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Heart failure is a chronic disease punctuated by intermittent exacerbations that require hospitalization or intravenous diuretic therapy. The association of worsening heart failure events (WHFEs) with patient-centered outcomes in heart failure with reduced ejection fraction (HFrEF) remains unexplored.Patients with HFrEF completed an online survey assessing health status, medication adherence, treatment satisfaction, treatment burden, and medication costs and affordability. Patients with and without WHFEs were compared on all study variables, with adjustment for patient characteristics using linear or logistic regression. Overall, 512 patients (52.0% WHFEs) were included. Patients with WHFEs more commonly had depression (55.3% vs 24.0%), anxiety (46.2% vs 17.9%), and insomnia (77.8% vs 44.7%; P0.001 for all). Patients with WHFEs had lower adjusted mean Kansas City Cardiomyopathy Questionnaire values (52.9 vs 56.0) and Satisfaction with Medications Questionnaire values (70.5 vs 72.6) and higher Treatment Burden Questionnaire scores (51.1 vs 45.1; P0.001). Medication-related beliefs and long-term concerns were independently associated with nonadherence in patients with WHFE (adjusted odds ratios: 4.2 and 5.2, respectively; P0.01 for both). Patients with WHFE incurred 50.0% higher median monthly out-of-pocket HF prescription medication costs and less often perceived HF medications to be affordable.WHFE is associated with several adverse impacts on patients with HFrEF. Additional support is warranted to manage symptoms, comorbidities, and HF treatments to improve adherence and outcomes.

PURPOSE: Participation of racial and ethnic minority groups (REMGs) in cancer trials is disproportionately low despite a high prevalence of certain cancers in REMG populations. We aimed to identify notable practices used by leading US cancer centers that facilitate REMG participation in cancer trials. METHODS: The National Minority Quality Forum and Sustainable Healthy Communities Diverse Cancer Communities Working Group developed criteria by which to identify eligible US cancer centers—REMGs comprise 10% or more of the catchment area; a 10% to 50% yearly accrual rate of REMGs in cancer trials; and the presence of formal community outreach and diversity enrollment programs. Cancer center leaders were interviewed to ascertain notable practices that facilitate REMG accrual in clinical trials. RESULTS: Eight cancer centers that met the Communities Working Group criteria were invited to participate in in-depth interviews. Notable strategies for increased REMG accrual to cancer trials were reported across five broad themes: commitment and center leadership, investigator training and mentoring, community engagement, patient engagement, and operational practices. Specific notable practices included increased engagement of health care professionals, the presence of formal processes for obtaining REMG patient/caregiver input on research projects, and engagement of community groups to drive REMG participation. Centers also reported an increase in the allocation of resources to improving health disparities and increased dedication of research staff to REMG engagement. CONCLUSION: We have identified notable practices that facilitate increased participation of REMGs in cancer trials. Wide implementation of such strategies across cancer centers is essential to ensure that all populations benefit from advances in an era of increasingly personalized treatment of cancer.

Clinical trial results provide the critical evidence base for evaluating the safety and efficacy of new medicines and medical products. Efficacy and safety may differ among population subgroups depending on intrinsic/extrinsic factors, including sex, age, race, ethnicity, lifestyle, and genetic background. Racial and ethnic minorities continue to be underrepresented in cardiovascular and other clinical trials. Although barriers to diversity in trials are well recognized, sustainable solutions for overcoming them have proved elusive. We investigated barriers impacting minority patients' willingness to participate in trials and-based on literature review and evaluation, and input from key stakeholders, including minority patients, referring physicians, investigators who were minority-serving physicians, and trial coordinators-formulated potential solutions and tested them across stakeholder groups. We identified key themes from solutions that resonated with stakeholders using a transtheoretical model of behavior change and created a communications message map to support a multistakeholder approach for overcoming critical participant barriers.

e18643Background: By 2050, racial and ethnic minorities (REMs) will constitute > 50% of the US population. Despite a high prevalence of certain cancers in REM populations, < 10% REMs diagnosed with...

Patients with diabetes or metabolic syndrome frequently have higher triglycerides, lower high-density lipoprotein (HDL) cholesterol, and more particles containing apolipoprotein B (ApoB); this combination contributes significantly to their cardiovascular risk. Optimal management of dyslipidemia and increased atherosclerotic risk requires a fundamental understanding of diabetic dyslipidemia, the clinical evidence for different interventional strategies, and the potential benefit of achieving therapeutic targets. For this review, we considered guidelines, recent reviews, and clinical trial results. The features of dyslipidemia in type 2 diabetes and the metabolic syndrome are linked metabolically and are related to central adiposity and insulin resistance. Levels of ApoB and HDL cholesterol are particularly important markers of risk. Guidelines broadly agree that low-density lipoprotein (LDL) cholesterol should be reduced below population average levels. Additional or secondary strategies in patients with diabetes or the metabolic syndrome are to decrease non-HDL cholesterol, ApoB and/or LDL particle concentration, to increase HDL cholesterol, and to reduce triglycerides. Lifestyle changes and statins are the bedrock of treatment, although second-line treatment using fibrates or niacin will likely benefit many patients with residual risk. Ezetimibe, too, has a favorable effect on lipid profile and inflammatory biomarkers of risk. Dyslipidemia in type 2 diabetes and metabolic syndrome has a distinct profile, suggesting the need for a tailored therapy that targets the key features of lowered HDL cholesterol and raised triglycerides, in addition to the primary antiatherogenic strategy of lowering ApoB-containing lipoproteins, such as LDL. With the prominent failure of some recent intervention trials, new therapeutic strategies-particularly safe and effective means to raise HDL-are needed to manage dyslipidemia in this high-risk population.

Although obstructive sleep apnea and cardiovascular disease have common risk factors, epidemiologic studies show that sleep apnea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking, alcohol, obesity, diabetes, dyslipidemia, atrial fibrillation, and hypertension). Individuals with severe sleep apnea are at increased risk for coronary artery disease, congestive heart failure, and stroke. The underlying mechanisms explaining associations between obstructive sleep apnea and cardiovascular disease are not entirely delineated. Several intermediary mechanisms might be involved including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress. Other abnormalities such as disorders in coagulation factors, endothelial damage, platelet activation, and increased inflammatory mediators might also play a role in the pathogenesis of cardiovascular disease. Linkage between obstructive sleep apnea and cardiovascular disease is corroborated by evidence that treatment of sleep apnea with continuous positive airway pressure reduces systolic blood pressure, improves left ventricular systolic function, and diminishes platelet activation. Several systematic studies are necessary to explicate complex associations between sleep apnea and cardiovascular disease, which may be compounded by the involvement of diseases comprising the metabolic syndrome (i.e., central obesity, hypertension, diabetes, and dyslipidemia). Large-scale, population-based studies testing causal models linking among sleep apnea, cardiovascular morbidity, and metabolic syndrome are needed. Citation: Jean-Louis G; Zizi F; Clark LT; Brown CD; McFarlane SI. Obstructive sleep apnea and cardiovascular disease: role of the metabolic syndrome and its components. J Clin Sleep Med 2008;4(3):261–272.

