Non-adherence in Hypertension Management Deficit in Information or Trust?

Hypertension, a leading cause of cardiovascular morbidity and mortality worldwide, continues to challenge health professionals. There are too many patients with uncontrolled hypertension who end up with life altering or life ending complications. Over the years so much hypertension research has been conducted; and numerous effective antihypertensive drugs have been discovered and yet the rate of blood pressure control remains unacceptably low. It is high time that we focused our attention on the optimal use of the available knowledge and medications. More emphasis on teaching the patients and the public at large is required and patients need to have full trust of their health care providers in order to adhere to the prescriptions provided. If patients take their medications as prescribed and follow therapeutic lifestyle changes like physical activity and calorie and salt restrictions, there would be very few patients with uncontrolled hypertension and its complications.

Effects of Lifestyle Modification on Telomerase Gene Expression in Hypertensive Patients: A Pilot Trial of Stress Reduction and Health Education Programs in African Americans.

BACKGROUND: African Americans suffer from disproportionately high rates of hypertension and cardiovascular disease. Psychosocial stress, lifestyle and telomere dysfunction contribute to the pathogenesis of hypertension and cardiovascular disease. This study evaluated effects of stress reduction and lifestyle modification on blood pressure, telomerase gene expression and lifestyle factors in African Americans. METHODS: Forty-eight African American men and women with stage I hypertension who participated in a larger randomized controlled trial volunteered for this substudy. These subjects participated in either stress reduction with the Transcendental Meditation technique and a basic health education course (SR) or an extensive health education program (EHE) for 16 weeks. Primary outcomes were telomerase gene expression (hTERT and hTR) and clinic blood pressure. Secondary outcomes included lifestyle-related factors. Data were analyzed for within-group and between-group changes. RESULTS: Both groups showed increases in the two measures of telomerase gene expression, hTR mRNA levels (SR: p< 0.001; EHE: p< 0.001) and hTERT mRNA levels (SR: p = 0.055; EHE: p< 0.002). However, no statistically significant between-group changes were observed. Both groups showed reductions in systolic BP. Adjusted changes were SR = -5.7 mm Hg, p< 0.01; EHE = -9.0 mm Hg, p < 0.001 with no statistically significant difference between group difference. There was a significant reduction in diastolic BP in the EHE group (-5.3 mm Hg, p< 0.001) but not in SR (-1.2 mm Hg, p = 0.42); the between-group difference was significant (p = 0.04). The EHE group showed a greater number of changes in lifestyle behaviors. CONCLUSION: In this pilot trial, both stress reduction (Transcendental Meditation technique plus health education) and extensive health education groups demonstrated increased telomerase gene expression and reduced BP. The association between increased telomerase gene expression and reduced BP observed in this high-risk population suggest hypotheses that telomerase gene expression may either be a biomarker for reduced BP or a mechanism by which stress reduction and lifestyle modification reduces BP. TRIAL REGISTRATION: ClinicalTrials.gov NCT00681200.

Obesity and Cardiovascular Diseases in a High-Risk Population: Evidence-Based Approach to CHD Risk Reduction.

BACKGROUND: Obesity is becoming a worldwide public health problem and it is expected to worsen as its prevalence is increasing in children and adolescents. This report examined the distribution of major cardiovascular disease (CVD) risk factors and the effect of life-style changes on coronary heart disease (CHD) risk prediction in a high risk obese African Americans. METHODS: We examined the baseline distribution of CVD risk factors in 515 obese African Americans, with mean BMI of 42.9 ± 6.8 kg/m2, and prospectively the effect of a 6-month low-salt, low-fat diet and aerobic-exercise intervention program on risk reduction. RESULTS: Prevalence of hypertension, dyslipidemia, and diabetes mellitus were 57%, 27% and 24% respectively. Metabolic syndrome was present in 36% and 39% met two features of the syndrome. The 10-year risk prediction for developing CHD ranged from 4% to 17% for women and 6% to 29% for men. After 6 months of life-style changes, many of the risk factors improved, and the CHD risk scores decreased from 6% to 4% in the women and 16% to 13% in the men. CONCLUSION: The high prevalence and increasing incidence of obesity and associated cardiovascular risk emphasizes the need to focus on obesity reduction in this high risk population.

Blood Pressure Dipping and Urban Stressors in Young Adult African Americans.

