表柔比星诱导小鼠药物心肌病模型的建立及清醒状态下超声评价该模型的研究

目的建立表柔比星诱导的小鼠心肌病模型并探讨高频率超声心动图对其检测的可行性。方法按电脑随机数字表法随机将70只小鼠分为对照组和给药组各35只．两组各以第3、4、5天为超声检测时间点。给药组腹腔注射10mg／kg表柔比星,对照组注射同容量0．9％氯化钠溶液。每天监测心率,第3、4、5天超声心动图测量左心室舒张末期内径、收缩末期内径（LVEDD、LVESD）、左心室短轴缩短率（FS）、每分钟心输出量（CO）。第5天处死小鼠,取心肌组织行心肌病理学评价。结果与对照组相比,给药组小鼠心率呈下降趋势,第4天、第5天心率显著下降,差异有统计学意义（P〈0．05）。与基础状态比较,给药组小鼠第4天每分钟心输出量明显下降,差异有统计学意义[（11．8±2．7）mL／minm（7．6±2．2）mL／min,P〈0．05];第5天左心室舒张末期内径减少（P〈0．01）而左心室收缩末期内径无明显变化;第5天左心室短轴缩短率明显下降,差异有统计学意义（P〈0．05）。第5天给药组小鼠组织学评分中位数为2．5。与对照组相比,第5天小鼠心脏重量明显减轻,差异有统计学意义（P〈0．05）。第5天电镜检查显示给药组小鼠心肌细胞内水肿、线粒体肿胀、部分肌纤维断裂。结论通过腹腔注射表柔比星,短时间内能在小鼠诱导出药物心肌病模型。小鼠清醒状态下高频率超声能成功评价该模型。     

地高辛治疗心力衰竭的现代概念

l地高辛独特的抗心力衰竭机制,地高辛通过多种机制发挥对心力衰竭（心衰）的治疗作用：（1）抑制心肌细胞膜Na＋_K’ATP酶泵,使细胞内钙离子浓度增加,加强心肌收缩力,从而反射性降低末梢阻力．改善心排血量：并发挥利尿作用与减慢心率（介导交感神经作用）,最终降低左心室舒张末期压与心肌氧耗量。     

较大剂量地高辛能否进一步改善正常窦性心律的轻、中度心衰患者血液动力学和自主神经活性?

目的和背景已有研究表明地高辛能增强心肌收缩力并增大心率变异性。但是对于治疗安全范围很小的地高辛的量效关系，目前知之甚少。本研究旨在检验不同剂量地高辛对血液动力学和自主神经活性的影响。方法19例轻或中度心衰患者（超声心动图地＜0．凸）人选，其中NYHA分级11级者13例，Ill级者6例。按病因分类冠心病11例，疑酒精性心肌病4例，高血压病1例，瓣膜性心脏病1例，非特异性心肌病2例。所有病人均为正常窦性心律，人选前至少3个月内无心梗病史，均未接受地高辛及拟交感药物治疗。整个研究过程中除地高辛以外，病人的其他用药都恒定不…     

丹参对肝硬变犬门脉压力及胃粘膜血流的影响

通过胆总管结扎法，制造犬肝硬变门脉高压模型，并直接测定丹参注射液对肝硬变犬门脉压力及胃粘膜血流（GMBF）的影响。结果表明，静注丹参注射液后，肝硬变犬的门脉压力（PpV）、嵌塞肝静脉压（WHVP）、肝静脉压力梯度（HVPG）显著下降（P＜0．01），平均动脉压（MAP）、心率（HR）无显著变化（P＞0．05）。给药后10min，肝硬变及正常犬的GMBF显著增加（P＜0．05）．用药后30min达最高值（P＜0．01），60min后GMBF稍有下降．但与用药前比较仍有显著差异（P＜0．05）。说明丹参在降低肝硬变犬门脉压力的同时改善GMBF，对血压、心率无显著影响。为副作用小，兼具降低门脉压力与保护胃粘膜作用的药物。     