QT dispersion (QTD) reflects heterogeneity of myocardial repolarization, which is modulated by the central nervous system. Although largely studied in patients with cardiovascular disease, QTD is increased in acute stroke and this finding is an independent predictor of functional outcome and mortality following acute neurological events.The hypothesis of this study was to determine whether changes in QTD in patients presenting with ischemic stroke parallel changes in neurologic function.We retrospectively studied 30 consecutive patients (76+/-9 years, 50% male) who received thrombolytic therapy for acute ischemic stroke between September 1996 and August 2002, and had multiple electrocardiograms (ECGs). QTD was calculated from the admission ECG and the last available ECG (median 3 days) during hospital admission as the absolute difference between the maximum and minimum QT intervals in at least 11 of 12 leads. The National Institute of Health Stroke Scale (NIHSS) was used to assess neurological status on admission and discharge. DeltaQTD was calculated as the absolute difference between QTD measured on admission and on the last available ECG. Absolute changes in heart rate corrected QTD (DeltaQTDc) and NIHSS scores (DeltaNIHSS) were also calculated.DeltaQTD was significantly higher in the 27% of patients who died as compared to the survivors (44+/-26 ms vs. -2+/-21 ms, p.001). DeltaNIHSS correlated directly with DeltaQTD (r=0.57, p0.001) and with DeltaQTDc (r=0.60, p0.001). The NIHSS score changed in the same direction 3.1 units (95% CI: 2.0, 4.2) for every 10 ms change in QTD.DeltaQTD are associated with changes in neurological function in patients treated with thrombolytic therapy for acute ischemic stroke.

Objectives The purpose of this study was to determine the association of the F11 receptor (F11R) with human vascular disease. Background A molecule identified as critical for platelet adhesion to a cytokine-inflamed endothelial surface in vitro is F11R. The F11R is known to be expressed in platelets and endothelium and reported recently to be overexpressed in atherosclerotic plaques. Methods A novel enzyme-linked immunosorbent assay was developed for the measurement of soluble F11R in human plasma. The F11R levels, along with a number of other biomarkers, were measured in 389 male patients with known or suspected coronary artery disease (CAD) undergoing coronary angiography at a Veterans Administration Medical Center. Results Patients with normal or nonobstructive disease (CAD angiographic score of 0), mild-to-moderate disease (score of 1 to 3), and severe disease (score of 4 to 6) had median F11R plasma levels of 38.6 pg/ml (mean 260 ± 509.6 pg/ml), 45.2 pg/ml (mean 395.3 ± 752.7 pg/ml), and 105.8 pg/ml (mean 629 ± 831.7 pg/ml), respectively (p = 0.03). By multivariate analysis, the variables independently associated with CAD score were age, hyperlipidemia, chronic renal insufficiency, left ventricular function, and plasma F11R levels. The F11R was the only biomarker that was independently associated with CAD score. Consistent with the previously reported effects of tumor necrosis factor (TNF)-alpha on F11R expression in cultured endothelial cells, F11R levels correlated strongly with plasma TNF-alpha levels (r = 0.84; p Conclusions Plasma F11R is independently associated with the presence and severity of angiographically defined CAD. By virtue of its strong correlation to plasma TNF-alpha, F11R may be an important mediator of the effects of inflammation on the vessel wall. Strategies that block F11R may represent a novel approach to the treatment of human atherosclerosis.

The complement system has been implicated in the pathogenesis of atherosclerosis. In addition, complement activation and complement-mediated brain injury have been found in a variety of central nervous system diseases, including stroke. However, there are limited data about the value of complement components for prediction of stroke. Complement C3 and C4 levels, in addition to a variety of established biomarkers, were measured in 389 men with known or suspected coronary artery disease referred for coronary angiography for a variety of indications at a Veterans Affairs Medical Center. Patients were followed prospectively for the development of stroke, which was defined and classified according to criteria of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). All strokes were confirmed with magnetic resonance imaging or computed tomography. For the 97% of patients in whom 24-month follow-up data were available, there were 23 strokes (5.9%). By multivariate Cox proportional hazard analysis, complement C4 was an independent predictor of stroke, with a hazard ratio of 1.57 (95% confidence interval 1.03 to 2.39, p = 0.0358). The 24-month stroke-free survival rate for the patients whose complement C4 levels were equal to or below the median value for the entire cohort was 96.1% compared with 90.1% for patients whose complement C4 levels were above the median value, p = 0.0127 by log rank test). In conclusion, in a cohort of men across a spectrum of risk referred for coronary angiography, a single baseline determination of serum complement C4 level is an independent predictor of the future development of stroke.

The metabolic syndrome represents a specific clustering of cardiovascular risk factors in the same individual (abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, insulin resistance, a prothrombotic state, and a proinflammatory state). Almost 50 million American adults (about one in four) have the metabolic syndrome, which puts them at increased risk for the development of diabetes mellitus and cardiovascular disease. African Americans, especially African‐American women, have a high prevalence of the metabolic syndrome. This is attributable mainly to the disproportionate occurrence in African Americans of elevated blood pressure, obesity, and diabetes. Management of the metabolic syndrome consists primarily of modification or reversal of the root causes (overweight/obesity and physical inactivity) and therapy to reduce or control the risk factors. Although all components of the metabolic syndrome should be addressed, optimal control of atherogenic dyslipidemia and elevated blood pressure may reduce cardiovascular risk by more than 80%. Copyright © 2007 Wiley Periodicals, Inc.

There are limited data about the relative importance of the many different but inter-related inflammatory markers with respect to their ability to independently predict the presence and extent of coronary artery disease (CAD). In addition, studies demonstrating such associations have often been conducted in well-defined populations and have excluded patients with or not adjusted for co-morbidities associated with CAD. In a cohort of 389 men who underwent coronary angiography for a variety of clinical indications and across a spectrum of risk, the following inflammatory markers were measured at baseline to determine their relative abilities to predict angiographic outcomes: C-reactive protein, myeloperoxidase, tissue inhibitor of metalloproteinase-1, erythrocyte sedimentation rate, and white blood cell (WBC) count. This analysis was done in the context of traditional CAD risk factors and other co-morbidities associated with CAD (such as morbid obesity, renal dysfunction, heart failure, and so forth). WBC count was the only marker that was independently associated with angiographically documented CAD (p = 0.0184). Further, WBC count (odds ratio 1.31, 95% confidence interval 1.05 to 1.64, p = 0.0157) and plasma myeloperoxidase (odds ratio 1.35, 95% confidence interval 1.08 to 1.69, p = 0.0090) were the only inflammatory markers that were independently predictive of the presence of multivessel disease on coronary angiography. In conclusion, these data demonstrate that a simple baseline WBC count is independently associated with angiographic CAD, and that it can predict the presence of multivessel disease, even in the context of clinical CAD risk factors and other established inflammatory markers.

