Author + information
- ↵⁎Internal Medicine Cardiology, Philipps University, Baldingerstrasse, 35033 Marburg, Germany
Current criteria indicating implantable cardioverter-defibrillator (ICD) therapy for primary prevention of sudden cardiac death are poor, and non–evidence-based ICD implantations are more likely to have worse outcomes. Therefore, Iles et al. (1) examined late gadolinium enhancement (LGE) by using cardiac magnetic resonance imaging to predict appropriate device therapy in patients with ischemic and nonischemic cardiomyopathy. The study relies on the assumptions that myocardial fibrosis is the substrate of LGE and that fibrosis is associated with arrhythmias.
Well-documented links between fibrosis and LGE exist in patients who have experienced myocardial infarction in whom nonviable cardiomyocytes are replaced by collagen. This contiguous subendocardial or transmural area can be detected by a bright LGE pattern. Histological changes are very different in patients with dilative cardiomyopathies. Histopathological studies have shown that the myocardial remodeling can be associated with an increased collagen volume fraction, and in transmural left ventricular sections, the extent of fibrosis increased from epicardium to endocardium and from the right to the left side of the septum (2). LGE occurs as midwall (septal) streak (1) or is irregularly diffuse. Thus, in dilative cardiomyopathies, causes beyond fibrosis should be taken into account for LGE.
In the study by Iles et al. (1), all patients with ischemic cardiomyopathy exhibited LGE, and the ICD discharge rate was 14%, whereas it was 29% in patients with nonischemic cardiomyopathy and LGE. Also, based on the absence of differences in left ventricular ejection fraction and end-diastolic volume index, it was concluded that fibrosis predicts appropriate ICD therapy. However, it remains to be assessed whether indeed fibrosis or an increased wall stress was responsible for LGE and ICD therapy. Using echocardiography-based ventricular mass and geometry data, we suggest calculating wall stress and examining the contention that patients with ICD therapy exhibit increased wall stress.
In accordance with a role of wall stress for LGE, our recent study on 300 patients with dilative cardiomyopathy showed that a rise in wall stress (3) was associated with LGE (4). Most likely, higher wall stress is associated with an increased capillary leakage, and thus favors contrast medium emission into the interstitial space. Also, its venous clearance can be prolonged by an impaired redistribution. The link of LGE with arrhythmias would follow from experimental studies in which myocardial stretch and neurohumoral reactions predispose patients to arrhythmias involving, for example, stretch-activated cation channels.
The proposed subanalysis also could clarify whether LGE per se is an independent prognostic predictor or a dependent surrogate marker. Thus, in a study of 141 patients with dilated cardiomyopathy, the prognostic value of LGE regarding survival was found only by univariate, but not by multivariate, analysis (5). Increased wall stress thus could be the underlying mechanism of a worse prognosis and should be evaluated also as indicator for ICD therapy.
- American College of Cardiology Foundation
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