1,721,193 research outputs found
The year in cardiology 2012: Focus on cardiovascular disease prevention
Current data suggest that advances in cardiovascular (CV) treatment have resulted in significant reduction in CV mortality but also in prolongation of life with disability. Focus on CV prevention is likely to reverse this unfavourable trend. In this review we provide information on the new European guidelines on CV prevention and discuss biomarkers and vascular imaging techniques which can assist in refining CV risk prediction. Finally, we provide new information on lifestyle and pharmacological advances which are likely to result in significant CV risk reduction.© The Author 2013
Circulating interleukins, coronary artery disease, ischemic stroke and atrial fibrillation: Connecting the dots between inflammation and cardiovascular disease
The renin-angiotensin-aldosterone system: a crossroad from arterial hypertension to heart failure
The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in the regulation of blood pressure and volume homeostasis, promoting critical structural changes in every component of the cardiovascular system, including the heart and blood vessels. Consequently, the RAAS is a crucial therapeutic target for several chronic diseases of the cardiovascular system, spanning from arterial hypertension (AH) to heart failure (HF). AH represents a leading risk factor for the development of symptomatic HF, particularly with left ventricle (LV) preserved ejection fraction (HFpEF). LV diastolic dysfunction and cardiac remodelling are the first discernible manifestations of heart disease in patients with AH. Typically, AH develops many years before the diagnosis of overt HF, providing a therapeutic target for preventive strategies. Treatment of AH is based on different classes of antihypertensive drugs, which show differences in their capacity to prevent the evolution towards HF. The blockers of the RAAS are effective drugs to treat AH and prevent HF with reduced ejection fraction (HFrEF), but the evidence of the potential benefits in patients with HFpEF remains limited. In this review, the authors summarise data from several clinical trials of HFpEF and HFrEF, focusing on the mechanisms leading the transition from AH to HF and late complications
Angiotensin II and vascular damage in hypertension: Role of oxidative stress and sympathetic activation
Reactive oxygen species (ROS) are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. Physiologically, ROS generation is counteracted effectively by the rate of elimination. In hypertension, a ROS excess occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. Angiotensin II, the active peptide of the renin-angiotensin-system (RAS), is a significant stimulus for ROS generation within the vasculature. It was also documented that at the level of subfornical cerebral regions an inappropriate RAS stimulation may lead to an increased vascular sympathetic activity. More recently, in conditions of fetal undernutrition, it was also proposed an increased vascular sympathetic activity secondary to inappropriate RAS activation, leading to the development of hypertension in adult life. The present review will discuss the complex interaction between RAS activation, vascular ROS generation and increased sympathetic outflow in hypertension
Understanding the relationship between lung function and cardiovascular phenotypes in the young: opportunity for a better cardiovascular risk prevention in adulthood?
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