Right ventricular function impaired in children and adolescents with severe idiopathic scoliosis

Background

Although it is speculated that scoliosis may induce cardiac dysfunction, there is no report about evaluation of cardiac function, especially right cardiac function in patients with scoliosis. Therefore, we evaluated right ventricular function in idiopathic scoliotic patients with mild to severe curves and compared them with healthy children and adolescents matched in age, then explored relationship between scoliosis and right ventricular function.

Methods

Thirty-seven patients diagnosed with idiopathic scoliosis with a mean age of 16y/o (range, 8-25y/o) and an average spine curve of 77.5°Cobb (range, 30-157°) were studied by echocardiography. TAD was obtained using M-mode echocardiography. Similar examination was performed in a control group of 17 healthy individuals in matched-age. According to the different curve degree, all patients were divided into 3 groups (mild, moderate and severe). Comparison was done among the groups and the relationship between TAD and spine curve of Cobb was analyzed.

Results

Patients with severe scoliosis showed depressed TAD. There was good correlation between TAD and spine curve of Cobb.

Conclusions

Patients with severe scoliosis showed a significant lower right ventricular systolic function.     

Left ventricular false tendons

Left ventricular false tendons (LVFTs) are fibromuscular structures, connecting the left ventricular free wall or papillary muscle and the ventricular septum.There is some discussion about safety issues during intense exercise in athletes with LVFTs, as these bands have been associated with ventricular arrhythmias and abnormal cardiac remodelling. However, presence of LVFTs appears to be much more common than previously noted as imaging techniques have improved and the association between LVFTs and abnormal remodelling could very well be explained by better visibility in a dilated left ventricular lumen.Although LVFTs may result in electrocardiographic abnormalities and could form a substrate for ventricular arrhythmias, it should be considered as a normal anatomic variant. Persons with LVFTs do not appear to have increased risk for ventricular arrhythmias or sudden cardiac death.     

组织多普勒成像对射血分数正常的心衰患者左心功能评价

目的:探讨组织多普勒成像(TDI)技术评价射血分数正常的心衰患者左室长轴功能特点。方法:选取30名健康人(Ⅰ组)、EF>50%的心衰患者30名(Ⅱ组)和EF<50%的心衰患者30名(Ⅲ组)作为研究对象,采用TDI在二尖瓣环室间隔(ivs)、侧壁(l)、前壁(a)、后壁(p)、下壁(d)测量其Sm、DSm、IVCTm、TSm、Em、Am、IVRTm、TEm等指标。结果:Ⅰ组、Ⅱ组、Ⅲ组DSm、Sm逐渐减低,(P<0.05);而IVCTm、TSm逐渐升高(P<0.05);IVRTm、TEm在Ⅰ组、Ⅲ组、Ⅱ组逐渐升高(P<0.05);DSm及TEm在诊断EF>50%心衰患者心功能的指标中ROC曲线下面积最大,同样DSp及TEp在五个位点中ROC曲线下面积最大。结论:射血分数正常的心衰患者存在收缩减低;DSm及TEm是诊断EF>50%心衰患者心功能比较有效的指标;后壁是诊断的最佳位点。     

Tp-e间期、P波离散度对室性心律失常病情的预测价值

摘要 目的：探讨Tp-e间期、P波离散度(Pd)对室性心律失常病情的预测价值。方法：2016年6月到2018年6月选择在本院诊治的心绞痛患者110例,所有患者都给予动态心电图检查,记录Tp-e间期、Pd值与室性心律失常发生情况。随访患者的心绞痛复发情况,并判定预测价值。结果：在110例患者中,发生室性心律失常48例(失常组),发生率为43.6 %,其中偶发室早21例、频发室早19例、室早4例、心室颤动3例、室性心动过速1例。失常组的Tp-e间期、Pd值都显著高于非失常组(P<0.05)。随访至今,失常组的心绞痛复发率为45.8 %,显著低于对照组的8.1 %(P<0.05)。在失常组中,单因素与多因素logistics回归分析显示Tp-e间期、Pd都为影响患者心绞痛复发的重要因素(P<0.05)。ROC曲线分析显示Tp-e间期、Pd预测心绞痛复发的敏感性与特异性都在85.0 %以上。结论：心绞痛合并室性心律失常患者多伴随有Tp-e间期、Pd增加,也会增加患者的复发率,Tp-e间期、Pd对预测室性心律失常复发情况具有重要价值。     

