Supraventricular tachycardia causing heart failure

Houmsse, Mahmoud; Tyler, Jaret; Kalbfleisch, Steven J.

doi:10.1097/hco.0b013e328345b010

Cited by 34 publications

(22 citation statements)

References 47 publications

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“…AF can cause reductions in cardiac output (because of shorter diastolic filling time, loss of atrial contractile function, and elevated filling pressures) and tachycardia-induced myocardial dysfunction. 147 In turn, HF results in structural and electric remodeling changes that enhance susceptibility to AF (see below).…”

Section: Heart Failurementioning

confidence: 99%

The Clinical Profile and Pathophysiology of Atrial Fibrillation

Andrade

Khairy

Dobrev

et al. 2014

Circulation Research

982

364

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Atrial fibrillation (AF) is the most common arrhythmia (estimated lifetime risk, 22%–26%). The aim of this article is to review the clinical epidemiological features of AF and to relate them to underlying mechanisms. Long-established risk factors for AF include aging, male sex, hypertension, valve disease, left ventricular dysfunction, obesity, and alcohol consumption. Emerging risk factors include prehypertension, increased pulse pressure, obstructive sleep apnea, high-level physical training, diastolic dysfunction, predisposing gene variants, hypertrophic cardiomyopathy, and congenital heart disease. Potential risk factors are coronary artery disease, kidney disease, systemic inflammation, pericardial fat, and tobacco use. AF has substantial population health consequences, including impaired quality of life, increased hospitalization rates, stroke occurrence, and increased medical costs. The pathophysiology of AF centers around 4 general types of disturbances that promote ectopic firing and reentrant mechanisms, and include the following: (1) ion channel dysfunction, (2) Ca 2+ -handling abnormalities, (3) structural remodeling, and (4) autonomic neural dysregulation. Aging, hypertension, valve disease, heart failure, myocardial infarction, obesity, smoking, diabetes mellitus, thyroid dysfunction, and endurance exercise training all cause structural remodeling. Heart failure and prior atrial infarction also cause Ca 2+ -handling abnormalities that lead to focal ectopic firing via delayed afterdepolarizations/triggered activity. Neural dysregulation is central to atrial arrhythmogenesis associated with endurance exercise training and occlusive coronary artery disease. Monogenic causes of AF typically promote the arrhythmia via ion channel dysfunction, but the mechanisms of the more common polygenic risk factors are still poorly understood and under intense investigation. Better recognition of the clinical epidemiology of AF, as well as an improved appreciation of the underlying mechanisms, is needed to develop improved methods for AF prevention and management.

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Section: Heart Failurementioning

confidence: 99%

The Clinical Profile and Pathophysiology of Atrial Fibrillation

Andrade

Khairy

Dobrev

et al. 2014

Circulation Research

982

364

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“…The mean procedure, fluoroscopy and radiofrequency energy exposure durations were 104±39 minutes (45-195), 24±10 minutes and 191±90 seconds , respectively. Mean follow-up period was 4.8±3.2 years (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Mean values for pre-RFA left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) were 49.1±9.6 mm and 40.8±13.4% (23-57%), respectively.…”

Section: Resultsmentioning

confidence: 99%

“…The aim of treatment should be to achieve normal sinus rhythm by antiarrhythmic medication initially and then by means of curative ablation therapy, if unsuccessful. Ablation of the atrioventricular junction with implantation of a permanent pacemaker is considered as the last option (6). Currently, although ablative modalities have been proven to be safe and effective in the management of arrhythmias refractory to medical treatment, data on the efficacy of radiofrequency ablation (RFA) in children with TIC is limited.…”

Section: Introductionmentioning

confidence: 99%

Results of radiofrequency ablation in children with tachycardia-induced cardiomyopathy

