[Hypertrophic obstructive cardiomyopathy and double-chamber pacing. Long-term results in a consecutive series of 22 patients].
D LelloucheMikaïl NourredineDuval AmPénélope PujadasOlivier GartenlaubA CastaigneCachin JcPascal Guéret
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The authors report their experience with dual-chamber pacing in hypertrophy obstructive cardiomyopathy. 22 patients (14 women and 8 men) mean age 60 +/- 13 years were implanted between 1992 and 1998. The criteria for pace-maker implantation were the presence of severe symptoms related with hypertrophy obstructive cardiomyopathy (dyspnea, angina, syncope) and left ventricular outflow tract gradient at mean 30 mmHg. Before pacing, all patients received a medical therapy which included beta-blockers or calcium inhibitors. This treatment was considered as ineffective or responsible of side effects. Patients were followed-up at mean 35.1 +/- 20.3 months. During this period, symptoms improved (mean NYHA class 2.7 +/- 0.5 before pacing vs 1.4 +/- 0.5 after pacing) and left ventricular outflow tract lowered from 95.4 +/- 40.8 to 39.3 +/- 20.5 at 6 months. 34.3 +/- 23.4 at one year and 26.5 +/- 21 at the end of follow-up. Seven patients had RF ablation of atrio-ventricular junction for paroxysmal atrial fibrillation or for lack of hemodynamic improvement with pacing. This procedure permits a significative lowering of gradient and a better ventricular filling. In conclusion, dual-chamber pacing is effective for treatment of hypertrophy obstructive cardiomyopathy when medical therapy is ineffective or bad tolerated at condition of: perfect pacing with permanent ventricular capture and optimal AV delay; RF ablation of AV junction in one third of cases; medical therapy systematically associated in all patients.Keywords:
Ventricular outflow tract
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Abstract Previous studies have suggested an unexpectedly low incidence of atrial fibrillation in patients with congestive cardiomyopathy. To further investigate the incidence of chronic atrial fibrillation in these patients and its relationship to left atrial dimension and pressure, we retrospectively examined M‐mode echocardiographic and cardiac catheterization data from 54 patients with idiopathic (n = 29) and ischemic (n = 25) congestive cardiomyopathy. The incidence of atrial fibrillation (17%) was surprisingly low given the degree of left atrial enlargement (51 ± 5 mm; mean ± SD) and left atrial hypertension (19 ± 8 mm Hg). In addition, there were no significant differences in left atrial pressure or left atrial dimension between those congestive cardiomyopathy patients in sinus rhythm and those in atrial fibrillation, nor was there a higher incidence of secondary mitral regurgitation in patients in atrial fibrillation. Comparisons were also made between congestive cardiomyopathy patients and 21 patients with primary mitral valve disease and atrial fibrillation. Left atrial pressure was not significantly different between these groups. However, the mean left atrial dimension of the patients with mitral valve disease (56 ± 8 mm) was greater (P < 0.01) than that of patients with idiopathic (51 ± 6 mm) or ischemic (50 ± 4 mm) cardiomyopathy in sinus rhythm and also greater (P = 0.07) than left atrial dimension (51 ± 6 mm) of congestive cardiomyopathy patients in atrial fibrillation. Furthermore, massive enlargement of the left atrium (greater than 60 mm) was a common feature of mitral valve disease (33% incidence) but occurred only rarely in congestive car‐diomyopathy (5% incidence). We conclude that while left atrial volume and pressure loads may be important contributors to the pathogenesis of atrial fibrillation, these factors are not sufficient to produce the arrhythmia in most patients with congestive cardiomyopathy. Other variables such as disease duration or the degree of atrial fibrosis or inflammation may also be important in determining which patients with left atrial enlargement will develop atrial fibrillation. Furthermore, massive left atrial enlargement (left atrial dimension > 60 mm) is rarely associated with ischemic or idiopathic congestive car‐diomyopathy and suggests underlying primary mitral valve disease.