右室Tei指数与血清醛固酮水平对COPD患者发生房颤的预测价值研究

摘要 目的：探讨右室Tei指数、血清醛固酮水平对慢性阻塞性肺病(COPD)患者发生房颤的预测价值。方法：根据房颤的发生情况,将200例COPD患者分为房颤发生组和无房颤发生组。比较两组的病程、COPD严重程度、血清醛固酮(ALD)水平及右室Tei指数、肺动脉压、右心室横径的差异,分析右室Tei指数和ALD预测房颤发生的ROC曲线下面积、截断值、灵敏度及特异度。结果：房颤发生组病程(8.48±1.3和7.59±1.75)、右心室横径(40.52±2.74和36.27±2.4)、血清ALD(137.64±42.77和98.61±15.39)、右室Tei指数(0.37±0.12和0.31±0.07)、COPD、肺动脉高压的严重程度与无房颤发生组比较差异都有统计学意义(P<0.05)。logistic回归分析结果显示ALD、右室Tei指数、病程、和肺动脉高压程度为影响COPD患者发生房颤的独立影响因素。右室Tei指数预测房颤发生的ROC曲线下面积AUC=0.645,截断值为0.420,灵敏度为38.0%,特异度达到93.33%;ALD预测房颤发生的ROC曲线下面积为0.792,截断值为122.72 pg/mL,灵敏度为66.0%,特异度可达到98.0%。结论：右室Tei指数和血清醛固酮水平可作为慢性阻塞性肺病患者发生房颤的预测参考指标。     

Temperature effects on the Na and Ca currents in rat and hedgehog ventricular muscle

Cardiac transmembrane potentials and Na and Ca currents were recorded at different temperatures in rat and hedgehog ventricular muscle. At 35 degrees C in both species resting potential was about -80 mV and upstroke velocity (Vmax) of the action potential above 100 V/s. The shape of the action potential in hedgehog ventricular cells at 35 degrees C was similar to that in the rat showing a fast repolarization phase. When temperature was decreased, the membrane resting potential depolarized and action potential amplitude and Vmax declined. In rat ventricular cells at 10 degrees C, the resting potential was about -40 to -50 mV and Vmax was reduced to about 5 V/s. In hedgehog ventricular cells, however, the transmembrane potentials and Vmax were better maintained at low temperature. Phase 3 of the action potential was markedly prolonged below 20 degrees C in hedgehog but not in rat ventricular cells. When temperature was decreased to 10 degrees C the availability curve of the Na current shifted toward more negative potentials and ICa.peak declined in rat ventricular cells. In hedgehog cardiac preparations, the Na current was less influenced by the cooling and ICa.peak did not change very much at low temperatures. A transient inward current usually considered to induce cardiac arrhythmias could be recorded in rat ventricular cells below 20 degrees C but not in hedgehog preparations. These features of hedgehog cardiac membranes may contribute to the cold tolerance and the resistance to ventricular fibrillation during the hypothermia in mammalian hibernators.     