慢性阻塞性肺疾病患者血清细胞因子的变化及其临床意义

目的探讨研究COPD患者血清CK-MB、NO、IL-6、TNF-α的含量变化及临床意义。方法选A组38例患者及B组35例患者，测定其患者治疗前后的血清CK—MB、NO、IL-6、TNF-α的含量。结果A组患者血清CK—MB、NO、IL6、TNF-α的浓度明显高于B组患者P〈0．01）。治疗后，A组患血清CK-MB、NO、IM、TNF-α的浓度较治疗前明显下降（P〈0．01）。结论当COPD患者伴心力衰竭时，炎性细胞因子可显著升高，参与心肌损害，心肌收缩力减弱导致心衰作用。     

1月和6月龄mdx基因缺陷小鼠心肌病理改变与心功能变化的初步研究

目的：研究1月和6月龄mdx小鼠心肌病理和心功能改变。方法：1月和6月龄mdx小鼠各10只，以同龄同数量的C57BL6小鼠作为正常对照，颈动脉插管检测动脉和左心室内的血流动力学参数，评价各组小鼠的死亡率、生存时间和心功能。分析小鼠心脏大体形态和组织病理改变。结果：1月龄mdx小鼠大动脉和左心室内的血流动力学参数均与对照组无显著差异。与对照组相比，6月龄mdx小鼠心率显著增快（P〈0．05），生存时间显著缩短（P〈0．05），左心室内第5分钟心率和反映收缩功能的LVPSP、dp／dt及反映最大收缩舒张能力的△Pmax，以及反映舒张功能的．dp／dt的绝对值均显著降低或减小（分别P〈0．01，P〈0．01，〈0．05，〈0．01，〈0．01）。1月龄mdx小鼠心重／体重比显著低于对照组（P〈0．01），而6月龄mdx小鼠则显著增加（P〈0．01）。6月龄mdx小鼠心脏宽度和长径均显著超过对照组（均P〈0．01）。病理切片1月龄mdx小鼠心肌未见损害，6月龄mdx小鼠心肌存在散在的细胞坏死，炎性细胞浸润和胶原纤维含量增加。结论：6月龄mdx小鼠已存在心脏扩张和心肌病的病理改变，并开始出现心率增快、对外源性的心室内刺激耐受不良和心功能储备降低。     

期前收缩后心肌复极异常的临床意义探讨

目的：探讨期前收缩后心肌复极异常的临床意义。方法：分析247例期前收缩后心肌复极的变化情况。结果：期前收缩后伴与不伴有心肌复极异常的病因，心血管病分别为68／78例与58／169例，其中冠心病分别38／78例与18／169例，差异均有非常显著性意义（P＜0．01），冠心病期前收缩后T波倒置加深、ST段改变、T波改变伴ST段和／或U波异常较其它各疾病组明显增高，差异均具有显著性意义（P＜0．05）；频发与偶发室上性期前收缩及室性期前收缩所出现的各类型心肌复极异常差异均无显著性意义（P＞0．05）。结论：期前收缩后伴心肌复极异常主要见于心血管疾病，可提示为器质性期前收缩，有助于与功能性期前收缩相鉴别，对冠心病的诊断有一定意义。     

重组人脑钠肽对急性心肌梗死冠脉未通患者左室重塑和心功能的影响

目的研究重组人脑钠肽（rhBNP）对急性心肌梗死（AMI）冠脉未通患者左室重塑和心功能的影响。方法将103例AMI冠脉未通患者随机分为常规治疗组23例、地高辛组40例、rhBNP治疗组40例,并于AMI后1周、12周、24周分别进行超声心动图分析,测定左室心肌重量,左室收缩功能、舒张功能,了解rhBNP对AMI后左室重塑的阻抑作用。结果①AMI后24周时rhBNP组与常规治疗组和地高辛组比较,室间隔厚度、左室后壁厚度、左室舒张末内径和左室心肌重量指数均明显降低。地高辛组与常规治疗组各项指标比较差异无统计学意义。②AMI后1周时,地高辛组和rhBNP组左室收缩末期容积较常规治疗组降低（P〈0．01）,左室射血分数较常规治疗组升高（P〈0．05）,两组间差异无统计学意义（P〉0．05）。治疗后12周、24周时,rhBNP组左室舒张末期容积和收缩末期容积较同时间点常规治疗组和地高辛组均显著降低（P〈0．05）,而左室射血分数、E／A则显著升高（P〈0．05）。结论rhBNP能明显减轻心肌梗死后心肌肥厚和左室重塑,阻抑左室重塑过程,改善左室功能。     

