were analysed by the consensus of 2 experienced operators, who were unaware of clinical and follow-up data. The presence of DE was visually determined on post-contrast images. Muller et al. Prospective N=185 patients who Inclusion criteria: patients Scanner: 1.5-T scanner ICD implantation: Not described () cohort presented for evaluation of who presented for evaluation Cardiac function sequence: Outcomes: newly diagnosed NICM: of newly diagnosed NICM breath-hold steady-state and recent findings HR for likelihood of having: n=94 (51%) LGE+ (SSFP) pulse suggestive of cardiac Germany NHMRC level II n=91 (49%) LGE– sequence ICD implantation structural damage (impaired all-cause mortality global or regional LV DCM = 55% LGE sequence: 2D cardiac death function, LV enlargement, SIGN: acceptable Myocarditis = 35% segmented k-space heart transplantation HCM or hypertensive CM = increase of cardiac enzymes, gradient-echo sequence quality with a aborted SCD pericardial effusion or ECG 8% moderate risk of Contrast agent: 0.15 mmol/kg appropriate ICD discharge abnormalities) Storage disease = 2% bias gadobutrol (Gadovist) sustained VT Exclusion criteria: patients Patient characteristics: hospitalisation for HF Time delay: 10–15 minutes with history of MI or age = 51.2 ± 15.9 years; in LGE+ patients compared with those ischaemic scar on CMR as a LV function: End-diastolic that are LGE– sign of unrecognised male = 71%; volumes (EDV) and end-systolic myocardial damage due to volumes (ESV) were used to QRS interval = 103 ± CAD determine LVEF (EDV – ESV/EDV 23 milliseconds; x 100). LVEF (CMR) = 43.3 ± 16.0%; LGE diagnosis: LGE image NYHA class ≥II = 62%; analysis was conducted by 2 medications: ACE inhibitor = experienced independent 81%, ARB = 14%, -blockers investigators who visually judged = 89% the occurrence (presence vs absence), localisation and pattern Median follow-up: 21 months of LGE. Areas of LGE were
were analysed by the consensus of 2 experienced operators, who were unaware of clinical and follow-up data. The presence of DE was visually determined on post-contrast images. Muller et al. () Germany Prospective cohort NHMRC level II SIGN: acceptable quality with a moderate risk of bias N=185 patients who presented for evaluation of newly diagnosed NICM: n=94 (51%) LGE+ n=91 (49%) LGE– DCM = 55% Myocarditis = 35% HCM or hypertensive CM = 8% Storage disease = 2% Patient characteristics: age = 51.2 ± 15.9 years; male = 71%; QRS interval = 103 ± 23 milliseconds; LVEF (CMR) = 43.3 ± 16.0%; NYHA class ≥II = 62%; medications: ACE inhibitor = 81%, ARB = 14%, -blockers = 89% Median follow-up: 21 months Inclusion criteria: patients who presented for evaluation of newly diagnosed NICM and recent findings suggestive of cardiac structural damage (impaired global or regional LV function, LV enlargement, increase of cardiac enzymes, pericardial effusion or ECG abnormalities) Exclusion criteria: patients with history of MI or ischaemic scar on CMR as a sign of unrecognised myocardial damage due to CAD Scanner: 1.5-T scanner Cardiac function sequence: breath-hold steady-state (SSFP) pulse sequence LGE sequence: 2D segmented k-space gradient-echo sequence Contrast agent: 0.15 mmol/kg gadobutrol (Gadovist) Time delay: 10–15 minutes LV function: End-diastolic volumes (EDV) and end-systolic volumes (ESV) were used to determine LVEF (EDV – ESV/EDV x 100). LGE diagnosis: LGE image analysis was conducted by 2 experienced independent investigators who visually judged the occurrence (presence vs absence), localisation and pattern of LGE. Areas of LGE were ICD implantation: Not described Outcomes: HR for likelihood of having: ICD implantation all-cause mortality cardiac death heart transplantation aborted SCD appropriate ICD discharge sustained VT hospitalisation for HF in LGE+ patients compared with those that are LGE–