The conundrum of ventricular arrhythmia and cardiomyopathy: Which abnormality came first?

Abstract

Ventricular arrhythmia and cardiomyopathy often coexist. Many patients with abnormal ventricular function have either documented premature ventricular contractions (PVCs) or nonsustained ventricular tachycardia and have an increased risk of sudden death from ventricular fibrillation. Tachycardia is a treatable cause of cardiomyopathy. The culprit arrhythmia may be atrial tachycardia, atrial fibrillation, or another supraventricular arrhythmia. The syndrome of PVCs giving rise to ventricular dysfunction was recently described. Thus, a conundrum exists for clinicians in determining which abnormality (PVCs or cardiomyopathy) came first and gave rise to the other. Solving this dilemma is important because radiofrequency ablation for frequent PVCs can completely reverse the cardiomyopathy and normalize systolic ventricular function. In this article, we describe the present evidence for the syndrome of PVCs that can be ablated as a cause for cardiomyopathy. We include a case example and discussion to illustrate this concept and provide a stepwise approach to determining whether PVCs cause cardiomyopathy or vice versa.

Premature Ventricular Contraction-Induced Cardiomyopathy

“…47 It is particularly important to identify the primary disorder because of the potential reversibility of PVC-induced cardiomyopathy. 48,49 Patients can present with debilitating symptoms, particularly palpitations, or other symptoms such as chest pain, presyncope, syncope, or heart failure manifested by decreased effort tolerance, possibly as a result of decreased effective cardiac output. 3 The vast majority of these patients are healthy with no known structural heart disease, 4 but a detailed family history is required to help exclude familial dilated cardiomyopathy.…”

“…Given the reciprocal causal association between PVCs and cardiomyopathy where either 1 can lead to the other, it may be difficult to isolate the primary disorder. 49,55 In many patients, the onset of frequent PVCs relative to the onset of LV dysfunction is unknown. 47 It is particularly important to identify the primary disorder because of the potential reversibility of PVCinduced cardiomyopathy.…”

Reversible Dilated Cardiomyopathy: Into the Thaumaturgy of the Heart—Part 1

“…The mechanisms of TIC are not fully defined but include subclinical ischemia, abnormalities in energy metabolism, redox stress and calcium overload. 46,47 In animal models of high-rate atrial or ventricular pacing, ventricular impairment is also associated with changes in myocardial electrophysiology including prolongation of the action potential and spontaneous ventricular arrhythmias. Furthermore, persistent left bundle branch block leads to lateralization of gap junctions promoting functional anisotropy and apoptosis.…”

“…They suggest that otherwise young healthy individuals, without abnormal cardiovascular substrate having over 20,000 VEs per day, with no more than two morphologies, originating from outflow tracts or from the fascicles and with preserved myocardial wall thickness are the best candidates for presumption of VEinduced cardiomyopathy. 47 …”

Tachycardia‐Induced Cardiomyopathy: Evaluation and Therapeutic Options

“…3,4 Clinical Features and Diagnostic Approach TIC may follow any type of chronic cardiac arrhythmia: supraventricular tachyarrhythmias, such as inappropriate sinus tachycardia 8 ; atrial fibrillation [9][10][11] ; atrial flutter 9 ; automatic atrial tachycardia 6 ; atrioventricular (AV) nodal reentry tachycardia 6 ; automatic AV junctional tachycardia, 6 accessory pathway tachycardia, 6 and ventricular tachycardia 12,13 ; and frequent premature ventricular complexes (PVCs). [14][15][16] Further, TIC has been reported at any age group, from the fetus to the elderly. 3,4 The incidence of TIC is unknown; most reports have been small retrospective series or case studies involving mostly patients with atrial fibrillation.…”