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The association of electrocardiographic (ECG) abnormalities with cardiovascular disease and risk factors has been extensively studied in whites and African-Americans. Comparable data have not been reported in Hispanics/Latinos. The Hispanic Community Health Study/Study of Latinos (HCHS/SOL) is a multicenter, community-based, prospective cohort study of men and women of diverse backgrounds aged 18 to 74 years who self-identified as Hispanic/Latinos. Participants (n = 16,415) enrolled from March 2008 to June 2011. We describe the prevalence of minor and major ECG abnormalities and examined their cross-sectional associations with cardiovascular disease and risk factors. The Minnesota code criteria were used to define minor and major ECG abnormalities. Previous cardiovascular disease and risk factors were based on data obtained at baseline examination. Significant differences in prevalent ECG findings were found between men and women. Major ECG abnormalities were present in 9.2% (95% confidence interval 8.3 to 10.1) of men and 6.6% (95% confidence interval 5.8 to 7.3) of women (p <0.0001). The odds of having major ECG abnormalities significantly increased with age, presence of ≥3 cardiovascular risk factors, and prevalent cardiovascular disease, in both men and women. Significant differences in major ECG abnormalities were found among the varying groups; Puerto Ricans and Dominicans had more major abnormalities compared with Mexican men and women. In conclusion, in a large cohort of Hispanic/Latino men and women, prevalence of major abnormalities was low, yet strong associations of major ECG abnormalities with cardiovascular disease and risk factors were observed in both men and women., (Copyright © 2013 Elsevier Inc. All rights reserved.)

The increased prevalence of hypertension and cardiovascular disease in industrialized societies undoubtedly is associated with the modern high-sodium/low-potassium diet. Extensive experimental and clinical data strongly link potassium intake to cardiovascular outcome. Most studies suggest that the sodium-to-potassium intake ratio is a better predictor of cardiovascular outcome than either nutrient individually. A high-sodium/low-potassium environment results in significant abnormalities in central hemodynamics, leading to potential target organ damage. Altered renal sodium handling, impaired endothelium-dependent vasodilatation, and increased oxidative stress are important mediators of this effect. It remains of paramount importance to reinforce consumption of a low-sodium/high-potassium diet as a critical strategy for prevention and treatment of hypertension and cardiovascular disease., (Published by Elsevier Inc.)

Although initially adaptive, the changes that accompany hypertension, namely, cell growth, endothelial dysfunction, and extracellular matrix deposition, eventually can become maladaptive and lead to end-organ disease such as heart failure, coronary artery disease, and renal failure. A functional imbalance between angiotensin II (Ang II) and nitric oxide (NO) plays an important pathogenetic role in hypertensive end-organ injury. NO, an endogenous vasodilator, inhibitor of vascular smooth muscle and mesangial cell growth, and natriuretic agent, is synthesized in the endothelium by a constitutive NO synthase. NO antagonizes the effects of Ang II on vascular tone, cell growth, and renal sodium excretion, and also down-regulates the synthesis of angiotensin-converting enzyme (ACE) and Ang II type 1 receptors. On the other hand, Ang II decreases NO bioavailability by promoting oxidative stress. A better understanding of the pathophysiologic mechanisms involved in hypertensive end-organ damage may aid in identifying markers of cardiovascular susceptibility to injury and in developing therapeutic interventions. We propose that those antihypertensive agents that lower blood pressure and concomitantly restore the homeostatic balance of vasoactive agents such as Ang II and NO within the vessel wall would be more effective in preventing or arresting end-organ disease.

Cigarette smoking is a major risk factor for atherosclerosis and cardiovascular disease. CD36 mediates oxidized LDL (oxLDL) uptake and contributes to macrophage foam cell formation. We investigated a role for the CD36 pathway in nicotine-induced activation of macrophages and foam cell formation in vitro and in vivo. Nicotine in the same plasma concentration range found in smokers increased the CD36+/CD14+ cell population in human peripheral blood mononuclear cells, increased CD36 expression of human THP1 macrophages, and increased macrophage production of reactive oxygen species, PKCd phosphorylation, and peroxisome proliferator-activated receptor-? (PPAR?) expression. Nicotine-induced CD36 expression was suppressed by antioxidants and by specific PKCd and PPAR? inhibitors, implicating mechanistic roles for these intermediates. Nicotine synergized with oxLDL to increase macrophage expression of CD36 and cytokines TNF-a, monocyte chemoattractant protein-1, IL-6, and CXCL9, all of which were prevented by CD36 small interfering (si)RNA. Incubation with oxLDL (50 µg/ml) for 72 h resulted in lipid deposition in macrophages and foam cell formation. Preincubation with nicotine further increased oxLDL-induced lipid accumulation and foam cell formation, which was also prevented by CD36 siRNA. Treatment of apoE-/- mice with nicotine markedly exacerbated inflammatory monocyte levels and atherosclerotic plaque accumulation, effects that were not seen in CD36-/- apoE-/- mice. Our results show that physiological levels of nicotine increase CD36 expression in macrophages, a pathway that may account at least in part for the known proinflammatory and proatherogenic properties of nicotine. These results identify such enhanced CD36 expression as a novel nicotine-mediated pathway that may constitute an independent risk factor for atherosclerosis in smokers. The results also suggest that exacerbated atherogenesis by this pathway may be an adverse side effect of extended use of high concentrations of nicotine independent of their mode of administration. [ABSTRACT FROM AUTHOR]

