肥厚型心肌病患者的心电图特点分析

目的探讨肥厚型心肌病(HCM)患者的心电图特点。方法 36例已确诊的HCM患者,按肥厚部位分为室间隔肥厚21例,游离壁肥厚3例,心尖部肥厚6例,全心弥漫性肥厚6例,分析其心电图特点。结果 ST-T改变最多34例(94.4%),ST段下移的程度在4型间差异无统计学意义(P0.05),T波倒置振幅超过0.5 mV者26例(72.2%),T波倒置在心尖肥厚组多于间隔肥厚组(P0.05)。异常Q波13例(36.1%),病理性Q波多出现在室间隔肥厚型患者中,间隔肥厚为主患者中,11例(52.4%)存在病理性Q波,心尖肥厚、单纯游离壁肥厚组均仅1例心电图存在病理性Q波。结论 HCM患者的心电图表现呈多样性,特异性不高,但敏感性较高。ST段改变、T波倒置、异常Q波是肥厚型心肌病患者的主要心电图表现。     

肥厚型心肌病患者心电图分析

目的探讨肥厚型心肌病住院患者的心电图特点。方法对1994年5月～2005年7月北京大学人民医院和北京世纪坛医院收治的经超声心动图诊断为肥厚型心肌病的住院患者76例,分析其心电图特点。结果按肥厚的部位分为单纯室间隔肥厚或室间隔肥厚为主组(46例)、单纯心尖肥厚组(14例)、单纯游离壁肥厚组(6例)和弥漫性肥厚组(10例)。间隔肥厚为主组患者中,23例(50.0%)存在病理性Q波,其中间隔厚度超过2.0cm者10例(42.5%);而在另23例无病理性Q波患者,间隔厚度超过2.0cm者仅5例(21.7%)。心尖肥厚组和单纯游离壁肥厚组均仅1例心电图存在病理性Q波。QRS波群宽度在各组无显著性差异(p>0.05)。76例患者中,心电图符合左室肥厚(SV1 RV5≥4.0mV)诊断标准的23例(30.3%),符合RV4>RV5>RV6(或RV3>RV4>RV5)者34例(44.7%),ST-T改变共71例(93.4%),ST段下移超过0.1mV者53例(69.7%),T波深倒置振幅超过0.5mV者30例(39.5%)。T波深倒置在心尖肥厚组多于间隔肥厚组(P=0.02),但T波倒置深度与心尖肥厚程度无明显相关(p=0.40)。间隔肥厚为主组中梗阻型和非梗阻型各项心电图指标无显著性差异(p>0.05)。结论病理性Q波多出现在室间隔肥厚为主型患者,T波深倒置在心尖肥厚组多于间隔肥厚组,但T波倒置深度与心尖肥厚程度无明显相关。     

老年肥厚型心肌病与高血压左室肥厚患者临床特点的比较

目的 分析老年肥厚型心肌病与老年高血压左室肥厚患者的临床特点.方法 回顾性分析老年肥厚型心肌病患者(35例)与老年高血压左室肥厚患者(35例)的症状和体征及心电图、超声心动图的差异.结果 老年肥厚型心肌病患者均无高血压史.两组年龄、性别、脑血管病史及肥厚型心肌病家族史比较,差异均无统计学意义(均为P＞0.05).老年肥厚型心肌病患者中,晕厥者5例(14.3%),高血压左室肥厚患者中,无晕厥者,2组比较,差异有统计学意义(P＜0.05).老年肥厚型心肌病患者中无心脏杂音者9例(25.7%),明显少于高血压左室肥厚患者[23例(65.7%),P＜0.05].心电图示:老年肥厚型心肌病患者中,有异常Q波者10例(28.6%),较高血压左室肥厚患者的1例(2.9%)多(P＜0.05).老年肥厚型心肌病患者中心房颤动(房颤)及ST-T改变者分别为11例(31.4%)及34例(97.1%),明显多于高血压左室肥厚患者的3例(8.6%)及26例(74.3%),均为P＜0.05.超声心动图示:老年肥厚型心肌病患者的左室后壁厚度为(9.5±1.1)mm,明显薄于高血压左室肥厚患者的(12.6±1.0)mm(P＜0.01),左房内径老年肥厚型心肌病患者为(41.6±6.3)mm,高血压左室肥厚患者为(38.6±5.5)mm,两组差异有统计学意义(P＜0.05);老年肥厚型心肌病患者二尖瓣血流频谱E/A＜1者15例(42.9%),明显少于高血压左室肥厚患者的32例(91.4%),P＜0.05.老年肥厚型心肌病患者有主动脉瓣钙化者7例(20.0%),高血压左室肥厚患者20例(57.1%),二者差异有统计学意义(P＜0.05),室间隔厚度、左室内径与射血分数2组相似(均为P＞0.05).结论 老年肥厚型心肌病患者临床表现有晕厥者多,心脏有明显的杂音,心电图有异常Q波及房颤者较多,超声心动图显示左室不对称性肥厚多;高血压左室肥厚患者左室肥厚多为对称性,合并主动脉瓣钙化者多.     

