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Reversal Of Cardiomyopathy In Patients With Congestive Heart Failure Secondary To Tachycardia Using Radiofrequency Ablation

Posted on:2014-04-29Degree:MasterType:Thesis
Country:ChinaCandidate:D H ZhaoFull Text:PDF
GTID:2254330425950251Subject:Internal medicine
Abstract/Summary:PDF Full Text Request
BackgroundCHF is perceived as a final common pathophysiological destination of variety heart diseases. Despite contemporary progression in research of CHF and new drug and devices such as Beta-blockers, angiotensin converting enzyme (ACE) inhibitors and aldosterone receptor blockers, cardiac resynchronization therapy had been widely used, which are proved by many evidence based medicine of benefit to improve the long-term outcome of the disease, long-term prognosis is still poor with the approximately5years survival rate of45-59%. CHF caused by primary cardiovascular diseases, including coronary atherosclerosis, hypertension, valvular heart disease, and cardiomyopathy are regarded as irreversible due to the process of cardiac remodeling. The term remodeling implies changes that result in the rearrangement of normally existing structures. However, cardiomyopathy secondary to tachycardia, called tachycardiainduced cardiomyopathy (TCM), is considered to be a reversible cause of congestive heart failure with an improvement of cardiac function after successful radiofrequency catheter ablation or rate control.TCM is known to occur in a variety arrhythmias including atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia, and ventricular tachycardia. AV nodal reentry tachycardia and AV reentrant tachycardia, though commonly indicated for ablation, rarely resulted in TCM. Atrial fibrillation (AF), characterized of irregularity of heart rhythm and asynchrony, is a common cause of TCM. In AF patients with potentially TCM, enlargement of end-systolic anteroposterior left atrial diameter (LAD) is developed due to the increase atrial pressure and left atrial remodeling. For these patients, ablation is no longer indicated because of low cardioversion rate and high recurrent rate. A large amount of atrial fibrillation patients with heart failure may not be included in the study. It is likely that the incidence of TCM is underestimated. Kasper et al. reported that, of673patients with cardiomyopathy, only1case was considered to be TCM. Medi et al reported the incidence of TCM was10%in patients with atrial tachycardiac (AT) for ablation procedure.PVCs related cardiomyopathy has occurred in patients ranged from high burden of PVCs to repetitive monomorphic VT and incessant VT. Yarlagadda et al. demonstrated that significant reduction in left ventricular ejection fraction was observed in patients with17,000ectopic beats daily. According to Takemoto et al., threshold of PVCs counts of20%total heartbeats over24h may develop cardiomyopathy. It is believed that high PVCs burden would result in an overall increase in the average heart rate and eventually lead to develop of cardiomyopathy. Unlike the other tachycardia, Huizar et al. thought that the main mechanism by which PVCs caused cardiomyopathy to be due to the asynchrony induced by frequent PVCs. They observed no gross histopathologic and mitochondrial abnormalities in canine model of left ventricular systolic dysfunction. Both increase of heart rate and asynchrony in patients with high PVCs burden accelerate the left ventricular dysfunction.Presenting symptoms of heart failure were more common in patients with TCM. Medi et al. reported that a series of30patients with TCM secondary to AT demonstrated a slower ventricular response compared with patients without cardiomyopathy, thus they less complained symptoms of palpitation. We hypothesized that patients with rapid ventricular response may be more likely to present early with symptom of palpitation than patients with slower ventricular rate tachycardia. These patients may seek for appropriate medical treatment earlier before heart failure developed. Patients with TCM were more likely not to be aware of tachycardia episodes and presented shortness of breath after deterioration of the left ventricular systolic function.Rapid pacing in animal models is responsible for the development of heart failure and eventually lead to myopathic change. In paced animal models of TCM, increased left ventricular end diastolic diameter (LVEDD), mitral regurgitation (MR), elevated LV end-diastolic pressure, and decreased ejection fraction were observed. In ultrastructural layer, disturbances in structure and function of the cardiomyocyte result in ventricular remodeling. The neurohumoral changes manifested in tachycardia-induced cardiomyopathy are similar to those manifested in other causes of heart