M H Alderman

Albert Einstein College of Medicine, New York City, New York, United States

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Publications (124)1184.34 Total impact

  • Pamela Singer, Hillel Cohen, Michael Alderman
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    ABSTRACT: Although higher sodium intake is known to increase blood pressure, its association with cardiovascular mortality is less established. We examined the association of baseline sodium intake in a hypertensive cohort with all-cause and cardiovascular mortality over a mean follow-up of 18.6 years.
    American Journal of Hypertension 08/2014; 28(3). DOI:10.1093/ajh/hpu141 · 3.40 Impact Factor
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    ABSTRACT: Despite all available therapies, the rates of hospitalization and death from heart failure (HF) remain unacceptably high. The most common reasons for hospital admission are symptoms related to congestion. During hospitalization, most patients respond well to standard therapy and are discharged with significantly improved symptoms. Post-discharge, many patients receive diligent and frequent follow-up. However, rehospitalization rates remain high. One potential explanation is a persistent failure by clinicians to adequately manage congestion in the outpatient setting. The failure to successfully manage these patients post-discharge may represent an unmet need to improve the way congestion is both recognized and treated. A primary aim of future HF management may be to improve clinical surveillance to prevent and manage chronic fluid overload while simultaneously maximizing the use of evidence-based therapies with proven long-term benefit. Improvement in cardiac function is the ultimate goal and maintenance of a "dry" clinical profile is important to prevent hospital admission and improve prognosis. This paper focuses on methods for monitoring congestion, and strategies for water and sodium management in the context of the complex interplay between the cardiac and renal systems. A rationale for improving recognition and treatment of congestion is also proposed.
    Heart Failure Reviews 06/2014; 20(1). DOI:10.1007/s10741-014-9438-7 · 3.99 Impact Factor
  • M.H. Alderman, H. Cohen, S. Madhavan, S. Kivlighn
    Hipertensión y Riesgo Vascular 07/2013; 17(1):38. DOI:10.1016/S1889-1837(00)71010-5
  • Journal of Hypertension 01/2011; 29:e17. DOI:10.1097/00004872-201106001-00045 · 4.22 Impact Factor
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    M H Alderman
    Journal of Human Hypertension 02/2008; 22(1):1-3. DOI:10.1038/sj.jhh.1002269 · 2.69 Impact Factor
  • M Alderman, J S Redfern
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    ABSTRACT: Serum uric acid represents an important, independent risk factor for cardiovascular and renal disease in patients with hypertension, heart failure, or diabetes. Elevated serum uric acid is highly predictive of mortality in patients with heart failure or coronary artery disease and of cardiovascular events in patients with diabetes. Although the mechanism(s) by which uric acid may play a pathogenetic role in cardiovascular disease is unclear, hyperuricemia is associated with deleterious effects on endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemrheology, and aggregation. Whether a reduction in uric acid impacts CV and renal disease remains to be determined. However, recent findings from LIFE in hypertensive patients with LVH suggest the possibility that a treatment-induced decrease in serum uric acid may indeed attenuate cardiovascular risk. Almost one third of the treatment benefit of a losartan-based versus atenolol-based therapy on the composite endpoint (death, myocardial infarction, or stroke) may be ascribed to differences in achieved serum uric acid levels. Clearly, randomized clinical trials are needed to investigate further the long-term cardioprotective benefits issue of reducing hyperuricemia in hypertensive patients.
    Therapeutische Umschau 10/2004; 61(9):547-52.
