Tai-Yang Luo

Late Gadolinium Enhancement Amount As an Independent Risk Factor for the Incidence of Adverse Cardiovascular Events in Patients with Stage C or D Heart Failure

Background: Myocardial fibrosis (MF) is a risk factor for poor prognosis in dilated cardiomyopathy (DCM). Late gadolinium enhancement (LGE) of the myocardium on cardiac magnetic resonance (CMR) represents MF. We examined whether the LGE amount increases the incidence of adverse cardiovascular events in patients with stage C or D heart failure (HF). Methods: Eighty-four consecutive patients with stage C or D HF, either ischemic or non-ischemic, were enrolled. Comprehensive clinical and CMR evaluations were performed. All patients were followed up for a composite endpoint of cardiovascular death, heart transplantation, and cardiac resynchronization therapy with defibrillator (CRT-D). Results: LGE was present in 79.7% of the end-stage HF patients. LGE distribution patterns were mid-wall, epi-myocardial, endo-myocardial, and the morphological patterns were patchy, transmural, and diffuse. During the average follow-up of 544 days, 13 (15.5%) patients had endpoint events: 7 patients cardiac death, 2 patients heart transplantation, and 4 patients underwent CRT-D implantation. On univariate analysis, LGE quantification on cardiac magnetic resonance, blood urine nitrogen, QRS duration on electrocardiogram, left ventricular end-diastolic diameter (LVEDD), and left ventricular end-diastolic volume (LVEDV) on CMR had the strongest associations with the composite endpoint events. However, on multivariate analysis for both Model I (after adjusting for age, sex, and body mass index) and Model II (after adjusting for age, sex, BMI, renal function, QRS duration, and atrial fibrillation on electrocardiogram, the etiology of HF, LVEF, CMR-LVEDD, and CMR-LVEDV), LGE amount was a significant risk factor for composite endpoint events (Model I 6SD HR 1.037, 95%CI 1.005–1.071, p = 0.022; Model II 6SD HR 1.045, 95%CI 1.001–1.084, p = 0.022). Conclusion: LGE amount from high-scale threshold on CMR increased the incidence of adverse cardiovascular events for patients in either stage C or D HF.

Anatomic properties of coronary arteries are correlated to the corrected thrombolysis in myocardial infarction frame count in the coronary slow flow phenomenon.

BackgroundCoronary slow flow phenomenon (CSFP) is an important, angiographic clinical entity, but its etiology remains unclear. The purpose of this study was to explore the potential role of local coronary anatomic properties in the genesis of CSFP. MethodsOne hundred and thirty-one consecutive patients with CSFP and 131 patients with angiographically normal coronary flow were prospectively enrolled after documenting coronary flow by corrected thrombolysis in myocardial infarction frame count (CTFC). Local anatomic parameters including the tortuosity index (TI), the ostial-to-middle diameter ratio, the ostial-to-middle cross-sectional area ratio, and the number of distal branches (NDB) of arteries at end-systole were compared between patients with CSFP and controls. ResultsFor each major coronary artery, CSFP patients had higher TI and NBD compared with controls (all P<0.05). The diameter ratio and cross-sectional area ratio of the three major coronary arteries were higher in the CSFP group (P=0.004 and 0.020, respectively). The TI (r=0.476, P<0.001) and NDB (r=0.186, P=0.004) were significantly correlated with CTFC. However, the higher TI (&bgr;=0.424, P<0.001) was the only independent correlate to CTFC. Multivariate logistic analysis revealed that TI (adjusted odds ratio 1.17, 95% confidence interval 1.11–1.23, P<0.001) and NDB (adjusted odds ratio 2.20, 95% confidence interval 1.50–3.21, P<0.001) were independent predictors of CSFP. ConclusionThe presence of CSFP was associated with higher tortuosity and more distal branches in coronary arteries, indicating that the anatomic properties of coronary arteries could also play a role in the pathogenesis of CSFP.