稳心颗粒协同地高辛控制持续性及永久性房颤心室率的疗效观察

目的观察稳心颗粒协同地高辛控制持续性及永久性房颤心室率的疗效。方法共入选住院及专科门诊持续性和永久性房颤患者40例，全部病例均间断长期（4周以上）服用地高辛0．125mg／d-0．250mg／d，日常轻体力活动时心率仍大于100／min，加服稳心颗粒（每日3次，每次1包，共服4周），期间服用地高辛剂量不变，并且不用其抗心律失常药物。加服稳心颗粒前及疗程结束后检查常规12导联心电图，08：00-09：00静息20min测血压及心率，Holter检查计数24h总心率、平均心率、最快心率及最慢心率，并计数其他心律及频度，查血脂、血糖、心肌酶谱、肝肾功能及血尿常规。结果加服稳心颗粒后有86例患者自觉胸闷、气短、心悸及乏力症状减轻，其有效率达90％，静息时心率及24h Holter总心率、平均心率、最快心率较治疗前明显减慢（P〈0．05或P〈0．01），平均收缩压及舒张压较治疗前降低不显著，心电图QRS波群形态及时间、Q-T间期无明显改变。6例病人出现消化道症状，2例病人出现头晕，但均可耐受。结论稳心颗粒协同小剂量地高辛控制持续性及永久性房颤心室率效果较好，副反应少。     

期前收缩后心肌复极异常80例临床分析

目的探讨期前收缩后心肌复极异常的临床意义。方法分析250例期前收缩后心肌复极的变化情况。结果期前收缩伴心肌复极异常组和无复极异常组，心血管疾病分别为70／80例与58／170例，其中冠心病分别39／80例与18／170例，差异有显著性意义（P〈0．01）。冠心病期前收缩后T波倒置加深、ST段改变、T波改变伴ST段和／或U波异常较其它各疾病组明显增高，差异均有显著性意义（P〈0．05）。结论期前收缩后伴心肌复极异常主要见于心血管疾病，可提示为器质性期前收缩，有助于与功能性期前收缩相鉴别。对冠心病的诊断有一定意义。     

Acute effects of alcohol on left ventricular dynamics during isometric exercise in normal subjects

The aim of this study was to assess whether drinking social amounts of alcohol impairs myocardial contractility in normal humans. To that end, 17 healthy volunteers performed isometric handgrip exercise before and 60 minutes after an intake of 1 g/kg body weight of ethanol within 60 minutes. Left ventricular M-mode echocardiogram, systolic time intervals, and sphygmomanometric arterial blood pressure were recorded before and at the end of 4-min handgrip at 30% of maximum voluntary contraction. The blood ethanol concentration (mean +/- SD) was 24.4 +/- 2.0 mmol/liter. At rest, ethanol increased heart rate (p less than 0.05), and decreased left ventricular end-diastolic diameter (p less than 0.05), end-systolic diameter (p less than 0.01), and circumferential systolic wall stress (p less than 0.05). The indices of left ventricular performance were unchanged except for the maximum circumferential fiber shortening velocity which was increased after ethanol (p less than 0.001). The cardiac response to isometric exercise was similar before and after ethanol except that the handgrip-induced rise in systolic wall stress was smaller postingestion (p less than 0.05). This study does not support the view that drinking small to moderate amounts of alcohol brings about myocardial depression in normal humans. Although preload, afterload, and heart rate were altered by ethanol at rest, myocardial contractility was not impaired even during the afterload stress imposed by isometric exercise.     