Aims To determine the prognostic value of baseline plasma adiponectin levels in patients with known or suspected coronary artery disease referred for coronary angiography. Methods and results Adiponectin was measured in 325 male patients with stable angina, troponin-negative unstable angina, and non-ST-segment elevation myocardial infarction (MI) undergoing coronary angiography at a Veterans Administration Medical Center. The patients were then followed prospectively for the occurrence of all-cause mortality, cardiac mortality, and MI. Follow-up data at 24 months were available for 97% of the patients. Adiponectin was the only biomarker to independently predict the individual endpoints of all-cause mortality, cardiac mortality, and MI. The 24-month survival rates for patients in the lower (≤4.431 mg/L), middle (>4.431 and ≤8.008 mg/L), and upper (>8.008 mg/L) tertiles of plasma adiponectin values were 95.0, 90.4, and 83.5%, respectively ( P = 0.0232 by log-rank test). Furthermore, when patients with chest pain were risk-stratified into those with and without a non-ST-segment elevation acute coronary syndrome (NSTEACS), adiponectin remained an independent predictor of both all-cause mortality and cardiac mortality in the NSTEACS subgroup. Conclusion In a cohort of male patients undergoing coronary angiography, a single baseline determination of plasma adiponectin is independently predictive of the subsequent risk of death and MI.

Anemia has been shown to be an independent risk factor for the development of adverse cardiovascular outcomes in a variety of patient populations. In the case of patients presenting with acute coronary syndrome (ACS), anemia has been demonstrated to be a powerful and independent predictor of 30-day outcomes. However, there are limited and conflicting data about the long-term independent predictive value of anemia in patients with ACS. This is in contrast to non-ACS populations in which anemia has been shown to be an independent predictor of long-term outcomes. The present study investigated the long-term prognostic significance of anemia in a well-characterized cohort of 193 men with ACS who were referred for coronary angiography at a Veterans Affairs Medical Center. All patients were followed prospectively for the development of death or acute myocardial infarction (AMI), and follow-up data were available for all patients at 24 months. After controlling for a variety of baseline clinical, laboratory, and angiographic variables, hemoglobin (analyzed as a continuous variable and as a categorical variable using the World Health Organization cutoff of 13 g/dl for men) was a strong and independent predictor of the composite end point of death or AMI at 24 months when using a Cox proportional hazards model. At 24 months, the event-free survival was 64% in the group with a hemoglobin level13 g/dl compared with 81% in the group with a hemoglobin levelor = 13 g/dl (p = 0.0065 by log-rank test). In conclusion, these data demonstrate that baseline anemia is a strong and independent predictor of death or AMI at 2 years in patients with ACS.

Background: Factor XI deficiency has been associated with bleeding diathesis mostly secondary to trauma and post-operatively depending on the severity of deficiency. Cases with factor XI deficiency having undergone cardiac surgery and coronary intervention after appropriate replacement therapy have been reported in the past. The presence of inhibitor in factor XI deficiency poses a hematological challenge and literature regarding coronary intervention in such patients is limited. Immunosuppressive therapy, plasma exchange and factor VII product transfusions have been used prior to cardiac interventions in few such reported cases. Method: We report our approach in such a case of Percutaneous Transluminal Coronary Angioplasty in a 72-year-old male of Jewish origin who has congenital factor XI deficiency complicated with acquired inhibitor. Results: In some cases, the acuity of the coronary syndrome may mandate immediate coronary intervention. However, patient’s history of factor XI deficiency and acquired inhibitor pose a major dilemma of further course of action. We performed percutaneous balloon angioplasty in this case with no anti-coagulant and with favorable outcome. Conclusion: Under these circumstances of significant coagulation disorder and based on the case report, we recommend that balloon angioplasty be undertaken with no additional anti-coagulation other than Aspirin.

African Americans (AA) have the highest coronary heart disease mortality rate of any ethnic group in the United States. Data from the National Cholesterol Education Program Evaluation ProjecT Utilizing Novel E-Technology (NEPTUNE) II survey were used to assess ethnic differences in low-density lipoprotein cholesterol (LDL-C) goal achievement.NEPTUNE II surveyed patients with treated dyslipidemia to assess achievement of treatment goals established by the Adult Treatment Panel III of the National Cholesterol Education Program. United States physicians working in primary care or relevant subspecialties enrolled 10 to 20 consecutive patients (May to September 2003), and patient data were recorded in Personal Digital Assistants and uploaded to a central database via the internet.Among 4,885 patients receiving treatment for dyslipidemia, 79.7% were non-Hispanic white (NHW) and 8.4% were AA. Non-Hispanic white and AA patients had significantly different frequencies of treatment success, with 69.0% and 53.7%, respectively, having achieved their LDL-C goal (P.001). African-American patients were more likely to be in the highest risk category, and less likely to be using lipid drug therapy, taking high-efficacy statins, and receiving care from a subspecialist, but the difference in goal achievement remained significant (P.001) after adjustment for these and other predictors of treatment success.The frequency of treatment success in dyslipidemia management was significantly lower in AA than NHW patients. Additional research is needed to elucidate reasons for this disparity and to evaluate strategies for improving goal achievement among AA patients receiving therapy for dyslipidemia.

Objectives Our purpose was to develop a risk score to predict in-hospital mortality for percutaneous coronary intervention (PCI) using a statewide population-based PCI registry. Background Risk scores predicting adverse outcomes after PCI have been developed from a single or a small group of hospitals, and their abilities to be generalized to other patient populations might be affected. Methods A logistic regression model was developed to predict in-hospital mortality for PCI using data from 46,090 procedures performed in 41 hospitals in the New York State Percutaneous Coronary Intervention Reporting System in 2002. A risk score was derived from this model and was validated using 2003 data from New York. Results The risk score included nine significant risk factors (age, gender, hemodynamic state, ejection fraction, pre-procedural myocardial infarction, peripheral arterial disease, congestive heart disease, renal failure, and left main disease) that were consistent with other reports. The point values for risk factors range from 1 to 9, and the total risk score ranges from 0 to 40. The observed and recalibrated predicted risks in 2003 were highly correlated for all PCI patients as well as for those in the higher-risk subgroup who suffered myocardial infarctions within 24 h before the procedure. The total risk score for mortality is strongly associated with complication rates and length of stay in the 2003 PCI data. Conclusions The risk score accurately predicted in-hospital death for PCI procedures using future New York data. Its performance in other patient populations needs to be further studied.

