Key result
The presence of late gadolinium enhancement in non-ischaemic dilated cardiomyopathy was associated with increased left ventricular end-diastolic wall stress (4.5 vs 3.6 kPa, P=0.025).
Why the study?
Is the occurrence of late gadolinium enhancement associated with increased left ventricular wall stress and mass in patients with suspected non-ischaemic dilated cardiomyopathy?
Observational (n=300)
Is the occurrence of late gadolinium enhancement associated with increased left ventricular wall stress and mass in patients with suspected non-ischaemic dilated cardiomyopathy?
The presence of late gadolinium enhancement on CMR in non-ischaemic dilated cardiomyopathy is associated with increased left ventricular wall stress and mass, suggesting a link between mechanical stretch and myocardial tissue changes.
LGE presence may mark higher wall stress in non-ischaemic DCM; leaves open prognostic value and need for longitudinal confirmation.
AIMS: Occurrence of late gadolinium enhancement (LGE) as assessed by cardiac magnetic resonance (CMR) imaging has been attributed to various myocardial injuries. We hypothesized that LGE is associated with left ventricular (LV) wall stress. METHODS AND RESULTS: We examined 300 patients with suspected non-ischaemic dilated cardiomyopathy. Cardiac magnetic resonance was used to assess LV volume, mass, wall stress, and LGE. Increased LV end-diastolic wall stress (> 4 kPa) was found in 112 patients (37 %), and increased end-systolic wall stress (>18 kPa) in 121 patients (40%). Presence of LGE was observed in 93 patients (31%). End-diastolic (94 ± 43 vs. 79 ± 42 ml/m(2), P = 0.006) and end-systolic LV volumes (62 ± 44 vs. 44 ± 37 ml/m(2), P < 0.001) and LV mass (95 ± 34 vs. 78 ± 31 g/m(2), P < 0.001) were increased in patients exhibiting LGE. In particular, LV end-diastolic and end-systolic wall stress were increased (4.5 ± 2.8 vs. 3.6 ± 3.0 kPa, P = 0.025; 19.6 ± 9.1 vs. 17.5 ± 8.2 kPa, P = 0.045). Late gadolinium enhancement was observed more frequently than would be expected from random occurrence in patients with increased end-diastolic (39 vs. 26%, P = 0.020) and end-systolic wall stress (41 vs. 24%, P = 0.002). Both normal end-diastolic and end-systolic wall stress had a high negative predictive value for LGE (75 and 76%). CONCLUSIONS: The present study shows that occurrence of LGE in cardiomyopathy is associated with increased LV wall stress and mass. Suspected causes are an increased capillary leakage by stretch, impaired contrast agent redistribution, or increased diffusion distances. It is proposed that LGE should be considered as a potential prognostic determinant of heart failure and severe arrhythmias.
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Alter et al. (2011) conducted an observational in suspected non-ischaemic dilated cardiomyopathy (n=300). Presence of late gadolinium enhancement (LGE) vs. Absence of LGE was evaluated on Left ventricular end-diastolic wall stress (kPa) (p=0.025). The presence of late gadolinium enhancement in non-ischaemic dilated cardiomyopathy was associated with increased left ventricular end-diastolic wall stress (4.5 vs 3.6 kPa, P=0.025).
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