Servier (Germany)

Objective: Inadequate treatment is one reason for poor hypertension control and prognosis in patients with hypertension. Guidelines recommend antihypertensive combination therapy for patients at increased risk or major co-morbidities. We analyzed antihypertensive prescription patterns and co-morbidities in patients with newly diagnosed hypertension. Design and method: In a database of several German statutory health insurance companies covering the period from 2011–2013 we analyzed the occurrence of newly diagnosed hypertension and major co-morbidities (diabetes, myocardial infarction, heart failure, stroke and renal dysfunction) by ICD code during 2012. We also analyzed the linked prescription data for antihypertensives by ATC code. Results: Of 2,077,889 persons at least 18 years of age, 32.2% carried the diagnosis hypertension, of which 7.9% (53,118) were newly diagnosed in 2012 (incidence 2.6%). Newly diagnosed patients received antihypertensive medication in 78.2%, while 21.8% received none. 70.8% of the treated patients were initiated on monotherapy, 13.2% on combination therapy and 16.0% on fix-dose combination. In the monotherapy group, 43.5% received ACE inhibitors, 32.2% beta-blockers, 8.2% angiotensin II receptor blockers, 7.7% diuretics and 7.7% were prescribed calcium channel blockers. When free combination treatment was prescribed, 73.5% contained beta-blockers, 72.9% contained ACE inhibitors, 40.6% contained diuretics and 25.7% contained calcium channel blockers. Among newly diagnosed patients on monotherapy, 28.7% had at least one major co-morbidity, while in patients without antihypertensive treatment, at least one major co-morbidity existed in 18.0%. Conclusions: The majority of patients with newly diagnosed hypertension is initiated on monotherapy suitable for patients at low risk, while one fifth of patients remains untreated. However, in both groups a significant number of patients have at least one major co-morbidity, suggesting in part inadequate risk management.

Enhanced heart rate (HR) is a compensatory mechanism in chronic heart failure (CHF), preserving cardiac output, but at the cost of increased left ventricular (LV) oxygen consumption and impaired diastolic function. The HR reduction (HRR) induced by the If current inhibitor ivabradine prevents LV systolic dysfunction in CHF, but whether HRR improves LV diastolic function is unknown. LV diastolic function and remodeling were assessed in rats with CHF after coronary ligation after long-term (90 days, starting 7 days after ligation) and delayed short-term (4 days, starting 93 days after ligation) ivabradine treatment (10 mg·kg·d). Long- and short-term HRR reduced LV end-diastolic pressure, LV relaxation, and LV end-diastolic pressure-volume relation. Simultaneously, LV hypoxia-inducible factor-1α expression was reduced. Long-term and, to a more marked extent, short-term HRR increased endothelial cell proliferation, associated after long-term HRR with the prevention of CHF-related LV capillary rarefaction. Long-term and, to a lesser extent, short-term HRR increased endothelial nitric oxide synthase expression, associated after long-term HRR with improved nitric oxide-dependent coronary vasodilatation. Long-term HRR induced by ivabradine improves diastolic LV function probably involving attenuated hypoxia, reduced remodeling, and/or preserved nitric oxide bioavailability, resulting from processes triggered early after HRR initiation: angiogenesis and/or preservation of endothelial nitric oxide synthase expression.

In a monocenter, placebo-controlled, double-blind, parallel-group study, 20 patients with acute symptoms of rhinosinusitis were treated with either fusafungine (CAS 1393-87-9, Locabiosol Dosier-Spray) (n = 10) or placebo nasal spray (n = 10). One patient from the placebo group was withdrawn from the study on the day of inclusion for noncompliance reasons. At the beginning of the 2-week treatment period, absence of an acute exacerbation of sinusitis with, e.g., opacity or fluid in any of the sinuses, was documented by computed tomography. Efficacy of treatment was assessed using objective measurements (e.g. sonography, rhinomanometry, acoustic rhinometry, and endoscopy) as well as scores recorded by the investigator on 6 consecutive visits before and after 1, 3, 7, 10, and 14 days of treatment, and by the patients on a diary card. Drug safety was evaluated on the basis of twice-daily assessment of general well-being and side effects. Statistical analysis of the data evidenced a positive effect of fusafungine as early as by the first 24 h of treatment (reduction of symptom score D0-->D1: p < 0.01), which was not seen in the placebo group (p = 0.2174). In the final assessment, both investigator and patients rated global efficacy better with fusafungine. In some instances, the intergroup difference achieved statistical significance (patient diaries, p = 0.0342). Side effects such as reactions at the application site mainly occurred in patients in the placebo group, who rated tolerability markedly worse than patients taking fusafungine (p = 0.0304; patient diaries, p = 0.0170).