The Sequential Change in Left Ventricular Function among Various Cardiovascular Diseases: A 12-Year Study.

Background: This 12-year study aimed to compare the longitudinal change in left ventricular diastolic dysfunction (LVDD) between healthy elderly, coronary artery disease (CAD), and hypertension (HTN) patients. Methods: From 2008 to 2020, 1476 patients were included, and 3181 echocardiography examinations were conducted. Finally, 130 participants (36 healthy elderly (79.39 ± 9.51 years old), 51 with CAD (68.31 ± 12.09 years old), and 43 with HTN (68.31 ± 12.09 years old)) with more than a 10-year follow-up period were included in the final analysis. Results: The change in diastolic function was different among these subjects according to the integrated score index (elderly vs. HTN, p = 0.01; CAD vs. HTN, p = 0.01), septal E/e' ratio (elderly vs. HTN, p < 0.001; CAD vs. HTN, p = 0.01), lateral E/e' ratio (elderly vs. HTN, p < 0.001; CAD vs. HTN, p < 0.001), and NYHA functional class (elderly vs. HTN, p = 0.03; CAD vs. HTN, p < 0.001). Additionally, per one-year increase in age, the integrated score index increased 0.2 in the healthy elderly, 0.15 in the CAD, and 0.06 in the HTN patients (all p < 0.05). Conclusion: Under aggressive treatment, diastolic function was relatively preserved in HTN subjects with aging in comparison with elderly and CAD subjects.

Association between Exosomal miRNAs and Coronary Artery Disease by Next-Generation Sequencing.

BACKGROUND: Among various bio-informative molecules transferred by exosomes between cells, micro RNAs (miRNAs), which remain remarkably stable even after freeze-and-thaw cycles, are excellent candidates for potential biomarkers for coronary artery disease (CAD). METHODS: Blood samples were collected from the coronary arteries of 214 patients diagnosed with three-vessel CAD and 140 without CAD. After precipitation extraction, the amounts of exosomes were found to decrease with increased age and three-vessel CAD. Next-generation sequencing was performed to further explore the possible relationship between exosomal miRNAs and CAD. RESULTS: Eight exosomal miRNAs showed altered expression associated with CAD. The up-regulated miRNAs in CAD were miRNA-382-3p, miRNA-432-5p, miRNA-200a-3p, and miRNA-3613-3p. The down-regulated miRNAs were miRNA-125a-5p, miRNA-185-5p, miRNA-151a-3p, and miRNA-328-3p. CONCLUSION: We successfully demonstrated particular exosomal miRNAs that may serve as future biomarkers for CAD.

A Novel Integrated Score Index of Echocardiographic Indices for the Evaluation of Left Ventricular Diastolic Function.

BACKGROUND: We propose a novel integrated score index, which could be used to quantify and grade left ventricular (LV) diastolic function. METHODS: We enrolled 629 participants [393 healthy subjects, 145 with hypertension (HTN), 24 with hypertrophic cardiomyopathy (HCM), and 67 with coronary artery disease (CAD)]. This score index was with a score of 1 for an E/A ratio < 1, a score of 1 for a septal e'/a' ratio ≤ 0.8, a score of 2 for a lateral e'/a' ratio ≤ 1, a score of 2 for a septal E/e' ratio ≥10-15, a score of 3 for a lateral E/e' ratio ≥8-15, and a score of 1 for a deceleration time >240 ms. The sum of each score was considered as the final value in this scoring method (either a septal or a lateral E/e' ratio > 15 was given a total score of 10, regardless of the other measurements). RESULTS: After analysis, the AUROC of this integrated score index for predicting any diastolic dysfunction (discriminated by the American Society of Echocardiography guidelines) was 0.962, and the AUROC of the method from the logistic regression was 0.970. The mean values of the score index for the groups were 3.81 ± 0.12 in healthy, 6.48 ± 0.19 in HTN, 7.35 ± 0.46 in HCM, and 6.62 ± 0.29 in CAD. Using the score index, the healthy subjects obtained lower scores compared with those of HTN (p = 0.00), HCM (p = 0.00), and CAD (p = 0.00). Therefore, this score index could discriminate patients with diseases with impaired diastolic function from the healthy subjects when the total sum of the score was equal to or greater than 4. CONCLUSIONS: If the presently used methods cannot allow the clear diagnosis of LV diastolic dysfunction, this integrated score index might be helpful for discriminating diseases with impaired diastolic function.

A triglyceride-raising APOA5 genetic variant is negatively associated with obesity and BMI in the Chinese population.

