Objectives:Myocardial work is estimated from noninvasive pressure-strain loop for advanced assessment of left ventricular function. Postsystolic shortening and diastolic dyssynchrony of left ventricle were noted early in hypertension. Their novel effects on myocardial work will be illustrated in this study.Methods:We recruited 43 newly diagnosed hypertensive patients (mean age 51.3 ± 12.5 years, 55.8% men) and 32 age-matched and sex-matched healthy individuals (mean age 52.7 ± 10.5 years, 37.5% men) as control. Pressure-strain loop derived myocardial work incorporated global longitudinal strain from speckle tracking echocardiography with brachial artery cuff pressure. Postsystolic strain index (PSI) was defined by the percentage of postsystolic shortening over peak strain. Diastolic dyssynchrony was assessed by standard deviation of time to peak early diastolic strain rate (TDSr-SD) of 18 segments, and maximal difference of time to peak early diastolic strain rate (TDSr-MD) between any two segments.Results:After multivariate regression analysis, global myocardial work index (GWI) was independently correlated with TDSr-SD (B = −0.498, P = 0.001) and TDSr-MD (B = −0.513, P = 0.001). Global myocardial constructive work (GCW) was independently correlated with TDSr-SD (B = −0.334, P = 0.025) and TDSr-MD (B = −0.397, P = 0.007). Global myocardial wasted work (GWW) was independently correlated with PSI (B = 0.358, P = 0.019). Global myocardial work efficiency (GWE) was lower in hypertensive patients than healthy control (P = 0.001). The untreated hypertensive patients were different from the healthy individuals with higher TDSr-SD, TDSr-MD, GWI, GCW, GWW, and PSI (all P < 0.05).Conclusion:In conclusion, the effect of diastolic dyssynchrony mainly influenced constructive work, whereas postsystolic shortening affected wasted work in early untreated hypertension.
Background: Moderate to severe tricuspid regurgitation (TR) is known to cause right ventricular (RV) failure and death. Although TR is traditionally classified as primary or secondary, recently, a new class of TR called idiopathic TR has been proposed, with varying definitions among different studies. Methods: The data were retrospectively collected for the period of January to June 2018 for 8711 patients from the patient cohort of the National Cheng Kung University Hospital echocardiography laboratory. A total of 670 patients (7.7%) with moderate-tosevere TR were included. Idiopathic TR was diagnosed strictly using a new systematic approach. Results: The distribution of significant TR included 74 (11.0%) primary TR cases, 48 (7.2%) with pacemaker-related TR, 267 (39.9%) with left heart disease, 24 (3.6%) with congenital heart disease, 6 (0.9%) with RV myopathy, 105 (15.7%) with pulmonary hypertension, and 146 (21.8%) with idiopathic TR. The mean age in primary and idiopathic TR groups was older (p = 0.004), with lower estimated pulmonary pressure (p < 0.001), higher RV fraction area change (FAC, p < 0.001), and tricuspid annulus systolic velocity (S', p = 0.004) compared with functional TR group. Multivariate analysis showed that idiopathic TR (p = 0.002) and primary TR (p = 0.008) had better RV FAC than functional TR. Conclusion: Idiopathic TR was associated with better RV function than the other secondary TRs. Thus, idiopathic TR should be strictly defined and regarded as a distinct type of TR.
Background: The efficacy, safety, and clinical outcomes for patients switch to generic rosuvastatin, compared with patients taking other brand-name atorvastatin, is unclear. Method: We retrospectively collected electronic medical records from January 1, 2013, to December 31, 2020, of patients who switched medication, because of hospital policy, from brand-name to generic rosuvastatin after March 14, 2018. we only considered patients who had taken the medication at least 1 year prior to and 1 year after that date. We also collected records of patients who consistently used brand-name atorvastatin during the same period. The efficacy of lipid control, potential adverse effects, clinical outcomes of major cardiovascular events (MACE), and medical expenses were compared between the 2 groups. Propensity score matching (PSM) was conducted to balance potential cofounders. Result: After 1:1 PSM, 592 patients were enrolled in the rosuvastatin and atorvastatin groups, and no significant difference was observed in their total cholesterol (TC) level difference (−4.38 ± 23.0 vs. −3.72 ± 26.95 mg/dL, P = 0.702), low-density lipoprotein (LDL-C) (−2.38 ± 19.89 vs. −2.42 ± 23.63 mg/dL, P = 0.976), or glycated hemoglobin (−0.05% ± 0.7% vs. −0.08% ± 0.76%, P = 0.543). No significant differences were noted in their cumulative MACE (2.70% vs. 3.89%, log-rank P = 0.265) after the switch date, and each person in the generic group had a 16% average reduction in their medical expenses. Conclusion: Switching to generic rosuvastatin led to comparable lipid-lowering efficacy, safety, and clinical outcomes and fewer medical expenses compared with consistently using brand-name atorvastatin.
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