No abstract

BackgroundCardiovascular diseases are the leading cause of death in the majority of developed and developing countries. African countries are currently facing an increase in both cardiovascular and transmitted diseases. In addition, cardiovascular risk varies among different socioeconomic groups. Thus, we determined the prevalence of modifiable cardiovascular risk factors in apparently healthy public-sector workers and investigated possible relationships with socioeconomic status.MethodsWe employed a cross-sectional study comprising 42.2% (n = 615) of the public-sector workers at Agostinho Neto University, 48% (n = 294) male and 52% (n= 321) female, with ages between 20 and 72 years and from various socioeconomic groups. The study was conducted from February 2009 to December 2010. Personal, anthropometric, biochemical, hemodynamic, socioeconomic, and physical activity data were collected.ResultsThe prevalence rates of cardiovascular risk factors were as follows: hypertension, 45.2% (men 46.3%, women 44.2%, P > 0.05); hypercholesterolemia, 11.1% (men 10.5%, women 11.5%, P > 0.05); low high-density lipoprotein (HDL) cholesterol, 50.1% (men 36.9%, women 62.3%; P < 0.05); hypertriglyceridemia, 10.6% (men 12.6%, women 8.7%, P > 0.05); smoking, 7.2% (men 10.2%, women 4.4%; P < 0.05); diabetes, 5.7% (men 5.5%, women 5.9%, P > 0.05); overweight, 29.3% (men 27.3%, women 31.2%, P > 0.05); obesity, 19.6% (men 9.2%, women 29.0%; P < 0.05); sedentary lifestyle, 87.2% (men 83.0%, women 91,0%, P < 0.05); and left ventricular hypertrophy, 20% (men 32.0%, women 9.0%; P < 0.05). At least one risk factor was present in 27.7% of the sample; 15.2% had two risk factors, and 31.4% had three or more risk factors. Among the individuals with low socioeconomic status, 41.0% had three or more risk factors.ConclusionsThe results of this study suggest the existence of a high prevalence of multiple risk factors for cardiovascular disease in apparently healthy public-sector workers in Angola. The workers in lower socioeconomic groups had higher incidences of hypertension, smoking, and left ventricular hypertrophy.

The gut microbiota, the ecosystem formed by a wide symbiotic community of nonpathogenic microorganisms that are present in the distal part of the human gut, plays a prominent role in the normal physiology of the organism. The gut microbiota’s imbalance, gut dysbiosis, is directly related to the origin of various processes of acute or chronic dysfunction in the host. Therefore, the ability to intervene in the gut microbiota is now emerging as a possible tactic for therapeutic intervention in various diseases. From this perspective, evidence is growing that a functional dietary intervention with probiotics, which maintain or restore beneficial bacteria of the digestive tract, represents a promising therapeutic strategy for interventions in cardiovascular diseases and also reduces the risk of their occurrence. In the present work, we review the importance of maintaining the balance of the intestinal microbiota to prevent or combat such processes as arterial hypertension or endothelial dysfunction, which underlie many cardiovascular disorders. We also review how the consumption of probiotics can improve autonomic control of cardiovascular function and provide beneficial effects in patients with heart failure. Among the known effects of probiotics is their ability to decrease the generation of reactive oxygen species and, therefore, reduce oxidative stress. Therefore, in this review, we specifically focus on this antioxidant capacity and its relationship with the beneficial cardiovascular effects described for probiotics.

Coronary artery disease is the leading cause of death in the developed world and in developing countries. Acute mortality from acute myocardial infarction (MI) has decreased in the last decades. However, the incidence of heart failure (HF) in patients with healed infarcted areas is increasing. Therefore, HF prevention is a major challenge to the health system in order to reduce healthcare costs and to provide a better quality of life. Animal models of ischemia and infarction have been essential in providing precise information regarding cardiac remodeling. Several of these changes are maladaptive, and they progressively lead to ventricular dilatation and predispose to the development of arrhythmias, HF and death. These events depend on cell death due to necrosis and apoptosis and on activation of the inflammatory response soon after MI. Systemic and local neurohumoral activation has also been associated with maladaptive cardiac remodeling, predisposing to HF. In this review, we provide a timely description of the cardiovascular alterations that occur after MI at the cellular, neurohumoral and electrical level and discuss the repercussions of these alterations on electrical, mechanical and structural dysfunction of the heart. We also identify several areas where insufficient knowledge limits the adoption of better strategies to prevent HF development in chronically infarcted individuals.