Measurement of myocardial native T1 in cardiovascular diseases and norm in 1291 subjects

Table 3 Sample size calculation using native ShMOLLI T1-mapping for clinical studies and trials, arranged according to Cohen’s d effect size (largest to smallest)

	Departure of focally abnormal myocardium from reference myocardium (within subjects)		Departure of reference myocardium from healthy myocardium [19] (between groups)
	Cohen-d	Paired, n>	Cohen-d	Unpaired, n>
Patients with normal CMR	N/A	N/A	0.14	1604
Cardiac Amyloidosis (AL)	4.58	2	–	–
Cardiac Amyloidosis (ATTR)	3.91	4	1.28	9
Aortic Stenosis	3.39	6	0.68	146
Takotsubo Cardiomyopathy	3.33	6	1.06	32
Dilated Cardiomyopathy	3.09	6	0.56	104
Pheochromocytoma	3.02	6	0.09	3880
Myocarditis (acute)	2.92	6	0.52	120
Obesity	2.81	8	0.21	716
Hypertension	2.36	8	0.57	100
Myocarditis(previous)	2.30	10	0.0	N/A
Cardiac Sarcoidosis	2.28	10	0.0	N/A
Cardiac Iron-Overload^a	2.06	10	13.30	4
Chronic CAD	2.06	10	0.47	146
Hypertrophic Cardiomyopathy	1.59	16	0.15	1398
Atrial Fibrillation^a	1.47	18	0.29	376
Anderson-Fabry Disease^a	0.82	50	2.81	8

All abbreviations are as per Tables 1 and 2. Focally abnormal myocardium: myocardium affected by either late gadolinium enhancement (LGE) or by regional wall motion abnormalities (RWMA) defined as severe hypokinesia, akinesia or dyskinesia on cines in patients with Takotsubo cardiomyopathy. Reference myocardium: myocardium not affected by RMWA or LGE. ^aindicates material from extended analysis period included to address peer review

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