肥厚型心肌病出现巨大倒置T波的临床意义

日本学者曾描述一种伴有巨大倒置 T 波的、局限于心尖部的肥厚型心肌病。本研究以西方病人为对象,比较伴有和没有巨大倒置T 波的肥厚型心肌病的临床、二维超声心动图、放射性同位素心室显像以及48小时动态心电图的特征。方法 A 组27例病人伴有而 B 组56例病人没有巨大倒置 T 波(波幅≥10mm)。临床特征包括诊断时年龄、家族史、胸疼,呼吸困难和昏厥等。在心电图上观察左室肥厚程度、有无右室肥厚以及异常 Q 波。二维超声心动图评价左室壁厚度、心室大小、室间隔不对称     

伴有高血压的肥厚型心肌病误诊分析

目的对伴有高血压的肥厚型心肌病的诊断进行探讨。方法以心电图、X线检查、超声心动图、冠状动脉造影及左室造影等检查方法,诊断12例肥厚型心肌病。结果12例肥厚型心肌病均伴有高血压,其中11例刚开始误诊为冠心病。心电图7例有左室肥厚表现,10例有胸前导联T波倒置、ST段水平压低,2例出现病理性Q波等;X线检查胸正位片心胸比例正常11例,1例>0.5;超声心动图示室间隔舒张期平均厚度1.64±0.35cm;左室后壁舒张期平均厚度1.08±0.11cm;IVSd/LVPWd平均1.51±0.34;冠状动脉造影及左室造影示冠状动脉造影8例正常,3例轻度不规则病变、血管狭窄程度<30~40%。结论肥厚型心肌病易出现误诊,但只要提高警惕,针对心电图及心脏杂音的特点,提出预见性诊断,进行针对性的检查,可以减少误诊。     

肥厚型心肌病临床心电图表现

肥厚型心肌病是以心肌非对称性肥厚,心室内腔变小为特征,其心电图表现是:ST—T改变:大部分出现ST段下移,T波低平、倒置。左室高电压、左室肥厚。出现病理性Q波,少数病人可在V_4～V_6或近Ⅱ、Ⅲ、aVF中出现深Q波。室间隔Q波(Ⅰ、aVL、V_5、V_6)的消失。出现各种心律失常。如室间隔肥厚深Q多在Ⅱ、Ⅲ、aVF导联出现。对于Q波的变认:因某些肢体导联和左胸导联中可出现Q波,但其时间应小于0.03s,深度应小于后继R波的1/4。正常人V_5、V_6导联中可出现q波。当额面电轴有偏时,Ⅲ和     

肥厚型心肌病患者的心电图改变

肥厚型心肌病的病理改变主要以心室肌肥厚为特征,并且还会影响到左心室以及室间隔,很多是非对称性左室肥厚。该病的心电图异常率和患者有无症状、室间隔肥厚程度密切相关。而ST-T异常是肥厚型心肌病较常见的心电图表现之一。本文主要对肥厚型心肌病,尤其是心尖肥厚型心肌病的心电图改变现象进行综述。     

心尖肥厚型心肌病的临床诊断探讨

目的 了解心尖肥厚型心肌病的临床表现和辅助检查特点。方法 总结２９例心尖肥厚型心肌病的临床表现和心电图,超声心动图,核素心肌断层显像,运动平板心电图及冠状动脉和左室造影的特征,确定心尖肥厚型心肌病的诊断方法。结果 心电图显示以胸导为主的导联Ｒ波振幅呈Ｖ４≥Ｖ５〉Ｖ３关系增高,同时伴有Ｔ波对称性深倒置,超声心动图和核素心肌断层显像显示心尖部肌肉肥厚,２０例活动平板心电图有心肌缺血,左心室造影心尖部肌     

