Of the equations studied, Salazar-Corcoran and Cockcroft-Gault appear to be the best for predicting Clcr.

Pulmonary arterial hypertension (PAH) is a disabling chronic disorder of the pulmonary vasculature, which is characterized by increased pulmonary artery pressure as a result of increased pulmonary vascular resistance. The pathology of PAH is characterized by pulmonary vascular vasoconstriction, smooth muscle cell proliferation, and thrombosis. These changes are a result of an imbalance between vasodilators (prostacyclin, nitric oxide, vasoactive intestinal peptide) and vasoconstrictors (thromboxane A2, endothelin, serotonin), growth inhibitors and mitogenic factors, and antithrombotic and prothrombotic factors. Recent advances in treatment are directed at restoring the balance between these systems. Endothelin receptor antagonists (bosentan, ambrisentan, sitaxsentan), phosphodiesterase type 5 inhibitors (sildenafil, tadalafil), and prostacylin (epoprostenol, iloprost, treprostinil, beraprost) represent the different classes of medications that are currently used in monotherapy and in combination to treat PAH. The purpose of this drug highlight is to provide the reader with an update of the pharmacotherapeutic treatment of PAH.

The most concerning adverse reaction with HMG-CoA reductase inhibitors (statins) is myotoxicity. Statins inhibit the production of mevalonate, a precursor of both cholesterol and coenzyme Q10, a compound believed to be crucial for mitochondrial function and the provision of energy for cellular processes. There is speculation that a reduction in coenzyme Q10 concentrations may promote the myopathies that have been associated with statin treatment as a result of mitochondrial damage. Although studies have repeatedly demonstrated a reduction in circulating coenzyme Q10 concentrations with statin therapy, it is unclear as to whether tissue levels of coenzyme Q10 are significantly affected. Coenzyme Q10 supplementation has been shown to reverse statin-induced decreases in circulating coenzyme Q10 concentrations, although the effect of supplementation on tissue coenzyme Q10 concentrations and any resulting clinical benefit has not been adequately assessed. Although there is not much of a safety concern with coenzyme Q10 supplementation, there is also not enough evidence to support its routine use for preventing the adverse effects of statin therapy, and it is therefore not recommended for this purpose at this time.

The ability of angiotensin converting enzyme (ACE) inhibitors to lower blood pressure may in part be due to the formation of vasodilatory prostaglandins. Inhibition of prostaglandin synthesis with aspirin may therefore theoretically attenuate the antihypertensive effect of ACE inhibitors. This trial studied the interaction between aspirin (ASA) and enalapril, an ACE inhibitor, and ASA and losartan, an angiotensin subtype 1 receptor antagonist. Seventeen essential hypertensive patients were studied, maintained on a stable dose of either enalapril (n = 7) or losartan (n = 10) monotherapy for > or =12 weeks before and throughout the study. Each patient received a 2-week course of placebo, 81 mg/day ASA, and 325 mg/day ASA, each treatment separated by a 2-week washout period. Blood pressure (BP) and serum thromboxane B2 (TXB2) samples were obtained at the end of each treatment period. Placebo was compared with each dose of ASA for each group. In both the enalapril and losartan groups, mean, systolic, and diastolic BP were unchanged with the addition of ASA. Concentrations of TXB2 were suppressed to <10% in both groups with ASA. This study demonstrates that 81 to 325 mg/day ASA exerts no significant effect on BP in essential hypertensives taking enalapril or losartan.

BACKGROUND:In 2005 the American Heart Association (AHA) released updated recommendations for blood pressure (BP) monitoring in order to ensure accurate BP measurements. OBJECTIVE: To determine if current methods of BP assessment in an ambulatory clinic result in significantly different BP measurements than those obtained by following the AHA recommendations and if these BP differences impact treatment decisions. RESEARCH DESIGN: Randomized prospective analysis. SETTING: University of New Mexico Hospital Adult Internal Medicine clinic. PATIENTS: Forty adults with hypertension METHODS: Patient BPs were measured using both the traditional triage method and the AHA-recommended method in cross-over fashion in random order. Two complete medical profile summaries were then constructed for each patient: one for each BP measurement obtained by each technique. These profiles were then reviewed by a panel of providers who provided hypothetical hypertension treatment recommendations. RESULTS: Individual BP results varied greatly between the two methods. SBP readings differed by ≥5 mmHg in either direction for 68% of patients while 78% of patient's DBP readings differed by ≥2 mmHg in either direction. Overall, 93% of patients had a BP difference of either ≥5 mmHg systolic or ≥2 mmHg diastolic. Five patients were determined to be at goal with the triage method, but were higher than their goal BP with the AHA method Significant differences were also seen in treatment recommendations for a given patient based on the differences seen between the two obtained BP readings. The number of patients with treatment variations between their two profiles ranged from 13% to 23% depending on the reviewing provider (p<0.01 for all providers). CONCLUSION: Inaccurate BP assessment is common and may impact hypertension treatment decisions.KEY WORDS: blood pressure measurement; hypertension.