scholarly journals Importance of regurgitant fraction for left ventricular end-systolic wall stress to end-systolic volume ratio in patients with chronic mitral regurgitation.

1988 ◽  
Vol 52 (5) ◽  
pp. 426-430
Author(s):  
MICHIAKI EJIRI ◽  
SHIGETAKE SASAYAMA ◽  
MASATOSHI FUJITA ◽  
SHIGERU YOKAWA
Keyword(s):  
Mitral Regurgitation ◽  
Volume Ratio ◽  
Wall Stress ◽  
Left Ventricular ◽  
Regurgitant Fraction ◽  
Systolic Volume ◽  
End Systolic Volume ◽  
Systolic Wall Stress

scholarly journals Genetic relevance and determinants of mitral leaflet size in hypertrophic cardiomyopathy

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Hyemoon Chung ◽  
Yoonjung Kim ◽  
Chul-Hwan Park ◽  
Jong-Youn Kim ◽  
Pil-Ki Min ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Nuclear Dna ◽  
Wall Stress ◽  
Left Ventricular ◽  
Mitral Leaflet ◽  
Systolic Volume ◽  
Left Atrial Wall ◽  
Lv Mass ◽  
End Systolic Volume ◽  
Sarcomeric Genes

Abstract Background Whether mitral leaflet elongation is a primary phenotype of hypertrophic cardiomyopathy (HCM) is controversial. We investigated the genetic relevance and determinants of mitral leaflet size by performing extensive gene analyses in patients with HCM. Methods Anterior mitral leaflet (AML) lengths were measured in HCM patients (n = 211) and age- and sex-matched controls (n = 30) using echocardiography with hemodynamic and chamber geometric assessments. We analyzed 82 nuclear DNA (8 sarcomeric genes, 74 other HCM-associated genes) and mitochondrial DNA. Cardiac magnetic resonance imaging (CMR) was performed in the 132 HCM patients. Results Average indexed AML was significantly longer for HCM than for controls (17.2 ± 2.3 vs. 13.3 ± 1.6 mm/m2, P <  0.001). Average AML length correlated with body surface area (BSA), left ventricular (LV) end-systolic volume (P <  0.001) and LV mass by CMR (P < 0.001). Average indexed AML by BSA of pure-apical HCM was significantly shorter than other typed HCM (16.6 ± 2.0 vs. 17.4 ± 2.4 mm/m2, P = 0.025). Indexed AML was independently correlated with left atrial wall stress. The thin filament mutation group showed larger average AML (31.9 ± 3.8 vs. 29.6 ± 3.8 mm, P = 0.045), but this was not significant with the indexed value. No difference in AML size among subgroups was observed based on the presence of sarcomere protein or mitochondria-related gene variants (P > 0.05). Conclusion AML elongation was a unique finding of HCM. However, the leaflet size was more related to chamber geometry and hypertrophy pattern rather than genetic factors within overt HCM.

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