegian Multicenter Study of timolol and the Beta-Blocker Heart Attack Trial (BHAT) of propranolol. The combined strength of these long-term trials, comprising greater than 8,000 patients, demonstrates a consistent and statistically significant reduction in mortality after MI. Both the Norwegian timolol study and BHAT further document a substantial reduction in mortality in patients stratified according to risk groups, with a reduction in mortality after complicated or uncomplicated first MI or in patients with prior MI. These 2 studies also document a reduction in sudden death mortality in the first year after MI. Data regarding subendocardial MI is more variable, but the Norwegian timolol study documents a substantial reduction in mortality after subendocardial MI. Based on this review, we recommend treatment of all patients who can tolerate beta blockade after acute MI, beginning in the late hospitalization phase and continuing for at least 2 years.

Adrenergic beta-Antagonists↗
PubMed1983

Ethmozine suppression of single and repetitive ventricular premature depolarizations during therapy: documentation of efficacy and long-term safety.

This study reports a total of 1677 patient days' experience with the use of Ethmozine to suppress ventricular premature depolarizations. A total of 39 patients were studied on three placebo-controlled protocols. Ethmozine, given at a mean total daily dose of 830 mg +/- 318 mg on a dosing schedule of every 8 hours, resulted in a mean plasma Ethmozine level of 0.42 micrograms/ml +/- 0.28 micrograms/ml. In addition to reducing ventricular premature depolarizations from 11,049/24 hr during placebo to 2231/24 hr during Ethmozine therapy (80% reduction), the drug also resulted in a 95% reduction in paired forms and a 99% reduction in total runs of ventricular tachycardia. Ethmozine is extraordinarily well tolerated with only mild side effects of dizziness, perioral tingling, and euphoria, with no serious toxicity requiring discontinuation of therapy. Ethmozine demonstrates great potential as an effective drug in suppressing ventricular premature depolarizations with minimal side effects or toxicity.

Adult↗
PubMed1983

Evaluation of metoprolol in suppressing complex ventricular arrhythmias.

This study documents the extent of suppression of premature ventricular beats which can be achieved with metoprolol, a semiselective beta-adrenergic blocking agent, at doses of 100 to 200 mg daily, utilizing a single-blind placebo-controlled 10-day protocol with continuous ambulatory electrocardiographic recording of 20 patients with cardiac disease and complex ventricular arrhythmias. Metoprolol (200 mg/day) resulted in suppression of 60% of total premature ventricular beats, with couplets (pairs) and ventricular tachycardia decreased 84% and 94%, respectively (all p less than 0.01). Exercise-induced premature ventricular beats, especially ventricular tachycardia, were effectively suppressed. The peak plasma metoprolol level to achieve these results was 72 +/- 34 ng/ml (mean +/- 1 standard deviation). At this plasma concentration, the mean 24-hour heart rate during normal activity was reduced from 78 +/- 8 beats/min (placebo) to 62 +/- 4 (metoprolol 200 mg/day) (p less than 0.001). Beta blockade also was demonstrated by a 20% reduction in heart rate during maximal Bruce exercise testing with metoprolol 200 mg/day. Although resting left ventricular function was not affected by metoprolol, pulmonary function tests show a statistically significant decrease in forced vital capacity, forced expiratory volume in 1 second, and forced expiratory flow rates (25-75) reversible with a beta-2 agonist.

Aged↗
PubMed1983

Analysis of ambulatory electrocardiograms in 15 patients during spontaneous ventricular fibrillation with special reference to preceding arrhythmic events.

Fifteen patients sustained ventricular fibrillation during ambulatory electrocardiographic recording in a period of 3.5 years over which time 16,500 ambulatory electrocardiograms were analyzed (prevalence = 0.09% or 1/1,100). Eight patients died, and seven survived cardiopulmonary resuscitation. Quantitative analysis of hourly ventricular arrhythmias prior to ventricular fibrillation revealed an increased frequency of premature ventricular beats and ventricular tachycardia, especially in the 2 hours immediately before ventricular fibrillation. Ventricular fibrillation was initiated by ventricular tachycardia in all 15 cases. These runs of ventricular tachycardia were characterized by their unusual length (mean = 560 +/- 536 beats) and their rapid rate (241 +/- 45 beats/min). Although an R on T premature ventricular beat initiated ventricular tachycardia and ventricular fibrillation occasionally, the mean prematurity index of the initiating premature ventricular beat was not early (mean = 1.27 +/- 0.28). QT prolongation was present in only 3 of the 15 patients (mean QTc interval = 0.42 +/- 0.06). Left ventricular dysfunction (mean left ventricular ejection fraction = 34.9 +/- 9.9%) and coronary artery disease were nearly always present. The cardiac medications most frequently associated with these patients at the time of ventricular fibrillation were digitalis and quinidine.