老年人心尖肥厚型心肌病的临床特点

目的 了解老年人心尖肥厚型心肌病的临床特征及正确诊治方法。方法 分析7例老年心尖肥厚型心肌病患者的临床表现和心电图、超声心动图、心室造影及冠状动脉(冠脉)造影等检查特点，总结老年心尖肥厚型心肌病临床特征。结果 6例出现胸闷、胸痛，4例心界向左侧扩大，2例可闻第四心音。心电图显示胸导为主导联上R波增高、ST段压低及对称性T波倒置，5例经超声心动图证实心尖处心肌肥厚，5例左心室造影时呈“黑桃”样图形，1例冠脉造影有轻度狭窄。结论 老年人心尖肥厚型心肌病多属于黑桃型，可并存冠脉病变。心电图、超声心动图、心室造影及冠脉造影等检查有助于该病的诊断。     

肥厚梗阻性心肌病化学消融前后心电图变化及其意义

目的分析肥厚梗阻性心肌病(HOCM)化学消融前后的心电图变化及其临床意义。方法 HOCM 76例经皮室间隔心肌化学消融术与梗阻程度较轻的29例肥厚型心肌病作对照研究,以常规12导联同步心电图V1-Ptf(-mm·s)、V1~3R波增高、左室高电压、左室导联ST-T段压低、前间壁或下壁导联病理性Q波、前壁导联T波倒置为观察指标。比较入院时两组心电图相关参数的差别;观察梗阻组手术后心电图即刻改变,及半年后与术前的差别;观察对照组药物治疗6个月后心电图改变及其与入院时的差别。结果 1梗阻组V1~3R波幅度增加病例显著低于对照组(14.5%vs 41.4%,P0.01);T波倒置梗阻组显著低于对照组(51.3%vs 93.1%,,P0.001);2梗阻组术后即刻心电图:典型STEMI样变化及其演变,心律失常呈多样化;梗阻组消融术后半年V1-Ptf已较术前明显降低[(0.036±0.012)vs(0.051±0.014),P0.001];病理性Q波病例数较术前显著增加(94.7%vs 28.9%,P0.001);3对照组药物治疗后半年V1-Ptf显著降低[(0.039±0.010)vs(0.047±0.010),P0.001];结论 HOCM室间隔心肌化学消融是一有效治疗方法,左室高电压和ST-T改变较前改善;病理性Q波是心肌化学消融成功的标志之一,V1-Ptf可作为梗阻型心肌病化学消融中长期疗效观察指标,药物是肥厚型心肌病的基础治疗措施。     

Relation of electrocardiographic abnormalities and patterns of left ventricular hypertrophy identified by 2-dimensional echocardiography in patients with hypertrophic cardiomyopathy

Distribution of left ventricular (LV) hypertrophy was assessed by wide-angle, 2-dimensional (2-D) echocardiography in 153 patients with hypertrophic cardiomyopathy and compared with the scalar electrocardiogram in the same patients. The most common electrocardiographic alterations were S-T segment changes and T-wave inversion (61%), LV hypertrophy (47%), abnormal Q waves (25%), and left atrial enlargement (24%). LV hypertrophy on the electrocardiogram was significantly more common in patients with the most extensive distribution of LV hypertrophy on 2-D echocardiogram involving substantial portions of both the ventricular septum and LV free wall (type III; 51 of 69, 74%) than in those with more limited distribution of LV hypertrophy (21 of 84, 25%; p less than 0.001). Most patients with hypertrophic cardiomyopathy and normal electrocardiograms (13 of 23) had localized (type I) hypertrophy, but only 4 had the extensive type III pattern of hypertrophy. Abnormal Q waves were significantly more common in those patients without hypertrophy of the anterior, basal septum (type IV; 15 of 27, 56%) than in those with basal septal hypertrophy (23 of 126, 18%; p less than 0.001); abnormal Q waves were uncommon in extensive type III distribution of hypertrophy (13 of 69, 19%). Thus, although no single electrocardiographic abnormality is characteristic of hypertrophic cardiomyopathy, 2-D echocardiography clarifies the significance of certain electrocardiographic patterns: (1) LV hypertrophy on the electrocardiogram, although present in only about half of the study group, was a relatively sensitive (74%) marker for extensive (type III) LV hypertrophy; (2) abnormal Q waves cannot be explained by ventricular septal hypertrophy alone; and (3) a normal electrocardiogram was most commonly a manifestation of localized LV hypertrophy.     

