无呼吸机支持下小鼠主动脉弓缩窄致心肌肥厚模型的建立

目的: 小鼠主动脉弓缩窄(transverse aortic constriction,TAC)是压力超负荷诱导的左心室肥厚及其进展为心力衰竭的实验研究中最常用的外科技术之一,以前一般在动物插管和通气的情况下进行TAC操作,这使得该过程需要呼吸机,且手术操作费时费力,本研究的目的是详细描述建立一种小鼠无气管插管和不使用呼吸机通气的微创TAC技术。方法：雄性C57BL/6小鼠(2-4月龄,20-30 g)用戊巴比妥钠腹膜内注射麻醉,实施胸骨部分切开术后暴露主动脉弓,用缝线穿过主动脉弓下方并将主动脉弓系在钝的27号针上后拔出针头,假手术组操作过程同TAC组,但不进行结扎。结果：TAC后4周小鼠心重体重比明显高于假手术组,心肌肥大标志基因心房钠尿肽（atrial natriuretic peptide,ANP）、脑钠肽(brain natriuretic peptide,BNP)表达显著升高,左心室射血分数和左心室短轴缩短率明显降低,而且手术过程中以及术后28天内死亡率只有5%。结论：通过微创TAC手术小鼠死亡率低,并能高效诱导心肌肥厚和心功能降低。     

Association Between Lipid Profiles and Left Ventricular Hypertrophy: New Evidence from a Retrospective Study

ObjectiveTo explore the association between lipid profiles and left ventricular hypertrophy in a Chinese general population.MethodsWe conducted a retrospective observational study to investigate the relationship between lipid markers [including triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein (HDL) cholesterol, non-HDL-cholesterol, apolipoprotein A-I, apolipoprotein B, lipoprotein[a], and composite lipid profiles] and left ventricular hypertrophy. A total of 309,400 participants of two populations (one from Beijing and another from nationwide) who underwent physical examinations at different health management centers between 2009 and 2018 in China were included in the cross-sectional study. 7,475 participants who had multiple physical examinations and initially did not have left ventricular hypertrophy constituted a longitudinal cohort to analyze the association between lipid markers and the new-onset of left ventricular hypertrophy. Left ventricular hypertrophy was measured by echocardiography and defined as an end-diastolic thickness of the interventricular septum or left ventricle posterior wall > 11 mm. The Logistic regression model was used in the cross-sectional study. Cox model and Cox model with restricted cubic splines were used in the longitudinal cohort.ResultsIn the cross-sectional study, for participants in the highest tertile of each lipid marker compared to the respective lowest, triglycerides [odds ratio (OR): 1.250, 95%CI: 1.060 to 1.474], HDL-cholesterol (OR: 0.780, 95%CI: 0.662 to 0.918), and lipoprotein(a) (OR: 1.311, 95%CI: 1.115 to 1.541) had an association with left ventricular hypertrophy. In the longitudinal cohort, for participants in the highest tertile of each lipid marker at the baseline compared to the respective lowest, triglycerides [hazard ratio (HR): 3.277, 95%CI: 1.720 to 6.244], HDL-cholesterol (HR: 0.516, 95%CI: 0.283 to 0.940), non-HDL-cholesterol (HR: 2.309, 95%CI: 1.296 to 4.112), apolipoprotein B (HR: 2.244, 95%CI: 1.251 to 4.032) showed an association with new-onset left ventricular hypertrophy. In the Cox model with forward stepwise selection, triglycerides were the only lipid markers entered into the final model.ConclusionLipids levels, especially triglycerides, are associated with left ventricular hypertrophy. Controlling triglycerides level potentiate to be a strategy in harnessing cardiac remodeling but deserve to be further investigated.     

