[Role of right heart failure in cardiac resynchronization].
ABSTRACT During recent years cardiac resynchronization has become an important tool in the treatment of patients with signs and symptoms of heart failure and desynchronized contraction of the left ventricle. Among patients with heart failure, right ventricular involvement can occur because the underlying disease affects both ventricles or because the reduction of left ventricular function impairs the right ventricular function by altered coupling and increased right ventricular afterload. Irrespective of the underlying cause the reduction of right ventricular function confers an adverse prognosis that is further aggravated by the presence of pulmonary hypertension. The present article describes the relevance of reduced right ventricular function for the clinical syndrome of heart failure, the role of right ventricular resynchronization in patients with predominant right heart failure and the possible effects of left ventricular resynchronization on a preexisting impairment of right ventricular function.
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ABSTRACT: The purpose of this research was to evaluate right ventricular (RV) remodeling after six months of cardiac resynchronization therapy (CRT). Cardiac resynchronization therapy is beneficial in patients with end-stage heart failure. The effect of CRT on RV size is currently unknown. Accordingly, the effects of CRT on RV size, severity of tricuspid regurgitation, and pulmonary artery pressure were evaluated. Fifty-six consecutive patients with end-stage heart failure (52% ischemic cardiomyopathy), left ventricular (LV) ejection fraction (EF) < or =35%, QRS duration >120 ms, and left bundle branch block were included. Clinical parameters, LV volumes, LVEF, LV dyssynchrony, and RV chamber size were assessed at baseline and after six months of CRT; LV dyssynchrony was assessed using tissue Doppler imaging. Clinical parameters improved significantly; LV dyssynchrony was acutely reduced after CRT and remained unchanged at six-month follow-up. Left ventricular EF improved significantly from 19 +/- 6% to 26 +/- 8% (p < 0.001), and LV end-diastolic volume decreased from 257 +/- 98 ml to 227 +/- 86 ml (p < 0.001). Right ventricular annulus decreased significantly from 37 +/- 9 mm to 32 +/- 10 mm, RV short-axis from 29 +/- 11 mm to 26 +/- 7 mm, and RV long-axis from 89 +/- 11 mm to 82 +/- 10 mm (all p < 0.001). Left ventricular and RV reverse remodeling were only observed in patients with substantial LV dyssynchrony at baseline. Finally, significant reductions in severity of tricuspid regurgitation and pulmonary artery pressure were observed. Cardiac resynchronization therapy results in significant reverse LV and RV remodeling after six months of CRT in patients with LV dyssynchrony. Moreover, CRT leads to a reduction of the severity of tricuspid regurgitation and a decrease in pulmonary artery pressure.Journal of the American College of Cardiology 12/2005; 46(12):2264-9. · 15.34 Impact Factor
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ABSTRACT: The predictive value of radionuclide ventriculography was studied in 34 patients with depressed left ventricular ejection fraction (less than 40%) and clinically evident congestive heart failure secondary to atherosclerotic coronary artery disease. In addition to left ventricular ejection fraction, right ventricular ejection fraction and extent of left ventricular paradox were obtained in an attempt to identify a subgroup at increased risk of mortality during the ensuing months. The 16 patients who were alive after a 2 year follow-up period had a higher right ventricular ejection fraction and less extensive left ventricular dyskinesia. When a right ventricular ejection fraction of less than 35% was used as a discriminant, mortality was significantly greater among the 21 patients with a depressed right ventricular ejection fraction (71 versus 23%), a finding confirmed by a life table analysis. Depressed right ventricular function was further linked to more severely compromised left ventricular function, as confirmed by a greater reduction in left ventricular ejection fraction and by an increased extent of left ventricular dyskinesia. These patients had a greater prevalence of chronic obstructive pulmonary disease and previous inferior myocardial infarction but the differences between groups were not statistically significant. It appears that the multiple factors contributing to the reduction in right ventricular ejection fraction make it a useful index not only for assessing biventricular function, but also for predicting patient outcome.Journal of the American College of Cardiology 09/1983; 2(2):217-24. · 15.34 Impact Factor
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ABSTRACT: We sought to investigate the effect of intrinsic conduction over the right bundle on the maximum rate of left ventricular pressure rise (LVdP/dt(max)) during left ventricular (LV) pacing compared to biventricular (BiV) pacing. Simultaneous BiV pacing and LV pacing both improve LV function in patients with heart failure and LV asynchrony. We studied the hemodynamic effect of intrinsic conduction leading to ventricular fusion during LV pacing. In 34 patients with New York Heart Association functional class III or IV, sinus rhythm with normal atrioventricular (AV) conduction, left bundle branch block, QRS >130 ms, and optimal medical therapy, LVdP/dt(max) was measured invasively during LV and simultaneous BiV pacing. The AV interval was varied in four steps starting (AV1) with an AV interval 40 ms shorter than the intrinsic PQ time and decreased with 25% for each step. At AV1, LVdP/dt(max) was 996 +/- 194 mm Hg/s for LV pacing and 960 +/- 200 mm Hg/s for BiV pacing (p = 0.0009), with all patients showing ventricular fusion during LV pacing. At AV2, 21 patients had ventricular fusion with a LVdP/dt(max) of 983 +/- 213 mm Hg/s and 957 +/- 202 mm Hg/s for LV and BiV pacing, respectively. In the remaining 13 patients without fusion these values were 919 +/- 164 mm Hg/s and 957 +/- 174 mm Hg/s, respectively. The difference between LV and BiV at AV2 is significantly higher when fusion is present (p = 0.01). The LVdP/dt(max) is higher in LV than in BiV pacing provided that LV pacing is associated with ventricular fusion caused by intrinsic activation.Journal of the American College of Cardiology 12/2005; 46(12):2305-10. · 15.34 Impact Factor