少见类型肥厚型心肌病的超声心动图诊断与鉴别诊断

分析少见类型肥厚型心肌病患者的超声心动图特点 ,提高超声心动图对该病诊断的准确性。利用Acuson12 8XP10彩色电脑声像仪分析了 38例经临床及超声心动图诊断为肥厚型心肌病患者的有关资料 ,采取二维超声心动图多切面、多角度观测室间隔、游离壁厚度和活动幅度以及二尖瓣活动特点 ;M型超声心动图Ⅱa区、Ⅳ区测量房室腔内径及室壁厚度 ;多普勒超声心动图记录左室流出道血流速度、二尖瓣频谱形态及二尖瓣返流速度。 38例肥厚型心肌病患者中 ,以Ⅲ型最为多见 ,占 4 5%。少见类型中心尖肥厚型 2例 ,心尖最厚达 33mm ;后下壁及下间隔肥厚型各 1例 ;对称型肥厚者 2例 ;高血压合并肥厚型心肌病者 2例。肥厚型心肌病的肥厚心肌分布比较复杂 ,少见类型肥厚型心肌病的诊断更应注意多切面、多角度进行探查 ,避免漏诊及误诊。     

Feasibility of identifying amyloid and hypertrophic cardiomyopathy with the use of computerized quantitative texture analysis of clinical echocardiographic data

Ultrasound tissue characterization, the evaluation of certain physical properties of a tissue based on its acoustic properties, is an evolving application in echocardiography. The ability to identify acutely and chronically injured tissue has been demonstrated in a number of animal studies, but data in humans are limited. The present study tested the hypothesis that quantitative echocardiographic texture analysis, a method of evaluating the spatial pattern of echoes in echocardiographic images, would differentiate amyloid and hypertrophic cardiomyopathy from normal myocardium. Routine clinical echocardiographic data were obtained on 34 subjects at the Mayo Clinic (10 normal subjects, 10 patients with amyloid heart disease, 8 patients with hypertrophic cardiomyopathy and 6 patients with left ventricular hypertrophy due to hypertension). Standard videotape recordings of these echocardiograms were analyzed at the University of Iowa. Echocardiographic data were digitized with use of a calibrated, 256 gray level digitization system. Quantitative texture analysis was performed on data from the ventricular septum and posterior left ventricular wall in end-diastolic and end-systolic, short-axis and long-axis echocardiographic images. The gray level run length texture variables were able to discriminate hypertrophic cardiomyopathy and amyloid heart disease from normal myocardium and from each other (p less than 0.0083 for comparisons of the quantitative texture features of amyloid versus hypertrophic cardiomyopathy versus normal by multivariate analysis of variance). The texture of the myocardium in hypertensive left ventricular hypertrophy not associated with amyloid or hypertrophic cardiomyopathy was in general not significantly different from that of normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)     

Echocardiographic assessment of right ventricular obstruction in hypertrophic cardiomyopathy.

Echocardiography was used to evaluate the incidence, flow dynamics and morphological characteristics of right ventricular obstruction in 91 patients with hypertrophic cardiomyopathy. Color flow mapping was used to define the sites of obstruction in the left and right ventricles. Ventricular obstruction was considered to be present if the flow velocity was less than 2.0 m/s as measured by continuous wave Doppler. The thickness of both the right ventricular free wall and anterior ventricular septum was measured to assess the magnitude and extent of hypertrophy. Right ventricular obstruction was present in 14 patients of whom 6 (43%) had left ventricular obstruction also. The right ventricular obstructions were found in the outflow tract (9 patients), mid-base septal bulge (2 patients) and apical trabecular region (3 patients). Doppler waveform was confined to systole in all patients with obstruction in the outflow tract and in one of the patients with mid-base septal bulge. Moreover, the flow wave persisted into early diastole in 4 patients, including 2 with apical trabecular obstruction. The thickness of both the right ventricular free wall and anterior ventricular septum suggested that these hypertrophied regions were the sites of right ventricular obstruction. Thus, echocardiography was useful in evaluating right ventricular obstruction in hypertrophic cardiomyopathy.     

