Pure right ventricular infarction

The case is reported of a patient with chronic emphysema andcor pulmonale who developed the signs of acute myocardial infarctionwhich were initially interpreted as being localized in the postero-inferiorwall of the left ventricle. The patient rapidly developed thefeatures of massive right heart failure in the absence of pulmonarycongestion, a condition thought to be due to pulmonary emboli.The autopsy, however, revealed a pure right ventricular infarct,which covered more than half of the pre-existent right ventricularmyocardium, in the setting of marked right ventricular hypertrophyinfraction. The case furthermore shows that the possibilityof pure right ventricular infarction should be evaluated inall patients with puzzling right heart failure, in the courseof what initially is thought to be an acute left ventricularinfraction, is important since therapy with plasma volume expandersshould be used with great caution in such patients     

Alterations in cerebral blood flow in children with congestive heart failure due to ventricular septal defect

Objective: We aimed to investigate the effect of ventricular septal defect (VSD) and heart failure on cerebral blood flow (CBF) in children, whether heart failure treatment improves CBF, and if there is any relationship between CBF and serum N‐ terminal pro‐brain natriuretic peptide (NT‐proBNP) level.
Method: Forty children with VSD (13 with heart failure) aged between 1 and 36 months were studied. The control group comprised 25 healthy children in the same age group. Maximum, minimum, and mean blood flow velocities and pulsatility indices of the right and left middle cerebral arteries were assessed using transcranial Doppler ultrasonography. Measurements of CBF and serum NT‐proBNP levels were repeated in patients with heart failure a month post–heart failure treatment initiation. The groups were also compared in terms of defect diameters, cardiac structural changes, left ventricular systolic function, and findings related to pulmonary hypertension determined by echocardiography. Correlations between echocardiographic measurements and CBF parameters were analyzed.
Results: Although no significant difference was found between patient and control groups for CBF, right and left maximum CBF velocities significantly increased posttreatment in patients with heart failure (P = .04 and P = .01, respectively). Serum NT‐ proBNP levels in children with VSD associated with heart failure were significantly higher than those in children with VSD alone (P = .04) or in healthy children (P < .001). NT‐proBNP levels were negatively correlated with right and left maximum CBF velocities (r = −0.39, P = .013 and r = −0.32, P = .043, respectively).
Conclusion: Although no significant difference was found in CBF velocity among the study groups, increase in the CBF velocity post heart failure treatment and negative correlations between CBF velocity and both the VSD diameter and NT‐proBNP levels indicate that the hemodynamic status due to VSD associated with heart failure has an effect on CBF.     

右房左室起搏治疗慢性心力衰竭伴室内传导阻滞患者的初步临床观察

观察右房 左室起搏治疗慢性心力衰竭 (简称心衰 )的临床效果。选择 1 6例充血性心衰患者 (NYHA分级Ⅲ Ⅳ级 ) ,男 1 0例、女 6例 ,年龄 6 8.4± 6岁 ;均为窦性心律 ,合并有Ⅰ度房室阻滞 ,完全性左束支阻滞。按安置起搏器的模式分为右房 左室起搏治疗组 (LV组 ,n =6 ) ,右房双室起搏治疗组 (BiV组 ,n =1 0 )。左室起搏电极分别放置于心大静脉左室侧后分支 9例 ,心大静脉左室后分支 7例。观察起搏治疗前后左室心功能参数、6min步行距离、左室壁运动的同步性及体表心电图的变化。结果 :BiV组左室射血分数 (LVEF)由术前的 0 .2 3提高至 0 .31 (P <0 .0 0 1 ) ;在LV组LVEF由术前的 0 .2 4提高至 0 .33(P <0 .0 0 1 ) ;左室舒张末期容积指数在二组分别由术前的 1 4 9± 5 1ml/m2 和 1 5 3±5 3ml/m2 下降至 1 1 6± 38ml/m2 和 1 2 1± 4 1ml/m2 (P均 <0 .0 0 1 ) ;室间隔与左室后壁运动的延迟时间在二组分别由术前的 1 95± 94ms和 1 97± 89ms下降至 1 7± 6 0ms及 1 6± 5 6ms(P均 <0 .0 0 1 )。 6min步行距离则分别由术前的4 0 3± 5 3m和 4 0 1± 5 9m提高至 4 4 1± 6 2m和 4 4 2± 6 7m(P均 <0 .0 5 )。结论 :初步临床观察提示右房 左室起搏治疗与右房双室起搏治疗相比 ,同样可有效地改善慢性心衰?     

