Hispanic Ethnicity and the Risk of Cardiovascular Disease in the United States: The Behavioral Risk Factor Surveillance System 2013

BACKGROUND: Although the leading cause of death among Hispanics living in the United States (US) is cardiovascular disease (CVD), the association between Hispanic ethnicity and CVD has been scarcely explored. OBJECTIVE: To examine whether being Hispanic is associated with an increased risk of CVD compared with the non-Hispanic US adult population in 2013. METHODS: Secondary data analysis of a cross-sectional 2013 Behavioral Risk Factor Surveillance System survey in 2013 (n=486,905). The main exposure variable was Hispanic ethnicity (Mexican, Puerto Rican, Cuban or Spanish origin) and the main outcome variable was self-reported CVD (myocardial infarction/coronary artery disease/angina). The main covariates were sex, age, education, income, healthcare access, exercise, body mass index, current smoking, heavy drinking, diabetes, hypertension and hyperlipidemia. Unadjusted and adjusted logistic regressions were used to assess the effect between ethnicity and self-reported CVD. Odds ratios (OR) and 99% confidence intervals (CI) were calculated. RESULTS: In total, 12% of the study participants were Hispanic (n=57,257). Approximately 24% of Hispanics were 25-34 y/o while (21%) of non-Hispanic were \u3e65 y/o. After adjustment, Hispanics were 30% less likely to report CVD compared with non-Hispanics (OR=0.7; 99%; CI=0.6-0.8). Compared with men, women had a 40% decreased risk of having CVD (OR=0.60; 99% CI=0.5-0.6). Advanced age, lower educational attainment, income \u3c$15,000/year, lack of exercise, smoking, non-heavy drinking, diabetes, hypertension and hyperlipidemia increased statistically significantly the likelihood of reporting CVD. CONCLUSION: The findings suggest that, in general, Hispanics residing in the US are significantly less likely to self-declare if they had a CVD compared with non-Hispanic Americans. These data suggest that although Hispanics are generally poorer and have less access to education and health services, their self-perceived health is better than in non-Hispanic residents of the US

OX-HDL: A Starring Role in Cardiorenal Syndrome and the Effects of Heme Oxygenase-1 Intervention

In this review, we will evaluate how high-density lipoprotein (HDL) and the reverse cholesterol transport (RCT) pathway are critical for proper cardiovascular-renal physiology. We will begin by reviewing the basic concepts of HDL cholesterol synthesis and pathway regulation, followed by cardiorenal syndrome (CRS) pathophysiology. After explaining how the HDL and RCT pathways become dysfunctional through oxidative processes, we will elaborate on the potential role of HDL dysfunction in CRS. We will then present findings on how HDL function and the inducible antioxidant gene heme oxygenase-1 (HO-1) are interconnected and how induction of HO-1 is protective against HDL dysfunction and important for the proper functioning of the cardiovascular-renal system. This will substantiate the proposal of HO-1 as a novel therapeutic target to prevent HDL dysfunction and, consequently, cardiovascular disease, renal dysfunction, and the onset of CRS

OX-HDL: A Starring Role in Cardiorenal Syndrome and the Effects of Heme Oxygenase-1 Intervention

In this review, we will evaluate how high-density lipoprotein (HDL) and the reverse cholesterol transport (RCT) pathway are critical for proper cardiovascular–renal physiology. We will begin by reviewing the basic concepts of HDL cholesterol synthesis and pathway regulation, followed by cardiorenal syndrome (CRS) pathophysiology. After explaining how the HDL and RCT pathways become dysfunctional through oxidative processes, we will elaborate on the potential role of HDL dysfunction in CRS. We will then present findings on how HDL function and the inducible antioxidant gene heme oxygenase-1 (HO-1) are interconnected and how induction of HO-1 is protective against HDL dysfunction and important for the proper functioning of the cardiovascular–renal system. This will substantiate the proposal of HO-1 as a novel therapeutic target to prevent HDL dysfunction and, consequently, cardiovascular disease, renal dysfunction, and the onset of CRS