Endocardial Fibrotic Lesions Have a Greater Effect on Peak Longitudinal Strain than Epicardial Fibrotic Lesions in Hypertrophic Cardiomyopathy Patients

Abstract

Peak longitudinal strain (PLS) of the left ventricular (LV) myocardium by transthoracic echocardiogram (TTE) is useful to detect LV myocardial damage. We hypothesized that myocardial fibrosis (MF) in the LV myocardium may influence PLS. Eighteen hypertrophic cardiomyopathy (HCM) patients (14 males; 58 ± 17 years old) underwent 1.5 Tesla cardiac magnetic resonance (CMR) and TTE. Patients with previous myocardial infarction were excluded. We used TTE to assess whole-layer PLS in an American Heart Association-defined 17-segment LV model. Whole-layer PLS was calculated using Echo PAC, version 113 (GE Healthcare). MF was assessed by T1-weighted CMR of the LV endocardial layer, the LV epicardial layer, or both the LV endocardial and epicardial layers for each lesion. Of the 306 segments, MF was detected in the LV endocardial layer only (13 segments), in the LV epicardial layer only (9 segments), or in both LV endocardial and epicardial layers (59 segments). PLS values were significantly lower in segments with MF affecting only the LV endocardial layer (7% ± 4%) (P < 0.05) and where MF was observed in both the LV endocardial and epicardial layers (9% ± 5%) (P = 0.001) compared with segments without MF (13% ± 7%). No significant difference in PLS values was detected between the MF segments for the LV epicardial layer only (10% ± 6%) and those without MF (13% ± 7%) (P > 0.05). In HCM patients, fibrotic lesions in the LV endocardium have a greater adverse effect on PLS than those in the LV epicardium. Our results are significant for HCM patients with fibrotic lesions within the LV endocardium.

Novel Approaches in Cardiac Imaging for Non-invasive Assessment of Left Heart Myocardial Fibrosis

“…In patients with Collagen deposition may influence myocardial function based on its localization in different muscle layers too. Funabashi et al (9) showed a greater reduction in GLS in subjects with HCM in which MF affected the endocardium compared to those with fibrotic lesions extended exclusively at the epicardium. Haland et al (10) showed that the electromechanical dispersion, defined as the time delay between the beginning of the QRS and peak longitudinal strain in the 16 ventricular segments, correlates with fibrosis in CMR and is predictive of malignant ventricular arrhythmias.…”

HCM

“…In this issue of International Heart Journal, Funabashi, et al discuss the effect of endocardial fibrotic lesions on the peak longitudinal strain of left ventricular myocardium in hypertrophic cardiomyopathy patients. 8) Based on their hypothesis that myocardial fibrosis in LV myocardium influences peak longitudinal strain, 18 HCM patients underwent CMR and echocardiographic examination to assess whole layer peak longitudinal strain. Myocardial fibrosis assessed with T1-weighted CMR was detected in the LV endocardial layer only (13 segments), in the LV epicardial layer only (9 segments), and in both the LV endocardial and epicardial layers (59 segments) of 306 segments.…”

Current Status and Challenges of NRF2 as a Potential Therapeutic Target for Diabetic Cardiomyopathy

“…[1][2][3] Eventually, the structure and function of the heart become impaired without coronary artery disease and hypertension, a disorder known as diabetic cardiomyopathy (DCM). [4][5][6][7] Although ischemic heart disease is the most frequent cause of heart failure and death in diabetic patients, DCM is increasingly recognized as a clinically relevant entity. [6][7][8][9] It is estimated that about 12% of the diabetic patients develop DCM.…”

“…[4][5][6][7] Although ischemic heart disease is the most frequent cause of heart failure and death in diabetic patients, DCM is increasingly recognized as a clinically relevant entity. [6][7][8][9] It is estimated that about 12% of the diabetic patients develop DCM. 10) The pathogenesis of DCM is predominantly related to the overgeneration of reactive oxygen species (ROS) as well as impaired antioxidant ability in diabetes mellitus.…”