The Medical Journal of Basrah University

Introduction

Cardiomyopathy is a primary heart muscle disorder with myriad causes and clinical presentations. The cardiomyopathies are often named according to the underlying etiology, like hypertensive, ischaemic, myocarditis and infiltrative cardiomyopathy ^1 - 6. The normal heart rate of 60 to 90 bpm allows normal left ventricular function ¹. A sustained heart rate increase in a tachyarrhythmia pattern may well induce a cardiomyopathy called tachycardia-induced cardiomyopathy (TIC). ^1 - 6 It is a type of dilated cardiomyopathy (DCM) caused mainly by recurrent paroxysmal or incessant tachycardia or by disturbing the rhythm of various mechanisms. ^1 - 6 It may manifest months or years after the onset of the arrhythmia. ³ Tachycardia - induced cardiomyopathy might well be rate dependent, as faster tachycardia develops TIC earlier. ⁵ This entity was first reported in 1913 by Gossage and Braxton Hicks in a patient with atrial fibrillation who presented with heart failure (HF). ² The association of tachyarrhythmias with heart failure is quite common, but what distinguish TIC are mainly the heart failure’s full or partial resolution and the regaining of normal left ventricular function after a period of sinus rhythm stabilization or after reasonable control of the heart rate within the arrhythmia. ^2 - 5 TIC can occur in a basically structurally normal heart where the arrhythmia purely precipitates the myocardial function suppression and the occurrence of heart failure. It may also occur in pathological heart diseases where the arrhythmia potentiates or worsens the left ventricular function impurely. ⁵ The most common arrhythmias causing TIC are atrial fibrillation (AF), atrial flutter (AFl) and atrial tachycardia (AT), whether paroxysmal, persistent or chronic permanent. ^7 , 12 Incessant type of atrioventrcular tachycardia (AVRT) like permanent junctional reciprocating tachycardia (PJRT) is a well-known cause of heart failure and cardiomyopathy in young and childhood age groups. ⁹ Ventricular premature beats (VPCs) may induce DCM if they are frequent enough to impair LV function. ^8 , 13 Other supraventricular tachycardias (SVT), including atrioventriculo nodal reentry tachycardia (AVNRT), rarely induces DCM and heart failure, possibly because they are almost paroxysmal. ⁶ Recognizing the arrhythmia as a cause of DCM and heart failure is clinically highly important for resolving the DCM and regaining normal LV function. ^{2 , 4 , 5 , 14} We are reporting 24 cases of TIC patients who regained full or partial normal LV function and resolution of the DCM after controlling the arrhythmia. Physicians need a high degree of suspicion to diagnose TIC and cannot forget tachycardia as an underlying etiology of DCM and HF.

Patients and methods

Twenty four patients who were diagnosed as DCM with heart failure are recognized and included in this study; the DCM is associated with cardiac arrhythmia. The cases were seen from 2006 to 2017 in a single private clinic of the author. Full histories were taken, concentrating on which symptoms started first, for the total duration of the HF symptoms. If the palpitation symptoms preceded the shortness of breath (SOB), the patient was labeled as group A (GrA). If the SOB symptoms preceded the palpitation, the patient was enrolled in group B (GrB). If it was unclear which symptoms started first, they were included in group C (GrC). All the patients had gone through basic cardiac investigations, including 12-leads electrocardiogram (ECG), chest X-ray (CXR), an echocardiogram (ECHO) assessing the LV cavity’s sizes in diastole and systole and calculating the left ventricular ejection fraction (LVEF). A Holter monitor was done in almost all the patients before treatment and within the course of therapy. All the tests were repeated periodically during the follow-up period, according to the patients’ attendance at the follow-up. Eight patients had atrial flutter, 10 patients had atrial fibrillation, four patients had VPCs and two patients had PJRT. The treatment included therapies for HF and for arrhythmia. Sinus rhythm stabilization was the main and only index of arrhythmia control. The arrhythmia therapy included either antiarrhythmic drug therapy (in 18 patients) or catheter radiofrequency ablation therapy (in 6 patients). According to the HF’s clinical status, the treatment of HF included diuretics, an angiotensin-converting enzyme (ACE) inhibitor, and isosorbide and beta blockers. DC cardio version was used in 5 patients to revert their sinus rhythm during the early stages of the arrhythmia treatment. Assessment of the HF’s improvement depended on a) regression in New York Heart Association (NYHA) functional class, b) improvement in LVEF and c) a reduction in cardiac size by CXR, expressed by a reduction in the cardiothoracic (C/T) ratio. Confounders implicated in the aetiology of tachycardia such as thyrotoxicosis and pheochromocytoma were excluded by appropriate tests. The DCM’s improvement grade was based on the increase in LVEF, which is classified in as a full recovery of LVEF for more than 50% or a partial recovery for values from 45% to 49%. The total follow-up period ranged from three months to two years.

Results

Twenty-four patients were included in this study after fulfilling the selection criteria. Nine patients were males, and 15 were females. The ages ranged from 10 years to 55 years. DCM was diagnosedclinically by cardiologist, and provisionally structural pathological causes were excluded via clinical history, ECG, echocardiography findingsa specific tests. A diagnostic coronary angiography was done in 5 patients, which revealed normal coronary arteries. The arrhythmia symptoms preceding the HF symptoms were seen in 20 patients (GrA). The total palpitation symptoms’ duration ranged from two months to three years. In two patients, the arrhythmia symptoms and the HF co- exist for the symptoms’ total duration (GrC). In the remaining two patients, the HF symptoms of SOB preceded the arrhythmia symptoms (GrB), according to the patient’s history. The NYHA functional class was in the level of II-IV at time of presentation and in NYHA I after variable times, ranging from seven days to three months, after stabilizing SR. The LVEF values rose remarkably, from an average of 20% to 32% to an average of 45% to 58% after the arrhythmia control (Figure-1). The cardiac size assessed by the C/T ratio in the CXR showed marked reduction after controlling the arrhythmia (Figure-2).

The recovery period for LV function after the arrhythmia control varied from one week to six months and correlated to the total duration of the arrhythmia and HF symptoms. Figures-3(A, B, C and D) show the remarkable improvement of LVEF and cardiac size after the atrial flutter reversion to sinus rhythm by catheter radiofrequency ablation therapy (CRFAT). Similar changes are seen in Figure 4 (A, B, C, D), showing a patient with atrial fibrillation, and Figure 5 (A, B, C, D), showing a patient with VPCs.

Figure 1. The improvement in LVEF before (A) and after (B) arrhythmia control in the 24 patients.

Figure 2. chest X ray cardiac size improvement assessed by cardiothoracic ratio (C/T ratio) before (C/T B) and after (C/T A) arrhythmia control.

Figure 3A. The 12-leads ECG showing atrial flutter.

Figure 3B. The electrophysiology trace showing the reversion of atrial flutter in sinus rhythm with catheter ablation therapy.

Figure 3C. The twelve leads ECG with sinus rhythm after catheter ablation therapy.

Figure 3D. Patient No 1.The reduction in cardiac size 10 months after stabilizing the sinus rhythm.