BackgroundRecent studies suggest the significance of right ventricular (RV) function in the outcome in patients with left ventricular dysfunction (LVSD); however, global assessment of RV remains to be determined by echocardiogram because of its complex geometry. This study aimed to validate RV outflow tract fractional shortening (RVOT-FS) in the evaluation of RV function and its prognostic value in patients with LVSD.MethodsThis study included eighty-one patients (62 ± 17 years, mean ± SD, male 79%) with reduced LV ejection fraction (LVEF) (≤40%). Two-dimensional echocardiogram of the parasternal short axis view was obtained at the level of the aortic root, and RVOT-FS was calculated as the ratio of end-diastole minus end-systole dimension to end-diastole dimension.ResultsRVOT-FS ranged from 0.04 to 0.8 (0.3 ± 0.2, mean ± SD), and correlated with LVEF (r = 0.33, p = 0.0028), RV fractional area change (r = 0.37, p = 0.0008) and brain natriuretic peptide level (r = -0.38, p = 0.0005). In Cox multivariate regression analysis, RVOT-FS [hazard ratio (HR) 0.028, 95% confidence interval (CI): 0.002-0.397]; p = 0.008] and New York Heart Association functional class III-IV [HR 2.233, 95% CI: 1.048-4.761]; p = 0.037] were independent factors to predict the events. During a median follow-up period of 319 days (1 to 1862 days), patients with RVOT-FS ≥ 0.2 showed a higher event-free rate than those < 0.2 by Kaplan-Meier analysis (log-rank test, p = 0.0016).ConclusionsOur data suggest that RVOT-FS is a simple parameter reflecting the severity of both ventricular function in patients with LVSD. In addition, RVOT-FS might be useful to predict adverse outcomes in such a patient population.

SummaryBackground: Epicardial adipose tissue expresses adiponectin protein, and its expression is significantly lower in patients with severe coronary artery disease (CAD) than in those without CAD. Transcoronary adiponectin levels are significantly decreased in nondiabetic but not in diabetic patients with CAD. Adiponectin is also an important adipocytokine that is linked to insulin resistance and reduces coronary microvascular function.Hypothesis: Adiponectin may play a significant role in the localized coronary circulation. The present study examines the local dynamics of adiponectin in the coronary circulation in nondiabetic individuals with normal coronary arteries and the relationship between adiponectin and coronary microvasculature function.Methods: We examined 22 consecutive nondiabetic patients whose coronary arteries were angiographically normal. Plasma levels of adiponectin were measured in blood samples that were simultaneously collected from the orifice of the left coronary artery (LCA) and the great cardiac vein (GCV). To evaluate the function of the coronary microcirculation, we

The circulating osteoprotegerin (OPG) level reflects a series of cardiovascular diseases; however, the source(s) of circulating OPG remain(s) to be determined. This study explored whether OPG is released in the coronary circulation and whether it is associated with cardiac structure and function. Fifty-six patients (67±10 years old, male 57%, hypertension 73%, coronary artery disease 50%) were enrolled, and blood samples were collected simultaneously from the orifice of the left coronary artery (CA) and the coronary sinus (CS) after angiography. The concentration of OPG was higher in the CS than in the CA (7.7±4.1 vs. 6.7±3.6 pmol/l, p<0.001). The trans-cardiac OPG concentration was significantly (p=0.019) decreased in patients who have been prescribed either an angiotensin converting enzyme inhibitor or an angiotensin II type 1 receptor blocker (ACEI/ARB). In patients subgroup who did not take an ACEI/ARB (n=27), the trans-cardiac OPG level was positively correlated with age (r=0.396, p=0.041) and relative wall thickness of left ventricle (r=0.534, p=0.004). In multivariate linear regression analysis, relative wall thickness remained to be the independent variable for the trans-cardiac OPG level (p=0.004). Moreover, trans-cardiac OPG was significantly (p=0.021) increased in patients with relative wall thickness greater than 0.45 but it did not differ if the left ventricular mass index was increased (≥116 for males, or ≥ 104 for females, g/m(2)) or not (p=0.627). This study suggests that OPG is secreted into the coronary circulation and is associated with concentric remodeling/hypertrophy of LV, possibly in interactions with the renin-angiotensin system.

In view of these findings, BVP therapy may contribute to the development of new therapeutic method for patients with severe CHF due to DCM.

