Sex- and/or ethnic-appropriate echocardiographic reference values are indicated for many measurements of LA and LV size, LV mass, and EF. Reference values for LV volumes and mass also differ across the age range.
Angiotensin II induces inflammatory activation of vascular smooth muscle cells and can cause left ventricular hypertrophy (LVH). Telmisartan is an angiotensin IIreceptor 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-naïve, 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.
In this study the authors evaluated correlation between aging and brachial endothelial and vascular smooth muscle dysfunction, changes in carotid geometry, and left ventricular remodeling. Vasomotor influences of brachial endothelium and brachial smooth muscle function to reactive hyperemia and nitroglycerin (400 microg, sublingual spray) were assessed by noninvasive ultrasound in 66 healthy subjects of different ages (20-82 years). Carotid intima-media thickness and left ventricular mass index were also assessed by ultrasound and compared with brachial hemodynamic parameters. All results were analyzed by linear regression analysis. The response of brachial artery diastolic diameter to reactive hyperemia decreased with aging (p<0.0001). Also, the response of brachial artery diastolic diameter to nitroglycerin increased relative to aging (p<0.004). Age-related correlations between increased carotid intima-media thickness and brachial artery diastolic diameter response to reactive hyperemia (p<0.01) as well as between increased carotid intima-media thickness and increased left ventricular mass index (p<0.001) were found. However, there was no correlation between brachial artery diastolic diameter response to reactive hyperemia and increased left ventricular mass index (p>0.05). The study showed that aging influences not only brachial endothelial vasomotor properties but also vascular and cardiac geometry. The authors believe that modern therapeutic approach should take these results into consideration to establish new vasculo-protective and cardioprotective strategies.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.