BACKGROUND: Blunted nocturnal blood pressure (BP) dipping is an early marker of cardiovascular risk that is prevalent among African Americans. PURPOSE: We evaluated relationships of BP dipping to neighborhood and posttraumatic stress and sleep in urban residing young adult African Americans. METHODS: One hundred thirty-six black, predominately African American, men and women with a mean age of 22.9 years (SD = 4.6) filled out surveys and were interviewed and had two, 24-h ambulatory BP recordings. RESULTS: Thirty-eight percent had BP dipping ratios < .10. Wake after sleep onset (WASO), neighborhood disorder and neighborhood poverty rates but not posttraumatic stress symptoms, and other sleep measures correlated significantly with dipping ratios. Models with the neighborhood measures that also included WASO increased the explained variance. CONCLUSIONS: Studies elucidating mechanisms underlying effects of neighborhoods on BP dipping and the role of disrupted sleep, and how they can be mitigated are important directions for future research.

Relationship of left ventricular hypertrophy and diastolic function with cardiovascular and renal outcomes in African Americans with hypertensive chronic kidney disease.

African Americans with hypertension are at high risk for adverse outcomes from cardiovascular and renal disease. Patients with stage 3 or greater chronic kidney disease have a high prevalence of left ventricular (LV) hypertrophy and diastolic dysfunction. Our goal was to study prospectively the relationships of LV mass and diastolic function with subsequent cardiovascular and renal outcomes in the African American Study of Kidney Disease and Hypertension cohort study. Of 691 patients enrolled in the cohort, 578 had interpretable echocardiograms and complete relevant clinical data. Exposures were LV hypertrophy and diastolic parameters. Outcomes were cardiovascular events requiring hospitalization or causing death; a renal composite outcome of doubling of serum creatinine or end-stage renal disease (censoring death); and heart failure. We found strong independent relationships between LV hypertrophy and subsequent cardiovascular (hazard ratio, 1.16; 95% confidence interval, 1.05-1.27) events, but not renal outcomes. After adjustment for LV mass and clinical variables, lower systolic tissue Doppler velocities and diastolic parameters reflecting a less compliant LV (shorter deceleration time and abnormal E/A ratio) were significantly (P<0.05) associated with future heart failure events. This is the first study to show a strong relationship among LV hypertrophy, diastolic parameters, and adverse cardiac outcomes in African Americans with hypertension and chronic kidney disease. These echocardiographic risk factors may help identify high-risk patients with chronic kidney disease for aggressive therapeutic intervention.

The metabolically healthy but obese phenotype in African Americans.

Obesity has become one of the leading public health concerns in the United States and worldwide. While obesity is associated with the metabolic syndrome, some obese individuals do not possess the constellation of the metabolic abnormalities and are referred to as metabolically healthy but obese (MHO) persons. Limited data exist on the prevalence and characteristics of the MHO in African Americans. The authors studied 126 obese African Americans and defined the MHO phenotype as an individual with a body mass index ≥30 kg/m(2) , high-density lipoprotein cholesterol ≥40 mg/dL, absence of type 2 diabetes mellitus, and absence of arterial hypertension. The correlates of the MHO phenotype with anthropometrical and metabolic indices were examined, as well as the effect of age on these correlates. Results showed that 36 (28.5%) of the individuals were identified with the MHO phenotype. Waist circumference (WC) and waist-to-hip ratio (WHR) were significantly lower (P<.05) in MHO than in non-MHO patients. While there were significant lower levels of low-density lipoprotein and triglycerides in MHO among patients younger than 40 years, the significance was lost among patients 40 years or older. This study indicates that increased WC and WHR may be early premetabolic syndrome markers in obese individuals and should warrant aggressive risk factor reduction therapy to prevent future development of related cardiovascular conditions.

Nocturnal blood pressure nondipping in obese African-Americans.

