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M M Mower

Publications and source records attributed to M M Mower.

At least 19 recordsLinked to original sources
PubMed2000

Biventricular pacing in end-stage heart failure improves functional capacity and left ventricular function.

BACKGROUND: Asynchronous patterns of contraction and relaxation may contribute to hemodynamic and functional impairment in heart failure. In 1993, we introduced biventricular pacing as a novel method to treat heart failure by synchronous stimulation of the right and left ventricles after an appropriate atrioventricular delay. The objectives of this study were to assess the early and long-term effects of this therapy on functional capacity and left ventricular function in patients with severe heart failure and left bundle branch block. METHODS AND RESULTS: Twelve patients with end-stage congestive heart failure, sinus rhythm and complete left bundle branch block were treated with biventricular stimulation at optimized atrioventricular delay. The NYHA functional class and maximal bicycle exercise capacity were assessed. Systolic and diastolic left ventricular function were studied with echocardiography and radionuclide angiography. Data was collected at various intervals during 1-year follow-up. Cumulative survival [95% CI] was 66.7% [40.0,93.4] at 1 year and 50 % [21.8, 78.2] at 2 and 3 years. Median NYHA class improved from class IV to class II at 1 year (p=0.008). After 6 weeks an increase in exercise capacity occurred, which was sustained. A less restrictive left ventricular filling pattern, an increase in dP/dt and left ventricular ejection fraction, and a decrease in mitral regurgitation were observed early and long-term. CONCLUSIONS: Biventricular pacing at optimized atrioventricular delay results in improvement in functional capacity, which is associated with improved systolic and diastolic left ventricular function, and a decrease in mitral regurgitation during short- and long-term follow-up.

Bundle-Branch Block↗
PubMed1997

Effect of varying pacing waveform shapes on propagation and hemodynamics in the rabbit heart.

The propagation characteristics of myocardium stimulated with anodal, cathodal, and equiphasic biphasic pacing pulses were examined in Langendorff-perfused rabbit hearts. Conduction velocity measurements were made using an array of bipolar extracellular electrodes, transmembrane potentials recorded using floating intracellular microelectrodes, and hemodynamics measured by fluid-filled catheter transducer systems. Anodal (A) stimulation pulses improved the electrical conduction at all the stimulus amplitudes tested in both longitudinal (e.g., 5 V 2-msec pulse: [A] 54.9 +/- 0.7 cm/sec; cathodal [C] 49.7 +/- 1.5 cm/sec) and transverse (e.g., 5 V 2 msec pulse: [A] 31.3 +/- 1.7 cm/sec; [C] 23.3 +/- 2.9 cm/sec) directions. Microelectrode recordings verified that increased conduction velocities of the anodal pulses were associated with faster upstrokes of the action potentials. The increased threshold associated with anodal pulses may be overcome by using a biphasic (B) waveform, in effect adding a second phase (e.g., 2-msec pulse: [A] 2.03 +/- 1.3 V; [C] 3.85 +/- 1.5 V; [B] 2.15 +/- 0.9 V). The conduction speeds achieved by the biphasic pulses were found to be comparable to the equivalent anodal pulses (e.g., 5 V 2-msec pulse: [B] 55.2 +/- 1.7 cm/sec longitudinal and 32.4 +/- 2.1 cm/sec transverse). It is postulated that the enhanced conduction by anodal and biphasic pulses may be due to preconditioning of the myocardium before stimulation, resulting in more vigorous action potential upstrokes. In preliminary experiments, it was observed that improved conduction elicited by these pulses also resulted in enhanced contractility as measured by shortened electromechanical delays and faster rate of rise of pressure development (dP/dtmax: [A] 25.4 +/- 0.4 mm Hg/sec; [C] 19.4 +/- 0.8 mm Hg/sec; [B] 25.7 +/- 1.2 mm Hg/sec, respectively). Use of novel hybrid pulses involving an anodal component may offer a way for implanted pacemakers to enhance the electro-mechanical response of the heart.

Action Potentials↗
PubMed1997

Overview of implantable cardioverter-defibrillator in reducing total mortality in the high-risk coronary patient.

The idea of an implantable cardioverter-defibrillator (ICD) was conceived in the mid- to late 1960s, and working circuits were built and tested at Sinai Hospital of Baltimore in the fall of 1969. After a number of years of preclinical testing, the device entered clinical trials at The Johns Hopkins Hospital in February, 1980, and received Food and Drug Administration (FDA) approval in 1985. The device appeared to be highly effective, but there was criticism that it had not been tested in a randomized fashion, and there was the feeling that drugs would eventually prove to be superior. In 1989, a series of randomized clinical trials were begun. One of these trials, the Multicenter Automatic Defibrillator Implantation Trial (MADIT), has concluded and the outcome has recently been published. The results are landmark in importance and lead the way towards rational treatment of serious ventricular arrhythmia patients in clinical practice.

Animals↗
PubMed1995

Automatic implantable cardioverter-defibrillator: history and future developments.

The clinical experience with automatic internal defibrillation is now extensive, with over 65,000 patients treated since the first implantation in 1980. The success of the technique is largely the result of the perseverance and foresight of Dr. Michel Mirowski, although many people were eventually involved. The author was privileged to participate almost from the very inception of the project. The early experiments and some of the difficulties along the way leading up to the present extensive favorable human experience are described.

