We have tried to explore the energy loss (EL) within the left ventricle in hypertension by using vector flow mapping (VFM) to detect left ventricular hemodynamic changes in hypertensive patients as early as possible and reflect changes of left ventricular function in hypertension by using EL. Twenty-one hypertensive patients with increased left ventricle mass index (LVMI), 14 hypertensive patients with normal LVMI and 22 control subjects were enrolled in this study. Systolic and diastolic EL derived from VFM within the left ventricle and E/e' by dual Doppler were recorded and analyzed. Compared with those of the controls, diastolic and systolic EL were significantly increased in hypertensive group (P<0.05). In diastole, EL=0.439×SBP (systolic blood pressure)–8.349; in systole, EL=0.385×SBP+0.644×LVMI–10.854. And the EL was positively correlated with E/e', but there was no significant correlation between EL and ejection fraction (EF) in the pooled population. The study shows that the increased EL can help us detect changes of left ventricular hemodynamic in hypertensive patients. It needs further investigation to prove whether EL within the left ventricle could be a new parameter to evaluate diastolic function. SBP and LVMI are the independent predictors for systolic EL, while SBP is the independent predictor for diastolic EL.
We tried to explore the value of contrast echocardiography (CEcho) on evaluating hypertrophic cardiomyopathy (HCM) with the inferior wall hypertrophy. A total of 114 patients with HCM were investigated. All the patients received CEcho and routine echocardiography (Echo), and 45 of them received cardiac magnetic resonance (CMR) and 47 of them received Holter. The frequency and percentage of inferior wall hypertrophy were analyzed in HCM patients, as well as the structure and function. The results showed that: (1) Inferior wall hypertrophy was detected in 55 patients (48%) by Echo, while 68 patients (60%) by CEcho. (2) There was no significant difference between CMR and CEcho in the measurement of inferior wall at end-diastole and end-systole. Thickness of inferior wall by CEcho tended to be higher than CMR. However, the inferior wall thickness measured by Echo was obviously lower than that by CMR (P < 0.05) and CEcho ( P < 0.05). (3) Bland-Altman plot suggested good consistency between CEcho and CMR in measuring inferior wall thickness. 95% CI of mean differences in inferior wall thickness between CEcho and CMR were smaller in HCM patients as compared with that between Echo and CMR. Unary linear regression analysis showed good degree of fitting between CEcho and CMR. (4) Holter showed that HCM patients with inferior wall hypertrophy were likely to have higher incidence of premature ventricular complexes (PVC) ≥ 500/24 h. We demonstrate that CEcho is rather sensitive in detecting inferior wall hypertrophy. Echo may underestimate the inferior wall thickness. The risk of ventricular premature beats may increase in HCM patients with inferior hypertrophy.