Restrictive cardiomyopathy
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Heart failure (HF) and atrial fibrillation (AF) are the most common cardiovascular conditions in clinical practice and frequently coexist. The number of patients with HF and AF is increasing every year. Aim . To analyze the effect of clinical course and management of HF and AF on the outcomes. Material and methods . The data of 1,003 patients from the first Russian register of patients with HF and AF (RIF-CHF) were analyzed. The endpoints included hospitalization due to decompensated HF, cardiovascular mortality, thromboembolic events, and major bleeding. Predictors of unfavorable outcomes were analyzed separately for patients with HF with preserved ejection fraction (AF+HFpEF), mid-range ejection fraction (AF+HFmrEF), and reduced ejection fraction (AF+HFrEF). Results . Among all patients with HF, 39% had HFpEF, 15% — HFmrEF, and 46% — HFrEF. A total of 57,2% of patients were rehospitalized due to decompensated HF within one year. Hospitalization risk was the highest for HFmrEF patients (66%, p=0,017). Reduced ejection fraction was associated with the increased risk of cardiovascular mortality (15,5% vs 5,4% in other groups, p<0,001) but not ischemic stroke (2,4% vs 3%, p=0,776). Patients with HFpEF had lower risk to achieve the composite endpoint (stroke+MI+cardiovascular death) as compared to patients with HFmrEF and HFrEF (12,7% vs 22% and 25,5%, p<0,001). Regression logistic analysis revealed that factors such as demographic characteristics, disease severity, and selected therapy had different effects on the risk of unfavorable outcomes depending on ejection fraction group. Conclusion. Each group of patients with different ejection fractions is characterized by its own pattern of factors associated with unfavorable outcomes. The demographic and clinical characteristics of patients with mid-range ejection fraction demonstrate that these patients need to be studied as a separate cohort.
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Factors associated with the development of atrial fibrillation (AF) in general population have been described, but it is still unknown whether the same risk factors apply to heart failure (HF) patients. The aim of this study was to identify clinical factors related to various forms of AF in HF patients.The clinical and echocardiographic characteristics were assessed in 155 HF patients: 50 with sinus rhythm, 52 with non-permanent AF, and 53 with permanent AF.Multivariate logistic regression analysis showed that the increase in the NYHA class was an independent risk factor for both forms of AF. The occurrence of permanent AF in comparison to sinus rhythm group was independently associated with hs-C-reactive protein (CRP) elevation above 1 mg/dL (OR 1.87, 95% CI 1.05-3.35), left atrial dimension above 4 cm (OR 3.78, 95% CI 1.29-11.06) and tricuspid maximal pressure gradient elevation above 35 mm Hg (OR 5.01, 95% CI 1.38-18.27). The presence of coronary disease was independently associated with less frequent occurrence of permanent AF in comparison to sinus rhythm group (OR 0.21, 95% CI 0.06-0.67).More advanced congestive HF was associated with presence of both types of AF. Non-ischemic etiology of HF and elevated CRP are independently associated with permanent AF compared to sinus rhythm. Left ventricular diastolic dysfunction indicators (increased tricuspid maximal pressure gradient and left artial dimension) are independently associated with permanent AF.
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Objective To explore the changes and significances of BNP plasma concentration in the subjects of heart failure complicated with atrial fibrillation.Methods 116 patients with heart failure were divided into atrial fibrillation(AF) group and sinus rhythm(SR) group.Patients in the Group AF were divided into 2 groups depend on whether the heart rate was more than 80 bpm.Plasma BNP,NYHA classification and left atrial and left ventricular end diastolic diameter were measured in every subject in each group.Results Plasma BNP concentration in group SR was higher than that in group AF,in the same subgroup of NYHA class II and III,BNP level in group AF was significantly higher than that in group SR.Plasma BNP in patients with heart failure,the level of BNP were positively correlated with age(r = 0.675,P 0.01),AF duration(r = 0.669,P 0.01),left atrial size(r = 0.734,P 0.01),left ventricular size(r = 0.846,P 0.01),in group AF BNP had no significant difference in the two groups whether heart rate was more than 80 bpm or not.Conclusion BNP levels in patients with heart failure and atrial fibrillation are significantly higher than that in the group SR,and positively correlated with ages,AF duration,left atrial and left ventricular diameters.
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Obesity is a well-known risk factor for atrial fibrillation (AF) and heart failure (HF). Epicardial fat, the true visceral fat depot of the heart, has been associated with changes in both cardiac function and morphology. In this study, we evaluated whether ultrasound-measured epicardial fat thickness is related to AF and HF. A cross-sectional study was performed in 84 consecutive subjects with clinical and ECG-documented history of permanent (AF) or paroxysmal AF (PAF) who underwent echocardiographic epicardial fat thickness measurement. Sixty-four subjects had AF and 20 showed PAF. AF subjects had higher prevalence of heart failure (HF), defined by ejection fraction (EF)<50%, (p<0.01). Subjects with AF had higher epicardial fat thickness than PAF subjects (4.8±2.5 vs. 3.5±2.4 mm, p<0.05). As subjects were stratified by HF, epicardial fat thickness was lower (4.4±2.2 vs. 5.4±2.3 mm, p<0.05) in those with HF as compared to subjects without HF. This study showed for the first time that echocardiographic epicardial fat thickness is significantly higher in subjects with chronic AF when compared to those with PAF. It is plausible that permanent AF is related to long-term influence of epicardial fat. Epicardial fat reduction in HF subjects may reflect the overall fat mass reduction, commonly observed in these patients. It is also possible to hypothesize that epicardial fat pad may incur in fibrotic changes during chronic cardiac failure.
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