三维斑点追踪技术对慢性肾功能不全患者左心室收缩功能和右心室功能的评估价值研究

摘要 目的：探讨慢性肾功能不全患者应用三维斑点追踪技术对其左心室收缩功能和右心室功能的评估价值。方法：选择我院收治的慢性肾功能不全患者82例,根据患者肾功能将其分为轻度慢性肾功能不全组[慢性肾脏病（CKD） 2期,47例],中-重度慢性肾功能不全组（CKD 3~5期,35例）,另选取同期医院体检的健康志愿者30例作为对照组,应用二维超声及三维斑点追踪技术检测各组心脏指标,比较三组二维超声指标、三维斑点追踪技术指标,应用受试者工作特征（ROC）曲线分析三维斑点追踪技术对患者左心室收缩功能和右心室功能的评估价值。结果：中-重度慢性肾功能不全组室间隔舒张末期厚度（IVSTd）、肺动脉收缩压（PASP）显著高于轻度慢性肾功能不全组、对照组,右心室面积变化分数（RVFAC）、组织运动三尖瓣环位移（TAPSE）、左心室射血分数（LVEF）显著低于轻度慢性肾功能不全组、对照组（P<0.05）。中-重度慢性肾功能不全组左室整体圆周收缩期峰值应变（LGCS）、左室整体纵向收缩期峰值应变（LGLS）、右室整体圆周收缩期峰值应变（RGCS）右室整体纵向收缩期峰值应变（RGLS）、显著高于轻度慢性肾功能不全组、对照组,左室整体径向收缩期峰值应变（LGRS）、三维左室射血分数（3D-LVEF）、右室整体径向收缩期峰值应变（RGRS）、三维右室射血分数（3D-RVEF）显著低于轻度慢性肾功能不全组、对照组（P<0.05）。ROC曲线分析显示,三维斑点追踪技术对慢性肾功能不全患者左心室收缩功能和右心室功能的评估价值较高。结论：三维斑点追踪技术可以准确检测心脏的纵向运动、圆周运动、径向运动,为临床早期发现慢性肾功能不全患者的心脏功能异常提供依据。     

Quantitative analysis of cardiac electrical restitution

Electrical restitution (ER) of cardiac cells is an aggregate of events that rhythmically restore the initial conditions of electric signal (action potential) generation. Its analysis represents an important insight into cardiac arrhythmogenesis. The aim of this work is to theoretically substantiate and verify a novel approach allowing for the quantification of the individual ionic current components of ER. A method of analysis of the primary, initial conditions-setting restitution processes (apart from the secondary, test pulse-affected ones) is proposed. Both processes are described as sums of their measurable constituents. It is demonstrated that the optimum parameter of ER is the electric charge that is transferred through ionic channels and carriers during the test impulse. The theory was tested by using voltage-clamped canine ventricular preparations and by computer simulations. The experimental ER curve of canine ventricular muscle was constructed using action potential (AP) plateau voltage and half-repolarization time as parameters. At 30 degrees C and 0.5 Hz stimulation, the ER curve peaked, on average, after 400 ms with a 10% overshoot. Of this plateau elevation, 50% was due to 4-aminopyridine-sensitive transient outward current and 44% was due to verapamil-sensitive current. The delayed outward current antagonized the overshoot by about 6%. It was found that the initial conditions (i.e. the primary restitution processes) tend to strongly alter the plateau voltage of the premature AP. However, the final deviation is by about one order less. It is concluded that the voltage-dependent secondary processes counteract the effect of the primary processes, thereby suggesting strong negative feedback control of natural APs.     

Effect of thyroid hormone treatment on responses of the isolated working rat heart

Hearts from rats pretreated either with L-triiodothyronine (T3) or with L-thyroxine (T4) exhibited changed function curve characteristics on the working heart apparatus compared with hearts from vehicle-treated rats. There was no supersensitivity of the hyperthyroid myocardium to the inotropic effect of isoproterenol as estimated by pD2 values. There were significant increases in +dP/dt and -dP/dt in hyperthyroid working hearts over the entire range of the function curve. T3 hearts showed much shorter relaxation times and total contraction times throughout the function curve. T4 hearts showed significantly reduced relaxation times and total contraction times as compared with control at all left atrial filling pressures under 15 cm of water. At high filling pressures T4 heart relaxation times and total contraction times were not different from control, but were however, significantly increased from those of T3 hearts. Area under the left ventricular pressure curve was unchanged by thyroid hormone pretreatment. Heart weight increased about 15% following either T3 or T4 treatment while the increases in (+) or (-) dP/dt and the left ventricular developed pressure (LVDP) were about 20-30%. The increase in cardiac mass certainly played a role in the increased cardiac function. Potency of isoproterenol in hyperthyroid working heart preparations was unchanged from control. The pD2 values, as determined from +dP/dt data, were 8.8 +/- 0.15 for T3-treated hearts, 8.25 +/- 0.40 for T4-treated hearts, and 8.18 +/- 0.12 for euthyroid hearts. While the mechanism(s) for the altered performance of the hyperthyroid working heart are not absolutely known, possible biochemical and physiological changes which may be implicated are discussed.     

