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Richard Leonard Verrier, Ph.D.

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Overview
My research concentrates on the major public health problem of sudden cardiac death, which claims approximately 325,000 lives per year in the United States alone and occurs without prodromes in at least 30% of cases. The main challenges have been to elucidate the complex pathophysiologic factors involved and to develop novel approaches for identifying individuals at risk for this mode of demise.

In an extensive series of studies, my colleagues and I explored the mechanisms responsible for sudden arrhythmic death. Our investigations demonstrated the pivotal role played by sympathetic nerve activity in triggering life-threatening arrhythmias and defined contributions of beta-adrenergic receptors acting primarily on intracellular calcium handling. We also determined that vagus nerve activity opposes the deleterious influence of adrenergic activity by opposition to presynaptic release of norepinephrine and direct antagonism of second messenger effects. I developed an experimental model in canines that emulated the angerlike state and allowed us to demonstrate that intense behavioral arousal profoundly alters cardiac electrical instability and coronary reactivity, which in turn predispose to malignant arrhythmias. My group and I also systematically studied the impact of sleep states on coronary hemodynamic and cardiac electrophysiologic function. The knowledge base generated was published in Science, Circulation, New England Journal of Medicine, and other leading journals. My basic science studies on neural control of heart rhythm received NIH funding for more than 35 years.

My most significant contributions to clinical innovation emerged during my appointment at Harvard Medical School in Beth Israel Deaconess Medical Center’s Division of Cardiovascular Medicine. In collaboration with my junior colleague, Dr. Bruce D. Nearing, a biomedical engineer, I discovered and published in Science in 1991 evidence that a fundamental electrophysiologic phenomenon, “T-wave alternans,” a beat-to-beat fluctuation in the magnitude of this waveform, is capable of stratifying risk for life-threatening arrhythmia. An extensive series of experiments revealed that T-wave alternans is tracks effects of neural factors, myocardial ischemia, and other proarrhythmic influences. Conversely, antiarrhythmic physiologic and pharmacologic interventions reduce the magnitude of alternans. These findings provided essential scientific underpinnings for utilizing alternans as a clinical marker of arrhythmic risk and target for therapeutic interventions. We developed, patented, and implemented methodologies for quantifying alternans that are compatible with routine ambulatory ECG monitoring and exercise stress testing and employed them to demonstrate that this phenomenon is capable of assessing risk for arrhythmic events in >1,600 post-myocardial infarction and heart failure patients based on ambulatory ECGs recordings. Prediction was also demonstrated in >3,500 consecutive patients with preserved left ventricular function who were referred for routine exercise testing. In 2011, I was lead author of a clinical consensus guideline on T-wave alternans by international experts that was published in Journal of the American College of Cardiology.

In summary, my research program focuses on sudden cardiac death, with dual emphasis on elucidation of pathophysiologic mechanisms and translation from bench to bedside. Our patented, FDA-approved diagnostic risk assessment technology is now in use in clinics and hospitals worldwide.

Mentoring
Chemical Cardioversion of Atrial Fibrillation by Transatrial Delivery of Antiarrhythmic Agents into the Pericardial Space
Summer, 05/15/00 - 08/18/00
A Novel Approach for Prevention and Treatment of Atrial Fibrillation by Intrapericardial L-Arginine Administration
Summer, 06/18/01 - 08/10/01
Characterization of the Efficacy of Intrapericardially Delivered Autonomic Nerve Blocking Agents in Protection Against Ischemia/reperfusion-induced Arrhythmia in Pigs
Summer, 06/01/02 - 08/31/02

Research
The research activities and funding listed below are automatically derived from NIH ExPORTER and other sources, which might result in incorrect or missing items. Faculty can login to make corrections and additions.
  1. R01HL063968 (VERRIER, RICHARD L) May 10, 2001 - Mar 31, 2006
    NIH
    ANTIFIBRILLATORY MECHANISMS OF INTRAPERICARDIAL AGENTS
    Role: Principal Investigator
  2. P01ES008129 (GODLESKI, JOHN J) Jun 28, 1997 - Jun 30, 2003
    NIH
    MECHANISMS OF MORBIDITY/MORTALITY DUE TO AIR PARTICLES
    Role: Co-Principal Investigator
  3. R01HL050078 (VERRIER, RICHARD L) May 19, 1994 - Apr 30, 1999
    NIH
    DYNAMIC TRACKING OF CARDIAC ARRHYTHMOGENESIS IN SLEEP
    Role: Principal Investigator
  4. R01HL032905 (VERRIER, RICHARD L) Sep 30, 1985 - Jun 30, 1990
    NIH
    EFFECT OF SLEEP ON MYCARDIAL PERFUSION AND ARRHYTHMIAS
    Role: Principal Investigator
  5. R01HL035138 (VERRIER, RICHARD L) Sep 30, 1985 - Sep 29, 1989
    NIH
    STRESS, NEUROACTIVE PEPTIDES, AND CARDIAC ARRHYTHMIAS
    Role: Principal Investigator

Bibliographic
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Funded by the NIH National Center for Advancing Translational Sciences through its Clinical and Translational Science Awards Program, grant number UL1TR002541.