  • M. Alderman, J. S. Redfern
    Therapeutische Umschau 09/2004; 61(09):0547-0552. DOI:10.1024/0040-5930.61.9.547
  • Michael Alderman, Kala J V Aiyer
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    ABSTRACT: A substantial body of epidemiological and experimental evidence suggests that serum uric acid is an important, independent risk factor for cardiovascular and renal disease especially in patients with hypertension, heart failure, or diabetes. Elevated serum uric acid is highly predictive of mortality in patients with heart failure or coronary artery disease and of cardiovascular events in patients with diabetes. Further, patients with hypertension and hyperuricemia have a 3- to 5-fold increased risk of experiencing coronary artery disease or cerebrovascular disease compared with patients with normal uric acid levels. Although the mechanisms by which uric acid may play a pathogenetic role in cardiovascular disease is unclear, hyperuricemia is associated with deleterious effects on endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemorheology, and aggregation. Xanthine oxidase inhibitors (e.g., allopurinol) or a variety of uricosuric agents (e.g., probenecid, sulfinpyrazone, benzbromarone, and benziodarone) can lower elevated uric acid levels but it is unknown whether these agents reversibly impact cardiovascular outcomes. However, the findings of the recent LIFE study in patients with hypertension and left ventricular hypertrophy suggest the possibility that a treatment-induced decrease in serum uric acid may indeed attenuate cardiovascular risk. LIFE showed that approximately 29% (14% to 107%, p = 0.004) of the treatment benefit of a losartan-based versus atenolol-based therapy on the primary composite endpoint (death, myocardial infarction, or stroke) may be ascribed to differences in achieved serum uric acid levels. Overall, serum uric acid may be a powerful tool to help stratify risk for cardiovascular disease. At the very least, it should be carefully considered when evaluating overall cardiovascular risk.
    Current Medical Research and Opinion 04/2004; 20(3):369-79. DOI:10.1185/030079904125002982 · 2.37 Impact Factor
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    Hypertension 01/2004; 45(4):575-579. · 7.63 Impact Factor
  • M H Alderman, H W Cohen, J Fang
    Journal of Hypertension 01/2004; 22(Suppl. 1):S5. DOI:10.1097/00004872-200402001-00005 · 4.22 Impact Factor
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    ABSTRACT: Serum uric acid (SUA) has been proposed to be an independent risk factor for cardiovascular morbidity and death. Losartan is uricosuric, in contrast to atenolol and to other AII antagonists. The LIFE study was a double-masked, randomized, parallel-group trial in 9193 patients (54% female) with essential hypertension and left ventricular hypertrophy. The participants received once-daily losartan- or atenolol-based treatment. We used Cox regression analysis to compare regimens.Baseline SUA was significantly associated with increased cardiovascular risk (hazard ratio [HR] = 1.024 [95% C.I. 1.017–1.032] per 10 μmol/L, p
    American Journal of Hypertension 05/2003; 16(5). DOI:10.1016/S0895-7061(03)00105-5 · 3.40 Impact Factor
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    ABSTRACT: It has been hypothesized that the level of end-systolic wall stress (sigma(m)) is a feedback signal that regulates the level of hypertrophy. Thus, low levels of sigma(m) may signify inappropriate hypertrophy. To characterize left ventricular (LV) structure and systolic function in hypertensive subjects with low levels of sigma(m), we studied 763 patients. LV function was studied by midwall stress-shortening analysis. Partition values for sigma(m) were derived from a separate group of normal subjects, and the study population was divided into low stress (group I, n = 136), high stress (group III, n = 157), and intermediate stress group II (n = 470). LV chamber and myocardial function were characterized by relating shortening at the endocardium and at the midwall, respectively, to stress. As expected, group III patients had the highest values for systolic blood pressure and LV cavity size but the lowest values for wall thickness and relative wall thickness. Surprisingly, however, there were no significant differences among stress groups with regard to age or body mass index. Contrary to the hypothesis that low levels of stress are indicative of excessive hypertrophy, there were no significant differences among the 3 groups with regard to LV mass or any form of LV mass index. Furthermore, despite lower mean values for afterload, group I patients had significantly lower values for midwall shortening, and this finding was indicative of reduced myocardial function; stress-shortening plots demonstrated that 28% of group I patients fell below 95% CI compared with 10% of group II and only 5% of group III patients. Hypertensive subjects with low values for sigma(m) have more concentric LV geometry (higher relative wall thickness) and, on average, reduced myocardial function.