failure. In experimental models, elevated norepinephrine, renin, aldosterone and endothelin-1levels have been reported.The crosstalk of neurohumoral may play a complex role in the progression of tachycardia-induced cardiomyopathy.ObjectiveTachycardia-induced cardiomyopathy (TCM) is a reversible cause of heart failure. Little is known of the characteristics of tachycardia associated with the development of left ventricular (LV) dysfunction and the reversal of cardiomyopathy after cure of tachycardia. This study was aim to examine the reversal of cardiomyopathy in patients undergoing ablation with congestive heart failure secondary to tachycardia. SubjectsThe study population consisted of a consecutive series of625patients undergoing radiofrequency ablation for tachycardia between January2009and July2011at the center of NanFang Hospital, Guangzhou, China. Surface12-lead electrocardiogram (ECG) and echocardiography were routinely performed before ablation procedure in our center. History of symptoms such as dyspnea, palpitations and syncope were documented. LVEF was evaluated by echocardiography. Transthoracic echocardiography was performed in parasternal and apical views. Left ventricular ejection fraction (LVEF) was estimated using the Simpson’s method. Left ventricular dysfunction was defined as a left ventricular ejection fraction (LVEF) of <50%(n=27). Patients with left ventricular dysfunction who had coexisting structural heart diseases (n=10) were excluded in the study. A total of17patients were considered to have TCM.MethodsPre-ablation echocardiographic assessment was performed during intervals of three or more consecutive sinus beats in15of17patients. The remaining2patients with persistence atrial fibrillation were in tachycardia with a mean heart rate of115±7beats per min (bpm). At the time of follow-up echocardiography examination, all patients with TCM were in sinus rhythm at a rate of72±12bpm. Left ventricular end-diastolic diameter (LVEDD) was determined in all subjects. Structural heart diseases were excluded by clinical history, Holter monitoring, echocardiographic study, exercise testing and coronary angiography. NT-proBNP was measured routinely in patients with depressed left ventricular function or with symptoms suggesting heart failure after admission in hospital. Blood samples were obtained in EDTA from each subject. Plasma NT-proBNP levels were determined using a commercially available enzyme immunoassay run on the analyzer (Roche-Elecsys 2010HITACHI). All patients underwent electrophysiological study in the fasting state with local anesthesia, and after the signature of informed written consent. All antiarrhythmic drugs were discontinued a minimum of5half-lives before the procedure. Surface ECG leads filtered at30to500Hz were recorded. Multielectrode catheters were introduced percutaneously through the femoral veins. When left ventricular access was required, it was obtained by retrograde aortic method, and a single bolus of heparin (30IU/kg) was administered. When necessary, the3-dimensional electroanatomic mapping system was used. RFA was performed with continuous temperature feedback control of power output to achieve a target temperature of50℃and a maximum power of50W. After ablation, infusions of isoproterenol or programmed stimulation were performed to confirm absence of tachycardia. After ablation, patients with recorded impaired LV function without structural heart disease before procedure were evaluated by repeated echocardiography and NT-proBNP assessment after a follow-up of3months. Any patient with symptoms suggesting recurrence of tachycardia was reviewed by the treating electrophysiologists. If patients had recurrence of tachycardia during the follow-up, repeated ablation was performed and another3months follow-up was required.ResultsThe incidence of TCM was2.7%(12males; age,35.8±17.1years). Successful ablation was performed in16of17patients (94.1%). There was a significant improvement in left ventricular ejection fraction (36.7±7.5%vs.59.4±9.7%; P <0.001). The mean LVEDD before treatment was59.5±8.3mm (range,43to70), compared with51.9±7.4mm (range,40to67)(P=0.009) after3months follow-up. The levels of NT-proBNP decreased after ablation procedure, from4092.6±3916.6pg/ml to478.9±881.9pg/ml (P<0.001). After successful ablation, ventricular function normalized in15of17(88.2%) of patients at a mean of3months.ConclusionRestoration of LV function and reversal of LV remodeling can be achieved with successful elimination of tachycardia in the majority of patients. NT-proBNP level elevates in subjects with TCM and decreases sharply after ablation.
Keywords/Search Tags:Tachycardia, Cardiomyopathy, NT-proBNP, Heart Failure, Ablation
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