Effects of myocardial contractility on microemboli production by mechanical heart valves in a bovine model

Microemboli caused by mechanical heart valves have the potential to cause cerebrovascular events. We investigated the effects of myocardial contractility and heart rate on microemboli production in association with conventional and experimental mechanical heart valves implanted in the mitral position in a bovine model. In 10 calves, the mitral valves were replaced with mechanical valves. Doppler recordings were analyzed for high-intensity transient signals, which are ultrasound reflections from circulating microemboli. The animals were studied at rest, during pacing at 160 bpm, after dobutamine infusion, and after esmolol infusion. The incidence of high intensity transient signals was expressed as signal frequency (signals per hour) and as signal rate (signals per 100 heart cycles). With a 68% increase in the heart rate, signal frequency increased by 135%, but signal rate increased by only 41 %. With a 144% increase in myocardial contractility, signal rate increased by 264 %. With a 31 % decrease in contractility, signal rate decreased by 62 %. We conclude that microemboli production by mechanical heart valves varies with myocardial contractility and heart rate. The fact that contractility affects the incidence of high-intensity transient signals suggests that the microemboli are gaseous in nature, that their production is pressure driven, and that cavitation is a possible cause. It is likely that mechanical heart valve design is responsible for the quantity of microemboli production.     

Functional and morphological characteristics of compensated and decompensated cardiac hypertrophy in dogs with chronic infrarenal aorto-caval fistulas

The relation between cardiac hypertrophy, shunt size, myocardial contractility, capillary density, adrenergic responsiveness, and neurohumoral stimulation was evaluated in dogs with compensated and decompensated cardiac hypertrophy caused by an infrarenal aorto-caval shunt. Shunt size varied from 5 to 35 mm2 due to an inability to create a uniform size. Dogs that developed heart failure within 4 months had 25 +/- 2 mm2 shunts, whereas those that developed it after 4 months had 19 +/- 3 mm2 shunts; those that did not develop heart failure had 10 +/- 1 mm2 shunts. Hypertrophy developed at the same rate in all the dogs that developed heart failure, which occurred at a critical heart weight (hypertrophy) for a given load (shunt size). In the dogs with heart failure there was a decrease in myocardial contractility (tension = 5.7 +/- 0.6 vs. 7.3 +/- 0.3 g/mm2, p less than 0.05), a decrease in adrenergic responsiveness (maximal heart rate with isoproterenol = 203 +/- 7 vs. 249 +/- 5 beats/min, p less than 0.01), an increase in circulating neurohormones, and a decrease in urinary sodium excretion (0.4 +/- 0.1 vs. 5.0 +/- 1.3 meq/3 hr, p less than 0.01). None of these abnormalities occurred in dogs with compensated hypertrophy. There were no differences in cardiac capillary density between the control dogs and the dogs with compensated cardiac hypertrophy or heart failure. Thus, it would appear that if heart failure is to develop after an initial toleration of a sudden volume overload, it will develop at a given combination of cardiac hypertrophy and volume overload, with cardiac hypertrophy developing at the same rate in all cases. In this model, once heart failure develops, myocardial contractility and cardiac adrenergic responsiveness are decreased and there is pronounced neurohumoral activation. All these changes are absent in hearts with compensated hypertrophy.     

Myocardial oxygen consumption in aortic valve disease with and without left ventricular dysfunction.

