Jacob Klein
United States Department of Veterans Affairs
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Circulation | 1988
Paul Dubach; Victor F. Froelicher; Jacob Klein; Oakes Df; M. Grover-McKay; Robert Friis
The objective of this study was to demonstrate the causes, optimal definition, and predictive value of exercise-induced hypotension occurring during treadmill testing. This study included all patients referred for clinical reasons to the Long Beach Veterans Administration Medical Center treadmill laboratory and then followed for a 2-year period for cardiac events. The population consisted of 2,036 patients who underwent testing from April 4, 1984, to May 7, 1987, 131 of whom exhibited exercise-induced hypotension (6.4%). We found that exercise-induced hypotension is usually related to myocardial ischemia or myocardial infarction, is best defined as a drop in systolic blood pressure during exercise below the standing preexercise value, and indicates a significantly increased risk for cardiac events (3.2-fold, p less than 0.005). This increased risk was not found in those having no previous myocardial infarction or no signs or symptoms of ischemia during the exercise test, and the increased risk was also not found in those undergoing a treadmill test within 3 weeks after a myocardial infarction. Exercise-induced hypotension appeared to be reversed by revascularization procedures, but confirmation of a beneficial effect on survival requires a randomized trial. The clinical importance of this study is that we have demonstrated that a drop in systolic blood pressure below standing preexercise values during treadmill testing indicates an increased risk for cardiac events except in certain subsets of patients.
Circulation | 1996
David S. Krantz; Willem J. Kop; Frances H. Gabbay; Alan Rozanski; Marie Barnard; Jacob Klein; Yosef Pardo; John S. Gottdiener
BACKGROUND The morning peak in myocardial ischemia has been related to diurnal variations in physical and mental activities and to postural changes upon awakening. This study assesses (1) the effects of exogenous activity triggers at different times of the day and (2) the contribution of an endogenous (ie, activity- and posture-independent) circadian vulnerability for ambulatory ischemia. METHODS AND RESULTS Sixty-three stable coronary artery disease patients underwent ambulatory ECG monitoring and completed a structured diary assessing physical and mental activities. During 2519 hours of observation, a morning increase in ischemia coincided with increases in physical and mental activities, and an evening decrease in ischemia coincided with a decline in activities. During the morning, ischemic versus ischemia-free periods were more likely to occur with high levels of physical activity (P < .001). High physical activity triggered ischemia to a lesser but still significant extent (P < .05) in the afternoon but not in the evening (P = NS). High levels of mental activity triggered ischemia significantly during the morning (P < .04) and evening (P < .04) but not in the afternoon. When a residualized score procedure was used to correct ischemic time for each patients simultaneously measured activities, for hourly heart rates, or for activity-related heart rate fluctuations, the circadian variation in ischemia was still observed (P < .001), with a peak at 6 AM. A significant increase in ischemia occurred immediately after awakening (P < .05), but activity-adjusted increases in morning ischemia persisted (P < .05) for 2 hours after awakening. CONCLUSIONS Exogenous factors (physical and mental activities) are most potent as triggers of ischemia during the morning hours, and the postural change after awakening contributes to the morning increase in ischemia. There is also evidence for an endogenous, activity-independent circadian influence on ischemic susceptibility that is independent of exogenous factors and that sustains the increase in ischemia upon awakening.