    American heart journal 04/2002; 143(3):546-51. DOI:10.1067/mhj.2002.119764 · 4.56 Impact Factor
  • J. Fang, M. H. Alderman, J. V. Tu
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    ABSTRACT: Background and Purpose-Age-adjusted stroke mortality in the United States has declined in recent decades. However, the course of stroke incidence is less certain. To address this issue, we determined trends of stroke hospitalization and in-hospital case fatality during 1988-1997. Methods-Stroke hospitalization was estimated from National Hospital Discharge Survey as numerator and Current Population Survey as denominator. Hospitalization rates were determined and stratified by patient characteristics. Average length of hospital stay was also determined. In-hospital mortality was specified by sex, age, and other patient characteristics. The change in these rates over 10 years and average annual percent changes were calculated. Results-During 1988-1997, age-adjusted stroke hospitalization rate increased 18.6% (from 560 to 664/100000; P=0.043), while total hospitalization increased from 592 811 to 821 760. This increase was limited to persons aged greater than or equal to 65 years. Patients in the South had the highest stroke hospitalization rates, and those in the West had the lowest. Overall, 58% of strokes were classified as ischemic, 13% as hemorrhagic, and 29% as other. Over these 10 years, stroke patients having coincident diabetes, hypertension, and congestive heart failure increased 17.4% (P=0.17), 34% (P=0.05), and 31% (P=0.091), respectively. The average length of hospital stay fell from 11.1 to 6.2 days (44.1%; P=0.012). As a result, despite an increase in hospitalizations for stroke, the total person-days in hospital actually decreased by 22% (P=0.06). Conclusions-The declining age-adjusted stroke mortality in the United States has not been accompanied by a fall in hospitalization over recent years. Thus far, however, decrease in length of stay has more than offset increased admission. At the same time, the sharp drop in hospital case fatality rates suggests that continuing decline in stroke mortality may be due, in large part, to improved survival after acute stroke.
    Stroke 10/2001; 32(10):2221-2226. DOI:10.1161/hs1001.096193 · 6.02 Impact Factor
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    J Fang, M H Alderman
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    ABSTRACT: Age-adjusted stroke mortality in the United States has declined in recent decades. However, the course of stroke incidence is less certain. To address this issue, we determined trends of stroke hospitalization and in-hospital case fatality during 1988-1997. Stroke hospitalization was estimated from National Hospital Discharge Survey as numerator and Current Population Survey as denominator. Hospitalization rates were determined and stratified by patient characteristics. Average length of hospital stay was also determined. In-hospital mortality was specified by sex, age, and other patient characteristics. The change in these rates over 10 years and average annual percent changes were calculated. During 1988-1997, age-adjusted stroke hospitalization rate increased 18.6% (from 560 to 664/100 000; P=0.043), while total hospitalization increased from 592 811 to 821 760. This increase was limited to persons aged >/=65 years. Patients in the South had the highest stroke hospitalization rates, and those in the West had the lowest. Overall, 58% of strokes were classified as ischemic, 13% as hemorrhagic, and 29% as other. Over these 10 years, stroke patients having coincident diabetes, hypertension, and congestive heart failure increased 17.4% (P=0.17), 34% (P=0.05), and 31% (P=0.091), respectively. The average length of hospital stay fell from 11.1 to 6.2 days (44.1%; P=0.012). As a result, despite an increase in hospitalizations for stroke, the total person-days in hospital actually decreased by 22% (P=0.06). The declining age-adjusted stroke mortality in the United States has not been accompanied by a fall in hospitalization over recent years. Thus far, however, decrease in length of stay has more than offset increased admission. At the same time, the sharp drop in hospital case fatality rates suggests that continuing decline in stroke mortality may be due, in large part, to improved survival after acute stroke.
    Stroke 10/2001; 32(10):2221-6. · 6.02 Impact Factor
  • H W Cohen, S Madhavan, M H Alderman
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    ABSTRACT: To determine the relationship of moderately high and low concentrations of serum potassium with cardiovascular disease events among treated hypertensive patients. An observational cohort study with prospectively collected data. A worksite treatment program for mild hypertension. All program participants with baseline and at least one annual follow-up measure of serum potassium; 7,653 individuals with 6.7 years mean follow-up met these criteria. Outcome events were admissions to hospital because of cardiovascular disease, and deaths. The research question regarding serum potassium categories was formulated after data collection. The serum potassium concentration (mean +/- 2SD) of the study population was used to define low (3.0-3.5 mmol/l), high (5.1-5.9 mmol/l) and middle (3.6-5.0 mmol/l) categories. Individuals with low (n = 146) and high (n = 226) serum potassium had significantly greater risk for cardiovascular disease events than those in the middle category (n = 7,281). Multivariate adjusted hazard ratios from Cox models were 2.6 [95% confidence intervals (CI) 1.5-4.4] for the low potassium group and 1.7 (95% CI 1.0-2.7) for the high potassium group, with the middle group as reference. Among 1,679 individuals who regularly took diuretics, hazard ratios were 4.3 (95% CI 2.4-7.9) for the low potassium group and 6.7 (95% CI 2.8-15.9) for the high group. Neither low nor high potassium was significantly associated with outcome events for those not regularly using diuretics. These data confirm an association of mild hypokalemia with increased cardiovascular events among diuretic-treated hypertensive patients. In addition, we have found a similar increased cardiovascular risk associated with modest hyperkalemia among these patients. Whether modification of these serum potassium concentrations would alter that risk remains to be determined.