Aykan¹,

Karagöz²,

Akın³

et al. 2014

Anadolu Kardiyol Derg

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Objective: Tachycardia-induced cardiomyopathy (TIC) is a rare but potentially curable cause of dilated cardiomyopathy. Data on radiofrequency ablation (RFA) for TIC is limited. The aim of this study is to present our experience with RFA in children with TIC, retrospectively. Methods: The medical records of patients with TIC and those underwent RFA between 2000-2011 were systematically reviewed. Demographics and echocardiographic features were recorded. Tachycardia-induced cardiomyopathy is defined as dilatation of the heart chambers or heart failure with chronic or very frequent cardiac arrhythmia. Diagnosis was confirmed with normalization of functions after sinus rhythm has been achieved. Results: A total of 12 patients with a mean age of 6.3±4.1 years (in utero-11.5 years) at diagnosis were enrolled in the study consisting of 7 patients with permanent junctional reciprocating tachycardia and 5 patients with focal atrial tachycardia. The mean pre-RFA left ventricular end-diastolic diameter and left ventricular ejection fraction (LVEF) values were 49.1±9.6 mm (32-66) and 40.8±13.4% (23-57%), respectively. One month after RFA, the mean LVEF value was 62±4.9% (52-69), with only 2 out of 12 patients' LVEF values were still lower than 58%. Tachycardia recurrence was observed in 4 patients, 3 of which had successful repeated RFA procedure. Overall, cure for arrhythmia was achieved in 11 patients (92%), while reversal of heart failure achieved in all patients. In 1 patient permanent complete AV block was developed after the procedure. Conclusion: Treatment of tachycardia with RFA, particularly in patients with arrhythmia refractory to medical therapy, is a feasible and effective treatment option regardless of age. (Anadolu Kardiyol Derg 2014; 14: 625-30)

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“…The resulting hyper-workload on LV causes a deterioration of LV function or a reduction in functional reserve, which has been shown in the pathophysiology of tachycardia-induced cardiomyopathy. 22–24 Hyper-workload of LV may first cause LV diastolic deterioration, which has been shown in patients with hypertensive LV hypertrophy. 25, 26 Furthermore, Kitahori K. et al reported that RV hypertrophy due to pressure overload of the RV causes LV diastolic dysfunction while preserving ejection fraction through mechanical and molecular effects on the septum and LV myocardium.…”

Section: Discussionmentioning

confidence: 99%

Left and Right Ventricular Functional Dynamics Determined by Echocardiograms Before and After Lung Transplantation

Kato

Armstrong

Schulze

et al. 2015

The American Journal of Cardiology

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Impaired cardiac function is considered a contraindication for lung transplantation (LT). Since right ventricular (RV) function is expected to improve after LT, poor left ventricular (LV) function is often the determinant for LT eligibility. However, the changes in cardiac function before and after LT have not yet been elucidated. Therefore, we reviewed echocardiograms obtained from 67 recipients before and after LT. In a subset of 49 patients, both RV and LV longitudinal strains based on 2D speckle tracking echocardiography were analyzed. The cardiopulmonary exercise tests were also reviewed. All patients showed significant improvements in their exercise capacity after LT. RV-echo parameters improved in all patients following LT (RV fractional area change: 36.7±5.6 to 41.5±2.7%, RV strain: −15.5±2.9 to −18.0±2.1%, RV E/E’: 8.4±1.8 to 7.7±1.8; all p<0.05). Overall, the LV ejection fraction (LVEF) did not change (58.7±6.0 to 57.5±9.7%, p=0.385); however, 20 patients (30%) showed more than a 10% decrease in LVEF after LT (61.5±6.1 to 47.3±4.2%, p<0.001), and an increase in LV E/E’ (11.8±1.8 to 12.9±2.2, p=0.049). Multivariate logistic regression analysis revealed that pre-LT LV E/E’ was associated with decrease in LVEF after LT [odds ratio (OR) 1.381, 95%CI (confidential interval) 1.010–1.947, p=0.043]. Furthermore, patients with strain data showed lower pre-LT LV strain was independently associated with LVEF decrease after LT (OR 1.293, 95%CI 1.088–1.614, p=0.002). While RV function improves after LT, LV systolic and diastolic functions deteriorate in a sizable proportion of patients. Impaired LV diastolic function before transplant appears to increase the risk of LVEF deterioration after LT.

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Supraventricular tachycardia causing heart failure

Abstract: The aim of this review is to provide the reader with clinical presentation as well as the common SVTs causing heart failure, pathophysiology of SVT causing heart failure, evaluation and management of SVT causing heart failure, and prognosis of SVT causing heart failure.

Cited by 34 publications

References 47 publications

The Clinical Profile and Pathophysiology of Atrial Fibrillation

The Clinical Profile and Pathophysiology of Atrial Fibrillation

Results of radiofrequency ablation in children with tachycardia-induced cardiomyopathy

Left and Right Ventricular Functional Dynamics Determined by Echocardiograms Before and After Lung Transplantation

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