Subject(s)
Brain Injuries, Traumatic/therapy , Brugada Syndrome/chemically induced , Electrocardiography , Heart Rate/drug effects , Hypnotics and Sedatives/adverse effects , Propofol/adverse effects , Accidents, Traffic , Adult , Brain Injuries, Traumatic/diagnosis , Brain Injuries, Traumatic/physiopathology , Brugada Syndrome/diagnosis , Brugada Syndrome/physiopathology , Fatal Outcome , Humans , Male , Predictive Value of TestsABSTRACT
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.
Subject(s)
Echocardiography, Doppler/methods , Hypertension/diagnostic imaging , Myocardial Contraction , Peptidyl-Dipeptidase A/blood , Renin-Angiotensin System , Ventricular Dysfunction, Left/diagnostic imaging , Ventricular Function, Left , Adult , Aged , Biomarkers/blood , Biomechanical Phenomena , Chi-Square Distribution , Female , Fibrosis , Humans , Hypertension/complications , Hypertension/physiopathology , Linear Models , Male , Middle Aged , Multivariate Analysis , Natriuretic Peptide, Brain/blood , Peptide Fragments/blood , Predictive Value of Tests , Prognosis , Risk Factors , Stress, Mechanical , Torsion, Mechanical , Up-Regulation , Ventricular Dysfunction, Left/etiology , Ventricular Dysfunction, Left/physiopathology , Ventricular PressureABSTRACT
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.
Subject(s)
Churg-Strauss Syndrome , Cyclophosphamide/administration & dosage , Thrombosis , Ventricular Dysfunction, Left , Adult , Churg-Strauss Syndrome/complications , Churg-Strauss Syndrome/diagnostic imaging , Churg-Strauss Syndrome/drug therapy , Coronary Angiography , Female , Heart Atria/diagnostic imaging , Humans , Magnetic Resonance Angiography/methods , Thrombosis/diagnostic imaging , Thrombosis/drug therapy , Thrombosis/etiology , Ventricular Dysfunction, Left/diagnostic imaging , Ventricular Dysfunction, Left/drug therapy , Ventricular Dysfunction, Left/ethnologySubject(s)
Aspirin/administration & dosage , Glucosephosphate Dehydrogenase Deficiency/drug therapy , Glucosephosphate Dehydrogenase Deficiency/surgery , Percutaneous Coronary Intervention , Platelet Aggregation Inhibitors/administration & dosage , Aged , Drug Therapy, Combination , Glucosephosphate Dehydrogenase Deficiency/diagnosis , Humans , MaleABSTRACT
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.
