The scar: the wind in the perfect storm—insights into the mysterious living tissue originating ventricular arrhythmias

Fig. 1. A Left ventricular endomyocardial biopsy from a patient with idiopathic dilated cardiomyopathy. Increased interstitial fibrosis (blue staining) and cardiomyocytes with severe reduction of myofibrillar content is evident (red-stained cells with vacuolization of cytoplasm). Masson trichrome staining, 200 × magnification. B Right ventricular endomyocardial biopsy from patient with ARVD. Cardiomyocytes are bordered by a huge area of fibrofatty replacement haematoxylin and eosin staining, 200 × magnification. C Left ventricular endomyocardial biopsy from a patient with hypertrophic cardiomyopathy. Replacement fibrosis (blue staining) interrupting cardiomyocytes in short runs. Masson trichrome staining, 200 × magnification. D Left ventricular endomyocardial biopsy from a patient with sarcoidosis. Inflammatory infiltration with the evidence of a multinucleated giant cell with arcuate arrangement of nuclei (Langhans type). Hematoxylin and eosin, 200 × magnification

Fig. 2. Electrophysiological mechanisms responsible of initiation and maintenance of re-entrant VT. A If the activation wavefront propagates from a source region with a relatively small volume and the tissue going forward, the sink is substantially larger in volume; the propagation will slow and even block because of the insufficiency of available current from the source to activate the larger-volume sink. Conduction is possible in the opposite direction because of the favourable sink to source relationship, allowing reentry to occur. B In non-uniform anisotropic propagation typical of scarred tissue, block can occur in regions of abrupt change in fibres orientation relative to the direction of propagation. C The wavefront generated by the ectopic beat finds the tissue with longer refractoriness still refractory and blocks. Hence, the wavefront is forced around the site of block and eventually invades the tissue retrogradely, when it has recovered its excitability. Arrows indicate direction of wavefront propagation; red dots indicate conduction of block sites

Fig. 3. Examples of LGE pattern. A Ischemic LGE pattern, mainly transmural, involving apex and apical cap, anterior and inferior wall at the mid segment; B sub-endocardial LGE (< 50%) at the lateral wall, note the LGE involving the postero-medial papillary muscle; C diffuse sub-endocardial LGE in patient with cardiac amyloid; D sub-epicardial LGE involving lateral and inferior wall in a patient with myocarditis; E non-ischemic LGE in the area of maximal hypertrophy in a patient with apical hypertrophic cardiomyopathy (HCM); F patchy areas of LGE at the septum at the right ventricle insertion points in patients with HCM; G non-ischemic LGE involving the inferior wall (sub-epicardial) and the septum (midwall) in a patient with dilated cardiomyopathy; H non-ischemic LGE involving the infero-lateral wall and the RV free wall in a young patient with arrhythmogenic cardiomyopathy with involvement of both ventricles