The effect of residual strain on the diastolic function of the left ventricle as predicted by a structural model

The unloaded heart is not stress-free. It is subjected to residual stress and strain. Their extent and influence on the global performance of the left ventricle and on local phenomena in the ventricular wall are studied by model simulation. The analysis focuses on the equatorial region of the ventricle, with an approximate thick-walled cylindrical geometry. The in vivo myocardium is considered to be incompressible, consisting of fibers embedded in a fluid matrix, with transmurally varying anisotropic microstructure in accordance with morphological characteristics.

The results show that residual strain is transmurally distributed with a pattern and magnitude which agree well with measurements. The calculated residual strains are within mean ± one standard deviation of the measured ones. Their magnitude was found to increase with increasing opening angle and with increasing wall thickness. The residual strain was found to have several effects on ventricular function: At volumes higher than the reference one it gives rise to more uniform transmural distributions of stress and intramyocardial pressure; it causes about 50% increase in the ventricular compliance at high volumes and doubles the suction of atrial blood at low volumes, thus facilitating the diastolic filling. In addition, residual strains cause bias of in vivo measured strains from their true values. This may significantly affect physiological interpretation of measured ventricular deformations.

In conclusion, the present structural analysis predicts that residual strain has favorable effect on left-ventricular diastolic performance, and gives rise to more uniform ventricular stress distribution.     

A Parametric ROC Model‐Based Approach for Evaluating the Predictiveness of Continuous Markers in Case–Control Studies

Summary The predictiveness curve shows the population distribution of risk endowed by a marker or risk prediction model. It provides a means for assessing the model's capacity for stratifying the population according to risk. Methods for making inference about the predictiveness curve have been developed using cross‐sectional or cohort data. Here we consider inference based on case–control studies, which are far more common in practice. We investigate the relationship between the ROC curve and the predictiveness curve. Insights about their relationship provide alternative ROC interpretations for the predictiveness curve and for a previously proposed summary index of it. Next the relationship motivates ROC based methods for estimating the predictiveness curve. An important advantage of these methods over previously proposed methods is that they are rank invariant. In addition they provide a way of combining information across populations that have similar ROC curves but varying prevalence of the outcome. We apply the methods to prostate‐specific antigen (PSA), a marker for predicting risk of prostate cancer.     

急性重症病毒性心肌炎的临床特征分析

目的:探讨急性重症病毒性心肌炎的临床特征及心脏彩超和血清心肌损伤标志物对重症病毒性心肌炎的早期临床诊断价值。方法:回顾性分析2013年6月至2015年8月入住我院心脏科的临床诊断为急性心肌炎的患者27例,其中符合急性重症心肌炎诊断标准的患者10例,其余17例为非重症心肌炎,另选取10例入院检查后排除心血管疾病的患者为健康对照组。对三组患者的一般临床资料、心脏彩超结果及心肌损伤标志物结果进行分析,选取有统计学差异的指标行ROC曲线分析得出预测重症心肌炎的效能。结果:重症心肌炎组左室室间隔厚度、左室后壁厚度、左房内径、血浆B型尿钠肽较其余两组显著增高,进一步行ROC曲线分析提示左室室间隔厚度、左室后壁厚度预测重症心肌炎的敏感性分别为80%、70%,特异性均为94%,临界值分别为0.855 cm、0.875 cm。结论:急性心肌炎患者室壁厚度增加,当左室室间隔厚度0.855 cm或左室后壁厚度0.875 cm时需引起重视,警惕患者可能进展至重症病毒性心肌炎。     