OBJECTIVE--To assess whether and to what extent myocardial oxygen consumption is modified by hypertrophy and alterations in contractility in patients with aortic valve disease and to evaluate the influence of regression of left ventricular hypertrophy and improvement of contractility on myocardial oxygen consumption after successful aortic valve replacement. DESIGN--A cohort analytical study to investigate the influence of the "explanatory" variables of myocardial oxygen consumption by multiple regression analysis. A comparison of myocardial oxygen consumption in preoperative patients with that after operation in a group with comparable severity of aortic valve disease before operation (analysis of covariance). PATIENTS--In six controls and in 43 patients with aortic valve disease and normal coronary arteries standard haemodynamic variables were measured, left ventricular biplane cineangiography performed, and coronary sinus blood flow measured by thermodilution. The patients were divided into three groups: 19 preoperative patients with normal ejection fraction (greater than or equal to 57%) (group 1); nine preoperative patients with reduced ejection fraction (less than 57%) (group 2); 16 postoperative patients (one with preoperative and postoperative measurements (group 3). Postoperative evaluation was performed 12-51 months after surgery. MAIN OUTCOME MEASUREMENTS--Myocardial oxygen consumption/100 g left ventricular muscle mass and its suspected "explanatory" variables--that is, peak systolic left ventricular circumferential wall stress, heart rate, contractility (assessed by left ventricular ejection fraction), and left ventricular muscle mass index. RESULTS--Multiple regression analysis showed that the product of peak systolic stress and heart rate (p less than 0.0001) and ejection fraction (p less than 0.03) were positively correlated with myocardial oxygen consumption/100 g and that left ventricular muscle mass index (p less than 0.002) was negatively correlated with myocardial oxygen consumption/100 g (r = 0.72; n = 50 measurements). Myocardial oxygen consumption per 100 g at a given stress-rate product was higher in the controls than in group 1 (hypertrophied ventricles with normal ejection fraction) and was also higher in group 1 than in group 2 (hypertrophied ventricles with reduced ejection fraction). In a subgroup of the postoperative patients with complete regression of hypertrophy and normalisation of contractility, myocardial oxygen consumption per 100 g at a given stress-rate product was indistinguishable from that in controls. CONCLUSIONS--When the actual stress-rate product was used as an index of overall left ventricular performance the results suggested that mechanical efficiency was increased in hypertrophied ventricles especially when contractility was decreased. These changes in mechanical efficiency seemed to be reversible during the postoperative course when muscle mass and contractility returned to normal.     

Myocardial oxygen consumption in aortic valve disease with and without left ventricular dysfunction.

OBJECTIVE--To assess whether and to what extent myocardial oxygen consumption is modified by hypertrophy and alterations in contractility in patients with aortic valve disease and to evaluate the influence of regression of left ventricular hypertrophy and improvement of contractility on myocardial oxygen consumption after successful aortic valve replacement. DESIGN--A cohort analytical study to investigate the influence of the "explanatory" variables of myocardial oxygen consumption by multiple regression analysis. A comparison of myocardial oxygen consumption in preoperative patients with that after operation in a group with comparable severity of aortic valve disease before operation (analysis of covariance). PATIENTS--In six controls and in 43 patients with aortic valve disease and normal coronary arteries standard haemodynamic variables were measured, left ventricular biplane cineangiography performed, and coronary sinus blood flow measured by thermodilution. The patients were divided into three groups: 19 preoperative patients with normal ejection fraction (greater than or equal to 57%) (group 1); nine preoperative patients with reduced ejection fraction (less than 57%) (group 2); 16 postoperative patients (one with preoperative and postoperative measurements (group 3). Postoperative evaluation was performed 12-51 months after surgery. MAIN OUTCOME MEASUREMENTS--Myocardial oxygen consumption/100 g left ventricular muscle mass and its suspected "explanatory" variables--that is, peak systolic left ventricular circumferential wall stress, heart rate, contractility (assessed by left ventricular ejection fraction), and left ventricular muscle mass index. RESULTS--Multiple regression analysis showed that the product of peak systolic stress and heart rate (p less than 0.0001) and ejection fraction (p less than 0.03) were positively correlated with myocardial oxygen consumption/100 g and that left ventricular muscle mass index (p less than 0.002) was negatively correlated with myocardial oxygen consumption/100 g (r = 0.72; n = 50 measurements). Myocardial oxygen consumption per 100 g at a given stress-rate product was higher in the controls than in group 1 (hypertrophied ventricles with normal ejection fraction) and was also higher in group 1 than in group 2 (hypertrophied ventricles with reduced ejection fraction). In a subgroup of the postoperative patients with complete regression of hypertrophy and normalisation of contractility, myocardial oxygen consumption per 100 g at a given stress-rate product was indistinguishable from that in controls. CONCLUSIONS--When the actual stress-rate product was used as an index of overall left ventricular performance the results suggested that mechanical efficiency was increased in hypertrophied ventricles especially when contractility was decreased. These changes in mechanical efficiency seemed to be reversible during the postoperative course when muscle mass and contractility returned to normal.     