双向荧光差异凝胶电泳技术在心脏病蛋白质组学研究中的应用

目的:应用双向荧光差异凝胶电泳技术筛选与致心律失常性右心室心肌病引起的与心力衰竭密切相关的蛋白质标志物.方法:从本院的心脏病组织库中挑选6例病理诊断明确和各方面资料比较齐全的致心律失常性右心室心肌病引起心力衰竭的左心室心肌标本(来源于心脏移植的受体),以年龄、性别和种族等因素相匹配的因非心脏病死亡的6例正常心脏的左心室心肌作为本实验的对照,进行比较蛋白质组学研究,筛选在致心律失常性右心室心肌病引起的心力衰竭中差异表达的蛋白质,即蛋白质标志物,并应用免疫组织化学和免疫印迹杂交方法检验差异蛋白质的可靠性.结果:经二次重复实验共筛选出5个差异表达的蛋白质,其中有3个在致心律失常性右心室心肌病引起的心力衰竭中表达升高,而另有2个表达降低.经生物信息学分析,这5个差异蛋白质主要为心肌细胞的骨架蛋白或参与能量代谢和应急保护反应的蛋白质.其中的一个差异表达蛋白质--细胞骨架蛋白Desmin经免疫组织化学和免疫印迹杂交方法得到了进一步验证.结论:本研究应用双向荧光差异凝胶电泳技术筛选获得5个与致心律失常性右心室心肌病引起的心力衰竭密切相关的蛋白质标志物,这些标志物可能与心力衰竭发生的分子机制相关,并可能用于疾病的分层、判断预后及指导个性化治疗.     

Left and right ventricular diastolic dysfunction and diastolic heart failure: does one lead to the other?

Background and Objective Diastolic dysfunction of the left ventricle is a mechanical abnormality diagnosed primarily by echocardiogram, and can be distinguished into three separate degrees based on the severity of reduction in passive compliance and active myocardial relaxation. Methods A literature search was performed for basic science studies, clinical studies and major practice guidelines on the subject of diastolic dysfunction and diastolic heart failure. Important findings were analyzed and correlated with regard to clinical relevance. Results Left ventricular diastolic dysfunction appears to compromise exercise tolerance and is believed to contribute to the pathophysiology in patients with diastolic heart failure. In the clinical setting, however, oftentimes no clear distinction is made between echocardiographically diagnosed diastolic dysfunction and diastolic heart failure, and adequate treatment recommendations are sparse and aimed to prevent worsening and progression of clinical symptoms. To date, there is a lack of high powered trials assessing the possible progression rate from echocardiographically diagnosed diastolic dysfunction to the clinical diagnosis of diastolic heart failure. Furthermore, there are no solid indices to assess the degree of severity of diastolic dysfunction or its progression. Pure right ventricular diastolic dysfunction appears to be even less understood and under-recognized, although it may play a role in the development of both right and left heart failure. Currently there are few but interesting data on the possible interaction between ventricles with diastolic dysfunction and the overall affect on the development of heart failure. Conclusions The timeline and progression of diastolic dysfunction to diastolic heart failure have not been well established and warrant further investigation.     

Unusual localisation of a ventricular septal defect following blunt chest trauma

A 64 year old man presented with a traumatic ventricular septal defect following blunt chest trauma 40 years before. Echocardiography and left ventriculography were helpful in locating the unusual septal defect, which was subpulmonary. The shunt was small, but the anomalous chronic overload led to right ventricular failure. The surgical correction was thus too late to improve right ventricular function.


Keywords: ventricular septal defect; blunt chest trauma; heart failure     

快速右室起搏建立动物心力衰竭模型

为建立稳定的慢性终末期心力衰竭 (简称心衰 )动物模型 ,选择太湖梅山猪 12只 ,采用快速 (2 30次 /分 )右室起搏 4周 ,之后改用 190次 /分的频率维持右室起搏 4周。并应用超声心动图及心导管检查 ,观察猪在实验的不同阶段心功能参数。结果 :快速起搏 4周后 ,所有猪均出现明显的充血性心衰的表现 ;超声心动图显示心室壁变薄、射血分数、心输出量明显下降 ;心导管检查结果示肺动脉压、右房压、肺动脉楔压升高 ,而心输出量、每搏输出量和动脉压降低 ;在以 190次 /分维持 4周后 ,上述参数仍保持稳定。结论 :快速右室起搏可建立稳定、持久的慢性终末期心衰模型。     

Pacing in heart failure: improved ventricular interaction in diastole rather than systolic re-synchronization.

AIMS: To determine the mechanism by which left ventricular and biventricular pacing works. BACKGROUND: Pacing for congestive heart failure patients is employed in those with left bundle branch block on the basis that it will improve discoordinated contraction; however, the response is unpredictable. The authors propose that the mechanism of benefit is rather related to improvement of ventricular interaction in diastole (VID). VID is found in patients with a high left ventricular end-diastolic pressure (> 15 mmHg). Left ventricular pacing in these patients will delay right ventricular filling and allow greater left ventricular filling before the onset of VID. METHODS: The study group consisted of 18 congestive heart failure patients with an ejection fraction < 30% and with no more than Grade 1 mitral regurgitation. Group I comprised 10 patients with pulmonary capillary wedge pressure > 15 mmHg, four patients had a normal QRS duration and six had left bundle branch block. Group II comprised eight patients with pulmonary capillary wedge pressure < 15 mmHg, of whom five had a normal QRS duration. Haemodynamics were measured at baseline and during VDD pacing from either the left ventricle or right ventricle. RESULTS: The ratio of stroke volume/pulmonary capillary wedge pressure was calculated as an index of the relationship between left ventricular end-diastolic pressure and contractile function. This ratio was lower in group I than in group II patients (P = 0.005). In group I, haemodynamics were improved with left ventricular pacing (stroke volume/pulmonary capillary wedge pressure increased from 2.2 +/- 0.9 to 4.4 +/- 3.6, P = 0.03). In group II there was no response to either left ventricular or right ventricular pacing. The improvement with left ventricular pacing was unrelated to QRS duration (r = 0.09). CONCLUSIONS: Left ventricular pacing acutely benefits congestive heart failure patients with pulmonary capillary wedge pressure > 15 mmHg irrespective of left bundle branch block. The present data suggest that the mechanism of response may be an improvement in left ventricular filling rather than ventricular systolic re-synchronization.     

