Exaggerated myocardial torsion may contribute to dynamic left ventricular outflow tract obstruction in hypertrophic cardiomyopathy

Abstract

Background Dynamic left ventricular (LV) outflow tract obstruction (LVOTO) is associated with symptoms and increased risk of developing heart failure in hypertrophic cardiomyopathy (HCM). The association of LVOTO and LV twist mechanics has not been well studied in HCM. Aim To compare the pattern of LV twist in patients with HCM associated with asymmetrical septal hypertrophy with and without LVOTO. Methods Echocardiography (including speckle tracking) was performed in 212 patients with HCM, divided according to the absence (n = 130) or presence (n = 82) of LVOTO (defined as peak pressure gradient ≥30 mmHg either at rest and/or with Valsalva manoeuvre). Results Patients with LVOTO were older, had smaller LV dimensions, higher LV ejection fraction (LVEF), longer anterior mitral valve leaflet length, and higher early transmitral pulsed-wave to septal tissue Doppler velocity ratio (E/E’). On univariate analysis, peak twist was significantly higher in patients with LVOTO compared to patients without LVOTO (19.7 ± 7.3 vs 15.7 ± 6.0, p = 0.00015). Peak twist was similarly enhanced in patients with LVOTO manifesting only during Valsalva (19.2 ± 5.6, P = 0.007) and patients with resting LVOTO (19.9 ± 8.0, P = 0.00004) compared to patients without LVOTO (15.7 ± 6.0). Using stepwise forward logistic regression, LVEF, LV end-systolic dimension indexed to body surface area, anterior mitral valve leaflet length, E/E’ and peak twist were independently associated with LVOTO. Conclusion This study demonstrates that increased peak LV twist is independently associated with LVOTO in patients with HCM. Peak twist was similarly exaggerated in patients with only latent LVOTO suggesting it may play a contributory role to LVOTO in HCM.

Exploring the Potential of Proteome Analysis as a Promising Tool for Evaluation of Sudden Cardiac Death (SCD) in Forensic Settings: A Literature Review

“…The causes of SCD can be diverse. Among these, we cite structural causes such as cardiac remodeling, which arises in various heart diseases such as hypertrophic cardiomyopathy, dilated cardiomyopathy, and chronic heart failure [ 17 , 18 ] ( Figure 1 ). There are also coronary-related causes that include coronary spasm, atherosclerosis up to ischemia, and myocardial infarction.…”