Aged↗
PubMed1981

Effects of exercise training on left ventricular performance and myocardial perfusion in patients with coronary artery disease.

To determine the effects of exercise training on left ventricular performance and myocardial perfusion in coronary artery disease, rest and exercise radionuclide angiocardiography and thallium-201 scintigraphy were performed before and after 12 weeks of training in 16 coronary patients. After training, 15 of the 16 patients had improved exercise tolerance; total treadmill exercise duration increased from (mean +/- standard error of the mean) 491 +/- 37 to 602 +/- 31 seconds (p less than 0.01), and the estimated rate of oxygen consumption (VO2 max) increased from 29.4 +/- 1.4 to 33.8 +/- 1.2 ml/kg per min (p less than 0.001). Resting left ventricular ejection fraction increased from 52 +/- 4 to 57 +/- 4 percent (p less than 0.02); no change occurred in left ventricular functional reserve assessed by ejection fraction and regional wall motion response to exercise at the same rate-pressure product before and after training. Myocardial perfusion at equivalent pre- and post-training cardiac work loads during exercise and on redistribution was unchanged by training. It is concluded that in patients with coronary heart disease, physical training increases exercise tolerance, and results in minimal improvement in resting left ventricular systolic performance. Functional reserve of both left ventricular systolic performance and the coronary circulation appears to be unchanged by exercise training. These data suggest that the beneficial effects of training for 12 weeks in patients with coronary artery disease predominantly result from factors other than improvement in left ventricular pump performance or perfusion.

Adult↗
PubMed1981

Demonstration of training effect during chronic beta-adrenergic blockade in patients with coronary artery disease.

Attenuation of exercise-induced increases in heart rate and cardiac output by chronic beta-adrenergic blockade has been thought to compromise benefit of exercise training in patients with coronary artery disease (CAD). To assess this important issue, 35 CAD patients were evaluated by a 3-month walk-jog-cycle training program: 14 patients received no beta blocker (group 1), 14 received propranolol, 30-80 mg/day (group 2), and seven patients received propranolol, 120-240 mg/day (group 3). The extent of CAD, resting heart rate before training blood pressure and VO2 max were similar (p = NS) in each group. The maximal exercise heart rate (mean +/- SD, 147 +/- 21 beats/min in group 1 vs 120 +/- 10 beats/min in group 2 and 115 +/- 12 beats/min in group 3 (both p less than 0.05 vs group 1). The VO2 max before training was 25 +/- 5.0 ml/kg/min in group 1 vs 23 +/- 3.2 ml/kg/min in group 2 and 26 +/- 2.8 ml/Kg/min in group 3 (all p = NS). Training consisted of three 1-hour periods per week at a heart rate of 70-85% of the maximal pretraining heart rate. In each group, VO2 increased (p less than 0.05) after training: group 1, 27%; group 2, 30%; group 3, 46%. The double product was unchanged after training (p = NS) in each group. These data indicate that substantial training effects may be achieved in CAD patients despite therapeutic doses of beta blockers and a reduced training HR. Thus, there appears to be no indication to reduce beta blockers in CAD patients engaged in cardiac rehabilitation.

Adrenergic beta-Antagonists↗
PubMed1975

Efficacy of beta adrenergic blockade in coronary heart disease: propranolol in angina pectoris.

