M H Alderman

Yeshiva University, New York, New York, United States

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Publications (122)1127.4 Total impact

  • Pamela Singer · Hillel Cohen · Michael Alderman ·
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    ABSTRACT: Background: 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. Methods: Three thousand five hundred five subjects were participants in a worksite hypertension program. Sodium intake was estimated by 24-hour urine excretion. Mortality data were obtained from the U.S. National Death Index. Unadjusted and multivariable-adjusted associations between sodium quartiles (quartile I (QI) to quartile IV (QIV)) and mortality were assessed using Cox models. Results: Estimated mean ± SD sodium intake was 130±69 mmol overall (55±20 mmol in QI; 220±56 mmol in QIV). Baseline systolic blood pressure did not vary significantly between groups. Last available mean systolic blood pressure was highest in QI and lowest in QIV (137±16 vs. 134±14 mm Hg; P = 0.009). Overall there were 1,013 deaths (399 cardiovascular). Unadjusted models exhibited significant inverse relationships between sodium and mortality outcomes. In adjusted models, sodium intake was not significantly associated with cardiovascular mortality (QI vs. QIV: hazard ratio (HR) = 1.00; 95% confidence interval (CI) = 0.71-1.42; P = 0.99). A borderline significant direct association with all-cause mortality was observed (QI vs. QIV: HR = 0.81; 95% CI = 0.66-1.00; P = 0.05) driven partly by noncardiovascular deaths. Conclusions: Our study found no significant association between sodium intake and cardiovascular outcomes, although a significant association with all-cause mortality was observed. Although these findings suggest that sodium may not have a strong relationship with cardiovascular mortality, the inconsistent results cast doubt on whether a single measurement can reliably predict mortality over a prolonged follow-up period.
    American Journal of Hypertension 08/2014; 28(3). DOI:10.1093/ajh/hpu141 · 2.85 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 · 3.79 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
  • M. Gonzalez · M. Alderman · H. Cohen · J. Sealey · J. Laragh ·

    Journal of Hypertension 06/2011; 29:e17. DOI:10.1097/00004872-201106001-00045 · 4.72 Impact Factor
  • H.A. Aldrich · M.J. Roman · Simone G. de · M.H. Alderman · R.B. Devereux ·

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    ABSTRACT: The National Heart, Lung, and Blood Institute assembled an ad hoc working group to evaluate opportunities for new major clinical trials in the field of hypertension. The mandate of this working group was to consider the possible designs of major randomized clinical trials focused on clinical outcomes that might merit significant investment by the National Institutes of Health. The group concluded that the ideal pragmatic clinical trial would have a factorial design and include a population at elevated risk of cardiovascular disease events. Subjects would be randomized to a target of systolic blood pressure <130 versus 130 to 150 mm Hg for adequate separation of means. Initial treatment with thiazide diuretic would be followed by randomization to angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, beta-blocker, calcium channel blocker, or aldosterone antagonist. A third drug could be added according to a protocol. DNA, proteins, and metabolites would be collected in a sample adequate to assess differential impact of treatment on outcome as a function of genotype, proteomic, and metabolomic expression. Subclinical markers and images would also be measured in a sample of patients to develop evidence of ability to predict ultimate effect on clinical outcomes. This ideal trial would take place within a network, funded for at least a decade, aimed at connecting primary care providers with hypertension specialists. Within the network, substudies or independent studies would be coordinated to develop a continuously improving base of knowledge about the effective delivery of hypertension care.
    Hypertension 07/2005; 46(1):1-6. DOI:10.1161/01.HYP.0000168924.37091.58 · 6.48 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 · 2.65 Impact Factor
  • M H Alderman · H W Cohen · J Fang ·

