Ventricular and vascular remodelling effects of the angiotensin II receptor blocker telmisartan and/or the angiotensin-converting enzyme inhibitor ramipril in hypertensive patients.

Angiotensin II induces inflammatory activation of vascular smooth muscle cells and can cause left ventricular hypertrophy (LVH). Telmisartan is an angiotensin II receptor blocker with demonstrated beneficial effects on cardiac and vascular structure and function in animal models. The angiotensin-converting enzyme inhibitor ramipril also reduces ventricular and vascular remodelling. The open-label study observed 75 treatment-naive, moderately or severely hypertensive (systolic blood pressure 160-190 mmHg, diastolic blood pressure 90-110 mmHg) patients (age range, 42-58 years) treated with once-daily telmisartan 40 mg force-titrated to 80 mg after 1 month (n=25), once-daily ramipril 2.5 mg force-titrated to 5 mg after 1 month (n=25), or once-daily telmisartan 40 mg plus ramipril 2.5 mg (n=25); the total duration of treatment was 6 months. At baseline, blood pressure, left ventricular mass index (LVMI), carotid intima-media thickness (IMT) and carotid cross-sectional intima-media area (CSA) were measured. Measurements were repeated 1, 3 and 6 months after initiation of treatment. After 6 months, comparable blood pressure reductions were achieved with the three treatments. Reductions in LVMI after 6 months' treatment were 11.4%, 9.9% and 15.6% with telmisartan, ramipril, and telmisartan plus ramipril, respectively. Respective reductions in IMT were 14.6%, 12.0% and 18.2%, and for CSA were 7.8%, 4.3% and 11.5%. In conclusion, treatment with telmisartan or ramipril for 6 months resulted in regression of LVH and vascular remodelling. When a combination of telmisartan and ramipril was administered, additional regression and remodelling occurred.

[Systemic mixed connective tissue disease--Sharp's syndrome]. / Mesovita sistemska bolest vezivnog tkiva--Sarpov sindrom.

Sharp's syndrome is a systemic mixed connective tissue disease that is defined with specific ribonucleoprotein antibody (U1RNP). The key diagnostic criterion is positive antinuclear antibodies in stain form. The disease is primarily localized on joints, muscles and skin; however, there are not widely used diagnostic criteria. There are USA, Mexican and Japanese diagnostic criteria. A 18-year-old male who fulfilled Sharp's diagnostic criteria is presented in the paper. In this patient the disease was manifested in pleura and pericardium. We wish to point out the importance of immunologic approach to the aetiology of pleural and pericardial inflammatory effusions in young patients, as well as the therapeutical dilemmas in the treatment of the disease.