    Journal of Hypertension 08/2001; 19(7):1315-23. DOI:10.1097/00004872-200107000-00018 · 4.22 Impact Factor
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    H W Cohen, S Madhavan, M H Alderman
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    ABSTRACT: Psychological factors have been suspected of contributing to the development of cardiovascular disease. This study examined the relationship between a self-reported history of treatment for depression and subsequent myocardial infarction among treated hypertensive patients. Participants (5564) in a union-sponsored, hypertension control program in New York City, who entered the program during 1981-1994 without a history of cardiovascular disease and who were asked whether they had been treated for depression, were followed in a prospective cohort study. The primary outcome of interest was hospitalization or death due to myocardial infarction. At entry, 3.5% of men and 6.4% of women reported a history of treatment for depression. During 4.9 years (average) of follow-up, 112 fatal and nonfatal myocardial infarctions were recorded. The sex-adjusted relative risk of myocardial infarction was 2.24 (confidence interval = 1.13-4.45). Controlling for known cardiovascular risk factors with multivariate proportional hazards models, history of treatment for depression was significantly associated with subsequent myocardial infarction (hazard ratio = 2.10, confidence interval = 1.04-4.23). A self-reported history of treatment for depression is independently associated with subsequent myocardial infarction in treated hypertensive patients without prior cardiovascular disease. Whether additional or different treatment for depression will be cardioprotective is unknown and merits further study.
    Psychosomatic Medicine 01/2001; 63(2):203-9. DOI:10.1097/00006842-200103000-00002 · 4.09 Impact Factor
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    J Fang, S Madhavan, H Cohen, M H Alderman
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    ABSTRACT: The impact of serum potassium on mortality is inadequately defined. To determine the association of serum potassium with mortality. We analyzed NHANES I Epidemiological Follow-up Study data from 1974-1992. Of 2,992 subjects with baseline serum potassium, 156 were excluded because their vital status was not known. A total of 2,836 subjects with serum potassium within 2.7-5.4 mmol/L were studied. All-cause and cardiovascular mortality were assessed controlling for sociodemographic status, smoking, medical history, and clinical characteristics. At baseline, mean age was 46.6 years, and mean serum potassium was 4.07 mmol/L. Subjects were stratified into three groups by mean +/-1 standard deviation of serum potassium: low, 2.7-3.7 mmol/L (N = 477); middle, 3.8-4.4 mmol/L (N = 1,982); and high, 4.5-5.4 mmol/L (N = 377). The cardiovascular mortality rate per 1,000 person-years adjusted for age, gender, and race for the high serum potassium group (8.1) was significantly higher than the middle (5.3) and low (6.5) serum potassium groups. Further analysis, controlling for age, gender, race, smoking status, cholesterol, and history of diabetes, renal disease, and cardiovascular disease, revealed that the increased cardiovascular mortality among subjects with moderately increased serum potassium was most prominent in those reporting use of diuretics (hazard ratio, 2.65; 95% confidence interval [95% CI], 1.20 to 5.85) and those with abnormal renal function (hazard ratio, 1.89; 95% CI, 1.05 to 3.41). In this general population sample with mostly normal serum potassium, higher serum potassium was independently associated with increased cardiovascular mortality.