Angiographic evaluation of a new technique for common femoral artery access: The inguinal ligament-guided approach

☆ This study was partly supported by grants from the dation of China (nos. 81070166 and 81270284) and th Program of Beijing Municipal Commission of Education ( ⁎ Corresponding author at: Department of Cardiology, B Medical University, Beijing Institute of Heart, Lung, andBloo Road, Chaoyang District, Beijing 100029, China. Tel.: + 64456078. E-mail address: chshma@vip.sina.com (C.-S. Ma). 1 These authors take responsibility for all aspects of th bias of the data presented and their discussed interpret

Chronic heart failure in patients with nonalcoholic fatty liver disease: prevalence, clinical features, and relevance

Objective This study was performed to assess the prevalence of nonalcoholic fatty liver (NAFL) in patients with symptomatic congestive heart failure (CHF) and compare the clinical features with those of patients without NAFL. Methods In total, 102 patients with CHF were divided into NAFL and non-NAFL groups according to their hepatic ultrasonography findings. All patients underwent transthoracic echocardiography and cardiac magnetic resonance examination. Follow-up was performed for major cardiovascular events (MACE) and readmission due to heart failure at 1, 3, 6, and 12 months after the index hospitalization. Results NAFL was detected in 37 of 102 patients (36.27%). Compared with the non-NAFL group, patients with NAFL were younger, had a higher body mass index and left ventricular (LV) mass index, and had more severe fibrosis. MACE and readmission occurred in 15 patients in the NAFL group and 29 patients in the non-NAFL group, without a significant difference. Linear regression analysis revealed that after adjusting for confounders, NAFL was independently associated with the LV fibrosis size and the ratio of the LV fibrosis size to the LV mass index. Conclusions NAFL is present in more than one-third of patients with CHF and is associated with the severity of LV fibrosis.

Extracellular volume quantitation using dual-energy CT in patients with heart failure: Comparison with 3T cardiac MR

BACKGROUNDS Cardiac magnetic resonance (CMR) T1 mapping and the extracellular volume (ECV) have been developed to quantitative analysis of diffusely abnormal myocardial fibrosis (MF). However, dual-energy CT (DECT) has a potential for calculation of ECV. The aim of this study is to evaluate the feasibility and accuracy of DECT technique in determining the ECV in patients with heart failure, with 3T CMR as the reference. METHODS Thirty-five patients with various reasons of heart failure were enrolled in this study. Both DECT and CMR exams were completed within 24 h. ECVs were calculated, and the relationship between DECT-ECV, CMR-ECV, and other heart function parameters, including left ventricular end systolic and diastolic volume, cardiac output and ejection fraction (LVESV, LVEDV, CO, LVEF), Brain natriuretic peptide (BNP) was determined. All participants gave informed consent, and the study was approved by the institutional review board. RESULTS The median ECVs on DECT and CMR were 33% (95%CI: 32%-36%) and 30% (95%CI: 30% - 32%), respectively. A good correlation between myocardial ECV at DECT and that at CMR (r = 0.945, P < 0.001) was observed. Bland-Altman analysis between DECT and CMR showed a small bias (2.6%), with 95% limits of agreement of -0.4% and 5.6%. Interobserver agreement for ECV at DECT was excellent (ICC = 0.907). Both ECVs, for DECT and CMR, were inversely associated with LVEF and CO. CONCLUSION DECT-based ECV could be an alternative non-invasive imaging tool for myocardial tissue characterization. However, overestimation of the extent of diffuse MF is observed with use of DECT.

e0096 The study on the relations between aldosterone and atrial interstitial remodelling and atrial fibrillation

