Arthur J. Moss

Bio: Arthur J. Moss is an academic researcher from University of Rochester. The author has contributed to research in topics: Long QT syndrome & QT interval. The author has an hindex of 44, co-authored 117 publications receiving 29779 citations. Previous affiliations of Arthur J. Moss include University of Milan & University of California, Los Angeles.

Risk Stratification and Survival after Myocardial Infarction

Abstract: We assessed the role of physiologic measurements of heart function in predicting mortality after myocardial infarction. Most of the 866 patients enrolled in our multicenter study underwent 24-hour Holter monitoring and determination of the resting radionuclide ventricular ejection fraction before discharge. Univariate analyses showed a progressive increase in cardiac mortality during one year as the ejection fraction fell below 0.40 and as the number of ventricular ectopic depolarizations exceeded one per hour. Only four risk factors among eight prespecified variables were independent predictors of mortality: an ejection fraction below 0.40, ventricular ectopy of 10 or more depolarizations per hour, advanced New York Heart Association functional class before infarction, and rales heard in the upper two thirds of the lung fields while the patient was in the coronary-care unit. Various combinations of these four factors identified five risk subgroups with two-year mortality rates ranging from 3 per cent (no factors) to 60 per cent (all four factors).

Reduction in Inappropriate Therapy and Mortality through ICD Programming

Abstract: We randomly assigned 1500 patients with a primary-prevention indication to receive an ICD with one of three programming configurations. The primary objective was to determine whether programmed high-rate therapy (with a 2.5-second delay before the initiation of therapy at a heart rate of ≥200 beats per minute) or delayed therapy (with a 60-second delay at 170 to 199 beats per minute, a 12-second delay at 200 to 249 beats per minute, and a 2.5-second delay at ≥250 beats per minute) was associ ated with a decrease in the number of patients with a first occurrence of inappropriate antitachycardia pacing or shocks, as compared with conventional programming (with a 2.5-second delay at 170 to 199 beats per minute and a 1.0-second delay at ≥200 beats per minute). RESULTS During an average follow-up of 1.4 years, high-rate therapy and delayed ICD therapy, as compared with conventional device programming, were associated with reductions in a first occurrence of inappropriate therapy (hazard ratio with high-rate therapy vs. conventional therapy, 0.21; 95% confidence interval [CI], 0.13 to 0.34; P<0.001; hazard ratio with delayed therapy vs. conventional therapy, 0.24; 95% CI, 0.15 to 0.40; P<0.001) and reductions in all-cause mortality (hazard ratio with highrate therapy vs. conventional therapy, 0.45; 95% CI, 0.24 to 0.85; P = 0.01; hazard ratio with delayed therapy vs. conventional therapy, 0.56; 95% CI, 0.30 to 1.02; P = 0.06). There were no significant differences in procedure-related adverse events among the three treatment groups. CONCLUSIONS Programming of ICD therapies for tachyarrhythmias of 200 beats per minute or higher or with a prolonged delay in therapy at 170 beats per minute or higher, as compared with conventional programming, was associated with reductions in inappropriate therapy and all-cause mortality during long-term follow-up. (Funded by Boston Scientific; MADIT-RIT ClinicalTrials.gov number, NCT00947310.)

Diagnostic criteria for the long QT syndrome. An update.

Abstract: T he idiopathic long QT syndrome (LQTS) is a congenital disease with frequent familial transmission, characterized primarily by prolongation of the QT interval and by the occurrence of life-threatening tachyarrhythmias, particularly in association with emotional or physical stress.1-5 Among untreated symptomatic patients, lethality is high, with 20% mortality in the first year after the initial syncope and approximately 50% within 10 years3; however, the risk of death varies among different families. This poor prognosis has been significantly improved by the use of pharmacological or surgical antiadrenergic therapy or both, which has reduced long-term mortality to <5%.3,4,6 The availability of effective therapy for this often lethal disease emphasizes the importance of early and accurate diagnosis. Unfortunately, there is frequently a delay in the diagnosis of LQTS, and patients with syncope are often misdiagnosed, most commonly as affected by a seizure disorder. In its most characteristic presentation, with obvious QT prolongation and stress-induced syncope, the diagnosis of LQTS is quite straightforward for physicians aware of the disease. In cases of borderline QT prolongation and/or absence of symptoms, however, a correct diagnosis may be more difficult. It was for this reason that a first set of diagnostic criteria (Table 1) was proposed in 1985.3 The major merit of that proposal was that it provided a logical and quantitative approach to the clinical diagnosis of LQTS by giving a different weight to major and minor criteria. Its major limitation was that it used the traditional, but untested for diagnostic purposes, cutoff value of QT, >440 msec '2. This also resulted in a rather black-and-white situation in which patients were judged to have an entirely normal or abnormal duration of ventricular repolarization on the basis of a difference of a few milliseconds in a measurement fraught with difficulties, such as interobserver variability.7

ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction—Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)

Abstract: Although considerable improvement has occurred in the process of care for patients with ST-elevation myocardial infarction (STEMI), room for improvement exists.[1–3][1][][2][][3] The purpose of the present guideline is to focus on the numerous advances in the diagnosis and management of patients

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

Abstract: ACC/AHA : American College of Cardiology/American Heart Association ACCF/AHA : American College of Cardiology Foundation/American Heart Association ACE : angiotensin-converting enzyme ACEI : angiotensin-converting enzyme inhibitor ACS : acute coronary syndrome AF : atrial fibrillation

Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association

Abstract: WRITING GROUP MEMBERS Emelia J. Benjamin, MD, SCM, FAHA Michael J. Blaha, MD, MPH Stephanie E. Chiuve, ScD Mary Cushman, MD, MSc, FAHA Sandeep R. Das, MD, MPH, FAHA Rajat Deo, MD, MTR Sarah D. de Ferranti, MD, MPH James Floyd, MD, MS Myriam Fornage, PhD, FAHA Cathleen Gillespie, MS Carmen R. Isasi, MD, PhD, FAHA Monik C. Jiménez, ScD, SM Lori Chaffin Jordan, MD, PhD Suzanne E. Judd, PhD Daniel Lackland, DrPH, FAHA Judith H. Lichtman, PhD, MPH, FAHA Lynda Lisabeth, PhD, MPH, FAHA Simin Liu, MD, ScD, FAHA Chris T. Longenecker, MD Rachel H. Mackey, PhD, MPH, FAHA Kunihiro Matsushita, MD, PhD, FAHA Dariush Mozaffarian, MD, DrPH, FAHA Michael E. Mussolino, PhD, FAHA Khurram Nasir, MD, MPH, FAHA Robert W. Neumar, MD, PhD, FAHA Latha Palaniappan, MD, MS, FAHA Dilip K. Pandey, MBBS, MS, PhD, FAHA Ravi R. Thiagarajan, MD, MPH Mathew J. Reeves, PhD Matthew Ritchey, PT, DPT, OCS, MPH Carlos J. Rodriguez, MD, MPH, FAHA Gregory A. Roth, MD, MPH Wayne D. Rosamond, PhD, FAHA Comilla Sasson, MD, PhD, FAHA Amytis Towfighi, MD Connie W. Tsao, MD, MPH Melanie B. Turner, MPH Salim S. Virani, MD, PhD, FAHA Jenifer H. Voeks, PhD Joshua Z. Willey, MD, MS John T. Wilkins, MD Jason HY. Wu, MSc, PhD, FAHA Heather M. Alger, PhD Sally S. Wong, PhD, RD, CDN, FAHA Paul Muntner, PhD, MHSc On behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart Disease and Stroke Statistics—2017 Update