James M Galloway

Weill Cornell Medical College, New York City, New York, United States

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Publications (48)277.94 Total impact

  • Diabetes care 06/2013; · 7.74 Impact Factor
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    ABSTRACT: BACKGROUND AND AIMS: Diabetes remains a predictor of incident heart failure (HF), independent of intercurrent myocardial infarction (MI) and concomitant risk factors. Initial cardiovascular (CV) characteristics, associated with incident heart failure (HF) might explain the association of diabetes with incident HF. METHODS AND RESULTS: Participants to the 2nd Strong Heart Study exam, without prevalent HF or coronary heart disease, or glomerular filtration rate <30 mL/min/1.73 m(2), were analyzed (n = 2757, 1777 women, 1278 diabetic). Cox regression of incident HF (follow-up 8.91 ± 2.76 years) included incident MI censored as a competing risk event. Acute MI occurred in 96 diabetic (7%) and 84 non-diabetic participants (6%, p = ns). HF occurred in 156 diabetic (12%) and in 68 non-diabetic participants (5%; OR = 2.89, p < 0.001). After accounting for competing MI and controlling for age, gender, BMI, systolic blood pressure, smoking habit, plasma cholesterol, antihypertensive treatment, heart rate, fibrinogen and C-reactive protein, incident HF was predicted by greater LV mass index, larger left atrium, lower systolic function, greater left atrial systolic force and urinary albumin/creatinine excretion. Risk of HF was reduced with more rapid LV relaxation and anti-hypertensive therapy. Diabetes increases hazard of HF by 66% (0.02 < p < 0.001). The effect of diabetes could be explained by the level of HbA1c. CONCLUSIONS: Incident HF occurs more frequently in diabetes, independent of intercurrent MI, abnormal LV geometry, subclinical systolic dysfunction and indicators of less rapid LV relaxation, and is influenced by poor metabolic control. Identification of CV phenotype at high-risk for HF in diabetes should be advised.
    Nutrition, metabolism, and cardiovascular diseases: NMCD 09/2011; · 3.52 Impact Factor
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    ABSTRACT: Evaluate the quality of care provided patients with acute myocardial infarction and compare with similar national and regional data. Case series. The Strong Heart Study has extensive population-based data related to cardiovascular events among American Indians living in three rural regions of the United States. Acute myocardial infarction cases (72) occurring between 1/1/2001 and 12/31/2006 were identified from a cohort of 4549 participants. The proportion of cases that were provided standard quality of care therapy, as defined by the Healthcare Financing Administration and other national organizations. The provision of quality services, such as administration of aspirin on admission and at discharge, reperfusion therapy within 24 hours, prescription of beta blocker medication at discharge, and smoking cessation counseling were found to be 94%, 91%, 92%, 86% and 71%, respectively. The unadjusted, 30 day mortality rate was 17%. Despite considerable challenges posed by geographic isolation and small facilities, process measures of the quality of acute myocardial infarction care for participants in this American Indian cohort were comparable to that reported for Medicare beneficiaries nationally and within the resident states of this cohort.