The lipid-modifying effects of statin therapy in hypercholesterolemic African-Americans have not been well characterized. This study compared the efficacy and safety of rosuvastatin and atorvastatin treatment for 6 weeks in hypercholesterolemic African-American adults. In the African American Rosuvastatin Investigation of Efficacy and Safety (ARIES) trial (4522US/0002), 774 adult African-Americans with low-density lipoprotein cholesterolor = 160 andor = 300 mg/dl and triglycerides400 mg/dl were randomized to receive open-label rosuvastatin 10 or 20 mg or atorvastatin 10 or 20 mg for 6 weeks. At week 6, significantly greater reductions in low-density lipoprotein cholesterol, total cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B concentrations, as well as lipoprotein and apolipoprotein ratios, were seen with rosuvastatin versus milligram-equivalent atorvastatin doses (analysis of variance with Bonferroni-adjusted critical p0.017 for all comparisons). Rosuvastatin 10 mg also increased high-density lipoprotein cholesterol significantly more than atorvastatin 20 mg (p0.017). Although statistical comparisons were not performed, larger proportions of rosuvastatin-treated patients than atorvastatin-treated patients achieved National Cholesterol Education Program Adult Treatment Panel III low-density lipoprotein cholesterol goals. The median high-sensitivity C-reactive protein levels were significantly reduced statistically from baseline with rosuvastatin 20 mg and atorvastatin 20 mg among all patients and with rosuvastatin 10 and 20 mg and atorvastatin 20 mg in those patients with a baseline C-reactive protein level2.0 mg/L. The 2 study medications were well tolerated during the 6-week study period. In conclusion, rosuvastatin 10 and 20 mg improved the overall lipid profile of hypercholesterolemic African-Americans better than did milligram-equivalent doses of atorvastatin.

Background: Acute coronary syndrome is the leading cause of morbidity and mortality regardless of race or gender. Although multicenter trials have provided information on gender differences and racial disparities in access to healthcare and application of treatment guidelines, very few data are available that assess gender differences in clinical characteristics, treatment trajectory and the severity of coronary artery obstruction in predominantly African-descent populations. Methods: Using the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology/American Heart Association guidelines (CRUSADE) qualitative initiative, a retrospective chart review was conducted in 198 consecutive patients admitted to the SUNY Downstate University Hospital with the diagnosis of acute coronary syndrome from September 1 2003 to August 31 2004. Sociodemographics, clinical characteristics and treatment patterns for men and women were a...

Background— Most studies that are the basis of recommended volume thresholds for percutaneous coronary interventions (PCIs) predate the routine use of stent placement. Methods and Results— Data from New York’s Percutaneous Coronary Interventions Reporting System in 1998 to 2000 (n=107 713) were used to examine the impact of annual hospital volume and annual operator volume on in-hospital mortality, same-day coronary artery bypass graft (CABG) surgery, and same-stay CABG surgery after adjustment for differences in patients’ severity of illness. For a hospital-volume threshold of 400, the odds ratios for low-volume hospitals versus high-volume hospitals were 1.98 (95% CI, 1.17, 3.35) for in-hospital mortality, 2.07 (95% CI, 1.36, 3.15) for same-day CABG surgery, and 1.51 (95% CI, 1.03, 2.21) for same-stay CABG surgery. For an operator-volume threshold of 75, the odds ratios for low-volume versus high-volume operators were 1.65 (95% CI, 1.05, 2.60) for same-day CABG surgery and 1.55 (95% CI, 1.10, 2.18) for same-stay CABG surgery. Operator volume was not significantly associated with mortality. Also, for hospital volumes below 400 and operator volumes below 75, the respective odds of mortality, same-day CABG surgery, and same-stay CABG surgery were 5.92, 4.02, and 3.92 times the odds for hospital volumes of 400 or higher and operator volumes of 75 or higher. Conclusions— Higher-volume operators and hospitals continue to experience lower risk-adjusted PCI outcome rates.

The most recent national survey of compliance with the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) guidelines was completed before ATP III and showed significant underachievement of low-density lipoprotein (LDL) cholesterol goals. The NCEP Evaluation ProjecT Utilizing Novel E-Technology (NEPTUNE) II was a national survey conducted in 2003. Of the 4,885 patients, 67% achieved their LDL cholesterol treatment goal, including 89%, 76%, and 57%, respectively, in the 0 or 1 risk factor,or = 2 risk factors or coronary heart disease (CHD), and CHD risk equivalent categories. The percentage with triglyceride concentrationsor = 200 mg/dl (2.25 mmol/L) in each risk category who achieved their LDL cholesterol and non-high-density lipoprotein cholesterol goals was 64%, 52%, and 27%, respectively. Patients with diabetes (55%) and other CHD risk equivalents (40%) were less likely to have achieved their LDL cholesterol targets than those with CHD (62%). Of the 1,447 patients with cardiovascular disease, 75% could be classified as very high risk according to the new July 2004 NCEP Writing Group recommendations, and 17.8% of those at very high risk had an LDL cholesterol level of70 mg/dl (1.81 mmol/L). In conclusion, these results suggest improved lipid management compared with previous surveys. The largest treatment gaps were found for features new to ATP III as of July 2004, including goal achievement for patients with CHD risk equivalents and for non-high-density lipoprotein cholesterol targets. Most of those (75%) with cardiovascular disease in NEPTUNE II would be considered very high risk and candidates for aggressive therapy to reach the new optional treatment goals.

Black Americans with acute coronary syndromes (ACS) are at greater risk and have poorer outcomes than white Americans. The reasons for this appears, at least in part, to be due to a greater burden of baseline risk factors, longer delays prior to seeking medical care, and underutilization of aggressive treatment strategies in high-risk individuals. A guiding principle of treatment of ACS is that patients at highest risk should receive the most immediate and aggressive therapy. However, compared with whites, blacks with ACS paradoxically receive less aggressive medical therapy, and are less often referred for cardiac catheterization, percutaneous coronary interventions, and bypass surgery. Treatment is--but should not be--different in black Americans. Changing this and improving care for ACS in blacks requires better strategies for decreasing patient delays, earlier recognition and diagnosis of ACS, and more effective implementation of evidence-based treatment guidelines.

