Emerging concepts in heart failure management and treatment: focus on tachycardia-induced cardiomyopathy

Abstract

Tachycardia-induced cardiomyopathy is an entity characterized by reversible dysfunction of the left ventricle, which can be induced by different types of arrhythmia such as atrial fibrillation, atrial flutter, incessant supraventricular tachycardia and ventricular arrhythmia (more frequent causes). Correct identification of the causative arrhythmia and normalization of the heart rate (e.g through medical treatment, electrical cardioversion, ablation) can lead to recovery of left ventricular function. Tachycardia-induced cardiomyopathy should be suspected in patients with tachycardia and left ventricular dysfunction (heart failure setting), especially when there is no history of previous heart disease. Its usual phenotype is that of non-ischaemic/non-valvular dilated cardiomyopathy and it can occur in both children (main cause: permanent junctional reciprocating tachycardia) and adults (main cause: atrial fibrillation). With proper treatment, most cases recover within a few months, though there is a risk of relapse, especially when the causal arrhythmia reappears or its control is lost. This is a narrative review that comprehensively addresses the pathophysiology, clinical manifestations, and therapeutic management of tachycardia-induced cardiomyopathy. This article is part of the Emerging concepts in heart failure management and treatment Special Issue: https://www.drugsincontext.com/special_issues/emerging-concepts-in-heart-failure-management-and-treatment

Cardiomyopathies

“…Assessment of global longitudinal strain (GLS) is a more sensitive method for assessing left ventricular contractility 10 . In the case of involvement of the right heart, pulmonary hypertension also occurs, so an analysis of the dimensions of the right cavities, tricuspid valve, and GLS of the right ventricle is recommended [10][11][12] .…”

“…Hypertrophic cardiomyopathy (HCM) is a disease of the heart muscle caused in 60-70% of cases by mutation of genes responsible for the properties of the sarcomere and contractile apparatus of the heart. Genes that affect it are: cardiac troponin T -TNNT2 gene, cardiac troponin I -TNNI3 gene, regulatory myosin light chain -MYL2 gene, essential myosin light chain -MYL3 gene, cardiac myosin binding protein -C-MYBPC3 gene, cardiac beta myosin heavy chain -MIH7 gene, alpha cardiac actin -ACTC1 gene, tropomyosin 1 -TPM1 gene, cardiac troponin C -TNNC1 gene, junctophilin 2 -JPH2 gene, cysteine-glycine-rich protein 3 -CSRP3 gene, alpha galactosidase gene -GLA gene (Anderson-Fabry disease), genes related to the RAS MAP kinase pathway (Noonan syndrome), muscle LIM protein gene -MLP gene, gene encoding gamma 2 -regulatory subunit adenosine monophosphate will activate protein kinase -PRKAG2 gene and gene for encoding protein membrane that binds to lysosome 2 -LAMP2 gene 12 .…”

“…Left ventricular hypertrophy is the main feature of HCM. Analysis of the existence of hypertrophy or obstruction of the outflow tract of the left ventricle, diastolic function, the existence of ischemic heart disease, and the status of the mitral valve is essential 12 . The most common symptoms are rapid fatigue, dyspnea, anginal complaints, palpitations, presyncope, or syncope.…”

“…RCM has distinct morphologic and hemodynamic features that separate it from DCM and HCM: nondilated ventricle with normal wall thickness, stiff ventricular walls resulting in severe diastolic dysfunction and a restrictive filling pattern with elevated filling pressures, dilated atrium, and normal left ventricular systolic function. Idiopathic or primary RCM is a disorder manifested by the characteristic, above-mentioned morphological and physiological changes without the existence of any identified cause 12 . The cause may be unknown, and may be sought in sarcoma protein mutations, troponin I and essential myosin light chain gene mutation, in the presence of familial amyloidosis, transthyretin and apolipoprotein mutation, desminopathies, hemochromatosis, Anderson-Fabry disease, glycogen storage disease, scleroderma, endomyocardial fibrosis, hypereosinophilic syndrome, radiation (radiation-induced heart disease), chemotherapy, carcinoid heart disease, and metastatic disease 14 .…”

“…Although not pathognomonic, features of restrictive cardiomyopathy are reduced velocity, tissue Doppler analysis across the mitral valve (septal e' < 7 cm/sec, lateral e' < 10 cm/sec, E/e' > 14), and increased left atrial volume. In RCM, wall thickness is usually normal, although it can be increased by certain infiltrative processes (amyloidosis) or storage diseases (Anderson-Fabry disease) 5,12 . The use of brain natriuretic peptide (BNP) is important because it can help distinguish RM from constrictive pericarditis and noncardiac causes of dyspnea.…”