    Ethnicity & disease 01/2011; 21(3):294-300. · 1.12 Impact Factor
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    ABSTRACT: The Stop Atherosclerosis in Native Diabetics Study (SANDS) reported cardiovascular benefit of aggressive versus standard treatment targets for both low-density lipoprotein cholesterol (LDL-C) and blood pressure (BP) in diabetic individuals. In this analysis, we examined within trial cost-effectiveness of aggressive targets of LDL-C ≤70 mg/dL and systolic BP ≤115 mmHg versus standard targets of LDL-C ≤100 mg/dL and systolic BP ≤130 mmHg. Randomized, open label blinded-to-endpoint 3-year trial. SANDS clinical trial database, Quality of Wellbeing survey, Centers for Medicare and Medicaid Services, Wholesale Drug Prices. American Indians ≥ age 40 years with type 2 diabetes and no previous cardiovascular events. April 2003 to July 2007. Health payer. Participants were randomized to aggressive versus standard groups with treatment algorithms defined for both. Incremental cost-effectiveness. Compared with the standard group, the aggressive group had slightly lower costs of medical services (-$116) but a 54% greater cost for BP medication ($1,242) and a 116% greater cost for lipid-lowering medication ($2,863), resulting in an increased cost of $3,988 over 3 years. Those in the aggressively treated group gained 0.0480 quality-adjusted life-years (QALY) over the standard group. When a 3% discount rate for costs and outcomes was used, the resulting cost per QALY was $82,589. The use of a 25%, 50%, and 75% reduction in drug costs resulted in a cost per QALY of $61,329, $40,070, and $18,810, respectively. This study was limited by use of a single ethnic group and by its 3-year duration. Within this 3-year study, treatment to lower BP and LDL-C below standard targets was not cost-effective because of the cost of the additional medications required to meet the lower targets. With the anticipated availability of generic versions of the BP and lipid-lowering drugs used in SANDS, the cost-effectiveness of this intervention should improve. Published by Elsevier Inc on behalf of the National Lipid Association.
    Journal of Clinical Lipidology 01/2010; 4(3):165-72. · 2.74 Impact Factor
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    ABSTRACT: The Stop Atherosclerosis in Native Diabetics Study (SANDS) was a randomized open-label clinical trial in type 2 diabetics designed to examine the effects of intensive reduction of blood pressure, aggressive vs standard goals (< or =115/75 mm Hg vs < or =130/80 mm Hg), and low-density lipoprotein (LDL) cholesterol on the composite outcome of change in carotid intimal-medial thickness and cardiovascular events. The study demonstrated that in conjunction with a lower LDL cholesterol target of 70 mg/dL, aggressive systolic blood pressure-lowering resulted in a reduction in carotid intimal-medial thickness and left ventricular mass without measurable differences in cardiovascular events. The blood pressure treatment algorithm included renin-angiotensin system blockade, with other agents added if necessary. The authors conclude that both standard and more aggressive systolic blood pressure reduction can be achieved with excellent safety and good tolerability in patients with type 2 diabetes mellitus.
    Journal of Clinical Hypertension 10/2009; 11(10):540-8. · 2.36 Impact Factor
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    ABSTRACT: BACKGROUND: Lowering low-density lipoprotein cholesterol (LDL-C) with statins reduces atherosclerosis. LDL and high-density lipoprotein (HDL) are commonly measured by their cholesterol content, but non-HDL cholesterol, LDL particle number (LDL-P), or total apolipoprotein B (apoB) may better predict cardiovascular risk. Few studies have examined relations among lipoprotein levels and composition before and after interventions to lower LDL-C and non-HDL-C. OBJECTIVE: To measure changes in carotid artery intimal media thickness (CIMT) and lipid concentration and composition during 36 months of statin therapy. METHODS: Analyses were conducted on 418 diabetic individuals, with complete data and no prior cardiovascular events, who were randomized to aggressive (AG) versus standard (STD) treatment for LDL-C, non-HDL-C, and systolic blood pressure (SBP) as part of the Stop Atherosclerosis in Native Diabetics Study (SANDS). RESULTS: The AG group achieved average LDL-C and non-HDL-C of 71mg/dL and 100mg/dL and a decrease in CIMT. No significant interactions were observed between treatment effect and initial levels of LDL-C, non-HDL-C, HDL-C, triglycerides, apoB, or LDL-P. Decreases in LDL-C (p<.005) and non-HDL-C (p<.001) were independently correlated with CIMT regression in the AG group. Changes in apoB and LDL-P showed borderline correlations with CIMT regression (p=.07 and p=.09). CONCLUSIONS: In diabetic adults with no prior cardiovascular events, treatment to current targets for lipids and SBP reduces atherosclerosis progression and when more aggressive targets are met, atherosclerosis regresses. The aggressive targets for LDL-C and non-HDL-C appeared to be the main determinants of CIMT regression and were more predictive of this outcome than changes in LDL-P or apoB.