Comparison of M-mode echocardiography and angiography in the evaluation of left ventricular hypertrophy

The authors analysed in a group of 82 patients with a symmetric left ventricle and a homogeneous ventricular wall thickness the reliability of M-mode echocardiography in recognizing left ventricular hypertrophy. In concentric hypertrophies, a sufficient diagnostic criterion is ventricular wall thickness. Measurement of the interventricular septum offers a better correlation with angiographic values (r = 0.609, p less than 0.001) than measurement of the posterior wall (r = 0.358, p less than 0.01); a correct diagnosis can be determined in 84%. In excentric hypertrophies, the hypertrophy must be assessed on the basis of calculating the left ventricular mass. The most accurate of echocardiographic methods proved to be the calculation according to the authors' own formula (r = 0.760, p less than 0.001), which recognizes left ventricular hypertrophy correctly in 85%. The diagnostic correctness of Teichholz' formula is 80% and of the cubic formula 74%. Fortuin's equations proved to be of no value for documenting ventricular hypertrophy. In a group of 13 patients with hypertrophic cardiomyopathy, the correlation between angiographic and echocardiographic values of the left ventricular mass was very low (r = 0.534, p = 0.05).     

Value and limitations of two dimensional echocardiography in assessment of cardiomyopathy

Primary myocardial diseases have traditionally been classified into congestive, hypertrophic and restrictive varieties. M mode echocardiography has proved extremely valuable in distinguishing congestive cardiomyopathy with major ventricular dilation and poor contractile performance from hypertrophic cardiomyopathy with predominant left ventricular hypertrophy (septum greater than posterior wall) and normal pump performance, and restrictive disorders with symmetric ventricular wall thickening and normal or diminished contractile function. The contributions of two dimensional echocardiography to the evaluation of patients with congestive or restrictive cardiomyopathy have been limited to certain specific situations, such as the recognition of left ventricular mural thrombi.

Twenty-five patients with hypertrophic cardiomyopathy were studied to assess two dimensional echocardiography in the evaluation of patients with this disorder, Two dimensional echocardiography indicated that hypertrophy of the interventricular septum is not uniform from apex to base in all patients but may be greatest in the apical, mid or basal third. In addition, the anterior free wall of the left ventricle was involved in the hypertrophic process in approximately 50 percent of patients. Two dimensional echocardiography documented that the location of systolic anterior motion of the mitral valve in patients with hypertrophic cardiomyopathy is most often at the junction of the mitral valve leaflets and chordae ten-dineae, although the chordae themselves and even the papillary muscles may be involved in this movement. The heterogeneity of these characteristics may enable patients with hypertrophic cardiomyopathy to be classified into subsets of patients in whom meaningful therapeutic and prognostic implications may be derived. Finally, data derived from two dimensional echocardiography have shown that, although the left ventricle in hypertrophic cardiomyopathy conforms in some degree to the configuration of a catenoid, this geometric conformation is unlikely to account for the genesis of this disorder.     

Echocardiographic spectrum of hypertrophic cardiomyopathy.

Echocardiographic patterns in 15 patients with hypertrophic cardiomyopathy were compared with those in 30 healthy persons. Correlations with angiocardiographic data indicated that most of the anatomical abnormalities in hypertrophic cardiomyopathy can be assessed reliably by echocardiography. These include abnormal mitral valve motion, a reduction of the anteroposterior dimension of the left ventricular outflow tract and of the left and right ventricular cavities, increased thickness of the interventricular septum and the posterior left ventricular wall. Comparision of the haemodynamic and echocardiographic data showed that some degree of abnormal mitral valve motion during systole may occur in the absence of left ventricular outflow tract obstruction. On the other hand, it need not always be present with left ventricular outflow tract obstruction. Other, hitherto unrecognized, abnormalities in hypertrophic cardiomyopathy detected by this technique were: (1) Aortic valve regurgitation in three out of nine patients with evidence of left ventricular cutflow tract obstruction at cardiac catheterization. (2) Left ventricular inflow tract obstruction at the mitral valve level associated with gross septal hypertrophy (five cases). (3) Abnormal forward displacement of the posterior mitral valve leaflet and of the chordae tendineae during systole in 10 patients, in seven of whom there was confirmatory angiocardiographic evidence. Seven patients with miscellaneous cardiac disorders are described in whom asymmetric septal hypertrophy was revealed by echocardiography. In one of these patients coexisting hypertrophic cardiomyopathy was excluded histologically; thus asymmetrical septal hypertrophy is not confined to patients with hypertrophic cardiomyopathy.     