Despite widespread clinical application of propranolol (P) in angina pectoris, convincing evidence of its efficacy has been incomplete, thereby resulting in continued controversy. Its antianginal effectivess was investigated in 20 patients with documented coronary heart disease in a 44-wk study incorporating a prolonged 12-wk lead-in period, individualization of P dosage in a 6-wk dose-finding period, and a 24-wk doule-blind crossover phase. On double-blind placebo, patients had 10.5 +/- 2.1 anginal attacks and consumed 12.8 +/- 3.0 nitroglycerin tablets (NTG) each week compared to 6.6 +/- 1.5 anginal episodes (- 37%, p less than 0.001) and 8.0 +/- 1.7 NTG (-38%, p less than 0.001) when on P. No patient experienced more angina with P than with placebo. In addition, time to onset of chest pain during treadmill exercise was prolonged by P from 190 +/- 16 to 248 +/- 22 sec (+31%, p less than 0.02) and ST depression was reduced from 1.7 +/- 0.21 to 0.99 +/- 0.18 mm (-42%, p less than 0.05). There was correlation (r = 0.64 p less than 0.01) between per cent declines in anginal frequency and resting double product with P. Thus, propranolol favorably altered several indices of myocardial ischemia in severe coronary heart disease. This investigation clearly documents the clinical efficacy of optimal beta adrenergic blockade in coronary disease and provides objective justification for the judicious application of propranolol in treatment of angina pectoris.

Adult↗
PubMedDate not supplied

A clinic's perspective on screening, recruitment and data collection.

This paper summarizes the approach of one university cardiology section with over a decade of experience in conducting National Institutes of Health and pharmaceutical cardiovascular trials. Many of the organizational and personnel issues discussed can be directly applied to most university cardiovascular clinical research settings. Other aspects reflect a very specialized approach but key features can be modified or adapted to smaller individual research clinics. In terms of organizational features, our multi-hospital recruitment effort is co-ordinated by a weekly clinical research conference which is attended by all nurse coordinators and cardiology fellows. Centralization of all clinic facilities and non-invasive laboratories, the central computer facility, and the availability of clinical research inpatient hospital beds facilitate our clinical research effort. An expanded role of the nurse co-ordinator is considered pivotal to trial performance. Suggestions are made as to the identification and recruitment of ideal nurse co-ordinators, maximizing their productivity, and retaining them. The key feature is the physicians' acceptance of the nurse co-ordinator as a colleague. The roles of the principal investigator and clinical cardiology fellows are delineated, and suggestions made for data entry and computer technical expertise to optimize nurse co-ordinator efficiency, allowing total focus on recruitment and follow-up.

Data Collection↗
PubMedDate not supplied

Doppler echocardiography: application to the assessment of successful thrombolysis of prosthetic valve thrombosis.

Prosthetic valve thrombosis remains a significant problem despite anticoagulation therapy and advances in valve design. Thrombolytic therapy offers an alternative approach to valve replacement in patients with high surgical risk. In this article we discuss three cases in which Doppler echocardiography was used to confirm the diagnosis of prosthetic mitral valve obstruction and serially monitor the response of valvular hemodynamic measurements to thrombolysis with intravenous streptokinase. These cases illustrate how the Doppler technique, in addition to allowing the noninvasive diagnosis of prosthetic valve obstruction, is presently the ideal tool to follow serially the effect of thrombolytic therapy on prosthetic valve function.

Aged↗
PubMedDate not supplied

Factors influencing clinical outcomes after revascularization in the asymptomatic cardiac ischemia pilot (ACIP). ACIP Study Group.

BACKGROUND AND AIM: The Asymptomatic Cardiac Ischemia Pilot is the first randomized trial where revascularization involved choice of either coronary bypass or angioplasty used in an early or a delayed symptom-driven approach. One-year outcomes were favorable (reduced recurrent ischemia and adverse outcomes) for an early revascularization strategy (within 4 weeks), compared with an early medical strategy when revascularization was delayed until symptom-driven. This ancillary study examined variables influencing outcomes after these 2 revascularization approaches (early vs. delayed until symptom-driven). METHODS: Participants were clinically stable coronary disease patients with stress-induced and daily life ischemia who underwent revascularization. Characteristics associated with clinical outcomes occurring within the year following revascularization were examined using Cox regression analysis. RESULTS: A total of 262 patients received revascularization; 170 in the early approach and 92 in the delayed symptom-driven approach. Thirty-three patients had adverse outcomes (death, nonfatal myocardial infarction, or repeat revascularization) during 1-year follow-up. The most important independent predictor of improved outcome during the follow-up year was attempted revascularization of > or = 66% of vessels with significant stenosis for the early (risk ratio [RR] 0.25, 95% confidence interval [CI] 0.09-0.67) and the delayed (RR 0.21, CI 0.08-0.58) approaches. Factors such as age, stress test results, and coronary angiographic findings did not predict clinical outcome. CONCLUSIONS: Our findings are important in the planning of a large trial with longer follow-up.