Abstract: Cardiovascular disease is emerging as a leading cause of morbidity and mortality in Latin America. Population-based data regarding the prevalence of hypertension and hypertension subtypes in Andean Hispanic populations are scarce. The authors performed a population-based study that included 1878 Peruvian Andean adults to determine: (1) the prevalence, awareness, and control of hypertension and (2) the relative frequency of hypertension subtypes (systolic vs. diastolic). The prevalence of hypertension was 15.7% (95% confidence interval [CI], 14.0%–17.4%), did not differ by gender, and increased steeply with age, particularly in women. Awareness, treatment, and control rates were 47.9%, 39.5%, and 14%, respectively. Diastolic blood pressure increased until age 50 years and reached a plateau thereafter, whereas mean arterial pressure continued to increase with age even after age 50 years. Furthermore, in sharp contrast with the United States population, the predominant type of hypertension was systodiastolic (41.7%; 95% CI, 35.1%–48.5%). Isolated systolic hypertension accounted for only 29.3% of cases (95% CI, 23.9%–35.4%) and was responsible for a minority of cases in all age groups before age 70 years. Hypertension subtypes in this Andean population seem to differ significantly from those present in the United States population, with a much larger proportion of systodiastolic and diastolic hypertension even with advanced age. These differences result from interactions between hemodynamic and structural factors, and further studies aimed at characterizing their genetic and environmental determinants and implications in end-organ damage and prognosis in this population may contribute to understanding the pathophysiology of hypertension. [Copyright &y& Elsevier]

Cigarette smoke (CS) is the most important source of preventable morbidity and mortality in the United States. Recent clinical studies have suggested that, in addition to being a major cardiovascular risk factor, CS promotes the progression of kidney disease. The mechanisms by which CS promotes the progression of chronic kidney disease have not been elucidated. Here we demonstrate for the first time that human mesangial cells (MCs) are endowed with the nicotinic ACh receptors (nAChRs) α4, α5, α7, α2, α3, and α4. Studies performed in other cell types have shown that these nAChRs are ionotropic receptors that function as agonist-regulated Ca2+ channels. Nicotine induced MC proliferation in a dose-dependent manner. At 10-7 M, a concentration found in the plasma of active smokers, nicotine induced MC proliferation (control, 1,328 ± 50 vs. nicotine, 2,761 ± 90 counts/minute (cpm); P < 0.05) and increased the synthesis of fibronectin (50%), a critical matrix component involved in the progression of chronic kidney disease. We and others have shown that, in response to PKC activation, MC synthesize reactive oxygen species (ROS) via NADPH oxidase. In the current studies we demonstrate that PKC inhibition as well as diphenyleneiodonium and apocynin, two inhibitors of NADPH oxidase, prevented the effects of nicotine on MC proliferation and fibronectin production, hence establishing ROS as second messengers of the actions of nicotine. Furthermore, nicotine increased the production of ROS as assessed by 2′,7′-dichlorofluorescein diacetate fluorescence (control, 184.4 ± 26 vs. nicotine, 281.5 ± 26 arbitrary fluorescence units (AFU); n = 5 experiments, P < 0.05). These studies unveil previously unrecognized mechanisms that indict nicotine, a component of CS, as an agent that may accelerate and promote the progression of kidney disease. [ABSTRACT FROM AUTHOR]

: BackgroundCalcium channel blockers such as amlodipine are effective antihypertensive agents. In this study we investigated the effects of amlodipine on vascular oxidative stress, expression of the lectin-like oxidized low-density lipoprotein receptor (LOX-1), and endothelial function in angiotensin (Ang) II-infused rats.: MethodsSprague-Dawley rats were treated with Ang II (0.7 mg/kg/day subcutaneously injected by mini-pump), with or without amlodipine (10 mg/kg/day by gavage), for 5 days and compared with control rats. Levels of aortic ring superoxide (O2−) and peroxynitrite (ONOO−) were determined, and systolic blood pressure (SBP) and endothelium-dependent relaxation were evaluated.: ResultsCompared with control rats, Ang II-infused rats developed hypertension (175 ± 3 v 135 ± 2 mm Hg, P < .05), aortic hypertrophy (16.9 ± 1.3 v 13.2 ± 0.3 mg/cm, P < .05), left ventricular hypertrophy (0.236 ± 0.003 v 0.204 ± 0.004 g/100 g body weight, P < .05), and impaired endothelium-dependent relaxation (ED50: 6.6 ± 0.2 v 8.0 ± 0.2 −log mol/L acetylcholine concentration, P < .05). Compared with control rats, Ang II-infused rats also had higher aortic levels of LOX-1 mRNA expression, O2−production (1005 ± 140 v 608 ± 159 counts/min/mg, P < .05), ONOO− production (1875 ± 295 v 782 ± 115 counts/min/mg, P < .05), and plasma free 8-F2α-isoprostanes (67.4 ± 19.1 v 27.2 ± 6.1 pg/mL, P < .05). In Ang II-infused rats SBP, aortic hypertrophy, endothelial dysfunction, LOX-1 expression, aortic O2− and ONOO− production, and plasma free 8-F2α-isoprostane levels were significantly reduced by amlodipine treatment.: ConclusionsAmlodipine has antihypertensive and antioxidant activity in vivo, which effectively inhibits many of the oxidative stress-dependent mechanisms involved in Ang II-mediated cardiovascular injury. [Copyright &y& Elsevier]