    Journal of Clinical Lipidology 10/2009; 3(5):322-331. · 2.74 Impact Factor
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    ABSTRACT: Type 2 diabetes is accepted as a cause of heart failure, but direct cause-effect evidence independent of incident myocardial infarction (MI), hypertension and other coexisting risk factors is less well studied. We tested the hypothesis that diabetes predisposes to heart failure independently of hypertension and intercurrent MI. We evaluated 12-year incident heart failure in 2740 participants (1781 women) without prevalent cardiovascular or severe kidney disease, at the time of the first exam of the Strong Heart Study cohort. Intercurrent MI was censored as a competing risk event. Diabetes was present in 1206 individuals (44%), and impaired fasting glucose (IFG) in 391 (14%). Diabetic participants more frequently had hypertension and/or central obesity (both P < 0.0001). Incident heart failure was ascertained in 64 participants with normal fasting glucose (NFG; 6%), 26 (7%) with IFG and 201 with diabetes (17%, hazard ratio = 4.04 vs. NFG, P < 0.0001). In Cox analysis adjusting for age, sex, obesity, central fat distribution, hypertension, antihypertensive medications, prevalent atrial fibrillation, glomerular filtration rate, urinary albumin/creatinine ratio, plasma cholesterol, Hb1Ac, smoking habit, alcohol use, educational level and physical activity, diabetes was associated with a two-fold greater risk of incident heart failure than NFG (hazard ratio = 2.45, P < 0.0001). Diabetes maintained 1.5-fold greater risk of heart failure than NFG (P < 0.03) even when intercurrent MI (n = 221) was censored as a competing risk event, similar to the adjusted hazard ratio for heart failure in hypertension. Type 2 diabetes is a potent, independent risk factor for heart failure. Risk of heart failure in diabetic patients cannot be fully explained by incident MI and coexisting cardiovascular risk factors. Mechanisms directly related to diabetes and impairing cardiac function should be studied and identified.
    Journal of hypertension 10/2009; 28(2):353-60. · 4.02 Impact Factor
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    ABSTRACT: This secondary analysis from the SANDS (Stop Atherosclerosis in Native Diabetics Study) trial examines the effects of lowering low-density lipoprotein cholesterol (LDL-C) with statins alone versus statins plus ezetimibe on common carotid artery intima-media thickness (CIMT) in patients with type 2 diabetes and no prior cardiovascular event. It is unknown whether the addition of ezetimibe to statin therapy affects subclinical atherosclerosis. Within an aggressive group (target LDL-C <or=70 mg/dl; non-high-density lipoprotein cholesterol <or=100 mg/dl; systolic blood pressure <or=115 mm Hg), change in CIMT over 36 months was compared in diabetic individuals >40 years of age receiving statins plus ezetimibe versus statins alone. The CIMT changes in both aggressive subgroups were compared with changes in the standard subgroups (target LDL-C <or=100 mg/dl; non-high-density lipoprotein cholesterol <or=130 mg/dl; systolic blood pressure <or=130 mm Hg). Mean (95% confidence intervals) LDL-C was reduced by 31 (23 to 37) mg/dl and 32 (27 to 38) mg/dl in the aggressive group receiving statins plus ezetimibe and statins alone, respectively, compared with changes of 1 (-3 to 6) mg/dl in the standard group (p < 0.0001) versus both aggressive subgroups. Within the aggressive group, mean CIMT at 36 months regressed from baseline similarly in the ezetimibe (-0.025 [-0.05 to 0.003] mm) and nonezetimibe subgroups (-0.012 [-0.03 to 0.008] mm) but progressed in the standard treatment arm (0.039 [0.02 to 0.06] mm), intergroup p < 0.0001. Reducing LDL-C to aggressive targets resulted in similar regression of CIMT in patients who attained equivalent LDL-C reductions from a statin alone or statin plus ezetimibe. Common carotid artery IMT increased in those achieving standard targets. (Stop Atherosclerosis in Native Diabetics Study [SANDS]; NCT00047424).
