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Although beta-blockers have been endorsed by guidelines committees for the treatment of patients with hypertension, particularly those with significant CVD and high CVD risk, there are concerns about conventional beta-blockers related to poorer clinical outcomes compared with other classes of antihypertensive agents, as well as deleterious effects on quality of life and lipid and carbohydrate metabolism. beta-Blockers comprise a heterogeneous group of antihypertensive agents, including nonselective agents, cardioselective, nonvasodilating agents, and vasodilating agents that either combine beta-nonselectivity with alpha-blockade or possess cardioselectivity without alpha-blockade. The pharmacologic, mechanistic, and hemodynamic differences between conventional, nonvasodilating beta-blockers and vasodilating beta-blockers are discussed in this review, with a focus on the cardioselective vasodilating beta-blocker nebivolol. These differences may have important clinical implications, particularly in the treatment of complicated hypertension, such as that associated with patients with diabetes or the cardiometabolic syndrome, elderly patients, and African American patients, suggesting that mechanism of action may be an important consideration when choosing a beta-blocker., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

Beta-blockers have played a key role in the management of hypertension-related cardiovascular disease for decades, and continue to be recommended as a mainstay of therapy in national guidelines statements. Recent data have shown less optimal reductions in total mortality, CVD mortality, and CVD events with beta-blockers compared with renin-angiotensin system-blocking agents or calcium channel blockers. The beta-blocker class, however, spans a wide range of agents, and the growing concern about the risk-benefit profile of beta-blockers should not be generalized to later-generation vasodilating beta-blockers such as carvedilol and nebivolol. A growing database from hypertension studies confirms the clinical efficacy and safety of vasodilating beta-blockers, and outcome studies indicate that these agents can play an important role in global CVD reduction in patients with hypertensive or ischemic heart failure., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

Out-of-hospital sudden cardiac death occurs in approximately 300,000 individuals each year in the United States, a total that represents about half of all annual deaths from coronary heart disease. Beta-blockers were the first class of drugs investigated for the prevention of sudden cardiac arrest because of their ability to reduce ventricular arrhythmias. Numerous randomized, controlled trials have now established the importance of beta-blockade in preventing sudden cardiac death. Clinical evidence reveals the association between beta-blockade and improved survival, and trials explore the role for beta-blockers in the prevention of sudden cardiac death.

Beta-blockers are an established class in the management of hypertension, and numerous randomized, controlled trials have shown that these drugs can prevent cardiovascular events in this population. However, beta-blockers are underutilized in managing the general hypertensive population. This phenomenon may stem in part from concerns about side effects. On the contrary, beta-blockers demonstrate comparable efficacy, safety, and tolerability compared with other classes of antihypertensive drugs. Because beta-blockers offer unique cardiovascular protection, they should be considered an integral part of the treatment regimen for patients with hypertension who are at risk for cardiovascular events.

Data from large clinical trials indicate that beta-blocker therapy can be successfully initiated and adjusted upward in most patients with stable chronic heart failure who already take standard heart failure therapy. Such therapy typically includes ACE inhibitors, diuretics, and digoxin. With optimal titration and maintenance strategies, beta-blockers are effective and well tolerated in these patients. It is recommened that all patients with clinically stable mild to moderate chronic heart failure (NYHA class II or III), no contraindications to beta-blocker use, and an LVEF less than 40% should be treated with beta-blockers. Based on the results of recent clinical trials on heart failure, beta-blocker therapy should be initiated at a low dose and slowly tirtrated upward as tolerated. A patient's heart failure should be stable for at least 2 weeks before the dose is adjusted upward. Slow titration facilitates maximal tolerability. In primary care practice, physicians should apply titration strategies and target dosed that have been demonstrated to reduce morbidity and mortality in clinical trials. Although worsening heart failure or other adverse events occur in a minority of patients who take beta-blockers, these effects can be managed by adjusting the dose of ACE inhibitor or diuretic, or both, or by temporarily withholding the beta-clocker. Currently, professional treatment guidelines recommend beta-blocker therapy in combination with ACE inhibitors an diuretics as the standard of care in the treatment of heart failure.

Finding the optimal combination of drugs in the correct dosages, which requires careful monitoring over time, is key to slowing the disease process and prolonging life. For most patients, treating heart failure involves correcting underlying left ventricular dysfunction, thereby slowing the remodeling process.