    Journal of General Internal Medicine 01/2001; 15(12):885-90. · 3.42 Impact Factor
  • M H Alderman
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    ABSTRACT: The positive relation of sodium intake and blood pressure, first recognized a century ago, has been well established in ecological, epidemiological, and experimental human studies. Equally well established is the association of increasing blood pressure and cardiovascular morbidity and mortality. Indeed, the pharmacological capacity to reduce blood pressure has produced one of the great public health accomplishments of the 20th century. These two facts-the positive relation of blood pressure to strokes and heat attacks and the positive association of sodium intake to blood pressure-underlie the hypothesis that a reduction in sodium intake, by virtue of its hypotensive effect, might prevent strokes and heart attacks. Moreover, even if the effect on blood pressure were in the range of a 1- to 2-mm Hg decline in blood pressure for every 75- to 100-mmol difference in sodium intake, the impact of such a change, applied to the whole population, would be enormous. The problem with this appealing possibility is that a reduction in salt consumption of this magnitude has other-and sometimes adverse-health consequences. The question, therefore, is whether the beneficial hypotensive effects of sodium restriction will outweigh its hazards. Unfortunately, few data link sodium intake to health outcomes, and that which is available is inconsistent. Without knowledge of the sum of the multiple effects of a reduced sodium diet, no single universal prescription for sodium intake can be scientifically justified.
    Hypertension 12/2000; 36(5):890-3. DOI:10.1161/01.HYP.36.5.890 · 7.63 Impact Factor
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    J Fang, S Madhavan, M H Alderman
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    ABSTRACT: An inverse relationship of dietary potassium to stroke mortality in a small community has been previously reported. To further assess this association in a larger sample, we examined data from the first National Health and Nutrition Examination Survey (NHANES I) Epidemiological Follow-up Study. We analyzed baseline data during 1971-1975 and follow-up through 1992. Dietary potassium intake, determined by 24-hour dietary recall at baseline, was available for 9866 subjects. Stroke mortality was recorded through 1992 follow-up. Mean age and dietary potassium at baseline were 55 years and 2084 mg/d; blacks reported significantly lower potassium intake than whites (1606 versus 2178 mg/24 h). During an average of 16.7 years of follow-up, there were 304 stroke deaths. For men, stratified by tertile of dietary potassium intake, age-adjusted stroke mortality rates per 1000 person-years for the lowest dietary potassium group were significantly higher than for the highest intake group, for both whites (1.94 versus 1.17; relative risk, 1.66; 95% CI, 1.32 to 2.14) and blacks (5.08 versus 1.19; relative risk, 4.27; 95% CI, 1.88 to 9. 19). For women, there was no significant difference in stroke mortality between similar levels of potassium intake for either whites (1.61 versus 1.42; relative risk, 1.13; 95% CI, 0.84 to 1.66) or blacks (2.46 versus 3.04; relative risk, 0.80; 95% CI, 0.21 to 2. 01). After stratification by hypertensive status, stroke mortality rates were significantly different by tertile of dietary potassium only for hypertensive men. There was no stroke mortality difference by potassium intake among hypertensive women or nonhypertensive men and women. Multivariate analysis, in which we controlled for caloric intake and other baseline cardiovascular risk factors, revealed that only among black men and hypertensive men was lower dietary potassium intake a predictor of stroke mortality. The previous finding of an association of increasing dietary potassium intake with decreasing stroke mortality has been detected only among black men and hypertensive men in this study.
    Stroke 08/2000; 31(7):1532-7. DOI:10.1161/01.STR.31.7.1532 · 6.02 Impact Factor

Publication Stats

6k Citations
1,184.34 Total Impact Points

Institutions

  • 1986–2014
    • Albert Einstein College of Medicine
      • • Department of Epidemiology & Population Health
      • • Department of Physiology & Biophysics
      New York City, New York, United States
    • Montefiore Medical Center
      New York, New York, United States
  • 2003
    • Sahlgrenska University Hospital
      • Department of Cardiology
      Goeteborg, Västra Götaland, Sweden
  • 2002
    • University of Massachusetts Medical School
      • Department of Medicine
      Worcester, Massachusetts, United States
  • 1996
    • University of Naples Federico II
      Napoli, Campania, Italy
  • 1990–1992
    • Cornell University
      • • Department of Medicine
      • • Cardiovascular Center
      Итак, New York, United States
  • 1991
    • York Hospital
      New York City, New York, United States