Arterial systemic hypertension is associated to right ventricular longitudinal diastolic dysfunction. This dysfunction involves the prolongation of active relaxation, which is independently associated with the degree of right ventricular hypertrophy and the impairment of passive wall properties, which is mainly due to ventricular interaction occurring under left ventricular pressure overload conditions.

No abstract

Background-Left ventricular wall motion (WM) abnormalities have recognized prognostic significance in patients with coronary or other heart diseases; however, whether abnormal WM predicts adverse events in adults without overt cardiovascular disease has not been assessed. Our objective was to determine whether echocardiographic WM abnormalities predict subsequent cardiovascular events in a population-based sample. Methods and Results-Participants (nϭ2864, mean age 60Ϯ8 years, 64% women) without clinically evident cardiovascular disease in the second Strong Heart Study examination who had complete echocardiographic WM assessment were studied. Echocardiographic assessment revealed that 5% of participants (nϭ140) had focal hypokinesia, and 1.5% (nϭ42) had WM abnormalities. Relationships between WM abnormalities and fatal and nonfatal cardiovascular events (including myocardial infarction, stroke, coronary artery disease, and heart failure; nϭ554) and cardiovascular death (nϭ182) during 8Ϯ2 years follow-up were examined. In Cox regression, after adjustment for age, gender, waist/hip ratio, systolic blood pressure, and diabetes mellitus, segmental WM abnormalities were associated with a 2.5-fold higher risk of cardiovascular events and a 2.6-fold higher risk of cardiovascular death (both PϽ0.0001). In similar multivariable models, global WM abnormalities were associated with a 2.4-fold higher risk of cardiovascular events (Pϭ0.001) and a 3.4-fold higher risk of cardiovascular death (Pϭ0.003). Conclusions-Echocardiographic

No abstract

This study shows the usefulness of pulsed Doppler tissue imaging to detect impairment of right ventricular myocardial function and to provide evidence about ventricular interaction in forms of hypertrophic cardiomyopathy which involve interventricular septum.

Rheumatoid arthritis (RA) is associated with enhanced atherosclerosis and impaired endothelial function early after the onset of the disease and cardiovascular (CV) disease represents one of the leading causes of morbidity and mortality. It is well known that disease modifying antirheumatic drugs (DMARDs) are able to improve the course of the disease and the quality of life of these patients, but little is known about the effects of DMARDs on CV risk and endothelial dysfunction. Our goal was to examine the effects of long‐term therapy with DMARDs on endothelial function and disease activity in early RA (ERA). Twenty‐five ERA patients (mean age 52 ± 14.6 years, disease duration 6.24 ± 4.10 months) without evidence of CV involvement were evaluated for disease activity score (DAS‐28), 2D‐echo derived coronary flow reserve (CFR), common carotid intima‐media thickness (IMT) and plasma asymmetric dimethylarginine (ADMA) levels at baseline and after 18 months of treatment with DMARDs (10 patients with methotrexate and 10 with adalimumab). DMARDs significantly reduced DAS‐28 (6.0 ± 0.8 vs. 2.0 ± 0.7; P < 0.0001) and improved CFR (2.4 ± 0.2 vs. 2.7 ± 0.5; P < 0.01). Common carotid IMT and plasma ADMA levels did not show significant changes. The present study shows that DMARDs, beyond the well known antiphlogistic effects, are able to improve coronary microcirculation without a direct effect on IMT and ADMA, clinical markers of atherosclerosis. Treatment strategies in ERA patients with high inflammatory activity must be monitored to identify beneficial effects on preclinical markers of vascular function.

In hypertensive patients free of coronary artery disease, the degree of reduction in CFR is associated with the excess of LVM beyond the values compensatory for individual haemodynamic load. This relation is also independent of the presence of LV hypertrophy.

In hypertensive patients free of coronary artery disease, 4-week nebivolol therapy induces a significant increase of the CFR. Nebivolol preserves coronary flow at rest despite the reduction of metabolic (O2 consumption) and hemodynamic (diastolic blood pressure) determinants. The increase of hyperemic coronary velocities appears due to the reduction of coronary resistance.