OBJECTIVES: Nondipping pattern of circadian blood pressure (BP) is associated with increased cardiovascular morbidity and mortality; however, limited data are available among obese African-Americans. We, therefore, aimed to evaluate the pattern of circadian BP variation and to identify clinical conditions associated with nondipping in this population. METHODS: A total of 211 obese African-Americans enrolled in a weight-reduction program underwent 24-h ambulatory BP monitoring. Nondipping was defined as a nocturnal BP reduction of less than 10%. RESULTS: Systolic BP (SBP) nondipping was present in 158 participants (74.9%) and diastolic BP (DBP) nondipping was present in 93 participants (44.1%). In multivariate logistic regression analyses, diabetes was associated with SBP nondipping (adjusted OR, 2.53; CI: 1.16-5.76; P=0.02), and increasing BMI (5 kg/m) was associated with DBP nondipping (adjusted OR, 1.46; CI: 1.17-1.83; P=0.001). In linear regression analyses, BMI was positively correlated to office, 24-h, daytime, and night-time SBP (P=0.03, 0.01, 0.03, and 0.005, respectively) and office, 24-h, daytime, and night-time PP (P=0.01, P<0.001, 0.001, and P=0.003, respectively). CONCLUSION: This study demonstrated an excessively high prevalence of nondippers and independent associations between diabetes and SBP nondipping and between BMI and DBP nondipping in an obese African-American population.

Malnutrition-inflammation modifies the relationship of cholesterol with cardiovascular disease.

In moderate and severe CKD, the association of cholesterol with subsequent cardiovascular disease (CVD) is weak. We examined whether malnutrition or inflammation (M-I) modifies the risk relationship between cholesterol levels and CVD events in African Americans with hypertensive CKD and a GFR between 20 and 65 ml/min per 1.73 m². We stratified 990 participants by the presence or absence of M-I, defined as body mass index <23 kg/m² or C-reactive protein >10 mg/L at baseline. The primary composite outcome included cardiovascular death or first hospitalization for coronary artery disease, stroke, or congestive heart failure occurring during a median follow-up of 77 months. Baseline total cholesterol (212 ± 48 versus 212 ± 44 mg/dl) and overall incidence of the primary CVD outcome (19 versus 21%) were similar in participants with (n = 304) and without (n = 686) M-I. In adjusted analyses, the CVD composite outcome exhibited a significantly stronger relationship with total cholesterol for participants without M-I than for participants with M-I at baseline (P < 0.02). In the non-M-I group, the cholesterol-adjusted hazard ratio (HR) for CVD increased progressively across cholesterol levels: HR = 1.19 [95% CI; 0.77, 1.84] and 2.18 [1.43, 3.33] in participants with cholesterol 200 to 239 and ≥240 mg/dl, respectively (reference: cholesterol <200). In the M-I group, the corresponding HRs did not vary significantly by cholesterol level. In conclusion, the presence of M-I modifies the risk relationship between cholesterol level and CVD in African Americans with hypertensive CKD.

Intensive blood-pressure control in hypertensive chronic kidney disease.

BACKGROUND: In observational studies, the relationship between blood pressure and end-stage renal disease (ESRD) is direct and progressive. The burden of hypertension-related chronic kidney disease and ESRD is especially high among black patients. Yet few trials have tested whether intensive blood-pressure control retards the progression of chronic kidney disease among black patients. METHODS: We randomly assigned 1094 black patients with hypertensive chronic kidney disease to receive either intensive or standard blood-pressure control. After completing the trial phase, patients were invited to enroll in a cohort phase in which the blood-pressure target was less than 130/80 mm Hg. The primary clinical outcome in the cohort phase was the progression of chronic kidney disease, which was defined as a doubling of the serum creatinine level, a diagnosis of ESRD, or death. Follow-up ranged from 8.8 to 12.2 years. RESULTS: During the trial phase, the mean blood pressure was 130/78 mm Hg in the intensive-control group and 141/86 mm Hg in the standard-control group. During the cohort phase, corresponding mean blood pressures were 131/78 mm Hg and 134/78 mm Hg. In both phases, there was no significant between-group difference in the risk of the primary outcome (hazard ratio in the intensive-control group, 0.91; P=0.27). However, the effects differed according to the baseline level of proteinuria (P=0.02 for interaction), with a potential benefit in patients with a protein-to-creatinine ratio of more than 0.22 (hazard ratio, 0.73; P=0.01). CONCLUSIONS: In overall analyses, intensive blood-pressure control had no effect on kidney disease progression. However, there may be differential effects of intensive blood-pressure control in patients with and those without baseline proteinuria. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Center on Minority Health and Health Disparities, and others.)

The relationship between flow-mediated dilatation of the brachial artery and intima-media thickness of the carotid artery to Framingham risk scores in older African Americans.

