The interplay between renin-angiotensin system activation, abnormal myocardial deformation and neurohumoral activation in hypertensive heart disease: a speckle tracking echocardiography study.

Angiotensin converting enzyme (ACE) promotes cardiac fibrosis. LV myocardial deformation and torsion are markers of subclinical myocardial dysfunction. We investigated the association of serum ACE levels with LV deformation markers in untreated hypertensives. In 120 untreated patients (age: 53.5 ± 11.2 years) with essential hypertension and 60 healthy controls, we measured (a) LV longitudinal, circumferential and radial strain (S), peak torsion and the percentage changes between peak twisting and untwisting at the end of early diastolic filling (%dpTw-UtwEDF) using speckle tracking echocardiography and (b) serum levels of ACE and NTproBNP. Compared to controls, patients had decreased longitudinal strain (-19.1 ± 2.9 vs. -21.7 ± 1.8%), increased peak twisting (19.1 ± 4.6 vs.14.0 ± 3.7 deg) but decreased %dpTw-UtwEDF (78 ± 8 vs. 86 ± 8%) and higher serum ACE levels (27.6 ± 8.0 vs 20.9 ± 7.1 U/ml) (p < 0.05 for all comparisons). Increasing serum ACE levels were related to impaired radial strain and longitudinal systolic SR (b = -0.41 and b = 0.31 respectively, p < 0.01), as well as to reduced %dpTw-UtwEDF (b = -0.37, p < 0.05). Furthermore, increasing serum ACE levels were related to increasing NTproBNP levels (b = 0.41, p < 0.01). In multivariate analysis, the above relations of serum ACE levels and LV function parameters remained significant after adjustment for other confounding factors (p < 0.01). The close link between serum ACE levels and impaired LV deformation suggests that activation of renin-angiotensin system is involved in the impairment of LV function resulting in elevated LV filling pressures causing the concomitant elevation of BNP levels in untreated hypertensive patients.

Rapid normalization of vasculitis-induced left ventricular dysfunction related with multiple cardiac thrombi.

We present a young female patient admitted in the emergency department with pulmonary edema, severely impaired left ventricular function, and simultaneous intracardiac thrombi in left and right ventricle as well as in right atrium, at echocardiography. A magnetic resonance tomography showed excess myocardial tissue edema and diffuse gadolinium enhancement. Blood analysis showed an elevated eosinophils count. The patient showed a rapid normalization of left ventricular function as well as resolution of intracardiac thrombi and myocardial tissue edema 3 months after proper treatment with cyclophosphamide and steroids for Churg-Strauss syndrome.

Inflammatory markers in coronary artery disease.

Coronary artery disease (CAD) is one of the most common manifestations of atherosclerosis. Inflammation is considered one of the major processes that contribute to atherogenesis. Inflammation plays an important role not only on the initiation and progression of atherosclerosis but also on plaque rupture, an event that leads to acute vascular events. Various biomarkers express different pathways and pathophysiologic mechanisms of cardiovascular disease, and inflammatory biomarkers express different parts of the atherogenic process, regarding the initiation and progression of atherosclerosis or the destabilization of the atherosclerotic plaque. Therefore, inflammatory biomarkers may prove to be useful in the detection, staging, and prognosis of patients with CAD. Furthermore, the fact that inflammatory processes are essential steps in the course of the disease offers future therapeutic targets for the interruption of the atherogenic process or for the management of acute events.