Direct thrombin inhibitors (DTI) are emerging as alternative anticoagulants to unfractionated heparin and indirect thrombin inhibitors in patients undergoing percutaneous coronary intervention (PCI). We review the pharmacological properties of these newer antithrombotic agents and evaluate the clinical data demonstrating their use in patients undergoing PCI].

Cardiovascular disease is a major cause of morbidity and mortality in people with diabetes and those with the metabolic syndrome. With the rising prevalence of these disorders that is now reaching epidemic proportions around the globe, cardiovascular disease is also expected to rise substantially. Although lifestyle and dietary interventions are the first-line approaches in the management of diabetes and the metabolic syndrome, pharmacotherapy is almost always necessary to achieve optimal control of glycemia, elevated blood pressure, microalbuminuria, dyslipidemia and other associated cardiovascular disease risk factors. Therapeutic agents that have beneficial cardiovascular effects are attractive choices in treating these high-risk patients. Thiazolidinediones have recently gained momentum due to an increase in interest in their insulin-sensitizing, pleiotrophic effects and their potential to reduce the risk of cardiovascular disease in people with diabetes and reduce diabetes itself. In this article, the beneficial cardiovascular effects of thiazolidinediones in people with insulin resistance and diabetes shall be reviewed, highlighting their antiatherosclerotic and anti-inflammatory role together with their potential effects on dyslipidemia, visceral obesity, hypertension and microalbuminuria.

The report of this working group focuses on ways to increase the number of cardiovascular specialists who are classified as members of an underrepresented minority (URM). The Association of American Medical Colleges (AAMC) defines URMs as blacks, Mexican Americans, mainland Puerto Ricans, and Native

The efficacy of statins in lowering low-density lipoprotein cholesterol (LDL-C) and reducing coronary heart disease risk is well established; however, recent evidence suggests that more aggressive lipid management, even beyond achievement of currently recommended LDL-C goals, may provide additional clinical benefits. A novel approach to the aggressive lowering of LDL-C is the combination of statins with agents that affect different aspects of cholesterol metabolism. Because absorption of cholesterol is an important contributor to cholesterol balance, the simultaneous inhibition of cholesterol absorption and cholesterol synthesis is an attractive approach to achieving greater LDL-C reductions. In clinical trials, the combination of the cholesterol absorption inhibitor ezetimibe with a statin resulted in greater improvements in lipids than statin monotherapy and allowed a greater percentage of patients to achieve treatment goals. In addition, this combination may offer benefits through reduction of phytosterols, chylomicron remnants, and C-reactive protein. Several ongoing trials are evaluating whether the benefit of simultaneously blocking cholesterol synthesis and intestinal cholesterol absorption translates into better clinical outcomes.

Background Coronary heart disease (CHD), the result of coronary atherosclerosis, is the largest single killer of Americans. Central to the pathogenesis of atherosclerosis are the deposition and retention of cholesterol in the arterial walls. Lipid modification, therefore, is key to CHD prevention. Methods Data from trials evaluating the safety and efficacy of several pharmacologic agents for dyslipidemia were thoroughly reviewed. Results Agents such as bile acid sequestrants, fibric acids, and nicotinic acid have a role in treating dyslipidemia. However, statins are the safest and most effective of the lipid-modifying drugs, reducing the incidence of CHD by as much as 21% to 43%. Despite the overall safety and efficacy of these agents, many patients undergoing statin therapy fail to achieve the treatment goals specified in the National Cholesterol Education Program Adult Treatment Panel III guidelines, often because of suboptimal use, tolerability problems, or lack of compliance. Although adverse effects of statins are generally mild and transient, more serious adverse effects, including myotoxicity, liver toxicity, and rhabdomyolysis, are still possible with statin monotherapy and are more common in patients receiving concomitant therapy with other drugs metabolized by the cytochrome P-450 enzyme system. Conclusions Because of the overall safety and efficacy of the statins, more patients with or at risk for CHD should be receiving aggressive therapy to lower low-density lipoprotein cholesterol levels and reduce CHD risk. (Am Heart J 2003;145:387-96.)

Background African Americans have greater precordial QRS voltages than whites, with concomitant higher prevalences of electrocardiographic (ECG) left ventricular hypertrophy (LVH) and lower specificity of ECG LVH criteria for the identification of anatomic hypertrophy. However, the high mortality associated with LVH in African American patients makes more accurate ECG detection of LVH in these patients a clinical priority. Methods Electrocardiograms and echocardiograms were obtained at study baseline in 120 African American and 751 white hypertensive patients enrolled in the Losartan Intervention For Endpoint (LIFE) echocardiographic substudy. The ECG LVH was determined using Sokolow-Lyon, 12-lead sum, and Cornell voltage criteria. Echocardiographic LVH was defined by LV mass indexed to height 2.7 >46.7 g/m 2.7 in women and >49.1 g/m 2.7 in men. Results After adjusting for ethnic differences in LV mass, body mass index, sex, and prevalence of diabetes, mean Sokolow-Lyon and 12-lead sum of voltage were significantly higher, but Cornell voltage was lower, in African Americans than in whites. As a consequence of these differences, when identical partition values were used in both ethnic groups, Sokolow-Lyon and 12-lead voltage criteria had lower specificity in African Americans than whites (44% v 69%, P = .007 and 44% v 59%, P = .10) but had greater sensitivity in African Americans (51% v 27%, P v 45%, P = .003). In contrast, Cornell voltage specificity was higher (78% v 62%, P = .09) but sensitivity was slightly lower (49% v 57%, P = 0.16) in African Americans. However, when overall test performance was compared using receiver operating curve analyses that were independent of partition value selection, ethnic differences in test performance disappeared, with no differences in accuracy of any of the ECG voltage criteria for the identification of LVH between African American and white hypertensive individuals. Conclusions When standard, non–ethnicity-specific thresholds for the identification of LVH are used, Sokolow-Lyon and 12-lead voltage overestimate and Cornell voltage underestimates the presence and severity of LVH in African American relative to white individuals. However, these apparent ethnic differences in test performance disappear when ethnic differences in the distribution of ECG LVH criteria are taken into account. These findings demonstrate that ethnicity-specific ECG criteria can equalize detection of anatomic LVH in African American and white patients.