Comparative cardiac dynamic effects of dobutamine and isoproterenol in conscious instrumented dogs

The cardiac dynamic consequences were evaluated of constant infusions of dobutamine and isoproterenol at graded dose levels into conscious, healthy instrumented dogs. Measurements were made of simultaneous changes in left ventricular internal diameter, pressure, aortic pressure and rate of rise of left ventricular pressure (dP/dt), as well as the left ventricular electrogram. From these primary variables, derived variables were computed using programs in a minicomputer system. The data showed that, with increasing doses of dobutamine there were significant linear increases in all measured indexes of myocardial contractility, such as the rate of rise of left ventricular pressure at a developed isovolumic pressure of 40 mm Hg (dP/dt/P₄₀), mean velocity of left ventricular fiber shortening, ejection fraction and stroke work. These changes in myocardial contractility occurred without changes in end-diastolic volume, mean aortic pressure or heart rate when dobutamine was infused in doses of 5 to 20 μg/kg per min. Isoproterenol also produced linear changes in indexes of myocardial contractility but in doses of 0.02 to 0.10 μg/kg per min, it produced a significantly higher heart rate at any given level of contractility than that produced by dobutamine. Cardiac minute work (heart rate × stroke work) was increased by both drugs. However, with infusions of isoproterenol the amount of cardiac minute work was significantly limited because of the changes in heart rate, whereas with dobutamine cardiac minute work could be increased to a higher level as a function of changes in myocardial contractility alone without changes in heart rate. These data suggest that dobutamine selectively increases myocardial contractility.     

钾通道开放剂对离体兔心缺血再灌注损伤的保护作用

目的观察非选择性三磷酸腺苷敏感性钾(KATP)通道开放剂Pinacidil和线粒体型KATP(mitoKATP)通道开放剂Diazoxide预处理对高钾停跳离体兔心缺血再灌注损伤的保护作用,以及mitoKATP通道阻断剂5-hydroxydecanoic acid sodiumsalt(5HD)应用后其心肌保护作用的变化。方法采用离体兔心Langendorff灌注实验模型。离体兔心40只随机等分成5组(n=8):对照组(C组)、Pinacidil组(P组)、Diazoxide组(D组)、5HD Pinacidil组(HP组)和5HD Diazoxide组(HD组)。离体兔心用标准Thomas停搏液(4℃,K 16mmol/L)至心停跳,45min后再灌注20min,于心脏停跳前灌注药物15min,对比观察Pinacidil、Diazoxide及其与5HD合用时对再灌注后心功能及冠状动脉血流的影响以及再灌注末心肌超微结构、蛋白含量、脂质过氧化物丙二醛(MDA)以及腺苷酸含量的变化。结果再灌注后P组、D组、HP组心功能的恢复率均明显高于C组,心肌MDA的含量、蛋白的漏出量明显低于C组,超微结构观察损伤较轻;但HP组心功能的恢复要差于P组,心肌MDA的含量、蛋白的漏出量明显高于P组;HD组与C组各检测指标比较差异无统计学意义。结论Pinacidil(10μmol/L)和Diazoxide(30μmol/L)预处理对离体兔心缺血/再灌注心肌具有保护效果,且其保护效果可以部分被5HD所阻断,提示心肌mitoKATP通道可能是产生心肌保护作用的靶点之一。     