    Journal of the American College of Cardiology 01/2009; 52(25):2198-205. · 14.09 Impact Factor
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    ABSTRACT: There are few published data on the incidence of fatal and nonfatal stroke in American Indians. The aims of this observational study were to determine the incidence of stroke and to elucidate stroke risk factors among American Indians. This report is based on 4549 participants aged 45 to 74 years at enrollment in the Strong Heart Study, the largest longitudinal, population-based study of cardiovascular disease and its risk factors in a diverse group of American Indians. At baseline examination in 1989 to 1992, 42 participants (age- and sex-adjusted prevalence proportion 1132/100 000, adjusted to the age and sex distribution of the US adult population in 1990) had prevalent stroke. Through December 2004, 306 (6.8%) of 4507 participants without prior stroke suffered a first stroke at a mean age of 66.5 years. The age- and sex-adjusted incidence was 679/100 000 person-years. Nonhemorrhagic cerebral infarction occurred in 86% of participants with incident strokes; 14% had hemorrhagic stroke. The overall age-adjusted 30-day case-fatality rate from first stroke was 18%, with a 1-year case-fatality rate of 32%. Age, diastolic blood pressure, fasting glucose, hemoglobin A(1c,) smoking, albuminuria, hypertension, prehypertension, and diabetes mellitus were risk factors for incident stroke. Compared with US white and black populations, American Indians have a higher incidence of stroke. The case-fatality rate for first stroke is also higher in American Indians than in the US white or black population in the same age range. Our findings suggest that blood pressure and glucose control and smoking avoidance may be important avenues for stroke prevention in this population.
    Circulation 10/2008; 118(15):1577-84. · 15.20 Impact Factor
  • High Blood Pressure & Cardiovascular Prevention 07/2008; 15(3):289.
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    ABSTRACT: Individuals with diabetes are at increased risk for cardiovascular disease (CVD), but more aggressive targets for risk factor control have not been tested. To compare progression of subclinical atherosclerosis in adults with type 2 diabetes treated to reach aggressive targets of low-density lipoprotein cholesterol (LDL-C) of 70 mg/dL or lower and systolic blood pressure (SBP) of 115 mm Hg or lower vs standard targets of LDL-C of 100 mg/dL or lower and SBP of 130 mm Hg or lower. A randomized, open-label, blinded-to-end point, 3-year trial from April 2003-July 2007 at 4 clinical centers in Oklahoma, Arizona, and South Dakota. Participants were 499 American Indian men and women aged 40 years or older with type 2 diabetes and no prior CVD events. Participants were randomized to aggressive (n=252) vs standard (n=247) treatment groups with stepped treatment algorithms defined for both. Primary end point was progression of atherosclerosis measured by common carotid artery intimal medial thickness (IMT). Secondary end points were other carotid and cardiac ultrasonographic measures and clinical events. Mean target LDL-C and SBP levels for both groups were reached and maintained. Mean (95% confidence interval) levels for LDL-C in the last 12 months were 72 (69-75) and 104 (101-106) mg/dL and SBP levels were 117 (115-118) and 129 (128-130) mm Hg in the aggressive vs standard groups, respectively. Compared with baseline, IMT regressed in the aggressive group and progressed in the standard group (-0.012 mm vs 0.038 mm; P < .001); carotid arterial cross-sectional area also regressed (-0.02 mm(2) vs 1.05 mm(2); P < .001); and there was greater decrease in left ventricular mass index (-2.4 g/m(2.7) vs -1.2 g/m(2.7); P = .03) in the aggressive group. Rates of adverse events (38.5% and 26.7%; P = .005) and serious adverse events (n = 4 vs 1; P = .18) related to blood pressure medications were higher in the aggressive group. Clinical CVD events (1.6/100 and 1.5/100 person-years; P = .87) did not differ significantly between groups. Reducing LDL-C and SBP to lower targets resulted in regression of carotid IMT and greater decrease in left ventricular mass in individuals with type 2 diabetes. Clinical events were lower than expected and did not differ significantly between groups. Further follow-up is needed to determine whether these improvements will result in lower long-term CVD event rates and costs and favorable risk-benefit outcomes. clinicaltrials.gov Identifier: NCT00047424.
