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The medium dose of atorvastatin over a 12-week period resulted in a significant reduction of arterial inflammation as well as various circulating biomarkers.

Background Despite the substantial overlap of obesity and metabolic disease, there is hetereogeneity with respect to cardiovascular risk. We sought to investigate preclinical differences in systolic and diastolic function in obesity, and specifically compare obese individuals with and without metabolic syndrome (MS). Methods and Results Obese individuals without cardiac disease with (OB/MS+, n=124) and without MS (OB/MS−, n=37) were compared to non-obese controls (n=29). Diastolic function was assessed by transmitral and tissue Doppler. Global longitudinal strain (LS) and time-based dyssynchrony were assessed by speckle tracking. Both Ob/MS− and OB/MS+ groups had similar ejection fraction but worse systolic mechanics as assessed by LS and dyssynchrony compared with non-obese controls. Specifically, OB/MS− had 2.5% lower LS (s.e. 0.7%, P=0.001 in multivariable-adjusted analyses) and 10.8 ms greater dyssynchrony (s.e. 3.3, P=0.002), and OB/MS+ had 1.0% lower LS (s.e. 0.3%, P<0.001) and 7.8 ms greater dyssynchrony (s.e. 1.5, P<0.001) compared with controls. Obesity was associated with impaired diastolic function regardless of MS status, as evidenced by greater left atrial diameter and left ventricular mass, though diastolic dysfunction was more pronounced in OB/MS+ compared with OB/MS− individuals. Conclusions Obesity is associated with subclinical differences in both systolic and diastolic function regardless of the presence or absence of MS, although MS appears to be associated with worse diastolic dysfunction. Compared to controls, ‘metabolically healthy’ obese had lower LS, greater dyssynchrony, and early diastolic dysfunction, supporting the notion that obesity per se may have adverse cardiovascular effects regardless of metabolic disease.

In Taiwan, the incidence of non-ST segment elevation acute coronary syndrome (NSTE-ACS) continues to increase in recent years. The purpose of this guideline is to help health care professionals in Taiwan to use adequate tests and treatments for management of NSTE-ACS. For rapid diagnosis, in addition to history and physical examination, 0/3 h rapid diagnosis protocol with high sensitivity cardiac troponin assay is recommended in this guideline. Dual antiplatelet and anticoagulation therapies are important parts in the initial treatment. Risk stratification should be performed to identify high risk patients for early coronary angiography. Through evaluation of the coronary anatomy and other clinical factors, the decision for coronary revascularization, either by percutaneous coronary intervention or coronary artery bypass grafting, should be decided by the heart team. The duration of dual antiplatelet therapy should be given for at least 12 months after discharge. Other secondary preventive medications are also recommended for long term use.

BackgroundMetabolic disease can lead to intrinsic pulmonary hypertension in experimental models. The contributions of metabolic syndrome (MetS) and obesity to pulmonary hypertension and right ventricular dysfunction in humans remain unclear. We investigated the association of MetS and obesity with right ventricular structure and function in patients without cardiovascular disease.Methods and ResultsA total of 156 patients with MetS (mean age 44 years, 71% women, mean body mass index 40 kg/m2), 45 similarly obese persons without MetS, and 45 nonobese controls underwent echocardiography, including pulsed wave Doppler measurement of pulmonary artery acceleration time (PAAT) and ejection time. Pulmonary artery systolic pressure was estimated from PAAT using validated equations. MetS was associated with lower tricuspid valve e′ (right ventricular diastolic function parameter), shorter PAAT, shorter ejection time, and larger pulmonary artery diameter compared with controls (P<0.05 for all). Estimated pulmonary artery systolic pressure based on PAAT was 42±12 mm Hg in participants with MetS compared with 32±9 and 32±10 mm Hg in obese and nonobese controls (P for ANOVA <0.0001). After adjustment for age, sex, hypertension, diabetes, body mass index, and triglycerides, MetS remained associated with a 20‐ms–shorter PAAT (β=−20.4, SE=6.5, P=0.002 versus obese). This association persisted after accounting for left ventricular structure and function and after exclusion of participants with obstructive sleep apnea.ConclusionsMetS is associated with abnormal right ventricular and pulmonary artery hemodynamics, as shown by shorter PAAT and subclinical right ventricular diastolic dysfunction. Estimated pulmonary artery systolic pressures are higher in MetS and preclinical metabolic heart disease and raise the possibility that pulmonary hypertension contributes to the pathophysiology of metabolic heart disease.

Octogenarian patients who developed STEMI tended to have multivessel disease. These patients had a high inhospital mortality rate that was most likely to be due to cardiogenic shock.

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BackgroundPatients with drug-refractory atrial fibrillation (AF) and pre-existing left atrial appendage occluder (LAAO) device may need pulmonary vein isolation (PVI). In this pioneer study, we investigated the impact of pre-existing LAAO on AF substrates and outcomes of PVI.MethodsFrom our AF registry, 65 drug-refractory patients with LAAO (72.1±11.4 years old; CHA2DS2-VASc score 3.7±2.1) were included for PVI. A balanced control group with 124 patients without LAAO receiving PVI (70.9±10.2 years old, CHA2DS2-VASc 3.6±1.9) were included for comparison.ResultsWe found PVI is feasible in patients with AF with pre-existing LAAO without new peridevice leak. Two patients with LAAO and one without LAAO had stroke during the procedure (2/65 vs 1/124, p=0.272). Complete isolation of left-sided PVs might not be achieved if the device covered the ridge joining the left atrial (LA) appendage to the body of LA. Local electrogram could be detected over LAAO and there was propagation of conduction over the occluder either under sinus rhythm or under atrial arrhythmia. LAAO might modulate LA substrate and induce peridevice fibrosis, peridevice LA flutter and complex fractionate atrial electrogram. The AF recurrent rate at 1 year was similar between the two groups (9.2% vs 8.8%).ConclusionsThis pioneer study first showed impacts of LAAO on LA substrate and PVI procedure.