The objective of this study was to investigate the relationship of flow-mediated dilatation and intima-media thickness (IMT) with coronary risk in African Americans (AAs). Endothelial dysfunction and IMT of carotid arteries are considered early steps in atherosclerotic disease process and have been used as surrogate markers of subclinical atherosclerosis. Data were collected on 106 AAs with a mean age of 64.0+/-6.6 years. Carotid artery IMT was measured with B-mode ultrasonography, as was brachial artery diameter at rest, during reactive hyperemia, and after nitroglycerin. Percent change in flow-mediated dilatation (%FMD) was defined as 100x(diameter during reactive hyperemia - resting diameter)/resting diameter. Percent change in nitroglycerin-mediated dilatation (%NMD) was defined as 100x(diameter with nitroglycerin-resting diameter)/resting diameter. The Framingham 10-year risk score (FRS) was calculated for each patient using the National Cholesterol Education Program (NCEP) risk score calculator and participants were categorized into 3 groups with FRS as <10%, 10% to 20%, and >20%. Thirty-eight participants had risk scores <10%, 26 had 10% to 20%, and 42 >20%. There was a significant inverse relation between %FMD and FRS (P<.0001) and between %NMD and FRS (P<.001). IMT was not statistically different among the risk groups. Endothelial dysfunction assessed by FMD significantly correlates inversely with FRS in AAs. FMD, an index of arterial compliance, appears to be a sensitive and reliable index of cardiovascular disease.

Heart failure in ALLHAT: did blood pressure medication at study entry influence outcome?

J Clin Hypertens (Greenwich). 2009;11:466-474. (c)2009 Wiley Periodicals, Inc.Lower heart failure (HF) rates in individuals taking chlorthalidone vs amlodipine, lisinopril, or doxazosin were unanticipated in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). HF differences appeared early, leading to questions about the possible influence of pre-enrollment antihypertensive drugs. A post hoc study evaluated hospitalized HF events. During year 1479 individuals had HF, with pre-entry antihypertensive medication data obtained on 301 patients (63%). Case-only analysis examined interactive effects (interaction odds ratio [OR, ratio of ORs]) of previous medication and ALLHAT treatment on HF outcomes, eg, did treatment effect differ by pre-entry antihypertensive class? Among cases, 39%, 37%, 17%, and 47% were taking pre-entry diuretics, angiotensin-converting enzyme inhibitors, beta-blockers, and calcium channel blockers, respectively. Interaction OR for year 1 HF for amlodipine vs chlorthalidone for patients taking vs not taking diuretics pre-entry was 1.08 (95% confidence interval [CI], 0.53-2.21; P=.83); for lisinopril vs chlorthalidone, 1.33 (95% CI, 0.65-2.74; P=.44); and for doxazosin vs chlorthalidone, 1.13 (95% CI, 0.57-2.25; P=.73). Controlling for other pre-entry antihypertensives yielded similar results. There was no significant evidence that pre-entry drug type explained observed hospitalized HF differences by ALLHAT treatment.

Posttraumatic stress disorder and nocturnal blood pressure dipping in young adult African Americans.

OBJECTIVE: To evaluate the relationship between posttraumatic stress disorder (PTSD) and nocturnal blood pressure (BP) dipping in young adult African Americans (AAs). PTSD is associated with physical illnesses including cardiovascular conditions. Sleep disturbances related to heightened arousal likely contribute to physical health risk; however, this possibility has not been studied. The studies that have found a relationship between PTSD and hypertension (HTN) have substantial representation of AAs. AAs have elevated rates of HTN and are more likely to exhibit an absence of the normal "dip" of BP at night. Nocturnal BP "nondipping" is an established risk factor for HTN and its cardiovascular complications. Nocturnal BP nondipping and sleep disturbances of PTSD have both been linked to sympathetic nervous system function. METHODS: Thirty healthy young adult AAs (60% female; mean age = 20.0 years; 17 with lifetime full or subthreshold PTSD, 4 with current symptoms) received 24-hour BP and actigraphy monitoring, filled out sleep diaries, and had structured clinical assessment of PTSD. RESULTS: There were significant associations of lifetime full and subthreshold PTSD and BP nondipping, and the degree of nocturnal dipping correlated with lifetime and current PTSD severity. CONCLUSION: Elevated nocturnal BP may be a link between PTSD and cardiovascular morbidity in AAs that can be targeted in prevention.

