Impact of race and gender on cardiac device implantations.

BACKGROUND: Pacemakers and implantable cardioverter-defibrillators (ICDs) are established therapies for life-threatening cardiac arrhythmias. Biventricular pacemakers (BiVP) can improve heart failure in selected patients as well. OBJECTIVE: This study sought to investigate the impact of gender and race on rates of implantation of pacemakers and ICDs in patients with reduced left ventricular ejection fraction (LVEF). METHODS: Data were obtained from ADVANCENT, a prospective multicenter registry enrolling patients with LVEF < or = 40% between June 2003 and November 2004. a total of 26,264 patients from 106 us centers were enrolled. the mean age was 66.4 years; 71.5% were male and 81.9% were white; 10,394 subjects (39.6%) had devices implanted. RESULTS: The overall rate of device implantation was higher in white subjects compared with nonwhite subjects (41.1% vs 32.5%, P <.0001). This was also true for the rates of implantation of all types of ICDs (28.6% vs 23.9%, P <.0001) and BiVP (11.2% vs 7.7%, P <.0001). After adjusting for age, gender, LVEF, New York Heart Association class, coronary artery disease, QRS duration, comorbidities, type of referring physician, and insurance type, nonwhite race remained an independent negative predictor of implantation of any device (odds ratio [OR] 0.86, 95% confidence interval [CI] 0.791 to 0.927), and any ICD (OR 0.88, 95% CI 0.817 to 0.964). Female gender was also independently associated with decreased implantation of any device (OR 0.70, 95% CI 0.66 to 0.76), and any ICD (OR 0.60, 95% CI 0.55 to 0.64). CONCLUSION: In this large cohort with reduced LVEF, minorities and women were significantly less likely to receive device implants. These findings were most pronounced in nonwhite women, and could not be explained by disparities in demographic or clinical characteristics.

Lipid-lowering drug use is associated with reduced prevalence of atrial fibrillation in patients with left ventricular systolic dysfunction.

BACKGROUND: Inflammation and oxidative stress have been implicated in the pathogenesis of atrial fibrillation (AF). Lipid-lowering drugs, particularly statins and fibrates, possess anti-inflammatory and antioxidant properties. OBJECTIVES: The purpose of this study was to assess the impact of lipid-lowering drug use on AF prevalence in patients with reduced left ventricular ejection fraction (LVEF). METHODS: Data were obtained from ADVANCENT(SM), a multicenter registry of patients with reduced LVEF (

The relationship between stature and the prevalence of atrial fibrillation in patients with left ventricular dysfunction.

OBJECTIVES: This study sought to determine the influence of stature on atrial fibrillation (AF) in high-risk patients with reduced left ventricular (LV) systolic function. BACKGROUND: Left atrial (LA) enlargement is a potent risk factor for AF. Because LA size is strongly associated with stature, we hypothesized that height and body surface area (BSA) are risk factors for AF, independent of other known associations. METHODS: Data were obtained from ADVANCENT, a multicenter registry of patients with impaired LV function. Height and BSA were divided into quartiles by gender. Statistical analysis was done using the Cochran Mantel-Haenszel statistic, and multivariable logistic regressions were used to adjust for the effects of known confounders on the association between stature and AF. RESULTS: A total of 25,268 patients were enrolled. The mean age was 66 years, and the cohort consisted mostly of white men (72%) and patients with ischemic cardiomyopathy (72%). The mean left ventricular ejection fraction was 31%. A history of AF was present in 7,027 patients (27.8%). The AF prevalence increased significantly between the lowest and highest quartiles for height (32% relative increase, p < 0.0001). In the multivariable analysis, the effect of height on AF risk persisted after adjusting for age, gender, race, left ventricular ejection fraction, heart failure class and etiology, hypertension, diabetes, and medication use (odds ratio 1.026/cm, 95% confidence interval [CI] 1.022 to 1.030). In the multivariable analysis, BSA was also an independent predictor of AF risk (odds ratio 4.221/m2, 95% CI 3.358 to 5.306). CONCLUSIONS: In patients with LV dysfunction, increasing stature portends a higher risk of AF independent of other traditional risk factors for the arrhythmia. This association seems to account for the higher prevalence of AF in men and may be useful for identification of a high-risk population.

Secondary prevention of coronary heart disease in elderly patients.

Coronary heart disease remains a leading cause of mortality in the United States, with 84 percent of persons 65 years or older dying from this disease. Secondary preventive measures, including lifestyle modification and pharmacotherapy, are important for elderly patients because of the variable impacts on morbidity and mortality rates and quality of life. Participating in light to moderate activities significantly decreases mortality rates in elderly patients. Smoking cessation translates into a reduction in overall mortality and morbidity rates at least equal to that of other preventive measures such as aspirin or beta-blocker therapy. Recent studies on the effects of lowering low-density lipoprotein cholesterol levels to below 100 mg per dL have shown a substantial reduction in coronary heart disease mortality and nonfatal myocardial infarction rates, with a persistent effect in patients older than 75 years. Hypertension, manifesting mostly as isolated systolic blood pressure elevation, also should be treated aggressively. Conventional medical therapies for hypertension (e.g., diuretics, beta blockers) and newer agents (e.g., calcium channel blockers, angiotensin-converting enzyme inhibitors), together with sodium restriction, have had a positive effect on cardiovascular mortality and morbidity rates in older patients. With the increasing prevalence of obesity, insulin resistance, and type 2 diabetes, interventions targeting weight reduction and glucose control should be emphasized. Whereas weight-loss strategies are poorly defined in this population, the management of diabetes through dietary modification, exercise, and medications is similar across age groups. The target hemoglobin A1C level is less than 7 percent. Elderly patients are prone to depression and social isolation, and they are more likely to have a lower socioeconomic status than younger patients, which may negatively affect participation in rehabilitation programs and compliance with medical advice and therapy. Strategies aimed at these factors have shown variable results and remain ill-defined.