Inflammation is thought to have a role in the pathogenesis of atherosclerotic coronary artery disease (CAD), and the measurement of markers of inflammation has been suggested to improve the identification of individuals at risk for this disease. The incidence of CAD in women is not accounted for by conventional risk factors, and the association of CAD and the antiinflammatory cytokine transforming growth factor beta1 (TGF-beta1) in this population is unknown. Associations among TGF-beta1, the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha), and CAD severity in inner city women were examined. Fifty-three women requiring angiography (mean age, 60.7 years) were stratified as having on of the following conditions: 0 vessel disease (VD) (n = 20), 1 (VD) (n = 10), 2 VD (n = 9), or 3 VD (n = 14). Fasting serum cytokine levels were determined by enzyme-linked immunosorbent assay. Serum TGF-beta1 was lower in patients with extensive disease (2 and 3 VD versus 0 and 1 VD). The lowest TGF-beta1 levels (

Percutaneous balloon mitral valvuloplasty (PBMV) provides an effective alternative to surgery in a selective group of patients with symptomatic mitral stenosis. The Inoue balloon technique involves transseptal catheterization followed by catheter manipulation to cross the mitral valve. The authors describe a case of successful percutaneous balloon mitral valvuloplasty in a patient with severe mitral stenosis and pulmonary hyperten sion. Left ventricular systolic pressure was used as a guide to locate and to advance the balloon catheter across the mitral valve. This technique to cross the mitral valve has not been reported in the literature.

Previous studies using intracoronary electrocardiography have demonstrated that ST-T alternans can develop during standard balloon coronary angioplasty. Total occlusion with a large amount of myocardium in jeopardy is the postulated prerequisite. In this study, the authors used perfusion balloons instead of standard balloons, so coronary perfusion was maintained and ischemia was minimized. Fourteen patients with standard balloon technique and 11 patients with perfusion balloon technique were studied. The ST segment was less elevated during perfusion angioplasty (0.15 ±0.05 mV vs 1.04 ±0.19 mV, p

We have shown previously that a hepatic lipase allele (designated 2 514T) is common among African Americans and contributes to low hepatic lipase activity in this population. To identify other hepatic lipase alleles as- sociated with low hepatic lipase activity in this population, the coding region and intron-exon boundaries of the he- patic lipase gene were sequenced in 20 African American men with low hepatic lipase activity. Two polymorphisms (N193S and L334F) were associated with low post-heparin plasma hepatic lipase activity and were much more com- mon in African Americans than in whites. This fi nding, together with our previous data on the 2 514T allele, in- dicates that at least three different hepatic lipase polymor- phisms associated with low hepatic lipase activity are com- mon among African Americans. Analysis of hepatic lipase haplotypes revealed that 97% of African Americans have at least one hepatic lipase allele that is associated with low he- patic lipase activity.— Nie, L., S. Niu, G. L. Vega, L. T. Clark, A. Tang, S. M. Grundy, and J. C. Cohen. Three polymor- phisms associated with low hepatic lipase activity are com- mon in African Americans. J. Lipid Res. 1998. 39: 1900- 1903.

The -514 polymorphism in the hepatic lipase gene (LIPC) is associated with decreased hepatic lipase activity. In the present study, the interaction between body mass index (BMI), the -514 polymorphism, and hepatic lipase activity was examined in 118 white men and in 51 African American men. BMI was significantly positively correlated with hepatic lipase activity in both populations. BMI was similar in men with genetic differences in hepatic lipase activity, indicating that high hepatic lipase activity did not cause increased BMI. The data therefore suggest that high BMI leads to increased hepatic lipase activity. The actions of BMI and the -514 polymorphism on hepatic lipase activity appear to be additive and independent, rather than synergistic. This finding indicates that hepatic lipase activity is a multifactorial trait, determined in part by polymorphism within the LIPC gene as well as by factors that influence BMI.—Nie, L., J. Wang, L. T. Clark, A. Tang, G. L. Vega, S. M. Grundy, and J. C. Cohen. Body mass index and hepatic lipase gene (LIPC) polymorphism jointly influence postheparin plasma hepatic lipase activity. J. Lipid Res. 1998. 39: 1127–1130.

The sudden death of a competitive athlete is a personal tragedy with great impact on the lay and medical communities.1 Sudden deaths in athletes are usually caused by previously unsuspected cardiovascular disease.2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Such an event often assumes a high public profile because of the generally held perception that trained athletes constitute the healthiest segment of our society. The death of a well-known elite athlete often emphasizes this visibility.1 21 Athletic field catastrophes strike to the core of our sensibilities and often galvanize us. They also inevitably raise a number of practical and ethical issues. This statement is a response to these considerations and represents the consensus of a panel appointed by the American Heart Association Science Advisory and Coordinating Committee. The panel comprised cardiovascular specialists, other physicians with extensive clinical experience with athletes of all ages, and a legal expert. The panel (1) assessed the benefits and limitations of preparticipation screening for early detection of cardiovascular abnormalities in competitive athletes; (2) addressed cost-efficiency and feasibility issues as well as the medical and legal implications of screening; and (3) developed consensus recommendations and guidelines for the most prudent, practical, and effective screening procedures and strategies (the recommendations are listed at the end of this statement). This endeavor seems particularly relevant and timely, given the large number of competitive athletes in this country, recent public health initiatives on physical activity and exercise, and the staging of the 1996 Olympic Games in the United States. The competitive athlete has been described as one who participates in an organized team or individual sport requiring systematic training and regular competition against others while placing a high premium on athletic excellence and achievement.20 The …

To evaluate the impact of a unique school-based program of exercise, health education, and behavior modification on health knowledge, health behaviors, coronary risk factors, and cardiovascular fitness in minority adolescents.A total of 346 students from an inner-city public high school participated in health promotion intervention or regular physical education volleyball classes. Subjects were African-American (47%), Asian-American (9%), Hispanic (21%), white (3%), and other (19%). The health promotion curriculum consisted of 11 weeks of daily circuit training exercise and health lecture-discussions.The groups were similar in age, height, weight, ethnicity, and socioeconomic status. Following intervention both boys (P.001) and girls (P.006) significantly improved health knowledge test scores. Significant benefits for girls included improved dietary habits (P.05), reduced cholesterol (P.004), and higher estimated V(O2)max (P.0001). There were no other significant changes in boys.The results suggest that a school-based health promotion program of exercise and health lecture-discussion is beneficial for multiethnic, inner-city adolescents, especially females.

We sought to determine the role of an abnormal ankle-brachial index (ABI) in an African-American population with suspected coronary artery disease (CAD) referred for diagnostic coronary angiography. In this population, an ABIor =0.90 predicted the presence ofor =3-vessel or left main CAD with a sensitivity of 85% and specificity of 77%. However, a normal ABI did not predict absence of 1- or 2-vessel CAD. These results suggest that in this population, the ABI can be used to increase the pretest probability of severe CAD.