Differing effects of antihypertensive drugs on the incidence of diabetes mellitus among patients with hypertensive kidney disease.

BACKGROUND: The African American Study of Kidney Disease and Hypertension was a multicenter trial of African Americans with hypertensive kidney disease randomized to an angiotensin-converting enzyme inhibitor (ramipril), a beta-blocker (metoprolol succinate), or a calcium channel blocker (amlodipine besylate). We compared the incidence of type 2 diabetes mellitus (DM) and the composite outcome of impaired fasting glucose or DM (IFG/DM) for the African American Study of Kidney Disease and Hypertension interventions. METHODS: Cox regression models were used to evaluate (post hoc) the association of the randomized interventions and the relative risk (RR) of DM and IFG/DM and to assess the RR of DM and IFG/DM by several prerandomization characteristics. RESULTS: Among 1017 participants, 147 (14.5%) developed DM; 333 (42.9%) of 776 participants developed IFG/DM. Respective DM event rates were 2.8%, 4.4%, and 4.5% per patient-year in the ramipril-, amlodipine-, and metoprolol-treated groups. The RRs of DM with ramipril treatment were 0.53 (P = .001) compared with metoprolol treatment and 0.49 (P = .003) compared with amlodipine treatment. Respective IFG/DM event rates were 11.3%, 13.3%, and 15.8% per patient-year in the ramipril-, amlodipine-, and metoprolol-treated groups. The RRs of IFG/DM with ramipril treatment were 0.64 (P<.001) compared with metoprolol treatment and 0.76 (P = .09) compared with amlodipine treatment. The RRs of DM and IFG/DM with amlodipine treatment compared with metoprolol treatment were 1.07 (P = .76) and 0.84 (P = .26), respectively. CONCLUSION: Ramipril treatment was associated with a significantly lower risk of DM in African Americans with hypertensive kidney disease than amlodipine or metoprolol treatment.

Effect of diet and exercise on pulse pressure and cardiac function in morbid obesity: analysis of 24-hour ambulatory blood pressure.

Blood pressure is a major risk factor for cardiovascular events, although the role of pulse pressure, an independent predictor of arterial stiffness, has recently been emphasized. This study examines the baseline relationship between body mass index (BMI) and blood pressure indexes in 215 obese African Americans enrolled in a diet-exercise program. The subject population was 77% female, with a mean +/- SD age of 46.7+/-10.7 years and a mean BMI of 42.5+/-7.5 kg/m2. In addition, the authors prospectively examined the effect of weight loss on cardiovascular parameters in a subset of 25 participants. The results show a closer significant correlation between pulse pressure and BMI (b=1.97 kgm-1; p=0.001) than between systolic blood pressure and BMI (b=1.58 kgm-1; p=0.020). After 3 months of diet and exercise, average reductions were as follows: BMI, 4.2 kg/m2 (p<0.01); systolic blood pressure, 7.2 mm Hg (p<0.01); pulse pressure, 4.8 mm Hg (p<0.01); and cardiac output, 975 mL/min (p<0.01). Compliance index increased by 0.1 mL/mm Hg/m2 (p=0.03). The results highlight the potential value to cardiovascular health of a modest reduction in body weight in obese individuals.

The impact of body mass index on pulse pressure in obesity.

OBJECTIVE: Pulse pressure, a marker of arterial vascular properties, has been linked to cardiovascular diseases and complications. This study examined the impact of excess body mass and cardiovascular disease risk factors on pulse pressure (PP). DESIGN: Cross-sectional and prospective study. METHODS: Baseline data consist of 219 obese African Americans, with mean +/- SD age of 46.8 +/- 10.9 years enrolled in a diet and exercise program of weight reduction. A non-invasive monitoring device was used to acquire 24 hourly ambulatory blood pressures. Pulse pressure was calculated as the difference between the average 24-h systolic and diastolic blood pressure and studied as a continuous variable and according to quartiles. The cross-sectional association of pulse pressure with body mass index (BMI) was examined using multivariate linear regression and proportional odds models that controlled for cardiovascular disease risk factors. In addition, we examined prospectively, in 36 participants, the effect of weight loss on pulse pressure, using the Wilcoxon signed ranked test. RESULTS: At baseline, a 5 kg/m2 increase in BMI was independently associated with a 35% risk [relative risk (RR) = 1.35, confidence interval (CI) = 1.10-1.65, P < 0.01] in the general study population and 19% (RR = 1.19, CI = 1.07-1.56, P = 0.04) in obese normotensives for increasing PP by one quartile after adjustment for other significant variables. After 3 months of diet and exercise intervention, BMI decreased by an average of 10.6% (P < 0.01) and resulted in an 8.8% (P < 0.01) reduction in PP. CONCLUSIONS: In the context of obesity, increasing BMI is independently associated with decreasing arterial compliance, as reflected in PP. This association highlights the potential value to cardiovascular health of any reduction in body weight in obese individuals.