Journal of the American College of Cardiology | 1989
Peter Callaham; Victor F. Froelicher; Jacob Klein; Mona Risch; Paul Dubach; Robert Friis
The purposes of this study were 1) to determine the prognosis of silent ischemia in an unselected group of patients referred for exercise testing, and 2) to assess whether age or the presence of myocardial infarction or diabetes mellitus influences the prevalence of silent myocardial ischemia during exercise testing. The design was retrospective, with a 2 year mean follow-up period. The study group consisted of 1,747 predominantly male in-patients and outpatients referred for exercise testing at a 1,200 bed Veterans Administration hospital. The main result was that the mortality rate was significantly greater (p = 0.02) among patients with abnormal ST segment depression than in patients without ST depression. The presence or absence of angina pectoris during exercise testing was not significantly related to death. The prevalence of silent ischemia was not significantly different among patients categorized according to myocardial infarction or diabetes mellitus status, but was directly related to age. It is concluded that, in patients with an ischemic ST response to exercise testing, the presence or absence of angina pectoris during the test does not alter the risk of death. The prevalence of silent ischemia during exercise testing is not statistically different among patients with recent, past or no myocardial infarction or with insulin-dependent or noninsulin-dependent diabetes mellitus.
Journal of the American College of Cardiology | 1989
Jacob Klein; Victor F. Froelicher; Robert Detrano; Paul Dubach; Ray Yen
The failure of exercise-induced ST segment depression to consistently predict prognosis in patients after myocardial infarction could be a result of population differences and the rest electrocardiogram (ECG). These hypotheses were tested by studying 198 veterans who survived a myocardial infarction, underwent a submaximal predischarge treadmill exercise test and were followed up for cardiac events for 2 years. During the 2 years, 29 deaths, 19 reinfarctions and 28 revascularization procedures were documented. The prevalence of death or reinfarction was two times higher in patients who had exercise-induced ST depression than in patients who did not. However, in the 55 patients without Q waves, the risk increased to 11 times for an abnormal ST response. These findings suggest that exercise-induced ST depression only predicts high risk in patients after myocardial infarction whose ECG at rest does not exhibit Q waves and that differences in the prevalence of rest ECG patterns are the most likely explanation for the failure of agreement among prior studies.
American Journal of Cardiology | 1989
Paul Dubach; Victor F. Froelicher; Jacob Klein; Robert Detrano
The objective of this study was to predict the prognosis of patients who become symptomatic after having undergone coronary artery bypass grafting (CABG) using clinical and exercise test responses. A retrospective analysis was performed of all veterans referred for clinical indications to a Veterans Administration Medical Center for a treadmill test after having undergone CABG. Of 2,044 patients who were exercise tested from April 1984 to May 1987, 296 had previously undergone CABG. Clinical data considered included age, sex, medication and symptom status, history of myocardial infarction, type of myocardial infarction and time from CABG. The exercise test responses considered were MET level, maximal heart rate, maximal systolic blood pressure, chest pain pattern and ST-segment response. During a 2-year follow-up after exercise testing, there were 15 deaths, 11 nonfatal myocardial infarctions, 6 repeat CABGs and 3 percutaneous transluminal coronary angioplasties. Although MET level and maximal heart rate were significantly related to prognosis and no patient who exceeded 8 METs died, the predictive power of these exercise test responses was low and ST-segment depression was not predictive at all. The inability of the exercise electrocardiogram to predict cardiac events in patients after CABG requires the use of other methods of testing to identify those who need invasive studies and intervention.
American Heart Journal | 1993
Jacob Klein; Erwin A. Rodrigues; Daniel S. Berman; Florence Prigent; Susan Y. Chao; Tamara Maryon; Alan Rozanski
Disease-a-month : DM | 1988
Victor F. Froelicher; Duarte Gm; Oakes Df; Jacob Klein; Paul Dubach; András Jánosi
Journal of the American College of Cardiology | 2002
Jacob Klein; Ariel Karawan; Noa Abeles-Raviv; Renat Reens; Dani Bitran; Dan Tzivoni
Journal of the American College of Cardiology | 1991
Jacob Klein; Frances H. Gabbay; Robert H. Howell; David S. Krantz; Susan M. Hedges; Daniel S. Berman; Alan Rozanski
/data/revues/00028703/v131i4/S0002870396902744/ | 2011
C. Noel Bairey Merz; Mady Moriel; Alan Rozanski; Jacob Klein; Daniel Berman