Effect of beta-adrenergic blockade on dynamic electrical restitution in vivo

The slope of the action potential duration (APD) restitution curve may be a significant determinant of the propensity to develop ventricular fibrillation, with steeper slopes associated with a more arrhythmogenic substrate. We hypothesized that one mechanism by which beta-blockers reduce sudden cardiac death is by flattening the APD restitution curve. Therefore, we investigated whether infusion of esmolol modulates the APD restitution curve in vivo. In 10 Yorkshire pigs, dynamic APD restitution curves were determined from measurements of APD at 90% repolarization with a monophasic action potential catheter positioned against the right ventricular septum during right ventricular apical pacing in the basal state and during infusion of esmolol. APD restitution curves were fitted to the three-parameter (a, b, c) exponential equation, APD = a.[1 - e((-b.DI))] + c, where DI is the diastolic interval. Esmolol decreased the maximal APD slope, 0.68 +/- 0.14 vs. 0.94 +/- 0.24 (baseline), P = 0.002, and flattened the APD restitution curve at shorter DIs, 75 and 100 ms (P < 0.05). To compare the slopes of the APD restitution curves at similar steady states, slopes were also computed at points of intersection between the restitution curve and the lines representing pacing at a fixed cycle length (CL) of 200, 225, 250, 275, and 300 ms using the relationship CL = APD + DI. Esmolol decreased APD restitution slopes at CLs 200-275 ms (P < 0.05). Esmolol flattens the cardiac APD restitution curve in vivo, particularly at shorter CLs and DIs. This may represent a novel mechanism by which beta-blockers prevent sudden cardiac death.     

Coronary flow reserve and the J curve relation between diastolic blood pressure and myocardial infarction.

The results of several large studies of hypertension and follow up studies on insured people have indicated that the lower the blood pressure the better for longevity. These studies excluded subjects with overt ischaemia. More recently long term studies of hypertension that included patients with more severe forms of hypertension and did not exclude those with overt ischaemia have shown a J shaped relation between diastolic blood pressure during treatment and myocardial infarction; the lowest point (the J point) was at a diastolic blood pressure (phase V) between 85 and 90 mm Hg. The J curve seems to be independent of treatment, pulse pressure, and the degree of fall in diastolic blood pressure and is unlikely to be caused by poor left ventricular function. The most probable explanation is that subjects who have severe stenosis of the coronary artery as well as hypertension have a poor coronary flow reserve, which makes the myocardium vulnerable to coronary perfusion pressures that are tolerated by patients without ischaemia, particularly at high heart rates. An optimal diastolic blood pressure (phase V) for such patients is about 85 mm Hg, though particular caution is appropriate when treating very old patients (84 and over) and patients aged 60-79 who have isolated systolic hypertension.     

Pressure-volume relationship in the right ventricle]

The curve of the pressure-volume relationships of the right ventricular cavity is not a mono-exponential one. It can be characterized by the presence of two successive segments: linear and exponential. The points that constitute the first of them could not be subjected to Starling's law. This is material for the physiopathology of the tamponade.     

缺血对心室浦肯野纤维跨膜电位和起搏离子流的影响

采用细胞内微电极和双微电极电压箝制术观察缺血对绵羊心室浦肯野纤维跨膜电位和起搏离子流（Ｉｆ）的影响。结果：模拟缺血液灌流３０ｍｉｎ,浦肯野纤维最大舒张电位（ＭＤＰ）、动作电位幅度（ＡＰＡ）明显减少;动作电位时程ＡＰＤ５０,ＡＰＤ９０明显缩短（ｎ＝１５Ｐ＜０．０１）;起搏离子流（Ｉｆ）,幅度降低,激活曲线向超极化方向移位,最大激活时间及半最大激活时间延长（ｎ＝１３Ｐ＜０．００１）。上述结果表明：心肌缺血时,心室浦肯野细胞跨膜电位及正常起搏活动不是增强,而是减弱。提示缺血性室性心律失常不是由于正常心室自律活动异常增强引起     

Force regulation by Ca2+ in skinned single cardiac myocytes of frog.

