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Dive into the research topics where Dennis M. McNamara is active.

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Featured researches published by Dennis M. McNamara.


Journal of Heart and Lung Transplantation | 2003

Impact of β-blocker therapy on functional capacity criteria for heart transplant listing

Amar L Pohwani; Srinivas Murali; Michael M Mathier; Tammy Tokarczyk; Robert L. Kormos; Dennis M. McNamara; Guy A MacGowan

BACKGROUNDnPeak exercise oxygen consumption is a widely used parameter to determine the need for transplant listing in patients with severe heart failure. Currently, beta-blocker therapy is known to benefit patients with severe heart failure, although it has minimal or no effects on peak exercise oxygen consumption. This raises the hypothesis that peak exercise oxygen consumption transplant-listing criteria are not valid for patients with heart failure who receive beta-blocker therapy.nnnMETHODSnWe compared outcomes in patients with chronic heart failure who underwent heart transplant evaluation with peak exercise oxygen consumption </= 14.0 ml/kg/min and who were treated with beta-blockers (n = 48) or who were not treated with beta-blockers (n = 55).nnnRESULTSnOutcomes were significantly better for patients treated with beta-blockers (combined end-points of death, transplantation as United Network for Organ Sharing [UNOS] Status 1 or 2, and ventricular assist device placement, p = 0.0001). The 1-year survival was 92% and 3-year survival was 71% in the patients treated with beta-blockers, and 69% and 48% in the patients not treated with beta-blockers (compared with UNOS transplant survival data of 92% 1-year and 77% 3-year survival rates).nnnCONCLUSIONSnPatients with chronic heart failure and severe functional impairment who were treated with beta-blockers have significantly better outcomes compared with similarly functionally impaired patients who were not treated with beta-blockers, and these patients would not be expected to derive a survival benefit from transplantation. Thus, in patients treated with beta-blockers, the use of peak exercise oxygen consumption as a criterion to list for heart transplantation may no longer be valid. Alternatively, non-usage of beta-blockers may be a criterion to list for transplantation.


Clinical Transplantation | 2008

Aggressive steroid weaning after cardiac transplantation is possible without the additional risk of significant rejection.

Jeffrey Teuteberg; M.A. Shullo; R. Zomak; Dennis M. McNamara; Kenneth R. McCurry; Robert L. Kormos

Abstract:u2002Background:u2002 Chronic steroid use after cardiac transplantation (CTX) is accompanied by co‐morbidities that are dependent on length of exposure.


Circulation | 1999

AMPD1 Gene Mutation in Congestive Heart Failure New Insights Into the Pathobiology of Disease Progression

Arthur M. Feldman; Daniel R. Wagner; Dennis M. McNamara

In the late 19th century, Sir William Osler noted that patients with myocardial damage due to valvular heart disease had a highly variable clinical course. Some patients remained free of symptoms for a relatively prolonged period of time, whereas others rapidly decompensated.1 More recently, the presence of cardiac dilatation has been found to be a robust predictor of the development of symptomatic congestive heart failure.2 However, in large populations of patients with asymptomatic and nonischemic myocardial dilatation, only a relatively modest percentage developed symptomatic congestive failure during 11 years of follow-up.2 This marked variability in the progression of disease in different individuals led investigators to suspect that these differences might be attributable to variations in genetic background. This hypothesis was further supported by recent evidence suggesting that (1) dilated cardiomyopathy is familial in a larger percentage of cases than was originally recognized,3 (2) specific loci are associated with adult-onset autosomal dominant dilated cardiomyopathy,4 and (3) mutations affecting cytoskeletal proteins are associated with the development of dilated cardiomyopathy.5 However, investigators have not found molecular markers that would predict the development of congestive heart failure in the general population, nor have they identified genetic determinants that might affect the progression of the disease in individual patients.nnIn this issue of Circulation , Loh and colleagues6 provide the first evidence of a correlation between the presence of a genetic marker and the progression of heart failure in patients with dilated cardiomyopathies. Patients having a relatively common mutation in at least 1 allele of the adenosine monophosphate deaminase 1 ( AMPD1 ) gene experienced a significantly longer duration of heart failure symptoms before referral for transplantation evaluation and had a greater chance of surviving without a cardiac transplant than patients homozygous for the wild-type allele. If confirmed in a …


Journal of Heart and Lung Transplantation | 2001

Short-term survival with combined heart-kidney or combined heart-liver transplantation with allografts from a single donor.