Obese African Americans: the prevalence of dyslipidemia, hypertension, and diabetes mellitus.

CONTEXT: The prevalence of the cardiovascular disease risk factors, dyslipidemia, hypertension, and diabetes mellitus, is increased in the setting of obesity. OBJECTIVE: To determine whether the prevalence of these risk factors increases with increasing body mass index in an obese cohort, or whether there is a threshold for their appearance. DESIGN AND SETTING: Individuals with body mass index > or = 30 kg/m2 joined a weight reduction program in the Howard University General Clinical Research Center. PARTICIPANTS: Five hundred fifteen African Americans (aged 12-74 years, mean body mass index of 42.8 +/- 8.5 kg/m2). OUTCOME MEASURES: The cohort was divided by incremental increases in body mass index of 4.99 kg/m2, and the prevalence rates of hypertension (blood pressure > or = 140/90 mm Hg), dyslipidemia (total cholesterol > 200 mg/dL, or low-density lipoprotein > 130 mg/dL, or elevated ratio of total or low-density to high-density lipoprotein cholesterol) and diabetes mellitus (fasting blood glucose > or = 126 mg/dL or random blood glucose > 200 mg/dL) were determined for each group. RESULTS: The cohort prevalence rates were: dyslipidemia, 27.0%; hypertension, 56.9%; and diabetes mellitus, 24.1%. These rates are higher than those found in the African-American population by the third National Health and Nutrition Examination Survey. After adjusting for age and sex, there were no significant differences in the prevalence rates of these risk factors according to increasing body mass index, suggesting a threshold of between 30 kg/m2-34.99 kg/m2 for maximal appearance of these risk factors. CONCLUSION: The incidence rates of dyslipidemia, hypertension, and diabetes mellitus do not increase with a greater degree of obesity above a body mass index of 34.99 kg/m2.

Alcohol consumption and prognosis in patients with left ventricular systolic dysfunction after a myocardial infarction.

OBJECTIVES: We assessed the influence of alcohol intake on the development of symptomatic heart failure (HF) in patients with left ventricular (LV) dysfunction after a myocardial infarction (MI). BACKGROUND: In contrast to protection from coronary heart disease, alcohol consumption has been linked to cardiodepressant effects and has been considered contraindicated in patients with HF. METHODS: The Survival And Ventricular Enlargement (SAVE) trial randomized 2231 patients with a LV ejection fraction (EF) <40% following MI to an angiotensin-converting enzyme inhibitor or placebo. Patients were classified as nondrinkers, light-to-moderate drinkers (1 to 10 drinks/week), or heavy drinkers (>10 drinks/week) based on alcohol consumption reported at baseline. The primary outcome was hospitalization for HF or need for an open-label angiotensin-converting enzyme inhibitor. Analyses were repeated using alcohol consumption reported three months after MI. RESULTS: Nondrinkers were older and had more comorbidities than light-to-moderate and heavy drinkers. In univariate analyses, baseline light-to-moderate alcohol intake was associated with a lower incidence of HF compared with nondrinkers (hazard ratio [HR] 0.71; 95% confidence interval [CI] 0.57 to 0.87), whereas heavy drinking was not (HR 0.91; 95% CI 0.67 to 1.23). After adjustment for baseline differences, light-to-moderate baseline alcohol consumption no longer significantly influenced the development of HF (light-to-moderate drinkers HR 0.93; 95% CI 0.75 to 1.17; heavy drinkers HR 1.25; 95% CI 0.91 to 1.72). Alcohol consumption reported three months after the MI similarly did not modify the risk of adverse outcome. CONCLUSIONS: In patients with LV dysfunction after an MI, light-to-moderate alcohol intake either at baseline or following MI did not alter the risk for the development of HF requiring hospitalization or an open-label angiotensin-converting enzyme inhibitor.