Apolipoprotein A-V (apo A-V) exerts a potent triglyceride (TG)-lowering effect through enhanced intravascular TG-hydrolysis with increased uptake of TG-derived free fatty acids into muscle and adipose tissue. Genetic variants in the APOA5 gene were strongly associated with plasma TG concentrations. The aim of this study was to examine whether APOA5 genetic variation was associated with obesity. We genotyped the missense c.553 G>T polymorphism (p.G185C) in the APOA5 gene in 1,085 Chinese (333 obese subjects and 752 nonobese controls). We analyzed the association between the c.553 G>T polymorphism and obesity and related metabolic phenotypes. The T allele at the c.553 G>T polymorphism was associated with higher plasma TG concentrations. Each additional T allele was associated with an increased TG concentration of 53.5 mg/dl (95% confidence interval (CI) 29.6-76.0, P < 0.0001). However, the T allele was associated lower risk of obesity (odds ratio (OR), 0.48; 95% CI 0.32-0.73, P = 0.0004). Each additional copy of the T allele was associated with a BMI decrease of 0.73 kg/m(2) (95% CI 0.26-1.16, P = 0.002), equivalent to 2.11 kg in a person 1.7 m tall. We may then conclude that the TG-raising APOA5 genetic variant was associated with a decrease in BMI and reduced risk of obesity in the Chinese population.

Interaction of ADIPOQ genetic polymorphism with blood pressure and plasma cholesterol level on the risk of coronary artery disease.

BACKGROUND: The protective effect of +45T >G polymorphism in the adiponectin gene (ADIPOQ) on coronary artery disease (CAD) has been demonstrated in European populations, so this study investigated the effect of +45T >G polymorphism on the risk of CAD and its interactions with other metabolic risk factors in a Chinese population. METHODS AND RESULTS: The +45T >G polymorphism (rs2241766) of ADIPOQ was genotyped in 600 patients with angiographically diagnosed CAD and in 718 controls. The G allele at the +45T >G polymorphism was associated with a lower risk of CAD (odds ratio (OR), 0.76; 95% confidence interval (CI), 0.64-0.89; P=0.001). The protective effect of the G allele at +45T >G polymorphism was magnified at blood pressure <140/90 mmHg (OR, 0.65; 95%CI, 0.51-0.82; P=0.0004), but disappeared at blood pressure >or=140/90 mmHg (OR, 0.98; 95%CI, 0.76-1.28; P=0.93), indicating an interaction between +45T >G polymorphism and blood pressure on CAD risk (P=0.02 for interaction). A similar interaction was also observed between plasma cholesterol level and the +45T >G polymorphism. CONCLUSIONS: An association of ADIPOQ genetic polymorphism with CAD risk is modified by traditional risk factors, such as blood pressure and plasma cholesterol level.

Electrophysiological mapping and histological examinations of the swine atrium with sustained (> or =24 h) atrial fibrillation: a suitable animal model for studying human atrial fibrillation.

OBJECTIVES: Interventional elimination of chronic persistent atrial fibrillation (AFib) remains difficult. An animal model mimicking the clinical situation is important. METHODS AND RESULTS: Twenty-five adult pigs were implanted with a high-speed atrial pacemaker. After continuous pacing at 600 bpm for 6 weeks, 20 (91%) of the 22 survivals developed sustained AFib lasting for at least 24 h. Epicardial dense mapping revealed multiple coexisting reentrant wavelets in the left and the right atrium (LA and RA, respectively; 10.6 +/- 2.9 vs. 7.6 +/- 2.4 wavelets/cm(2)/s; p < 0.002). The mean local A-A intervals were 87.2 +/- 14.6 ms in the LA and 103.3 +/- 19.0 ms in the RA (p < 0.0002). Acute termination of sustained AFib was successful in 3 of the 5 pigs by propafenone, but in none of the 6 by dl-sotalol. Epicardial cryothermal ablation failed to terminate any AFib by compartmentalization of the RA free wall alone (4 pigs) or together with the LA appendage (4 pigs). Electron microscopic examination demonstrated diffuse perinuclear myolysis, myofibrillar fragmentation and mitochondrial crystal disruption in the atrium. CONCLUSIONS: Pacing-induced sustained AFib (> or =24 h) in adult pigs is a feasible and efficient animal model with electrophysiological and histological characteristics closely similar to those seen in humans.

Association of the human minK gene 38G allele with atrial fibrillation: evidence of possible genetic control on the pathogenesis of atrial fibrillation.

BACKGROUND: Human minK protein is the beta-subunit of I(Ks) potassium channel and plays an important role in cardiac cellular electrophysiology. We investigated the association between human atrial fibrillation and the polymorphism of minK gene (38G or 38S) with a case-control study. METHODS: We included 108 patients with atrial fibrillation and 108 control subjects. The case patients and control subjects were matched regarding age, sex, presence of valvular heart disease, and presence of left ventricular dysfunction. The genotype of minK was determined with polymerase chain reaction and restriction fragment analysis. RESULTS: The results showed an association between the minK 38G allele and atrial fibrillation. The odds ratios for atrial fibrillation in patients with 1 and 2 minK 38G alleles were 2.16 (95% CI 0.81-5.74) and 3.58 (95% CI 1.38-9.27), respectively, when compared with patients without minK 38G allele. In a logistic regression model, the odds ratio for atrial fibrillation was 1.80 (95% CI 1.20-2.71, P <.0046) for patients with 1 more minK 38G allele. CONCLUSION: We report the association between the minK 38G allele and clinical atrial fibrillation. Our findings suggest possible genetic control on the pathogenesis of atrial fibrillation.