Adult↗
PubMedDate not supplied

IPM, the Methodist Hospital, Houston.

The cardiac rehabilitation department at this institute combines three separate programs into a complete rehabilitation facility. The sequence of programs is designed to provide optimum conditions for maximum physiologic as well as psychologic improvement.

Cardiac Care Facilities↗
PubMedDate not supplied

Sudden death caused by bradycardia and asystole in a heart transplant patient with coronary arteriopathy.

The mechanism of death as a result of allograft ischemic heart disease is not well characterized. Ventricular tachycardia and fibrillation may not be the terminal events they often are in the general population. We report observations in a 41-year-old man with cardiac allograft arteriopathy who died suddenly while wearing an ambulatory monitor. The lethal rhythm was a progressive bradycardia terminating in asystole. Autopsy revealed epicardial and small vessel intramyocardial, coronary arteriopathy, and only mild allograft rejection. It is our belief that ischemia caused the bradycardic sudden death. We would like to hypothesize that prophylactic permanent pacemaker implantation may prevent bradycardic sudden death and improve survival in heart transplant patients with coronary disease.

Adult↗
PubMedDate not supplied

Evolution of hemodynamics after orthotopic heart and heart-lung transplantation: early restrictive patterns persisting in occult fashion.

Though successfully transplanted hearts respond in such a way that individuals remain remarkably asymptomatic, they do not function normally. Characterization of early hemodynamic patterns and their evolvement has not been done. The evolution of hemodynamic indices in 20 patients receiving orthotopic heart (n = 17) or combined heart-lung (n = 3) transplants is therefore documented. In 15 isolated heart recipients, right heart catheterization was performed at 24 to 48 hours, 1 to 2 weeks, 4 to 8 weeks, and greater than 3 months after surgery at the time of routine endomyocardial biopsy. Early, patients had elevated mean blood pressure (96 +/- 14 mm Hg, mean +/- standard deviation), mean right atrial pressure (15 +/- 6 mm Hg), right ventricular end-diastolic pressure (16 +/- 7 mm Hg), mean pulmonary artery pressure (30 +/- 7 mm Hg), and mean pulmonary capillary wedge pressure (19 +/- 6 mm Hg), but normal resting heart rate (96 +/- 14 beats/min) and cardiac output (5.6 +/- 1.6 L/min). Heart rate, blood pressure, and output did not change during follow-up, but right atrial pressure decreased dramatically (4 +/- 2 mm Hg at 3 months), as did right ventricular end-diastolic pressure (4 +/- 4 mm Hg), mean pulmonary artery pressure (21 +/- 8 mm Hg), and pulmonary capillary wedge pressure (11 +/- 4 mm Hg). Analysis of right heart filling dynamics revealed an abnormal inspiratory rise in mean right atrial pressure (15 +/- 6 and 27 +/- 7 mm Hg at 24 to 48 hours) that subsequently resolved. In eight patients whose resting follow-up right heart pressures normalized, rapid volume challenge uncovered occult restrictive right atrial pressure patterns that increased from 4 +/- 4 to 9 +/- 4 mm Hg after infusion of saline solution. Kussmaul's response was not apparent with prevolume infusion, but volume expansion caused appearance of this hemodynamic pattern. All patients had early evidence of tricuspid insufficiency, but in two patients, the Doppler regurgitant fraction was over 50%. These two individuals had hemodynamics similar to the other 15 patients initially, but in contrast, their right heart filling pressures did not change during follow-up. Other significant echocardiographic findings included enlarged atria and increased left ventricular mass in all patients. In two of three combined heart-lung transplant patients, similar hemodynamic patterns were evident. Rejection indices did not correlate with hemodynamic observations. Thus a characteristic evolvement of hemodynamics in heart and heart-lung transplants that mimic dynamics associated with restrictive myocardial disease is documented.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