Hypertension and concomitant diseases: a guide for evidence-based therapy.

Hypertension remains one of the leading causes of morbidity and mortality in the United States. Numerous antihypertensive agents are available today, and most hypertensive patients suffer from concomitant diseases/conditions. Many of these diseases/conditions require appropriate selection of antihypertensive agents. It gets quite complex to pick the initial and additional antihypertensive agents that are simultaneously beneficial in the management of these comorbidities. The authors believe this guide will assist physicians in picking the right agent to achieve goal blood pressure recommended by the Joint National Committee (JNC). In this paper, the introduction section briefly outlines some aspects of the pathophysiology of hypertension. This is followed by subsections that identify commonly encountered diseases/conditions that coexist with hypertension, and a list of antihypertensive drugs to be used for these conditions in the order of preference. The suggested choices are based on evidence from clinical trials, for the most part, and in some cases based on mechanisms of action of the drugs. The list of choices is then followed by concise explanations or rationale, including citations for the clinical trials or other relevant sources. Such a systematic approach and use of a handy flow chart would enhance appropriate blood pressure control and patient compliance and, hopefully, make a little dent in the rate of hypertension-related cardiovascular morbidity and mortality.

Cardiovascular risk reduction in hypertensive black patients with left ventricular hypertrophy: the LIFE study.

OBJECTIVES: We report on a subanalysis of the effects of losartan and atenolol on cardiovascular events in black patients in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. BACKGROUND: The LIFE study compared losartan-based to atenolol-based therapy in 9,193 hypertensive patients with left ventricular hypertrophy (LVH). Overall, the risk of the primary composite end point (cardiovascular death, stroke, myocardial infarction) was reduced by 13% (p = 0.021) with losartan, with similar blood pressure (BP) reduction in both treatment groups. There was a suggestion of interaction between ethnic background and treatment (p = 0.057). METHODS: Exploratory analyses were performed that placed LIFE study patients into black (n = 533) and non-black (n = 8,660) categories, overall, and in the U.S. (African American [n = 523]; non-black [n = 1,184]). RESULTS: A significant interaction existed between the dichotomized groups (black/non-black) and treatment (p = 0.005); a test for qualitative interaction was also significant (p = 0.016). The hazard ratio (losartan relative to atenolol) for the primary end point favored atenolol in black patients (1.666 [95% confidence interval (CI) 1.043 to 2.661]; p = 0.033) and favored losartan in non-blacks (0.829 [95% CI 0.733 to 0.938]; p = 0.003). In black patients, BP reduction was similar in both groups, and regression of electrocardiographic-LVH was greater with losartan. CONCLUSIONS: Results of the subanalysis are sufficient to generate the hypothesis that black patients with hypertension and LVH might not respond as favorably to losartan-based treatment as non-black patients with respect to cardiovascular outcomes, and do not support a recommendation for losartan as a first-line treatment for this purpose. The subanalysis is limited by the relatively small number of events.

Response of lipoprotein(a) levels to therapeutic life-style change in obese African-Americans.

Lipoprotein(a) (Lp(a)) is regarded as an independent risk factor for Atherosclerotic cardiovascular disease. The objectives of this study were: to determine the effects of diet and exercise on Lp(a) and to evaluate the relation of Lp(a) with the lipid profile (total serum cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol). Baseline Lp(a), body mass index (BMI) and the lipid profiles were measured in 343 Obese (BMI >30kg/m(2)) African-Americans. After a 3-month intervention of diet and exercise by 105 participants, their lipids were re-measured. Baseline Lp(a) levels ranged from 1.2 to 280mg/dl. Lp(a) was inversely associated with triglyceride (P<0.05). After the intervention, Lp(a) and HDL increased by a mean of 20 and 5%, respectively. Total cholesterol, triglycerides, LDL and BMI decreased by 7, 10, 11 and 8%, respectively. Women taking estrogen replacement had a negligible change in Lp(a) while participants taking HMG-CoA reductase inhibitors had an increase in Lp(a) levels by 30%.