    JAMA The Journal of the American Medical Association 04/2008; 299(14):1678-89. · 29.98 Impact Factor
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    ABSTRACT: The deceleration time of early mitral inflow (E) is shortened by left ventricular chamber stiffening and prolonged by impaired relaxation. For any given rate of deceleration of early mitral inflow, a higher E-wave velocity (E) is associated with a longer deceleration time. It is not known whether deceleration time normalized for E-velocity or its inverse (deceleration slope) better predicts cardiovascular (CV) events compared with deceleration time or E-velocity alone. We compared the prognostic value of deceleration time, E-velocity, deceleration time/E-velocity, and deceleration slope in 3102 American Indian participants in the Strong Heart Study, free of clinical CV disease and documented atrial fibrillation, in predicting fatal and nonfatal CV events. During a mean of 8.5 +/- 2.4 years, there were 637 fatal and nonfatal CV events. After adjustment for traditional CV risk factors, deceleration time/E-velocity (adjusted hazard ratio [HR], 1.09; 95% confidence interval [CI], 1.00-1.18; P = .04 for every 0.89 msec/[cm/s] [1 + standard deviation {SD}] increase) and deceleration slope (HR, 0.91; 95% CI, 0.82-1.00; P = .01 for every 91 msec [1 + SD] increase) predicted CV events, whereas deceleration time and E-velocity did not. When participants with restrictive-type filling (n = 74) were removed from the analysis, deceleration time/E-velocity (HR, 1.10; 95% CI, 1.01-1.20; P = .03 for every 0.89 msec/[cm/s] [1 + SD] increase) and deceleration slope (HR, 0.64; 95% CI, 0.36-0.91; P = .01 for every 91 msec [1 + SD] increase) predicted CV events even more strongly. In a large population-based sample with high prevalences of hypertension and diabetes, free of prevalent CV disease, deceleration time/E-velocity and deceleration slope predict CV events, whereas their components (deceleration time and E-velocity) do not. This suggests normalization of deceleration time for E-velocity or using its inverse (deceleration slope) more precisely captures prognostically significant prolongation of deceleration than does deceleration time alone.
    Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 12/2007; 20(11):1300-6. · 2.98 Impact Factor
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    ABSTRACT: This study analyzed which definition of the metabolic syndrome is more predictive of cardiovascular events in both diabetic and nondiabetic members of a population-based sample. A 10-year, longitudinal follow-up of the Strong Heart Study cohort has been evaluated. The analysis included 3,945 participants (2,384 female) with complete data (1,700 with diabetes and 1,468 with arterial hypertension) for evaluation of metabolic syndrome. Those with prevalent cardiovascular disease were excluded (n = 287, of whom 127 were female). Prevalence of metabolic syndrome was assessed based on the World Health Organization (WHO), the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III, and International Diabetes Federation (IDF) definitions. The main outcome was 10-year incidence of combined fatal and nonfatal cardiovascular events, including stroke, coronary heart disease, and congestive heart failure. Fatal and nonfatal cardiovascular events occurred in 1,120 participants. After adjusting for age, sex, and diabetes, metabolic syndrome by all definitions was significantly associated with higher incidence of cardiovascular events (all P < 0.0001). In nondiabetic individuals, incident cardiovascular event rates were about 30-40% higher in those with metabolic syndrome, without a significant difference among definitions (0.03 < P < 0.001), and remained significant in WHO and NCEP ATP III definitions even after further adjustment for obesity, hypertension, and low HDL cholesterol. In the diabetic group, metabolic syndrome risk for cardiovascular events was greatest using the WHO definition (P < 0.002 vs. other models). In individuals without diabetes, metabolic syndrome is associated with incident cardiovascular disease, especially with WHO and NCEP ATP III definitions. Metabolic syndrome also predicts higher cardiovascular event rates in diabetic participants, a prediction that is greatest using the WHO definition.