Srinivas Murali; Tammy Tokarczyk; J. Ristich; Kenneth R. McCurry; Guy A. MacGowan; Warren D. Rosenblum; Dennis M. McNamara; R. Shapiro; John J. Fung; Robert L. Kormos

institutions in the USA from 1990 through 1999 representing 24,489 patient-years followup. Mean followup was 3.95 yrs (range 0 10 yrs) with 35 % having 5 years of followup. RESULTS: Two distinct overlapping phases of risk for death were presentan early phase merging at 6 months with a constant phase (annual mortality 3.6%). The risk factors that have appeared in the current risk factor model that have not been seen in models from an earlier era at our institutions includein the early phase, obesity (p50.008), cachexia (p50.02), higher creatinine (p,0.0001), history of (h/o) cocaine use (p50.03), h/o significant pulmonary disease (p50.04), h/o cigarette use within 6 months of transplantation (p50.0001). In addition to these risk factors, this analysis identified earlier date of transplantation as being associated with increased mortality (p,0.0001; for transplant in 1990 the predicted probability of death at 3 yrs 5 20%, for transplant in 1997 probability of death at 3 yrs 5 14%). However, while the impact of each of the co-morbid disease risk factors on survival is relatively small (4 to 6% increase in mortality for each risk factor at 9 yrs), the additive effect was significant. INFERENCES: (1) These risk factors , reflecting co-morbid diseases might appear in this model for three reasonslonger followup (with increased power), neutralization of previously identified risk factors, liberalization of recipient criteria. (2) Whatever the reason for the emergence of co-morbid disease risk factors and their impact on survival, there is now clear evidence that, despite improving overall survival, these factors must be a consideration when deciding on transplantation versus alternative therapies, especially in this time of limited donor organ supply.


Archive | 2012

Clinical Investigations Implantable Cardiac Defibrillators and Sudden Death in Recent Onset Nonischemic Cardiomyopathy: Results From IMAC2

Richard Sheppard; Paul J. Mather; Jeffrey Alexis; Randall C. Starling; John P. Boehmer; Vinay Thohan; Daniel F. Pauly; David W. Markham; Mark Zucker; Kevin E. Kip; Dennis M. McNamara; Winston Salem


Archive | 2011

Pharmacogenomics and Pharmacogenetics in Heart Failure

Dennis M. McNamara; Arthur M. Feldman


Heart Failure: A Companion to Braunwald's Heart Disease (Second Edition) | 2011

Chapter 42 – Pharmacogenomics and Pharmacogenetics in Heart Failure

Dennis M. McNamara; Arthur M. Feldman


Journal of Cardiac Failure | 2009

ICDs and Sudden Death in Recent Onset Cardiomyopathy: Results from IMAC

Richard Sheppard; Paul J. Mather; Randall C. Starling; John Boehmer; Jeffrey Alexis; Vinay Thohan; Daniel F. Pauly; David W. Markham; Mark Zuker; Dennis M. McNamara


Heart Failure: Pharmacologic Management | 2007

Chapter 16. Pharmacogenetics

Richard Sheppard; Dennis M. McNamara


Journal of Cardiac Failure | 2006

Gender Differences in Myocardial Histology and Gene Expression in Recent Onset Cardiomyopathy: Implications for Recovery

Jeffrey Teuteberg; Karen M. Janosko; Randall C. Starling; Guillermo Torre-Amione; G. William Dec; Charles McTiernan; Dennis M. McNamara

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Srinivas Murali

Allegheny General Hospital

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Jeffrey Alexis

University of Rochester Medical Center

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Jeffrey Teuteberg

Cardiovascular Institute of the South

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