Objective To investigate the relations between aldosterone (Ald) and atrial interstitial remodelling and atrial fibrillation (AF). Methods 18 healthy male hybrid dogs aged 15–18 months were divided into three groups randomly, the control group (n=6), the Perindopril group (1 mg/kg/d, n=6), the Spironolactone group (10 mg/kg/d, n=6). To test the form and function of left atrial and plasma aldosterone levels before pacing and 4 weeks, 8 weeks after pacing, respectively. Observe the number of dogs maintained AF and duration of AF after cessation of pacing. Then, kill the animals and collect some tissues of left and right atrial to detect aldosterone levels and test the situation of atrial fibrosis by pathological examination. By comparing the similarities and differences between the three groups, to understand the impact of atrial interstitial remodelling and the occurrence and development of atrial fibrillation induced by aldosterone inhibitor. Results The levels of plasma aldosterone were no significant differences between the three groups before pacing (p>0.05), while 4 weeks and 8 weeks after pacing the plasma aldosterone levels and the aldosterone levels of atrial tissue 8 weeks after pacing of the other groups were significantly lower than those of the control group (p<0.05). In the control group, 4 weeks and 8 weeks after pacing the plasma aldosterone levels was significantly higher than that before pacing (p<0.05), while in the other two groups, there were no significant differences between before and after pacing (p>0.05). Pacing for 4 weeks and 8 weeks later, the diameter, end-systolic volume and end-diastolic volume of the left atrium of the control group dogs significantly increased than before pacing, and left atrial ejection fraction (LAEF) lower than before pacing significantly (p<0.05). Compared with the control group, those of the Perindopril group and Spironolactone group after pacing significantly reduced, but LAEF significantly increased (p<0.05). Compared with the control group, the number of dogs maintained atrial fibrillation of the two treatment groups after cessation of pacing significantly reduced, with a shorter average duration of atrial fibrillation. While there was not significant difference between the two treatment groups. The value of Collagen Volume Fraction (CVF) of the Control group was significantly higher than those of the other two groups (p<0.05), while no significant difference value between the two treatment groups (p>0.05). Conclusion The aldosterone receptor antagonist (spironolactone) and ACEI (Perindopril) can inhibit aldosterone levels and atrial fibrosis, improve the changes of atrial structure and function, and reduce the incidence and duration of atrial fibrillation. And the effects of the two drugs are similar.

e0095 The study on the relations between rennin-angiotensin-aldosterone system and atrial structural remodelling and atrial fibrillation

Objective To investigate the effects of perindopril and/or spironolactone on atrial structural and functional remodelling in atrial fibrillation (AF) dogs induced by chronic rapid atrial pacing, and research the relations between rennin-angioensin-aldosterone system (RAAS) and atrial interstitial remodelling and atrial fibrillation. Methods 24 healthy male hybrid dogs aged 15–18 months were paced for 8 weeks and randomly divided into four groups: control group, perindopril group (P), spironolactone group (S), and combination of perindopril and spironolactone group (P+S). The dogs in P group, S group, and P+S group respectively received perindopril (1 mg·kg−1·d−1) and/or spironolactone (10 mg·kg−1·d−1). Plasma Angiotensin II (Ang II) and aldosterone (Ald) were measured before and after 4 and 8 weeks pacing. Transthoracic echocardiographic examinations were performed before and after 8 weeks pacing. The number of dogs maintained AF and duration of AF after stopping of pacing were recorded. Atrial collagen volume fraction (CVF) was analysed by Masson staining after 8 weeks pacing. Results (1) Plasma Ang II and Ald were no significant differences between four groups before pacing. Compared with the control group, plasma Ang II and Ald after 4 and 8 weeks pacing in P group, S group and P+S group were significantly lower. In the control group, plasma Ang II and Ald levels after 4 and 8 weeks pacing was significantly higher than that before pacing; in the other groups, there were no significant differences. (2) Compared with the control group, the diameter, end-systolic volume and end-diastolic volume of the left atrium of P group, S group and P+S group after pacing significantly reduced, but LAEF significantly increased after 8 weeks pacing. (3) Compared with the control group, the rate of dogs maintained atrial fibrillation of three drug treatment groups after stopping of pacing significantly reduced, with a shorter average duration of AF. (4) Compared with the control group, the value of CVF in P group, S group and P+S group was significantly lower. Conclusion The occurrence and development of atrial fibrillation and atrial structural remodelling is closely related to RAAS activation. The RASS blockers can inhibit atrial fibrosis, improve the changes of atrial structure and function, and reduce the incidence and duration of atrial fibrillation in the atrial fibrillation dogs induced by chronic rapid atrial pacing.