    Diabetes care 08/2007; 30(7):1851-6. · 7.74 Impact Factor
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    ABSTRACT: The qualitative electrocardiographic strain pattern of ST depression (STD) and T-wave inversion is strongly associated with coronary heart disease and left ventricular hypertrophy and is an independent predictor of new-onset heart failure in hypertensive participants. However, whether quantitative measures of STD in the lateral precordial leads predict new heart failure is unclear. Digital electrocardiograms were examined in 2,059 American-Indian participants in the second Strong Heart Study examination with no history of heart failure. The absolute magnitude of ST segment deviation was measured using computer to the nearest 5 microV in leads V(5) and V(6). During 5.7 +/-1.4 years of follow-up, heart failure developed in 77 participants (3.7%). Participants who developed heart failure had greater STD in leads V(5) or V(6) (-11 +/- 35 vs 12 +/- 27 microV; p <0.001) than those who did not. In univariate Cox analyses, STD was a significant predictor of new heart failure, with each 10-microV greater STD associated with a 31% greater risk of heart failure (hazard ratio [HR] 1.31, 95% confidence interval [CI] 1.24 to 1.39). Increasing STD grouped according to quartiles was strongly associated with the development of heart failure, with stepwise increasing risk of heart failure compared with the lowest quartile of STD for the second (HR 2.39, 95% CI 0.77 to 7.40), third (HR 3.01, 95% CI 1.00 to 9.08), and fourth quartiles of STD (HR 9.06, 95% CI 3.26 to 25.16). In Cox multivariate analyses controlling for age, gender, diabetes, coronary heart disease, albuminuria, and other baseline risk factors, STD remained a significant predictor of incident heart failure (HR 1.22, 95% CI 1.13 to 1.32 per 10-muV increment in STD; p <0.001). In conclusion, increasing STD in lateral precordial leads is strongly associated with increased risk of developing heart failure independent of other risk factors for new heart failure.
    The American Journal of Cardiology 08/2007; 100(1):94-8. · 3.21 Impact Factor
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    ABSTRACT: Left ventricular wall motion (WM) abnormalities have recognized prognostic significance in patients with coronary or other heart diseases; however, whether abnormal WM predicts adverse events in adults without overt cardiovascular disease has not been assessed. Our objective was to determine whether echocardiographic WM abnormalities predict subsequent cardiovascular events in a population-based sample. Participants (n=2864, mean age 60+/-8 years, 64% women) without clinically evident cardiovascular disease in the second Strong Heart Study examination who had complete echocardiographic WM assessment were studied. Echocardiographic assessment revealed that 5% of participants (n=140) had focal hypokinesia, and 1.5% (n=42) had WM abnormalities. Relationships between WM abnormalities and fatal and nonfatal cardiovascular events (including myocardial infarction, stroke, coronary artery disease, and heart failure; n=554) and cardiovascular death (n=182) during 8+/-2 years follow-up were examined. In Cox regression, after adjustment for age, gender, waist/hip ratio, systolic blood pressure, and diabetes mellitus, segmental WM abnormalities were associated with a 2.5-fold higher risk of cardiovascular events and a 2.6-fold higher risk of cardiovascular death (both P<0.0001). In similar multivariable models, global WM abnormalities were associated with a 2.4-fold higher risk of cardiovascular events (P=0.001) and a 3.4-fold higher risk of cardiovascular death (P=0.003). Echocardiographic left ventricular WM abnormalities in adults without overt cardiovascular disease are associated with 2.4- to 3.4-fold higher risks of cardiovascular morbidity and mortality, independent of established risk factors.
