Figure 1
(A) Representative ECG of the same animal at baseline and after induction of the model showing p wave enlargement and QRS widening associated to a certain degree of intraventricular conduction defect. (B) Experimental preparation: electrodes connected to the CRT device used to pace the right atrium (1), the right ventricle (2), and the left ventricular endocardium (ENDO) or epicardium (EPI), respectively (3). Below, all raw physiological signals registered during the study. (C) Microphotograph (at 20× magnification) of a myocardial sample from a non-ischaemic cardiomyopathic heart stained with Masson’s trichrome showing extensive loss of myofibrils, vacuolated appearance of the sarcoplasm, hypertrophy of remaining cardiomyocytes and myocardial fibrosis. RV, right ventricle; LVP, left ventricular pressure; RVP, right ventricular pressure; ABF, aortic blood flow.

(A) Representative ECG of the same animal at baseline and after induction of the model showing p wave enlargement and QRS widening associated to a certain degree of intraventricular conduction defect. (B) Experimental preparation: electrodes connected to the CRT device used to pace the right atrium (1), the right ventricle (2), and the left ventricular endocardium (ENDO) or epicardium (EPI), respectively (3). Below, all raw physiological signals registered during the study. (C) Microphotograph (at 20× magnification) of a myocardial sample from a non-ischaemic cardiomyopathic heart stained with Masson’s trichrome showing extensive loss of myofibrils, vacuolated appearance of the sarcoplasm, hypertrophy of remaining cardiomyocytes and myocardial fibrosis. RV, right ventricle; LVP, left ventricular pressure; RVP, right ventricular pressure; ABF, aortic blood flow.

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