An analysis of the left ventricular response to isometric exercise

Analysis of the left ventricular response to isometric exercise was performed in a group of patients undergoing diagnostic cardiac catheterization. A normal response was observed in nine patients with normal resting hemodynamics (Group I). This response consisted of a significant increase in LV stroke work associated with minor changes (average increase of 2 mm. Hg) in LV end-diastolic pressure. Significant increases were consistently observed in the isovolumic indices of myocardial contractility. These findings indicate that the normal left ventricle responds to this form of exercise by improving its contractile state and to a minor degree by increasing preload, thus maintaining a constant stroke volume in the presence of an increased afterload.To test whether the increase in contractility observed during isometric exercise was related to the increase in heart rate, isovolumic indices of contractility were measured in eight patients during atrial pacing at a rate equal to that achieved during exercise. Isometric exercise was associated with a higher level of myocardial contractility than atrial pacing. In addition, a significant improvement in the isovolumic indices was observed in four out of five patients subjected to isometric exercise at a constant heart rate (atrial pacing). Thus, it seems that in addition to the “treppe” effect, other factors independent of heart rate are involved in augmenting myocardial contractility during isometric exercise.Ten patients (Group II) responded to exercise with a marked increase in LVEDP but little change in LV stroke work; five patients (Group III) responded with only a minor change in LVEDP (similar to Group I) but with no improvement in LV stroke work. Myocardial contractility also failed to increase in most of these patients. Isometric exercise uncovered abnormalities of LV performance not identified by the resting hemodynamics in a significant number of patients.     

Quantitative echocardiographic study of the left ventricular function in acute aortic infective endocarditis

Left ventricular (LV) function in 45 patients with native aortic valve infective endocarditis was studied in order to identify high surgical risk patients and the pattern of irreversible myocardial damage. LV function was studied by M-mode and 2D-echocardiography (LV volumes; ejection fraction, EF; peak systolic pressure to end-systolic volume ratio (PAP/ESV) as an index of myocardial contractility; LV mean systolic wall stress as an index of LV afterload and the radius to thickness ratio (R/Th). Thirteen patients underwent aortic valve replacement with an overall operative mortality of 15%. The cause of death was intractable heart failure. Different EF vs stress relationships could be described for different level of myocardial contractility: patients with intractable heart failure had a severely depressed myocardial contractility so that for a given level of LV stress, EF was significantly lower. High operative risk patients were identified by the PAP/ESV vs R/Th relation. All surgical deaths occurred in patients with a severely depressed myocardial contractility (PAP/ESV less than 2) and inadequate hypertrophy (R/Th greater than 4). Reversal of LV dysfunction in patients with moderately depressed myocardial contractility depended on the pattern of LV hypertrophy; a normal post-operative EF was achieved only in patients with adequate hypertrophy (R/Th less than 4).     

Effect of intravenous metoprolol on left ventricular performance in Q-wave acute myocardial infarction

To determine the effects of intravenous metoprolol on left ventricular (LV) function in acute myocardial infarction (AMI), 16 patients were studied within 48 hours of Q-wave AMI (mean ejection fraction 47 +/- 6%, mean pulmonary artery wedge pressure 22 +/- 6 mm Hg) with high fidelity pressure and biplane cineventriculography before and after intravenous metoprolol (dose 12 +/- 4 mg). Heart rate decreased from 90 +/- 13 to 74 +/- 11 beats/min (p less than 0.001), pulmonary arterial wedge pressure and LV end-diastolic pressure were unchanged (22 +/- 6 to 21 +/- 6 and 27 +/- 8 to 26 +/- 8 mm Hg, respectively), despite impaired LV relaxation (P = Poe-t/T) after intravenous metoprolol (T from 59 +/- 13 to 72 +/- 12 ms, p less than 0.001). Peak systolic circumferential LV wall stress decreased after beta-adrenergic blockade (330 +/- 93 to 268 +/- 89 g/cm2, p less than 0.05) and LV contractility decreased (dP/dtmax from 1,480 +/- 450 to 1,061 +/- 340 mm Hg/s, p less than 0.001). The ejection fraction decreased (48 +/- 7 to 43 +/- 7%, p less than 0.05) due to an increase in LV end-systolic volume (85 +/- 19 to 93 +/- 19 ml, p less than 0.05) since LV end-diastolic volume was unchanged (161 +/- 30 to 163 +/- 30 ml, difference not significant). In patients with Q-wave AMI, intravenous metoprolol reduces the major determinants of myocardial oxygen demand including heart rate, contractility and peak systolic wall stress. Further, despite decreased heart rate, (+)dP/dtmax, ejection fraction, isovolumic relaxation, LV end-diastolic pressure and end-diastolic volume remain unchanged.