Search

ObjectivesThe aim of the study was to evaluate the effectiveness of cardiac resynchronization therapy (CRT) in patients with refractory heart failure (HF) and incomplete left bundle branch block (“narrow” QRS), together with echocardiographic evidence of interventricular and intraventricular asynchrony.BackgroundCardiac resynchronization therapy has been proven effective in patients with HF and wide QRS by ameliorating contraction asynchrony.MethodsFifty-two patients with severe HF received biventricular pacing. The patients were eligible in the presence of echocardiographic evidence of interventricular and intraventricular asynchrony, regardless of QRS duration. The patient population was divided into group 1 (n = 38), with a QRS duration >120 ms, and group 2 (n = 14), with a QRS duration ≤120 ms.ResultsThe baseline parameters considered in the study were similar in both groups. At follow-up, CRT determined narrowing of the QRS interval in the entire population and in group 1 (p < 0.001), whereas a small increase in QRS duration was observed in group 2 (p = NS); in all patients and within groups, we observed improvement of New York Heart Association functional class (p < 0.001 in all), left ventricular ejection fraction (p < 0.001 in all), left ventricular end-diastolic and end-systolic diameter (p < 0.05 within groups), mitral regurgitation area (p < 0.001 in all), interventricular delay (p < 0.001 in all), and deceleration time (group 1: p < 0.001, group 2: p < 0.05), with no significant difference between groups. The 6-min walking test improved in both groups (group 1: p < 0.001; group 2: p < 0.01).ConclusionsCardiac resynchronization therapy determined clinical and functional benefit that was similar in patients with wide or “narrow” QRS. Cardiac resynchronization therapy may be helpful in patients with echocardiographic evidence of interventricular and intraventricular asynchrony and incomplete left bundle branch block.

In order to examine the relation between secondary hyperparathyroidism (sHPT) and left ventricular hypertrophy (LVH) in hemodialysis (HD) patients, were selected retrospectively 60 of 228 HD patients who had two echocardiography over a 12-16 months period (13.2 1.2 months). Patients were subdivided in three groups (G) according to PTH behaviour: G1 (n = 19), with PTH levels300 pg/ml not requiring with vitamin D receptor activators (VDRAs) treatment; G2 (n = 20), with a progressive increase of PTH levels to values300 pg/ml that required to start or to increase VDRAs therapy in 18/20 patients during follow-up; G3 (n = 21), with PTH levels300 pg/ml and50% reduction after VDRAs treatment. Parathormone levels correlated with left ventricular mass index (LVMi; r = 0.714; P0.001). Multiple regression analysis indicated that PTH levels were an independent predictor of LVMi (P0.001). Patients with baseline PTH levels300 pg/ml (n = 27) had higher LVMi with respect to those with PTH300 pg/ml (n=33), 197 50 vs 136 30 g/m2 (P0.01). In G1 LVMi did not change during follow-up. In G2 LVMi increased from 146 26 to 169 35 g/m2 (P=NS). In G3LVMi decreased from 210 44 to 154 42 g/m2 (P0.05). Parathyroid hormone seems to play an important role in the genesis and perpetuation of LVH, whereas treatment of sHPT with VDRAs may determine LVH regression or at least slow down its progression.

This article describes a case of cardiac resynchronization therapy (CRT) performed with dual site left ventricular pacing. The main clinical and functional long-term results are in agreement with the most recent data regarding traditional CRT. Furthermore, this innovative pacing modality allowed optimal inter- and intraventricular resynchronization.

OBJECTIVE: Cardiac resynchronisation therapy has proven to be effective in refractory heart failure (HF) patients with QRS >120-130 ms. Therefore, the aim of our study was to verify the long-term effectiveness of cardiac resynchronisation therapy in HF patients with echocardiographic evidence of mechanical asynchrony regardless of QRS duration. METHODS: One hundred and six patients with New York Heart Association class II-IV HF and echocardiographic documentation of interventricular and intraventricular asynchrony underwent biventricular stimulation. A clinical and functional evaluation was performed at baseline, 1, 3, 6 months, and every 6 months thereafter. RESULTS: After a median follow-up of 16 months, a significant improvement was noted in ejection fraction, left ventricular diameters, mitral regurgitation jet area, interventricular and intraventricular echocardiographic indexes of asynchrony, and the 6-min walking distance (P < 0.001 for all). Death rates for all causes and for cardiac causes were 18.2 (95% confidence interval 12.8-25.9) and 13.5 (95% confidence interval 9.0-20.3) per 100 person-years, respectively. Patients in New York Heart Association class IV had an almost three-fold increase in risk of dying as compared to class II-III (hazard ratio 2.97, 95% confidence interval 1.30-6.79). CONCLUSIONS: Interventricular and intraventricular asynchrony at echocardiography may be useful in identifying HF patients suitable for cardiac resynchronisation therapy, with results comparable to those obtained with QRS duration selection criteria.

To discuss the most relevant studies on the prognostic impact of echocardiographic left ventricular hypertrophy in hypertension.There is abundant evidence from epidemiological studies that increased left ventricular mass identifies hypertensive patients at increased risk of major cardiac and cerebrovascular events. Looking at the geometric patterns of the left ventricle, concentric remodelling and concentric left ventricular hypertrophy carry the highest risk for adverse events. Patients with left ventricular hypertrophy reversal as an effect of treatment are exposed to a lesser risk of events as compared with patients with persistence of left ventricular hypertrophy. Reversal of concentric remodelling predicts a lesser risk of adverse events compared with persistence of remodelling. Experimental evidence is accumulating that several haemodynamic and nonhaemodynamic factors which are able to promote progression of atherosclerosis through plaque growth and destabilization may also induce left ventricular hypertrophy by acting on myocyte and interstitium. Increased left ventricular mass may also be a causative factor for reduced pumping performance and arrhythmias.Increased left ventricular mass is a marker of cardiovascular risk because it reflects and integrates the long-term level of activity of factors inducing progression of atherosclerosis. Increased left ventricular mass may also mediate myocardial ischaemia with potential evolution towards heart failure and arrhythmias.