EBCT在原发性非黏液瘤性心脏心包肿瘤中的诊断价值

目的探讨原发性非黏液瘤性心脏心包肿瘤的EBCT特征,评价EBCT在心脏肿瘤诊断中的价值.方法经手术和病理证实的25例非黏液瘤性心脏心包原发肿瘤,男14例,女11例,年龄5个月～72岁,平均32.1岁,接受单层增强和/或电影序列EBCT扫描.结果良性肿瘤19例,恶性肿瘤6例,其中8例(脂肪瘤3例,单纯心包囊肿和淋巴管瘤各2例,血管瘤1例)与病理诊断一致.结论EBCT具有优良的时间、空间和密度分辨率,脂肪瘤、单纯囊肿、淋巴管瘤和血管瘤等有相对特征性表现,但对大部分肌源性、纤维瘤性等实质性肿瘤似无法做出准确的定性诊断.     

超声心动图测定小儿左室壁应力的临床应用

本文用超声心动图测定的左室内径及室壁厚度，结合袖带血压计测量的收缩压，计算了８０名正常儿童（４～１４岁）及２１例心脏病合并心力衰竭患儿的左室壁应力。结果显示：正常儿童室壁应力不受年龄和性别的影响，心力衰竭患儿室壁应力明显增加，经治疗部分心功能好转的患儿，其室壁应力有明显的下降。动态观察室壁应力的变化，可作为了解治疗效果的一项指标。     

Potential use of pericardial cTnI,Mg2+ and Ca2+ in the forensic investigation of seawater drowning in Greece: An initial assessment

The investigation of drowning constitutes one of the biggest problems in forensic practice. Elevated cardiac troponin I (cTnI) levels in biological fluids have been associated with myocardial damage, whereas increased Mg²⁺ and Ca²⁺ levels were found in cases of seawater drowning. The aim of this study was to examine the diagnostic utility of postmortem determination of cTnI, Mg²⁺ and Ca²⁺ in the pericardial fluid, in differentiating between cases of seawater drowning related to myocardial injury and those brought about by other causes. This study included 76 cases selected during a 2-year period from medicolegal autopsies. The cases were divided into three groups, according to the cause of death established based on macroscopic and microscopic evidence. The groups were: 1) seawater drowning (n = 23), 2) seawater drowning with histological evidence of myocardial infarction (n = 28), and 3) myocardial infarction unrelated to drowning (n = 25). cTnI was determined with an enzyme immunoassay; Mg²⁺ and Ca²⁺ with standard colorimetric assays. Pericardial cTnI levels were significantly lower in group 1 compared to groups 2 and 3. In contrast, pericardial Mg²⁺ and Ca²⁺ levels were both significantly higher in groups 1 and 2 compared to group 3. Our results suggest that the postmortem determination of pericardial cTnI levels may be useful in detecting previous myocardial damage as a contributory factor in death from seawater drowning and provide independent confirmation of the usefulness of pericardial Mg²⁺ and Ca²⁺ levels for differentiating between seawater drowning and fatal acute myocardial injury unrelated to the former.     

Coronary Microembolization with Normal Epicardial Coronary Arteries and No Visible Infarcts on Nitrobluetetrazolium Chloride-Stained Specimens: Evaluation with Cardiac Magnetic Resonance Imaging in a Swine Model

Objective

To assess magnetic resonance imaging (MRI) features of coronary microembolization in a swine model induced by small-sized microemboli, which may cause microinfarcts invisible to the naked eye.

Materials and Methods

Eleven pigs underwent intracoronary injection of small-sized microspheres (42 µm) and catheter coronary angiography was obtained before and after microembolization. Cardiac MRI and measurement of cardiac troponin T (cTnT) were performed at baseline, 6 hours, and 1 week after microembolization. Postmortem evaluation was performed after completion of the imaging studies.

Results

Coronary angiography pre- and post-microembolization revealed normal epicardial coronary arteries. Systolic wall thickening of the microembolized regions decreased significantly from 42.6 ± 2.0% at baseline to 20.3 ± 2.3% at 6 hours and 31.5 ± 2.1% at 1 week after coronary microembolization (p < 0.001 for both). First-pass perfusion defect was visualized at 6 hours but the extent was largely decreased at 1 week. Delayed contrast enhancement MRI (DE-MRI) demonstrated hyperenhancement within the target area at 6 hours but not at 1 week. The microinfarcts on gross specimen stained with nitrobluetetrazolium chloride were invisible to the naked eye and only detectable microscopically. Increased cTnT was observed at 6 hours and 1 week after microembolization.

