Jesús G Mirelis1, Javier Sánchez-González2, Esther Zorio3, Tomas Ripoll-Vera4, Rafael Salguero-Bodes5, David Filgueiras-Rama6, Esther González-López1, María Gallego-Delgado7, Rodrigo Fernández-Jiménez8, María Jesús Soleto4, Juana Núñez4, Gonzalo Pizarro9, Javier Sanz10, Valentín Fuster11, Pablo García-Pavía1, Borja Ibáñez12. 1. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; CIBER de enfermedades CardioVasculares (CIBERCV), Spain; Departamento de Cardiología, Hospital Universitario Puerta de Hierro, Majahonda, Madrid, Spain. 2. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; Departamento de Ciencia Clínica, Philips Healthcare, Spain. 3. Departamento de Cardiología, Hospital Universitario y Politécnico La Fe, Valencia, Spain. 4. Departamento de Cardiología, Hospital de Son Llàtzer & IdISPa, Palma de Mallorca, Spain. 5. Departamento de Cardiología, Hospital Universitario 12 de Octubre, Madrid, Spain. 6. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; CIBER de enfermedades CardioVasculares (CIBERCV), Spain; Departamento de Cardiología, Hospital Universitario Clínico San Carlos, Madrid, Spain. 7. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; CIBER de enfermedades CardioVasculares (CIBERCV), Spain. 8. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; CIBER de enfermedades CardioVasculares (CIBERCV), Spain; Department of Cardiology, The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, United States. 9. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; CIBER de enfermedades CardioVasculares (CIBERCV), Spain; Departamento de Cardiología, Complejo Hospitalario Ruber Juan Bravo, Universidad Europea de Madrid, Madrid, Spain. 10. Department of Cardiology, The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, United States. 11. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; Department of Cardiology, The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, United States. 12. Área de Fisiopatología del Miocardio, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Instituto de Salud Carlos III, Madrid, Spain; CIBER de enfermedades CardioVasculares (CIBERCV), Spain; Departamento de Cardiología, IIS-Hospital Fundación Jiménez Díaz, Madrid, Spain. Electronic address: bibanez@cnic.es.
Abstract
INTRODUCTION AND OBJECTIVES: Myocardial interstitial fibrosis, a hallmark of hypertrophic cardiomyopathy (HCM), has been proposed as an arrhythmic substrate. Fibrosis is associated with increased extracellular volume (ECV), which can be quantified by computed tomography (CT). We aimed to analyze the association between CT-determined ECV and malignant ventricular arrhythmias. METHODS: A retrospective case-control observational study was conducted in HCM patients with implantable cardioverter-defibrillator, undergoing a CT-protocol with continuous iodine contrast infusion to determine equilibrium ECV. Left ventricular septal and lateral CT-determined ECV was compared between prespecified cases (malignant arrhythmia any time before CT scan) and controls (no prior malignant arrhythmias) and among ECV tertiles. RESULTS: A total of 78 implantable cardioverter-defibrillator HCM patients were included; 24 were women, with a mean age of 52.1 ± 15.6 years. Mean ECV ± standard deviation in the septal left ventricular wall and was 29.8% ± 6.3% in cases (n = 24) vs 31.9% ± 8.5% in controls (n = 54); P = .282. Mean ECV in the lateral wall was 24.5% ± 6.8% in cases vs 28.2% ± 7.4% in controls; P = .043. On comparison of the entire population according to septal ECV tertiles, no significant differences were found in the number of patients receiving appropriate shocks. Conversely, we found a trend (P = .056) for a higher number of patients receiving appropriate shocks in the lateral ECV lowest tertile. CONCLUSIONS: Extracellular volume was not increased in implantable cardioverter-defibrillator HCM patients with malignant ventricular arrhythmias vs those without arrhythmias. Our findings do not support the use of ECV (a surrogate of diffuse fibrosis) as a predictor of arrhythmias in high-risk HCM patients.
INTRODUCTION AND OBJECTIVES:Myocardial interstitial fibrosis, a hallmark of hypertrophic cardiomyopathy (HCM), has been proposed as an arrhythmic substrate. Fibrosis is associated with increased extracellular volume (ECV), which can be quantified by computed tomography (CT). We aimed to analyze the association between CT-determined ECV and malignant ventricular arrhythmias. METHODS: A retrospective case-control observational study was conducted in HCM patients with implantable cardioverter-defibrillator, undergoing a CT-protocol with continuous iodine contrast infusion to determine equilibrium ECV. Left ventricular septal and lateral CT-determined ECV was compared between prespecified cases (malignant arrhythmia any time before CT scan) and controls (no prior malignant arrhythmias) and among ECV tertiles. RESULTS: A total of 78 implantable cardioverter-defibrillator HCM patients were included; 24 were women, with a mean age of 52.1 ± 15.6 years. Mean ECV ± standard deviation in the septal left ventricular wall and was 29.8% ± 6.3% in cases (n = 24) vs 31.9% ± 8.5% in controls (n = 54); P = .282. Mean ECV in the lateral wall was 24.5% ± 6.8% in cases vs 28.2% ± 7.4% in controls; P = .043. On comparison of the entire population according to septal ECV tertiles, no significant differences were found in the number of patients receiving appropriate shocks. Conversely, we found a trend (P = .056) for a higher number of patients receiving appropriate shocks in the lateral ECV lowest tertile. CONCLUSIONS: Extracellular volume was not increased in implantable cardioverter-defibrillator HCM patients with malignant ventricular arrhythmias vs those without arrhythmias. Our findings do not support the use of ECV (a surrogate of diffuse fibrosis) as a predictor of arrhythmias in high-risk HCM patients.
Authors: Aleksandra Karabinowska-Małocha; Ewa Dziewięcka; Paweł Banyś; Małgorzata Urbańczyk-Zawadzka; Maciej Krupiński; Małgorzata Mielnik; Jacek Łach; Aleksandra Budkiewicz; Piotr Podolec; Łukasz Żydzik; Sylwia Wiśniowska-Śmiałek; Katarzyna Holcman; Magdalena Kostkiewicz; Paweł Rubiś Journal: J Pers Med Date: 2022-02-17