    Journal of Hypertension 02/2004; 22(Suppl. 1):S5. DOI:10.1097/00004872-200402001-00005 · 4.72 Impact Factor
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    Hypertension 01/2004; 45(4):575-579. · 6.48 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 · 2.85 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 · 4.46 Impact Factor
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    ABSTRACT: The Omapatrilat in Persons with Enhanced Risk of Atherosclerotic events (OPERA) trial is a large clinical trial of omapatrilat, a vasopeptidase inhibitor, in patients with stage 1 isolated systolic hypertension (ISH). OPERA is the first study to examine whether effective antihypertensive treatment can provide survival and clinical end point benefits in older persons with this common condition. This 5-year multinational, randomized, double-blind, parallel-group, placebo-controlled, forced-titration study will be conducted in approximately 12,600 subjects randomized by approximately 1100 study centers worldwide over a recruitment period of approximately 2 years. The primary objective of OPERA is to determine whether treatment with once-daily omapatrilat (target dose 40 mg) will reduce cardiovascular (CV) morbidity and mortality in older (> or = 65 years) men and women with enhanced risk for atherosclerotic events due to stage 1 ISH plus other risk factors for which currently there is no evidence-based requirement for treatment. Blood pressure inclusion criteria are systolic blood pressure (SBP) 140 to 159 mm Hg (SBP 125 to 139 mm Hg in diabetic individuals) and diastolic blood pressure (DBP) <90 mm Hg. The primary end point is defined as the composite of fatal/nonfatal stroke, fatal/nonfatal myocardial infarction, fatal/nonfatal heart failure, and other CV mortality. Secondary end points include the individual components of the primary end point, CV mortality, and major cardiovascular end points, as well as effects on cognitive function and initiation of treatment for diabetes. Additional analyses will be conducted in men and women, in diabetic patients, in different risk classes and according to prior evidence of vascular disease.
    American Journal of Hypertension 02/2002; 15(2 Pt 1):193-8. DOI:10.1016/S0895-7061(01)02048-9 · 2.85 Impact Factor
  • C D Furberg · B M Psaty · M Pahor · M H Alderman ·
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    ABSTRACT: Several recent comparative trials in hypertension have reported that similar blood pressure reductions may not necessarily translate into similar reductions in risk for cardiovascular complications. Thus, the method used to lower blood pressure may be important. In the Antihypertensive and Lipid-Lowering Treatment To Prevent Heart Attack Trial (ALLHAT), low-dose chlorthalidone as the first-line drug was superior to doxazosin. The 25% higher risk for major cardiovascular events associated with doxazosin was attributed primarily to a doubling in the risk for heart failure. A meta-analysis of patients with type 2 diabetes mellitus suggested that despite achieving similar blood pressure reductions, angiotensin-converting enzyme inhibitors are superior to other antihypertensive drugs in reducing the risk for acute myocardial infarction and cardiovascular events, but not stroke. Although individual comparative trials have failed to show conclusively that calcium-channel blockers differ from other antihypertensive drugs, a meta-analysis that included all published trials concluded that calcium-channel blockers are inferior to other classes of drugs in reducing the risk for acute myocardial infarction and heart failure. These observations suggest not only that antihypertensive drugs may have important mechanisms of action apart from blood pressure lowering but also that effective treatment is not a matter of simply lowering blood pressure. These findings have potential implications for the regulatory approval of antihypertensive agents, revisions of treatment guidelines, the design of future randomized trials comparing different antihypertensive drugs and, most important, the selection of drugs for the treatment of hypertensive patients.
    Annals of internal medicine 01/2002; 135(12):1074-8. · 17.81 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. · 5.72 Impact Factor
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    ABSTRACT: African Americans with hypertension, particularly those with more severe blood pressure elevations, are generally less responsive to monotherapy from any antihypertensive class. These patients usually require treatment with drugs from > or = 2 antihypertensive classes to achieve adequate blood pressure control. The purpose of this study was to assess the antihypertensive efficacy and safety of losartan alone and in combination with hydrochlorothiazide (HCTZ) in African American adults with mild to moderate hypertension. In this 12-week, multicenter, double-blind, randomized, parallel-group, placebo-controlled study, African American patients were randomized in a 3:3:1 ratio to I of 3 treatment groups: placebo, losartan monotherapy (50 to 150 mg), or losartan plus HCTZ (50/0 to 50/12.5 to 100/25 mg). Doses were titrated at weeks 4 and 8 if sitting diastolic blood pressure (SiDBP) was > or = 90 mm Hg. Safety was assessed by determining the incidence of clinical and laboratory Adverse events and evaluating mean changes in pulse, body weight, electrocardiographic parameters, and laboratory test results. A total of 440 patients were randomized-188 to placebo, 193 to losartan monotherapy, and 59 to losartan/HCTZ; 391 completed the study. At week 12, the response rate with losartan monotherapy was 45.8%, with a significant (P < or = 0.01) lowering in mean SiDBP by 6.6 mm Hg compared with placebo; the response rate with placebo was 27.2%, with a mean SiDBP reduction of 3.9 mm Hg. Sitting systolic blood pressure (SiSBP) was significantly lowered with losartan monotherapy, by 6.4 mm Hg, compared with placebo (reduction of 2.3 mm Hg). The response rate with losartan/ HCTZ was 62.7%, with reductions in SiSBP and SiDBP of 16.8 mm Hg and 10.8 mm Hg, respectively (P < or = 0.01 vs placebo and losartan monotherapy). The incidence of clinical adverse events was comparable in the 3 treatment groups. The results of this study suggest that in African American patients, losartan monotherapy was significantly more effective than placebo in lowering SiSBP and SiDBP. Moreover, the losartan/ HCTZ combination regimen resulted in significant and clinically meaningful additional reductions in SiSBP and SiDBP compared with losartan monotherapy or placebo. Losartan monotherapy and the losartan/HCTZ regimens were generally as well tolerated as placebo.
    Clinical Therapeutics 08/2001; 23(8):1193-208. DOI:10.1016/S0149-2918(01)80101-6 · 2.73 Impact Factor
  • M Pahor · BM Psaty · M.H Alderman ·

    ACC Current Journal Review 05/2001; 10(3):27–28. DOI:10.1016/S1062-1458(01)00240-9
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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. · 3.45 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 · 6.48 Impact Factor

Publication Stats

6k Citations
1,127.40 Total Impact Points


  • 2014
    • Yeshiva University
      • Department of Epidemiology & Population Health
      New York, New York, United States
  • 1986-2014
    • Albert Einstein College of Medicine
      • • Department of Epidemiology & Population Health
      • • Department of Physiology & Biophysics
      New York City, New York, United States
  • 2005
    • University of Ottawa
      Ottawa, Ontario, Canada
  • 2003
    • Sahlgrenska University Hospital
      • Department of Cardiology
      Goeteborg, Västra Götaland, Sweden
  • 2002
    • University of Massachusetts Medical School
      • Department of Medicine
      Worcester, Massachusetts, United States
  • 1990-1992
    • Cornell University
      • • Department of Medicine
      • • Cardiovascular Center
      Итак, New York, United States
  • 1983-1988
    • New York Downtown Hospital
      New York, New York, United States
  • 1980-1981
    • Weill Cornell Medical College
      • Department of Medicine
      New York, New York, United States