    Circulation 08/2007; 116(2):143-50. · 15.20 Impact Factor
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    ABSTRACT: Brachial blood pressure is predictive of cardiovascular outcome; however central pressure may better represent the load imposed on the coronary and cerebral arteries and thereby bear a stronger relationship to vascular damage and prognosis. Relations of brachial and central pressures to carotid artery hypertrophy (intimal-medial thickness and vascular mass), extent of atherosclerosis (plaque score), and incident cardiovascular events were examined in the Strong Heart Study. Central pressures were calculated using radial applanation tonometry. Among 3520 participants, central and brachial pulse pressures were more strongly related to vascular hypertrophy and extent of atherosclerosis than were systolic pressures. Central pulse pressure was more strongly related to all 3 arterial measures than was brachial pulse pressure (r=0.364 versus 0.309 for plaque score; P<0.001 for comparison of Spearman correlation coefficient; r=0.293 versus 0.249 for intimal-medial thickness; P<0.002; r=0.320 versus 0.289 for vascular mass; P<0.05). Among the 2403 participants free of clinical cardiovascular disease at baseline, 319 suffered fatal or nonfatal cardiovascular events during mean follow-up of 4.8+/-1.3 years. After adjustment for age, gender, current smoking, body mass index, cholesterol:HDL ratio, creatinine, fibrinogen, diabetes, and heart rate, central pulse pressure predicted cardiovascular events more strongly than brachial pulse pressure (hazards ratio=1.15 per 10 mm Hg, chi(2)=13.4, P<0.001 versus hazards ratio=1.10, chi(2)=6.9, P=0.008). In conclusion, noninvasively-determined central pulse pressure is more strongly related to vascular hypertrophy, extent of atherosclerosis, and cardiovascular events than is brachial blood pressure. These findings support prospective examination of use of central blood pressure as a treatment target in future trials.
    Hypertension 07/2007; 50(1):197-203. · 6.87 Impact Factor
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    ABSTRACT: The myocardial performance index (MPI) introduced by Tei, a Doppler-derived echocardiographic measure that reflects both left ventricular (LV) systolic and diastolic function, has been shown to have prognostic value in several clinical settings, including myocardial infarction and congestive heart failure. There are scant data on the correlates and prognostic value of MPI in a population without overt cardiovascular (CV) disease. We investigated clinical and physiologic correlates of MPI, as assessed from echocardiographic Doppler recordings in 1,862 American Indian participants free of coronary or valvular disease or LV systolic dysfunction in the population-based strong heart study (SHS). We then assessed the prognostic value of MPI for incident CV events, including nonfatal stroke, coronary heart disease, congestive heart failure, and CV death. The study population was 59 +/- 8 years old (66% women); 48% had diabetes, 44% hypertension, and 54% were obese. In univariable analyses, MPI (mean = 0.24 +/- 0.17) showed significant negative associations with creatinine clearance, C-reactive protein (CRP), LV ejection fraction (EF), mitral valve E- and A-wave velocities, cardiac index (CI), stroke index (SI) and stroke index/pulse pressure (SI/PP), and significant positive associations with serum creatinine and total peripheral resistance index (TPRI) (all P < 0.05). There were no significant associations of MPI with hypertension or diabetes status, systolic or diastolic blood pressure, body mass index, hemoglobin A1C or LV mass. After adjusting for age, sex, diabetes, and hypertension, MPI remained weakly but significantly correlated with CRP, EF, CI, SI, SI/PP, mitral E- and A-wave velocities, and TPRI. MPI did not predict fatal and nonfatal CV events (risk ratio 1.06 per unit MPI, 95% C.I. 0.56-2.04; P = 0.85) at a mean follow-up of 7.1 +/- 2.2 years. In a population-based sample of adults with high prevalence of diabetes, hypertension, and obesity but without overt CV disease, MPI has weak associations with clinical and physiologic determinants of cardiac function. Moreover, MPI does not provide prognostic information for CV events in this population. Though conceptually attractive as a global measure of cardiac function, MPI has limited utility in a high-risk population without clinical CV disease.
