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.

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.

We propose a novel integrated score index, which could be used to quantify and grade left ventricular (LV) diastolic function.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).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.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.

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/m2 (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.

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 >= 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. (Circ J 2009; 73: 1934-1938)

Automaticity (postpacing impulse recovery time) of the sinus node or subsidiary pacemakers (or both) was determined by intracardiac recordings and atrial overdrive pacing in three patients with disease of the sinus node. Their electrocardiographic manifestations included sinus bradycardia, sinoatrial block, sinus arrest, afrioventricular junctional rhythm, and atrioventricular dissociation. One patient, who initially had syncope, demonstrated prolonged time for recovery of the sinus node (maximum corrected value, 3,485 msec) and impaired afrioventricular junctional automaticity (maximum corrected junctional recovery time, 1,460 msec). Of the remaining two patients without syncopal attacks, one had an adequate low atrial or junctional escape mechanism following cessation

embolism 87 Aspirin 119, 250 Atrial fibrillation 161 -function 134 -septal aneurysm 87 -size 150 Atrioventricular canal 231 -nodal tachycardia 264 -reentry tachycardia 264 Beriberi 92 Bernoulli equation 205 Bioelectrical impedance 127 Björk-Shiley convexo-concave valve 96 Blood flow 184 --velocity 173 Body fat 127 -mass 140 Bradycardia 268

The slow delayed rectifier potassium current (IKs) is unique in its slow activation and deactivation kinetics. It is important during cardiac repolarization, especially when the heart rate is fast. We compared the effects of quinidine, procainamide, sotalol, and amidarone on IKs and correlated the findings with the clinical reverse use-dependent effects of potassium channel blockers. Human minK RNA was obtained by reverse transcription-polymerase chain reaction using explanted human heart. The RNA was injected into Xenopus oocytes for heterologous expression of IKs. A two-electrode voltage clamp technique was performed to investigate the IKs. We demonstrated that quinidine, sotalol and procainamide had no effects on IKs up to a concentration of 300 µM while amiodarone inhibited IKs in a concentration-dependent manner starting from 10 µM. The inhibition by amiodarone was state-dependent with gradual unblocking after depolarization. The degree of inhibition was 53% immediately after depolarization and 19% at the end of a 5-second depolarization. IKs is 30 times more sensitive to amiodarone than to quinidine, sotalol, and procainamide. Quinidine, sotalol and procainamide have reverse use-dependent effects while amiodarone does not. This is compatible with the hypothesis that no inhibition of IKs at clinical concentrations contributes to the clinical reverse use-dependent effects.

To identify the disease locus of familial hypertrophic cardiomyopathy (FHC) in a Chinese family, a genetic linkage study was performed using polymorphisms from various chromosomal regions. This family has eight affected members, including a case with typical features of apical hypertrophic cardiomyopathy of the Japanese type. The results revealed significant evidence of linkage of polymorphisms on chromosome 11p13-q13 and FHC in this family with a maximal lod score of 3.38 at theta = 0.00. Our data suggest that the locus responsible for FHC in this family maps to chromosome 11 and that the molecular basis of FHC in the case of apical hypertrophic cardiomyopathy of the Japanese type might be similar to that of other affected members in the same family. Further studies are needed to elucidate the whole spectrum of the genetic basis of apical hypertrophic cardiomyopathy of the Japanese type.

We report the case of a 41-year-old male presenting with acute heart failure due to myxofibrosarcoma of the left atrium. Total resection was performed, followed by 4 courses of postoperative chemotherapy. Recurrence of the tumor was found 14 months later and resection was repeated with local irradiation and chemotherapy. Unfortunately, this failed to halt the spread of the malignancy and the patient died of brain metastasis. We conclude that cardiac myxofibrosarcoma is rare and highly malignant. Adjuvant chemotherapy and radiotherapy seemed ineffective in this case.

Seventy-eight patients with chronic nonrheumatic atrial fibrillation were studied by transesophageal echocardiography with regard to the left atrial appendage function and its relation to the coarseness of atrial fibrillation on electrocardiogram. These 78 patients (52 men and 26 women; mean age, 66 +/- 10 years; range, 40 to 94 years) were classified into two groups according to the presence of coarse (group 1, n = 46; those with the greatest amplitude of fibrillatory wave in lead V1 > or = 1 mm) or fine (group 2, n = 32; those without the coarse fibrillatory wave in lead V1) atrial fibrillation on a standard 12-lead electrocardiogram within 1 month of echocardiographic studies. There were no significant differences in age, sex, mean duration of atrial fibrillation, left ventricular end-diastolic dimension, left ventricular end-systolic dimension, left ventricular ejection fraction, and left atrial dimension between the two groups. In group 1, however, the left atrial appendage ejection fraction (24.4 +/- 14.2% vs 32.6 +/- 14.8%; p < 0.05) and the peak emptying velocity (21.7 +/- 12.6 cm/s vs 30.4 +/- 14.3 cm/s; p < 0.01) were lower than those in group 2. There were higher incidences of left atrial appendage spontaneous echo contrast (26/46 vs 7/32; p < 0.005) and thrombus (8/46 vs 0/32; p < 0.05) in group 1 patients. The coarse atrial fibrillation revealed a sensitivity of 80.0%, a specificity of 58.1%, a positive predictive value of 60.9%, and a negative predictive value of 78.1% for the presence of left atrial appendage spontaneous echo contrast and/or thrombus formation. In conclusion, in patients with coarse nonrheumatic atrial fibrillation, the left atrial appendage function is usually poor and the incidence of spontaneous echo contrast and thrombus formation appears to be higher in these patients.

Primary cardiac tumors are very rare and the majority of them are histologically benign and surgically curable. During a 30-year period from 1963 to January 1993, 45 cases of primary cardiac tumors were surgically excised at the National Taiwan University Hospital, representing 0.52% of 8,695 open heart surgical cases during the same period. In this series, 42 cases (94%) were benign tumors; 39 (88%) were myxoma (30 female, 9 male), and 32 (82%) originated in the left atrium. None were discovered in the left ventricle. In all but the first 6 cases, tumors in patients with myxoma in the left atrium were successfully excised by the transseptal approach. There were 3 patients with rare benign tumors: intracardiac goiter, rhabdomyoma, and hemangioma respectively. The intracardiac goiter was completely excised with no ectopic thyroid tissue after operation and the other 2 received palliative resection. The latter 2 patients suffered no recurrence. Rhabdomyosarcoma, leiomyosarcoma and malignant lymphoma were noted in one patient each, all of whom died of low cardiac output in the early postoperative course. In our experience, the majority of primary cardiac tumors were benign and located in the left atrium. The long-term result of surgical treatment of benign cardiac tumors is excellent, even incases of incomplete resection, while the results from surgical treatment of malignant tumors is poor.