Atrial and ventricular myocytes 200 to 300 microm long containing one to five myofibrils are isolated from frog hearts. After a cell is caught and held between two suction micropipettes the surface membrane is destroyed by briefly jetting relaxing solution containing 0.05% Triton X-100 on it from a third micropipette. Jetting buffered Ca2+ from other pipettes produces sustained contractions that relax completely on cessation. The pCa/force relationship is determined at 20 degrees C by perfusing a closely spaced sequence of pCa concentrations (pCa = -log[Ca2+]) past the skinned myocyte. At each step in the pCa series quick release of the myocyte length defines the tension baseline and quick restretch allows the kinetics of the return to steady tension to be observed. The pCa/force data fit to the Hill equation for atrial and ventricular myocytes yield, respectively, a pK (curve midpoint) of 5.86 +/- 0.03 (mean +/- SE.; n = 7) and 5.87 +/- 0.02 (n = 18) and an nH (slope) of 4.3 +/- 0.34 and 5.1 +/- 0.35. These slopes are about double those reported previously, suggesting that the cooperativity of Ca2+ activation in frog cardiac myofibrils is as strong as in fast skeletal muscle. The shape of the pCa/force relationship differs from that usually reported for skeletal muscle in that it closely follows the ideal fitted Hill plot with a single slope while that of skeletal muscle appears steeper in the lower than in the upper half. The rate of tension redevelopment following release restretch protocol increases with Ca2+ >10-fold and continues to rise after Ca2+ activated tension saturates. This finding provides support for a strong kinetic mechanism of force regulation by Ca2+ in frog cardiac muscle, at variance with previous reports on mammalian heart muscle. The maximum rate of tension redevelopment following restretch is approximately twofold faster for atrial than for ventricular myocytes, in accord with the idea that the intrinsic speed of the contractile proteins is faster in atrial than in ventricular myocardium.     

Simulated ischemia enhances L-type calcium current in pacemaker cells isolated from the rabbit sinoatrial node

Ischemic-like conditions (a glucose-free, pH 6.6 Tyrode solution bubbled with 100% N(2)) enhance L-type Ca current (I(Ca,L)) in single pacemaker cells (PCs) isolated from the rabbit sinoatrial node (SAN). In contrast, studies of ventricular myocytes have shown that acidic extracellular pH, as employed in our "ischemic" Tyrode, reduces I(Ca,L). Therefore, our goal was to explain why I(Ca,L) is increased by "ischemia" in SAN PCs. The major findings were the following: 1) blockade of Ca-induced Ca release with ryanodine, exposure of PCs to BAPTA-AM, or replacement of extracellular Ca(2+) with Ba(2+) failed to prevent the ischemia-induced enhancement of I(Ca,L); 2) inhibition of protein kinase A with H-89, or calcium/calmodulin-dependent protein kinase II with KN-93, reduced I(Ca,L) but did not prevent its augmentation by ischemia; 3) ischemic Tyrode or pH 6.6 Tyrode shifted the steady-state inactivation curve in the positive direction, thereby reducing inactivation; 4) ischemic Tyrode increased the maximum conductance but did not affect the activation curve; 5) in rabbit atrial myocytes isolated and studied with exactly the same techniques used for SAN PCs, ischemic Tyrode reduced the maximum conductance and shifted the activation curve in the positive direction; pH 6.6 Tyrode also shifted the steady-state inactivation curve in the positive direction. We conclude that the acidic pH of ischemic Tyrode enhances I(Ca,L) in SAN PCs, because it increases the maximum conductance and reduces inactivation. Furthermore, the opposite results obtained with rabbit atrial myocytes cannot be explained by differences in cell isolation or patch-clamp techniques.     

The changing spectrum of arrhythmogenic (right ventricular) cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a clinically and genetically heterogeneous heart muscle disorder associated with ventricular arrhythmias and risk of sudden death. The disease is heredo-familial, and mutations in desmosomal genes have been identified in about half of patients. Recent experimental models confirm this disease develops after birth due to progressive myocardial dystrophy. Genotype-phenotype correlations, including magnetic resonance and pathology studies on heart specimens, are currently demonstrating that the spectrum of the disease is wider than initially thought and usually referred to with the adjective "right ventricular", with the evidence of biventricular or even isolated left ventricular forms, so that it is increasingly identified simply as "arrhythmogenic cardiomyopathy". A revision of the diagnostic criteria encompassing familial, electrocardiographic, arrhythmic, morpho-functional and histopathologic findings, has been made to improve diagnostic sensitivity and specificity, in particular of the concealed forms and left-dominant subtypes of the disease. Experimental models are mandatory to gain an insight into the cascade of cellular and molecular events leading from gene defect to myocardial dystrophy in ARVC.