Occurrence of late gadolinium enhancement is associated with increased left ventricular wall stress and mass in patients with non‐ischaemic dilated cardiomyopathy

Abstract

AimsOccurrence 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 resultsWe 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 ¼ 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 ¼ 0.025; 19.6 + 9.1 vs. 17.5 + 8.2 kPa, P ¼ 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 ¼ 0.020) and end-systolic wall stress (41 vs. 24%, P ¼ 0.002). Both normal end-diastolic and end-systolic wall stress had a high negative predictive value for LGE (75 and 76%). ConclusionsThe 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.--

Diabetic cardiomyopathy—fact or fiction?

“…Since LV mass and volume predominantly determine ventricular wall stress [7,8], it appears that wall stress is a prognostic predictor in cardiomyopathy. As recently shown, increased end-diastolic wall stress amplifies ventricular hypertrophy, which can initiate a vicious cycle [4,9]. Thus, the prognostic value of LV wall stress should also be examined in DCM.…”

“…We recently examined 300 patients in whom the occurrence of LGE was related to increased LV wall stress and mass [4,6,7]. We suggested that stretch at the cellular level facilitates increased contrast agent distribution and its prolonged myocardial deposition.…”

From Heart Failure to Highly Unsaturated Fatty Acid Deficiency and Vice Versa: Bidirectional Heart and Liver Interactions

“…To obtain LV volumes (end-diastolic volume [LVEDV], and end-systolic volume [LVESV]), function (ejection fraction [LVEF]) and myocardial mass, a stack of short-axis views of the left ventricle from base to apex was acquired using electrocardiogram-gated steady-state free precession sequences (TrueFISP). 15,16 Wall stress was calculated using a thick-walled sphere model of the left ventricle. 12,17 The method was primarily derived from the law of LaPlace, but allows wall stress calculation for arbitrary wall diameters.…”

“…15,16,35 Increased wall stress precedes the development of LV hypertrophy. Type and extent of LV hypertrophy appear to be crucial prognostic determinants.…”

Replacement of Reduced Highly Unsaturated Fatty Acids (HUFA Deficiency) in Dilative Heart Failure: Dosage of EPA/DHA and Variability of Adverse Peroxides and Aldehydes in Dietary Supplement Fish Oils

“…On similar lines, we have shown in experimental animals that ω-3 fatty acids attenuate left ventricular (LV) dilatation, which is a major cause of heart failure progression [5] particularly when wall stress is increased [6,7,8]. Since the amount of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) administered was much higher than the daily 840 mg EPA/DHA used in post-myocardial infarction patients [9], the dose for patients with dilative heart failure remains unclear.…”