Current medical research and opinion
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β-blockers are a heterogeneous class, with individual agents distinguished by selectivity for β1- vs. β2- and α-adrenoceptors, presence or absence of partial agonist activity at one of more β-receptor subtype, presence or absence of additional vasodilatory properties, and lipophilicity, which determines the ease of entry the drug into the central nervous system. Cardioselectivity (β1-adrenoceptor selectivity) helps to reduce the potential for adverse effects mediated by blockade of β2-adrenoceptors outside the myocardium, such as cold extremities, erectile dysfunction, or exacerbation of asthma or chronic obstructive pulmonary disease. According to recently updated guidelines from the European Society of Hypertension, β-blockers are included within the five major drug classes recommended as the basis of antihypertensive treatment strategies. Adding a β-blocker to another agent with a complementary mechanism may provide a rational antihypertensive combination that minimizes the adverse impact of induced sympathetic overactivity for optimal blood pressure-lowering efficacy and clinical outcomes benefit.
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Cardiovascular disease (CVD) remains the most prevalent cause of premature death worldwide. It had been suspected for decades that increased activity of the sympathetic nervous system (SNS) might play a pathogenetic role in the development and progression of hypertension, heart failure (HF) and CVD. The use of microneurographic techniques to directly assess the SNS has allowed this field to advance considerably in recent years. ⋯ Sympathetic overactivity also drives increased cardiovascular risk in the settings of obesity, metabolic syndrome, chronic kidney disease and obstructive sleep apnoea, among other conditions. Thus, sympathetic overactivity is an important factor that drives patients through the CVD continuum, from the early appearance of cardiovascular risk factors, to impairments of the structure and function of components of the heart and arteries, to established CVD, and ultimately to a life-threatening cardiovascular event. A deeper understanding of the role of sympathetic overactivity in the pathogenesis of CVD and HF will support the optimization of therapeutic interventions for these conditions.