BackgroundMyocardial mechanical dyssynchrony induced by the presence of postinfarction scar and/or conduction abnormalities in patients with a left ventricular ejection fraction (LVEF) of < 35 % may be associated with a greater propensity toward inducing serious ventricular arrhythmia [(ventricular tachycardia (VT), ventricular fibrillation (VF)] and sudden cardiac death. The assessment of regional myocardial function using tissue Doppler echocardiography (TDE) allows for noninvasive analysis of regional mechanical dysfunction (LV mechanical dispersion).AimThe aim of this study was to evaluate the TDE-based mechanical dispersion as a potential echocardiographic predictor of VT/VF.MethodsThe study group consisted of 47 consecutive ambulatory patients with implanted cardiac resynchronization therapy–defibrillator (CRT-D) devices who were divided into two groups: Group 1 (n = 29) comprised patients with recorded episodes of VT/VF, in whom baseline TDE data were available, and group 2 (n = 18) comprised patients without registered VT/VF in the device memory within 4 years after implantation. LV mechanical dispersion was defined as the standard deviation of the time measured from the beginning of the QRS complex to the peak longitudinal strain in apical four-chamber and two-chamber views. A retrospective quantitative assessment of LV regional deformation was based on the color tissue velocity recordings.ResultsThe average time to event after implantation was 345 days. Patients with electrical events demonstrated greater mechanical dispersion: 99.14 ± 33.60 vs. 72.98 ± 19.70, p=0.002.ConclusionDuring the 4-year follow-up, patients with documented VT/VF were characterized by significantly higher LV mechanical dispersion as compared with patients without electrical events. Measurement of LV mechanical dispersion might be helpful in determining the risk of sudden cardiac death.
The study evaluates the influence of steatosis on hepatocytes proliferative potential, reflected by proliferating cell nuclear antigen (PCNA) expression in chronic hepatitis C (CHC) patients both in steatotic and non-steatotic areas of lobules. The liver histology was evaluated according to Kleiner's score. Nonalcoholic steatohepatitis (NASH) was also defined as the presence of lobular inflammation, hepatocyte ballooning and steatosis. Expression of PCNA was significantly in patients with definite NASH compared to those with simple steatosis, but not to those with borderline NASH. Advanced steatosis negatively influenced PCNA expression. NASH not only affects PCNA expression in staetotic, but also in non-steatotic lobule areas. Expression of PCNA could be an independent indicator of changes in hepatocyte metabolism in CHC patients. High NAS values and low PCNA expression may be a negative prognostic factor in predicting the further course of the disease.
Introduction Permanent right ventricle pacing leads to left ventricle remodeling, its systolic dysfunction and symptomatic heart failure in the long run. Valsartan is well known for its preventive anti-remodeling function in the post infarction heart remodeling. Objectives To assess the effect of valsartan on left ventricle remodeling in patients with second and third degree atrioventricular block with first-time implantation of dual chamber pacemaker. Methods This was a randomized, double-blind, placebo controlled single center study. One hundred eligible patients were assigned in a 1:1:1 fashion to receive placebo, valsartan 80mg or 160mg once daily, respectively. Echocardiographic assessment of left ventricle geometry, its systolic and diastolic function was performed at baseline and at twelve months. One patient from placebo group suffered stroke. We present the baseline date for 100 enrolled patients and follow-up data for 88 patients who have completed the study. Data in valsartan arms are pooled in one group. Concentration of soluble ST2 was measured in duplicates with Aspect Reader (Critical Diagnostics). Results Results are presented in table. Data are presented as mean and standard deviation. Table 1 Placebo (n=28) Valsartan (n=60) ANOVA Baseline 12 mths Baseline 12 mths sST2, ng/mL 36.0±16.0 39.4±15.3 35.1±15.2 19.9±6.5 0.01 LVEF, % 60±8 55±9 60±8 58±8 0.01 LVEDD, mm 48±5 50±4 48±6 49±5 NS LVESD, mm 29±4 32±5 29±5 31±4 NS LVEDV, mL 79±12 84±13 80±12 81±13 NS LVESV, mL 32±5 38±7 31±5 34±6 0.01 E/A 0.94±0.12 0.92±0.13 0.94±0.15 0.95±0.15 NS DecT, ms 211±38 226±43 223±45 218±37 0.01 IVRT, ms 98±14 108±17 101±17 99±18 0.01 Conclusion Valsartan has protective effect of left ventricle remodeling and function. It may be useful in prevention of pacing induced heart failure. Decrease in soluble ST2 concentration may help explain the alternative mechanism for protective role of valsartan. (NCT01805804)
A 29-year-old male patient was admitted to hospital with severe decompensated congestive heart failure (HF) with pleural effusion, ascites, peripheral oedema, and worsening dyspnoea in New York Heart Association class IV. He had already been diagnosed with hypereosinophilic syndrome (HES) with endomyocardial fibrosis, irreversible pulmonary hypertension, and chronic atrial fibrillation (AF). Previous diagnostic work-up confirmed chronic eosinophilic leukaemia with fusion gene FIP1L1-PDGFRA as the underlying cause of HES, and the patient was successfully treated with imatinib, although HF rapidly worsened. Endomyocardial fibrosis was diagnosed using magnetic resonance imaging with late gadolinium enhancement in left ventricular (LV) apical and mid-posterior regions. Electrocardiographic examinations revealed AF and right ventricular hypertrophy (Fig. 1A). Echocardiography showed cardiomegaly (Suppl. Video 1-see journal website) with normal LV systolic function biplane, LV ejection fraction 59%, significant mitral regurgitation (Fig. 1B, Suppl. Video 2-see journal website), and significant tricuspid regurgitation (Suppl. Video 3-see journal website) with a pressure gradient of 73 mmHg (Fig. 1C). LV diastolic function was restrictive with monophasic transmitral flow with E wave of 112 cm/s, medial e' wave of 5 cm/s, and E/e' med ratio equal to 22.4. Two-dimensional speckle tracking analysis revealed a severe segmental decline of longitudinal strain within anterior, lateral, and posterior walls with global longitudinal strain reduced to-14.2% (Fig. 1D). After intravenous diuretics and inotropic drugs, the patient's condition has improved and he lost 8 kg of weight. He was discharged home on oral treatment, and a readmission for right heart catheterisation and cardiac transplant evaluation was scheduled. However, before this could happen the patient unexpectedly died without witness. We have to consider imatinib cardiotoxicity as one of the presumed underlying causes of rapid HF progression [1, 2]. Myocardial cells may be extremely susceptible to cardiotoxic properties of tyrosine kinase inhibitors in patients with pulmonary hypertension [3]. This is the second report on the use of speckle tracking echocardiography in chronic eosinophilic leukaemia with cardiac involvement [4]. Similarities in distribution of disturbed myocardial strain and reduced global longitudinal strain are evident. Such casuistic reports may lead to better understanding and care of these unique patients.
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