    Echocardiography 05/2007; 24(4):340-7. · 1.26 Impact Factor
  • Diabetes Care. 01/2007; 30(7):1851-1856.
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    ABSTRACT: Abstract—Brachial blood pressure is predictive of cardiovascular outcome; however,central pressure may better represent the load imposed,on the coronary and cerebral arteries and thereby bear a stronger relationship to vascular damage,and prognosis. Relations of brachial and central pressures to carotid artery hypertrophy,(intimal-medial thickness and vascular mass), extent of atherosclerosis (plaque score), and incident cardiovascular events were examined in the Strong Heart Study. Central pressures were calculated using radial applanation tonometry. Among 3520 participants, central and brachial pulse pressures were more strongly related to vascular hypertrophy and extent of atherosclerosis than were systolic pressures. Central pulse pressure was more strongly related to all 3 arterial measures than was brachial pulse
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    ABSTRACT: The present article presents equations for the prediction of coronary heart disease (CHD) in a population with high rates of diabetes and albuminuria, derived from data collected in the Strong Heart Study, a longitudinal study of cardiovascular disease in 13 American Indian tribes and communities in Arizona, North and South Dakota, and Oklahoma. Participants of the Strong Heart Study were examined initially in 1989-1991 and were monitored with additional examinations and mortality and morbidity surveillance. CHD outcome data through December 2001 showed that age, gender, total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein cholesterol, smoking, diabetes, hypertension, and albuminuria were significant CHD risk factors. Hazard ratios for ages 65 to 75 years, hypertension, LDL cholesterol > or = 160 mg/dL, diabetes, and macroalbuminuria were 2.58, 2.01, 2.44, 1.66, and 2.11 in men and 2.03, 1.69, 2.17, 2.26, and 2.69 in women, compared with ages 45 to 54 years, normal blood pressure, LDL cholesterol <100 mg/dL, no diabetes, and no albuminuria. Prediction equations for CHD and a risk calculator were derived by gender with the use of Cox proportional hazards model and the significant risk factors. The equations provided good discrimination ability, as indicated by a c statistic of 0.70 for men and 0.73 for women. Results from bootstrapping methods indicated good internal validation and calibration. A "risk calculator" has been developed and placed on the Strong Heart Study Web site, which provides predicted risk of CHD in 10 years with input of these risk factors. This may be valuable for diverse populations with high rates of diabetes and albuminuria.
    Circulation 06/2006; 113(25):2897-905. · 15.20 Impact Factor

Publication Stats

1k Citations
277.94 Total Impact Points


  • 2009–2011
    • Weill Cornell Medical College
      New York City, New York, United States
    • Washington DC VA Medical Center
      Washington, Washington, D.C., United States
    • University of Maryland, Baltimore
      Baltimore, Maryland, United States
    • Northwestern University
      • Feinberg School of Medicine
      Evanston, Illinois, United States
  • 2008
    • University of Naples Federico II
      Napoli, Campania, Italy
  • 2002–2008
    • The University of Arizona
      Tucson, Arizona, United States
  • 2002–2007
    • Cornell University
      • Department of Medicine
      Ithaca, NY, United States
  • 2006
    • MedStar Health Research Institute
      Maryland, United States
    • University of Oklahoma Health Sciences Center
      • College of Public Health
      Oklahoma City, OK, United States
  • 2004
    • National Heart, Lung, and Blood Institute
      Maryland, United States