Echocardiographic spectrum of hypertrophic cardiomyopathy.

Echocardiographic patterns in 15 patients with hypertrophic cardiomyopathy were compared with those in 30 healthy persons. Correlations with angiocardiographic data indicated that most of the anatomical abnormalities in hypertrophic cardiomyopathy can be assessed reliably by echocardiography. These include abnormal mitral valve motion, a reduction of the anteroposterior dimension of the left ventricular outflow tract and of the left and right ventricular cavities, increased thickness of the interventricular septum and the posterior left ventricular wall. Comparision of the haemodynamic and echocardiographic data showed that some degree of abnormal mitral valve motion during systole may occur in the absence of left ventricular outflow tract obstruction. On the other hand, it need not always be present with left ventricular outflow tract obstruction. Other, hitherto unrecognized, abnormalities in hypertrophic cardiomyopathy detected by this technique were: (1) Aortic valve regurgitation in three out of nine patients with evidence of left ventricular cutflow tract obstruction at cardiac catheterization. (2) Left ventricular inflow tract obstruction at the mitral valve level associated with gross septal hypertrophy (five cases). (3) Abnormal forward displacement of the posterior mitral valve leaflet and of the chordae tendineae during systole in 10 patients, in seven of whom there was confirmatory angiocardiographic evidence. Seven patients with miscellaneous cardiac disorders are described in whom asymmetric septal hypertrophy was revealed by echocardiography. In one of these patients coexisting hypertrophic cardiomyopathy was excluded histologically; thus asymmetrical septal hypertrophy is not confined to patients with hypertrophic cardiomyopathy.     

Extreme cardiac hypertrophy in athletes. Morphological and functional echographic study

Cardiac hypertrophy is an adaptation phenomenon of the heart as a result of increased hemodynamic load due to intense and prolonged training in athletes. This is mainly seen in endurance athletes. In some cases cardiac hypertrophy can mimic hypertrophic cardiomyopathy, specially if hypertrophy is mainly localized at the interventricular septum as compared to the left ventricular free wall. In our study we tried to evaluate the different diagnostic features obtained by echocardiography and clinical examination in a group of 23 athletes with marked hypertrophy (all were participants to the 1984 Olympic Games held in Los Angeles) as compared to a group of 11 sportsmen with non-obstructive hypertrophic cardiomyopathy (HC). Cardiomyopathy was diagnosed on the basis of clinical, echocardiographic and angio-scintigraphic findings. The 23 athletes were selected on the basis of M-Mode and 2D echocardiographic thickness of the interventricular septum (IVS) which was in diastole greater than or equal to 15 mm. They were all asymptomatic, only 4 of the 23 athletes had ECG anomalies due to left axis deviation (LAS) and T wave inversion. Only 4 of the subjects with HC had a family history of HC. ECG changes were the following: T wave inversion (9 subjects), left axis deviation (LAD) (4 subjects), deep Q wave in D2-3, aVF, V5-6 (2 subjects) and low voltage R wave in V5-6 (1 subject). All the athletes had marked hypertrophy of the IVS. Interventricular septum thickness (IVST) was 15.7 +/- 0.6 mm, with a range from 15 to 17.5 mm. Posterior wall thickness (PWT) was 13.7 +/- 1.1 with a range from 12 to 16 mm. The sportsmen with HC had an IVST of 16.2 +/- 3.5 mm and a PWT of 11.3 +/- 1.5 mm. The IVST/PWT ratio was significantly lower (p less than 0.01) in the athletes (1.14 +/- 0.02) when compared to the group with HC (1.4 +/- 0.3). In 7 of the subjects with HC the hypertrophy was mainly localized at the anterolateral segment of the interventricular septum (in 4 of these subjects the hypertrophy involved also the antero-lateral part of the left ventricular free wall).(ABSTRACT TRUNCATED AT 400 WORDS)