PURPOSE The purpose was to evaluate the effects of a health promotion curriculum on health knowledge, behavior, cardiovascular fitness, and cardiovascular risk factors. METHODS A multi-ethnic, multi-cultural sample (n = 54) of 10th grade males and females participated in a study of cardiovascular health promotion and coronary risk factor reduction. The sample was comprised of Asian-Americans (39%), blacks (33%), Hispanics (11%), whites (2%), and others (15%). Intervention consisted of a 10-week health promotion curriculum of classroom education modules in physical activity, nutrition, smoking cessation, stress management and personal problem solving, and an exercise program of walking and running. A nonintervention control group served as a basis for comparison. Classroom and exercise sessions met on alternate days. RESULTS Following intervention, a significant treatment effect (P = .007) was observed in lowered total cholesterol, and significant within group improvements (P < .01) were observed in diet habits, percent body fat, and cardiovascular health knowledge. Comparisons of knowledge and social effects revealed higher cardiovascular health knowledge (P < .05) in subjects of nonsmoking compared to smoking parents, higher self-perception of health (P < .01) in more active vs less active subjects and better dietary habits (P < .07) in children whose parents were college educated compared to parents who did not attend college. CONCLUSIONS Preliminary findings suggest that a health promotion curriculum consisting of health education, behavior modification, and regular aerobic exercise lowers cholesterol, improves health behavior and increases health knowledge.

The right gastroepiploic artery (RGEA) is being successfully used as an arterial conduit in a selected group of patients undergoing coronary artery bypass graft surgery. However, myocardial ischemia may result due to spasm, occlusion, and stenosis of this graft. The anastamosis site at distal right coronary artery (RCA) or posterior descending artery (PDA) is the most common location for stenosis of an in situ gastroepiploic coronary bypass graft. Balloon angioplasty of such stenoses has been reported with optimal short-term results. Stent deployment would decrease the restenosis rate, so that repeat procedures could be minimized for these technically challenging lesions. We describe a case of successful deployment of a stent with monorail delivery system at the anastamotic site stenosis of an in situ gastroepiploic right coronary artery bypass graft. This percutaneous coronary intervention could prevent redo coronary artery bypass graft surgery. Cathet. Cardiovasc. Intervent. 49:197-199, 2000.

Approximately 60 million people in the United States have hypertension. More than half are either untreated or treated without blood pressure control, despite the well-known risks of hypertension and the established benefits of treatment. The major reason for inadequate control of hypertension is poor adherence to treatment. Approximately 50% of patients with hypertension fail to keep follow-up appointments, and only 60% take their medications as prescribed. Barriers to effective therapeutic adherence include poor doctor-patient communication, cost of antihypertensive therapy, and side effects of the drugs. To increase control of hypertension, compliance with therapy must be improved. Physicians and patients must be mutually committed to achieving control of blood pressure. Physicians should communicate instructions clearly and prescribe therapies that are effective, affordable, and have minimal or no adverse effects on patient quality of life or overall cardiac risk profile. The needs of special hypertensive populations (i.e., elderly, black, and young patients) must also be recognized and addressed. Patients must follow recommendations and alert their physicians to any problems with their medications--particularly those relating to side effects and cost. When selecting drug therapy it should be noted that older patients are sensitive to volume depletion and sympathetic inhibition. In this group of patients, initial drug doses should be low and increments smaller and more gradual than in younger patients. Black patients with hypertension show an accentuated response to diuretics and blunted responses to beta-blockers and angiotensin-converting enzyme (ACE) inhibitors as monotherapy. However, when used with a diuretic, there are no racial differences in the blood pressure lowering effects of beta-blockers and ACE inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)

Ischemic heart disease is the leading cause of death in the United States among Americans of African as well as of European ancestry. African Americans have the highest overall coronary heart disease (CHD) mortality rate and the highest out-of-hospital coronary death rates of any ethnic group in the United States, particularly at younger ages. The reasons for this excess CHD mortality among African Americans have not been fully elucidated but may be attributed to a high prevalence of coronary risk factors, patient delays in seeking medical care, limited access to and utilization of cardiac services, and undertreatment of high-risk individuals. The high prevalence of modifiable risk factors in African Americans provides a major opportunity for CHD prevention and risk reduction in this high-risk population. Hypertension, left ventricular hypertrophy (LVH), diabetes mellitus, cigarette smoking, obesity, physical inactivity, and multiple CHD risk factors all occur more frequently in African Americans than in whites. –7 The predictive value of most conventional risk factors for CHD appears to be similar for African Americans and whites. However, the risk of death and other sequelae attributable to some risk factors, such as hypertension and diabetes, is disproportionately greater for African Americans, –11 and current risk assessment algorithms may not have the same predictive value in African Americans as in whites. Hypertension and LVH are more prevalent, develop at younger ages, and are associated with three to five times higher mortality rates in African Americans than in whites. Moreover, African Americans experience greater cardiovascular and renal damage at any level of hypertension than do whites. Elevations in both diastolic and systolic blood pressures increase cardiovascular risk. However, elevated systolic blood pressure is a more powerful predictor of CHD, heart failure, stroke, end-stage renal disease, and overall mortality than is elevated diastolic blood pressure. LVH, when present, is more predictive of CHD morbidity and mortality than is hypertension, cigarette smoking, or hypercholesterolemia. Hypertension and LVH increase the predisposition to arrhythmia and potentially lethal silent ischemic events. –10,12 Both hypertension and LVH impart a particular risk for a poor outcome in African Americans. In a study of African Americans with LVH and coronary disease, LVH accounted for 40% of the attributable risk of death. In the Meharry–Hopkins physician cohort study, hypertension was the best predictor of cardiac events in African American physicians, whereas smoking, cholesterol, and a family history of CHD were better predictors of cardiac events in white physicians. Thus, both hypertension and LVH are common and important risk factors for CHD events in African Americans. Risk prediction algorithms that do not include hypertension and LVH may have less predictive value in African Americans than in other populations. The prevalence of diabetes in African Americans has tripled during the past 30 years, is two to three times greater than in whites, and is associated with a greater burden of macrovascular and microvascular disease complications. Individuals with diabetes are two to three times more likely to experience a CHD event than are nondiabetics, with approximately 60% of deaths in diabetics due to CHD. It is not known why diabetes is substantially more prevalent in African Americans and other high-risk minorities than in whites or why the disease appears to run a more aggressive clinical course in these populations. The cornerstones of effective cardiovascular disease prevention and risk reduction in patients with diabetes are glycemic control, vigorous modification of other CHD risk factors, and ongoing patient monitoring to facilitate early disease detection and prompt intervention. Most population-based surveys indicate that African Americans have lower total serum cholesterol levels and a similar or lower prevalence of hypercholesterolemia compared with whites. – 6,18 The relation between total cholesterol levels and CHD mortality was the same among 23,490 black men screened for the Multiple Risk Factor Intervention Trial (MRFIT) as among 325,384 white men during an average follow-up period of approximately 12 years. However, the first National Health and Nutrition Examination Survey epidemiologic folFrom the Division of Cardiovascular Medicine, State University of New York Health Science Center at Brooklyn, Brooklyn, New York. Requests for reprints should be addressed to Luther T. Clark, MD, Division of Cardiovascular Medicine, State University of New York Health Science Center at Brooklyn, 450 Clarkson Avenue, Brooklyn, New York 11203.

