Sulodexide improves pain-free walking distance in patients with lower extremity peripheral arterial disease: A systematic review and meta-analysis.

Peripheral arterial disease is associated with very high cardiovascular risk. The main symptom is intermittent claudication, which strongly affects the quality of life. Therefore, treatment goals in peripheral arterial disease consist of the reduction of cardiovascular events and the relief of symptoms. An increase in pain-free walking distance, evaluated based on the Initial Claudication Distance, was also a strong positive prognostic factor in patients with peripheral arterial disease. Our objective was to reassess whether sulodexide is effective in improving Initial Claudication Distance. For this, we searched the literature according to the PRISMA checklist for double blind clinical trials assessing the improvement in the Initial Claudication Distance after 90 days of standard therapeutic regimen with sulodexide in adult patients with peripheral arterial disease. We found and assessed for bias in 11 studies eligible for review and meta-analysis. Data extracted from those studies favoured the sulodexide group, showing an overall difference in Initial Claudication Distance of +68.9 (CI 95%; ± 11.9 m) at the end of treatment (p < 0.001). According to this review, sulodexide is effective in improving Initial Claudication Distance and consequently the quality of life in patients with peripheral arterial disease. Further studies are needed to assess the effects of this drug on disease progression in asymptomatic patients with peripheral arterial disease.

Clinical variables, not RAAS polymorphisms, predict blood pressure response to ACE inhibitors in Sardinians.

AIM: No definite factors predict blood pressure response to angiotensin-converting enzyme-inhibitors. The aim of this study was to test the association of gene polymorphisms of the renin-angiotensin-aldosterone system with essential hypertension and anthropometric variables, intermediate phenotypes and gene polymorphisms with blood pressure after fosinopril in a genetically homogeneous cohort. METHODS: A total of 630 essential hypertension patients, not previously treated or out of antihypertensive treatment for at least 6 months versus 219 normotensives (genotype frequencies, chi(2)). A total of 191 patients were randomly assigned to fosinopril 20 mg/day. Samples for plasma renin activity and aldosterone, 24-h urinary sodium (flame photometry) were collected. Gene polymorphisms--angiotensin-converting enzyme (insertion/deletion), angiotensin II type 1-receptor (A1166C), aldosterone synthase (-344C/T) and angiotensinogen (-6A/G)--were analyzed by standard techniques. The association of anthropometric variables, intermediate phenotypes and gene polymorphisms with blood pressure after 4 weeks therapy was tested by univariate analysis and analysis of covariance model (Intercooled Stata SE 9.2). RESULTS: No genetic polymorphisms were associated with essential hypertension, blood pressure response and intermediate phenotypes (p > 0.05). Systolic blood pressure after therapy was associated with baseline systolic blood pressure, age and sex. CONCLUSIONS: Our results confirm the difficulty in dissecting both essential hypertension and pharmacogenomics when analyzing the effect of single genes in complex multifactorial traits.