Conclusion

Coronary microembolization induced by a certain load of small-sized microemboli may result in microinfarcts invisible to the naked eye with normal epicardial coronary arteries. MRI features of myocardial impairment secondary to such microembolization include the decline in left ventricular function and myocardial perfusion at cine and first-pass perfusion imaging, and transient hyperenhancement at DE-MRI.     

Inhibition of CaMKII Attenuates Progressing Disruption of Ca2+ Homeostasis Upon Left Ventricular Assist Device Implantation in Human Heart Failure

In heart failure, left ventricular assist device (LVAD) implantation is performed to ensure sufficient cardiac output. Whereas some patients are subsequently weaned from LVAD support, other patients still need heart transplantation. To elucidate underlying mechanisms, we assessed the arrhythmogenic SR‐Ca²⁺ leak at the time of LVAD implantation (HF‐Im) and heart transplantation (HF‐Tx) and evaluated the effects of CaMKII‐inhibition. Human left‐ventricular cardiomyocytes were isolated, paced at 1 Hz for 10 beats to ensure SR‐Ca²⁺ loading and scanned for diastolic Ca²⁺ sparks (confocal microscopy). In HF‐Im, the high diastolic spark frequency (CaSpF) of 0.76 ± 0.12 × 100 μm^?1 × s^?1 could be reduced to 0.48 ± 0.10 × 100 μm^?1 × s^?1 by CaMKII inhibition (AIP, 1 μM). The amplitude of Ca²⁺ sparks, width, and length was not significantly altered. In sum, CaMKII inhibition yielded a clear tendency toward a reduction of the SR‐Ca²⁺ leak (n cells/patients = 76/6 vs. 108/6, P = 0.08). In HF‐Tx, we detected an even higher CaSpF of 1.00 ± 0.10 100 μm^?1 × s^?1 and a higher SR‐Ca²⁺ leak compared with HF‐Im (increase by 81 ± 33%, n cells/patients = 156/7 vs. 130/7, P < 0.05), which fits to the further decreased LV function. Here, CaMKII inhibition likewise reduced CaSpF (0.35 ± 0.09 100 μm^?1 × s^?1, P = 0.06) and significantly reduced spark duration (n sparks/patients = 58/3 vs. 159/3, P < 0.05). Conclusively, the SR‐Ca²⁺ leak was reduced by 69 ± 12% in HF‐Tx upon CaMKII inhibition (n cells/patients = 53/3 vs. 91/3, P < 0.05). These data show that the SR‐Ca²⁺ leak correlates with the development of LV function after LVAD implantation and may represent an important pathomechanism. The fact that CaMKII inhibition reduces the SR‐Ca²⁺ leak in HF‐Tx suggests that CaMKII inhibition may be a promising option to beneficially influence clinical course after LVAD implantation.     

Cardiac Index Declines During Long‐Term Left Ventricular Device Support

To investigate longitudinal trends in valvular and ventricular function with long‐term left ventricular assist device (LVAD) therapy, we analyzed hemodynamic and echocardiographic data of patients with at least 2 years of continuous LVAD support. All 130 patients who underwent HeartMate II implantation at our institution between 2005 and 2012 were reviewed. Twenty patients had hemodynamic and echocardiographic evaluations in both the early (0–6 months) and late (2–3 years) postoperative period. Patients on inotropic therapy or temporary mechanical support were excluded. The average times of early and late hemodynamic evaluations were 59 ± 41 days and 889 ± 160 days, respectively. Cardiac index (CI) declined by an average of 0.4 L/min/m² (P = 0.04) with concomitant increase in pulmonary capillary wedge pressure (PCWP; P = 0.02). The right atrial pressure to PCWP (RAP:PCWP) ratio decreased during LVAD support suggesting improvement in right ventricular function. While there was an increase in degree of aortic insufficiency (AI) at the late follow‐up period (P = 0.008), dichotomization by median decline in CI (?0.4 L/min/m²) indicated no difference in prevalence of AI among the groups. CI declined in patients with HeartMate II after 2 years of continuous support. An increase in preload and afterload was observed in those with the greatest decline in CI.