Although obstructive sleep apnea and cardiovascular disease have common risk factors, epidemiologic studies show that sleep apnea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking, alcohol, obesity, diabetes, dyslipidemia, atrial fibrillation, and hypertension). Individuals with severe sleep apnea are at increased risk for coronary artery disease, congestive heart failure, and stroke. The underlying mechanisms explaining associations between obstructive sleep apnea and cardiovascular disease are not entirely delineated. Several intermediary mechanisms might be involved including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress. Other abnormalities such as disorders in coagulation factors, endothelial damage, platelet activation, and increased inflammatory mediators might also play a role in the pathogenesis of cardiovascular disease. Linkage between obstructive sleep apnea and cardiovascular disease is corroborated by evidence that treatment of sleep apnea with continuous positive airway pressure reduces systolic blood pressure, improves left ventricular systolic function, and diminishes platelet activation. Several systematic studies are necessary to explicate complex associations between sleep apnea and cardiovascular disease, which may be compounded by the involvement of diseases comprising the metabolic syndrome (i.e., central obesity, hypertension, diabetes, and dyslipidemia). Large-scale, population-based studies testing causal models linking among sleep apnea, cardiovascular morbidity, and metabolic syndrome are needed.

To evaluate home blood pressure monitoring (HBPM) in an inner city cardiology practice.Retrospective study.Inner city cardiology practice.Consecutive patients were evaluated for hypertension and hador = 8 home blood pressure recordings during 2-4 weeks while clinically stable on a medical regimen.Blood pressure differences, blood pressure load, defined as %HBPM systolic blood pressure readings140 and/or diastolic blood pressure readings90 mm Hg.55 patients, (33 female, age 62 +/- 12.5 years). Office systolic, diastolic and mean BPs were higher than HBPM values (147 +/- 19 mmHg vs 139 +/- 17 mmHg, P =.0001), (86 +/- 10 mm Hg vs 79 +/- 10 mm Hg, P.0001), and (106 +/- 11 mm Hg vs 99 +/- 10 mmHg, P.0001) respectively. Office and home pulse pressure (PPs) were similar (61 +/- 17 mm Hg vs 60 +/- 17 mm Hg, P = .42). Office and home PPs were more strongly correlated (r = .78, P.0001) than were systolic (r = .51, P.0001), diastolic (r = .51, P.0001). Blood pressure load increased in a step-wise manner with increasing office blood pressure, 7.5% for patients with office blood pressure120/80 mm Hg to 73.5% in patients with office blood pressure160/100 mm Hg (P = .02). Office BPs showed 10/55 patients were normal or controlled (blood pressure140/ 90 mmHg) and 45 were high or uncontrolled (blood pressureor = 140/90 mmHg). HBPM reclassified 2/10 patients as high/uncontrolled whereas 17/45 patients became normal/controlled.Office systolic and diastolic BPs are 7-8 mm Hg higher than home recordings in ethnically diverse patients. Office and home PPs are more strongly correlated than systolic, diastolic or mean arterial BPs. Blood pressure load is related to office BPs. HBPM reclassified approximately one third of the patients. HBPM appears useful in managing minority populations with hypertension.

Numerous disparities in access to health care by race and gender have been identified in the literature. This study examines differences in the use of drug-eluting stents (DES) versus bare-metal stents (BMS) by race, payer, and income level. Data from New York State's Percutaneous Coronary Intervention Reporting System from July 2003 to December 2004 were used to examine use of DES (20,165 patients) relative to BMS (4,547 patients) by race, payer, and annual income level, controlling for a variety of patient and hospital characteristics. African-Americans were found to be less likely to receive DES than other races between July 2003 and March 2004 (adjusted odds ratio [OR] 0.56, 95% confidence interval [CI] 0.50 to 0.65) and between April 2004 and December 2004 (adjusted OR 0.74, 95% CI 0.61 to 0.90). These disparities were reduced (respective adjusted ORs 0.67, 95% CI 0.58 to 0.77 and 0.81, 95% CI 0.66 to 0.91) when controlling for admitting hospital and hospital volume, but were still significant. Medicaid/self-pay patients, and patients living in zip codes with median annual incomes between $20,000 and $30,000 were also less likely to receive DES in the first time period (adjusted respective ORs 0.80, 95% CI 0.68 to 0.93) and 0.85, 95% CI 0.75 to 0.96). In conclusion, African-Americans and low income groups receive DES less frequently than their counterparts compared with BMS. This is related to the hospitals where they are admitted, but not entirely.

Previous studies on outcomes following percutaneous coronary intervention (PCI) have shown an increased rate of in-hospital mortality and vascular complications in women compared to men. The impact of gender on post-PCI outcomes in African-Americans has not been reported.We retrospectively analyzed 835 consecutive African-American patients (n = 392 men and n = 443 women) who underwent PCI using a glycoprotein IIb/IIIa inhibitor (GPI) bolus-only strategy from January 2003 to August 2004 at a single institution. Baseline characteristics, procedural data, and in-hospital outcomes were recorded.Women were older and had a higher mean body mass index (BMI) compared to men. Men were more likely to be smokers, more often had triplevessel disease and left ventricular dysfunction compared to women. There were no deaths or repeat revascularizations in either group. After adjustment for baseline risk factors and procedural characteristics, there was no significant difference in the composite endpoint of in-hospital death, myocardial infarction (MI), and repeat revascularization between men and women (6.38% in men and 2.48% in women; p = 0.051), but women had a higher rate of major and minor bleeding (0.5 vs. 2.5; p = 0.019; and 0.5 vs. 2.3; p = 0.021, respectively). On multiple logistic regression analysis, female gender was an independent risk factor for bleeding post-PCI (adjusted odds ratio [OR]-5.6, 95% confidence intervals [CI]: 1.15-27.45).Although there is no difference in the in-hospital composite endpoint of death, MI, and repeat revascularization, African-American women are at increased risk for bleeding complications post-PCI, even when a GPI bolus-only strategy is used.