Nebivolol is a highly selective β1-adrenergic receptor antagonist with a pharmacologic profile that differs from those of other drugs in its class. In addition to cardioselectivity mediated via β1 receptor blockade, nebivolol induces nitric oxide-mediated vasodilation by stimulating endothelial nitric oxide synthase via β3 agonism. This vasodilatory mechanism is distinct from those of other vasodilatory β-blockers (carvedilol, labetalol), which are mediated via α-adrenergic receptor blockade. Nebivolol is approved for the treatment of hypertension in the US, and for hypertension and heart failure in Europe. While β-blockers are not recommended within the current US guidelines as first-line therapy for treatment of essential hypertension, nebivolol has shown comparable efficacy to currently recommended therapies in lowering peripheral blood pressure in adults with hypertension with a very low rate of side effects. Nebivolol also has beneficial effects on central blood pressure compared with other β-blockers. Clinical data also suggest that nebivolol may be useful in patients who have experienced erectile dysfunction while on other β-blockers. Here we review the pharmacological profile of nebivolol, the clinical evidence supporting its use in hypertension as monotherapy, add-on, and combination therapy, and the data demonstrating its positive effects on heart failure and endothelial dysfunction.

The Food and Drug Administration has banned the sale of ephedrine-based weight-loss products because of their association with many cardiovascular adverse effects. Bitter orange is now being used as a stimulant in "ephedra-free" weight-loss supplements but was recently implicated in adverse cardiovascular sequelae. To our knowledge, this report describes the first case of variant angina associated with bitter orange in a dietary supplement.

Vancomycin is well recognized as causing the nonallergic skin reaction known as red man syndrome; however, it is rarely suspected as causative in the setting of an immune-mediated skin reaction. We describe a 76-year-old Caucasian woman with a history of penicillin and sulfa allergies who was transferred to our medical center while receiving vancomycin for treatment of persistent methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia. After admission, the patient's pacemaker was explanted; cultures from the pacemaker grew MSSA. Based on the culture data and her allergy to penicillin, vancomycin was continued. On day 4 of therapy, the patient developed a papular rash with small blisters on her distal upper extremities. Furosemide, which she was receiving intermittently to maintain fluid balance, was initially suspected as the likely cause. Furosemide was withheld; however, the rash worsened and spread to her neck and torso. Results of skin biopsy confirmed a severe leukocytoclastic, necrotizing small-cell vasculitis that met the criteria for a hypersensitivity vasculitis associated with drug therapy. Five days after discontinuation of vancomycin, the vasculitis was resolving and continued to resolve throughout the remainder of her hospitalization. Furosemide was readministered without worsening of the vasculitis. Use of the Naranjo adverse drug reaction probability scale indicated that the likelihood of vancomycin being the cause of the vasculitis was probable (score of 5). Clinicians should be aware of vancomycin as a potential cause of small-vessel vasculitis.