Defibrillators, Implantable↗
PubMed1994

AVID necessity.

Explore the source record for details and available documents.

Anti-Arrhythmia Agents↗
PubMed1993

Clinical results with nonthoracotomy ICD systems.

The results of two separate US Food and Drug Administration clinical trials that involved endocardial and epicardial leads were compared with regard to patient demographics, detection and conversion characteristics, and subsequent clinical course including long-term survival experience. The patient groups, although not strictly contemporaneous, were sufficiently similar to allow meaningful comparisons. There were no significant differences in detection of induced arrhythmias and ability to convert them. The surgical mortality, infection rate, and incidence of other morbid complications were lower in patients who had received endocardial leads; however, the differences did not reach statistical significance. Survivals through 1 year of follow-up were uniformly high. These results suggest that the performance of the endocardial lead system is comparable to existing epicardial leads in similar patient populations.

Actuarial Analysis↗
PubMed1993

Relation between upper limit of vulnerability and defibrillation threshold in humans.

BACKGROUND: In the canine model, an upper limit of shock strength exists that can induce ventricular fibrillation during the vulnerable period of the cardiac cycle. This shock strength (the upper limit of vulnerability) closely correlates with the defibrillation threshold and supports the "upper limit of vulnerability" hypothesis of defibrillation. It is not known whether an upper limit of vulnerability exists in humans or whether this limit correlates with the defibrillation threshold. METHODS AND RESULTS: In 13 patients undergoing implantable cardioverter-defibrillator implantation, the shock strengths associated with a 50% probability of reaching the upper limit of vulnerability (ULV50) and a 50% probability of reaching the defibrillation threshold (DFT50) were determined by the up-down algorithm. The ULV50 was determined only for the mid-upslope of the positive T waves and for the mid-downslope of the negative T waves. No major complications occurred during surgery. An upper limit of vulnerability was demonstrated in each patient. The ULV50 was 300 +/- 138 V or 6.8 +/- 5.8 J, which was significantly lower than the DFT50 of 347 +/- 167 V (p = 0.038) or 9.1 +/- 7.3 J (p = 0.013). The correlation between the ULV50 and the DFT50 was significant (r = 0.90, p < 0.001 for voltage; r = 0.93, p < 0.001 for energy). CONCLUSIONS: An upper limit of vulnerability is present in humans. There is a significant correlation between the ULV50 and the DFT50, and the ULV50 is significantly lower than the DFT50.

Algorithms↗
PubMed1992

The automatic implantable cardioverter-defibrillator. Long-term clinical experience and outcome at a hospital without an open-heart surgery program.

From November 1982 through April 1989, 111 patients with refractory sustained ventricular tachycardia/fibrillation had the automatic cardioverter-defibrillator implanted at our institution, the first community hospital involved in implantation of such a device. We have reviewed our long-term clinical experience to assess the feasibility, learning curve, and efficacy of device implantation in a facility with cardiac electrophysiology expertise but without open-heart surgery facilities. All patients were considered inoperable or at high risk for other concomitant surgery. Eighty-six patients (77%) underwent uneventful implantation. Nine patients (8%) died prior to hospital discharge. Operative mortality declined from 10.9% to 5.4% during the first half (55 patients; November 1982 through September 1986) and second half (56 patients; October 1986 through April 1989) of the experience. Other postoperative complications occurred in 16 patients (14%), 12 of whom experienced complications during the first half of the experience. At 22 +/- 20 (mean +/- SD) months' follow-up, 78 (76%) of 102 patients discharged were alive, and 24 patients (24%) had died. Fifty patients (49%) had experienced at least one automatic cardioverter-defibrillator discharge associated with hypotensive symptoms. The actuarial incidence of sudden death at 1, 2, and 3 years was 1.2%, 5.5%, and 6.2%, respectively. We concluded that the automatic implantable cardioverter-defibrillator is an effective therapy for refractory ventricular tachycardia/fibrillation and that device implantation at community hospitals with an experienced cardiac electrophysiology team is both feasible and practical.

Adult↗
PubMed1992

Case report: myocardial ischemia: an overlooked substrate in syncope of aortic stenosis.

The cause of the syncope in aortic stenosis has been the subject of controversy partly because only a few patients have been monitored during their syncopal episodes. Among the mechanisms proposed are hypersensitive carotid sinus, complete A-V block, ventricular arrhythmias, and ischemic myocardial depression. It is now accepted that the syncope is caused by a vasodepressor response from stimulation of left ventricular baroceptors, resulting in reflex hypotension and bradycardia. This case report describes a patient who developed a syncopal episode during stress testing. Although the mechanism for the syncope is consistent with the vasodepressor response, ischemic changes were observed in the electrocardiogram before the development of syncope. Review of literature shows that, although different mechanisms for syncope have been described, all reported patients manifested myocardial ischemia before the development of their syncopal episodes even when the syncope was nonexertional and clearly caused by a vasodepressor response. The authors conclude that, independent of the mechanism proposed, myocardial ischemia is overlooked as an important substrate in which the syncopes are precipitated in aortic stenosis.

Aged↗