Atrial septal abnormalities and cryptogenic stroke: a paradoxical science.

Patent foramen ovale and/or atrial septal aneurysm occur in up to 20% of the general population, and have been linked to cryptogenic ischemic strokes in younger individuals. The pathophysiologic basis of this association remains unclear, with growing evidence suggesting a role for thrombosis and embolization. Aspirin and warfarin constitute the current mainstay of medical therapy, with a variety of secondary prevention studies assessing their impact on stroke recurrence. To date, the quality of published data preclude the development of strict recommendations, but a number of suggestions can be derived from available literature. Patients with isolated patent foramen ovale or atrial septal aneurysm and a first ischemic stroke respond well to either aspirin or warfarin therapy. On the other hand, oral anticoagulation seems to be the preferred medical therapy in higher-risk patients with both patent foramen ovale and atrial septal aneurysm or those with multiple strokes on aspirin. Percutaneous or surgical patent foramen ovale closures have been proposed as alternative therapies and seem effective in reducing stroke recurrence. In the absence of randomized, controlled trials comparing medical and invasive approaches, the adoption of a particular therapy should take into consideration the individual's preference, clinical presentation, risk profile, lifestyle, and the expertise of the local interventional and surgical teams.

Functional association of nox1 with p22phox in vascular smooth muscle cells.

The vascular NAD(P)H oxidases constitute important sources of ROS in the vessel wall and have been implicated in vascular disease. Vascular smooth muscle cells (VSMCs) from conduit arteries express two gp91phox homologs, Nox1 and Nox4, of which Nox1 is agonist-sensitive. Because p22phox has been shown to be functionally important in vascular cells stimulated with vasoactive hormones, the relationship of Nox1 and p22phox was investigated in VSMCs from rat and human aortas. Coimmunoprecipitation studies demonstrated that p22phox and hemagglutinin-tagged Nox1 associate in unstimulated VSMCs. These findings were confirmed by confocal microscopy, showing colocalization of the two proteins in their native states in the plasma membrane and submembrane areas of the cell. NADPH-driven superoxide production, as measured by electron spin resonance using 1-hydroxy-3-carboxypyrrolidine as a spin probe, is dependent on the coexpression of both subunits, suggesting the importance of the association for the functional integrity of the enzyme. These results indicate that in contrast to the neutrophil enzyme, VSMCs can use Nox1 rather than gp91phox as a catalytic center in the p22phox-based oxidase and that these two proteins are preassembled at or near the plasma membrane and submembrane vesicular structures in unstimulated cells.

Left atrial structure and function after percutaneous left atrial appendage transcatheter occlusion (PLAATO): six-month echocardiographic follow-up.

OBJECTIVES: This study was designed to evaluate the effects of percutaneous left atrial appendage transcatheter occlusion (PLAATO) on the anatomic and hemodynamic properties of the mitral valve (MV) and left upper pulmonary vein (LUPV). BACKGROUND: PLAATO is a device designed to seal the neck of the left atrial (LA) appendage and reduce embolization in patients with atrial fibrillation intolerant of warfarin. The impact of deployment of this device on adjacent structures has not been reported. METHODS: Patients with atrial fibrillation participating in the ongoing study for evaluation of PLAATO were enrolled. Transesophageal echocardiographies at baseline, one, and six months were reviewed to measure LA and LUPV dimensions, degree of mitral regurgitation, stability of the device, peak MV E-wave velocity, and peak systolic and diastolic flow velocities in the LUPV. Data were analyzed by a linear mixed model for repeated measures. RESULTS: Eleven patients (mean age of 72 +/- 7 years) completed six months of follow-up. Left upper pulmonary vein diameter (mean: 1.55, 1.61, 1.54 cm, p = 0.13) and peak systolic (mean: 0.38, 0.34, 0.31 m/s, p = 0.72) and diastolic flow velocities (mean: 0.39, 0.40, 0.42 m/s, p = 0.46) did not differ over the follow-up period. Left atrial size, mitral regurgitation severity, and MV peak E-wave velocities (mean: 0.94, 0.94, 0.82 m/s, p = 0.58) showed no significant change from baseline. The devices remained stable at their sites of deployment with minimal residual flow around them. CONCLUSIONS: PLAATO achieved an adequate seal of the neck of the left atrial appendage without significant effect on the structure or function of the LA and LUPV.

NAD(P)H oxidase-derived reactive oxygen species as mediators of angiotensin II signaling.

Angiotensin II has been shown to participate in both physiological processes, such as sodium and water homeostasis and vascular contraction, and pathophysiological processes, including atherosclerosis and hypertension. The effects of this molecule on vascular tissue are mediated at least in part by the modification of the redox milieu of its target cells. Angiotensin II has been shown to activate the vascular NAD(P)H oxidase(s) resulting in the production of reactive oxygen species, namely superoxide and hydrogen peroxide. In this article, we review what is known about the molecular steps that link angiotensin II and its receptor to production of reactive oxygen species and subsequent redox-mediated events, focusing on the structural and functional properties of the vascular NAD(P)H oxidases and their downstream mediators. As such, we provide a framework linking angiotensin II to crucial vascular pathologies, such as hypertension, atherosclerosis, and restenosis after angioplasty, by means of the NAD(P)H-dependent oxidases and their effector molecules.