SummaryAdiponectin has antiatherosclerotic properties and is also produced in the local coronary circulation. We previously reported that signifi cantly less adiponectin was produced in the coronary circulation of patients with than without coronary artery disease (CAD). The goal of this study was to determine whether adiponectin production in the coronary circulation could predict future cardiovascular events in patients with CAD.Forty-eight CAD patients whose left anterior descending coronary arteries required percutaneous coronary intervention (PCI) were enrolled. The amount of adiponectin production in the coronary circulation was defi ned as the plasma adiponectin level at the great cardiac vein minus that at the orifi ce of the left coronary artery. All patients were divided by adiponectin production level in the coronary circulation into the adiponectin-positive production group (> 0 µg/ mL) and adiponectin-negative production group (≤ 0 µg/mL). Median follow-up period was 66 months (maximum, 108 months). The primary endpoint was the combined occurrence of major adverse cardiovascular events (MACE), including rehospitalization due to unstable angina, heart failure, nonfatal myocardial infarction, revascularization with PCI or coronary artery bypass grafting, ischemic stroke, and cardiovascular death.Sixteen MACE occurred. The incidence of MACE was signifi cantly higher in the adiponectin-negative production group than in the adiponectin-positive production group (P = 0.02). In multivariate analysis, adiponectin-negative production was a predictor of MACE (P = 0.03). Kaplan-Meier analysis revealed that the MACE-free rate was signifi cantly lower in the adiponectin-negative production group than in the adiponectin-positive production group.Adiponectin production in the coronary circulation with CAD may be associated with MACE. (Int Heart J 2014; 55: 239-243)

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We encountered a case of wide QRS tachycardia with chronic atrial fibrillation in Wolff-Parkinson-White syndrome. Unique features were late onset of syncope attacks associated with this tachycardia at an advanced age of 72 years old without previous documentation of WolffParkinson-White syndrome on electrocardiogram. He had a high likelihood of sudden cardiac death. Catheter ablation using CARTO TM system easily led to a successful ablation of the accessory pathway. The mechanism of late onset of the wide QRS tachycardia was attributed to possible changes of electrophysiologic properties including the atrio-ventricular node and/or the accessory pathway, and the unique location of the accessory pathway. Case ReportA 72-year-old man was admitted for evaluation of frequent syncope or fainting attacks which had suddenly begun 1 month before admission in May 2002. He easily experienced syncope attacks on exercise. Thus, his daily life activities were limited. He was taking antihypertensive drugs (5 mg of enalapril and 25 mg of atenolol), digitalis glycosides (0.125 mg of digoxin) and warfarin potassium as anticoagulant therapy for~10 years because of a history of cerebral infarction associated with hypertension and non-valvular chronic atrial fibrillation (Af). An electrocardiogram (ECG) taken 1 year prior to the admission was Af with narrow QRS complex ( Fig. 1A) with no evidence of tachycardia and delta waves (mean heart rate; 64 beats per minute, QRS; 82 msec). While the ECG taken 2 months prior to the admission showed Af with intermittent delta waves (mean heart rate; 60 beats per minute) ( Fig. 2A).On admission, his blood pressure was 102/64 mmHg and pulse rate was 124 beats per minute and irregular. When his heart rate was over 150 beats per minute on exercise, his systolic blood pressure dropped under 70 mmHg with manifestation of fainting. There were no murmurs on cardiac auscultation. Routine blood test results were almost normal except for a coagulation time. An ECG (Fig. 1B) showed wide QRS complex tachycardia (mean heart rate; 138 beats per minute, QRS; 134 msec) with a slur at the initial portion of the QRS complex. This tachycardia was suppressed by an intravenous administration of procainamide, which is known to depress the conduction of the accessory pathway (1), and resulted in a dramatic decrease of the wide QRS complex (Fig. 2B). By contrast, the tachycardia was accelerated by an intravenous application of verapamil or digitalis glycosides (Fig. 2C), which are reported to depress the conduction of the atrio-ventricular (AV) node (2, 3). With this change of ECG, the patient experienced symptoms of hypotension and notable fainting. These findings suggested that this patient might have Wolff-Parkinson-White (WPW) syndrome. A chest radiograph showed a mild increase of the cardiothoracic ratio (CTR; 54%) and two-dimensional echocardiography revealed no evidence of cardiac abnormalities except for mild dilatation of the left atrium, such as Ebstein's anomaly and mitral leaflet prolapse which are...