The role of diastolic ventricular interaction in abnormal cardiac baroreflex function in chronic heart failure

Baroreflex abnormalities have been well documented in both patients with chronic heart failure and experimental animal models of heart failure. These abnormalities are associated with increased mortality and probably contribute to neurohumoral activation. While it is likely that several mechanisms contribute to reduced baroreflex sensitivity, it has been difficult to explain why baroreflex control mechanisms during acute volume unloading in patients with severe chronic heart failure should be directionally opposite to those in normal subjects. Volume unloading normally causes a reduction in baroreceptor activity, and hence an increase in sympathetic outflow; however, patients with chronic heart failure develop attenuated increases or paradoxical reductions in forearm vascular resistance, muscle sympathetic nerve activity, and noradrenaline spillover. It has been suggested that this probably represents paradoxical activation of left ventricular (LV) mechanoreceptors, but why LV receptors should behave in such a fashion has not been determined. In the setting of diastolic ventricular interaction, the filling of the left ventricle is constrained by the surrounding pericardium and right ventricle. In these patients, the reduction in right ventricular (RV) volume that normally occurs during acute volume unloading allows for an increase in LV end-diastolic volume (as opposed to the reduction in LV volume that normally occurs). We have demonstrated this to be important in some patients with chronic heart failure, and observed that baroreflex control of forearn vascular resistance was markedly impaired in these patients. We propose that the increase in LV volume that occurred during volume unloading would increase LV mechanoreceptor activity, and could therefore explain the paradoxical reductions in sympathetic outflow. As discussed, this has important therapeutic implications.     

Effects of milrinone for right ventricular failure after left ventricular assist device implantation

Right ventricular failure after left ventricular assist device implantation sometimes requires additional mechanical right ventricular support. The effectiveness of nitrates, prostaglandin, or nitric oxide inhalation in such cases has already been reported. However, there are few reports on the administration of phosphodiesterase inhibitor for right ventricular failure after left ventricular assist device implantation. We report two patients with right ventricular failure after left ventricular assist device implantation successfully treated with milrinone. Both had residual pulmonary hypertension due to high pulmonary vascular resistance after left ventricular assist device implantation. However, intravenous milrinone caused a significant reduction in pulmonary vascular resistance and an increase in left ventricular assist device flow. Milrinone acts as both an inotropic agent and a direct vasodilator, and thus may avoid the need for mechanical support for right ventricular failure due to residual pulmonary hypertension after left ventricular assist device implantation. Received: May 28, 2001 / Accepted: September 22, 2001     

Left and right heart Doppler stress echo in congestive heart failure

Doppler echocardiographic assessment of the left and right ventricular function at rest, during and 6 minutes after submaximal exercise was performed in 60 patients with a mean age of 43±11 years suffering from heart failure classified stage I-III according to the NYHA-criteria and 10 volunteers with a mean age of 36±9 years who served as a control group. At mitral (m) and tricuspid (t) valve early diastolic peak-flow velocity (VEm, VEt), atrial peak-flow velocity (VAm, VAt), speed-time integrals (Em, Et, Am, At) and the ratios (VE/VAm, VE/VAt, E/Am, E/At) were determined. The left ventricular end-diastolic diameter (LVEDD) and the right ventricular outflow tract (RVOT) were measured in addition. The left ventricular ejection fraction (LVEF) was decreased to <36% in 9 patients (group 1). In 51 individuals LVEF was found to be >35% but <50% or LVEF was shown to be >50% but VE/VAm-ratio was found to be <1 (group 2). Out of all the determined parameters, VE/VAt, VEt and VAm during exercise were found to be the most sensitive parameters for the detection of early to advanced grade left heart failure.     

探讨心衰超声指数评价慢性心力衰竭患者的临床运用价值

目的：探讨心衰超声指数评价慢性心力衰竭患者的临床运用价值。方法：选取2013年4月—2014年4月符合诊断标准的84例慢性心力衰竭患者(观察组)按照患者的临床症状分为I、II、III、IV级,另取40例门诊体检者(对照组)。对各级慢性心力衰竭患者、门诊体检者进行心衰超声指数评分,与氨基末端脑钠肽前体(NT-ProBNP)水平、左室射血分数、左房内径、左室舒张末径、纽约心功能分级进行比较。结果：门诊体检者、心功能I、II、III、IV级的慢性心力衰竭患者的心衰超声指数分别为0、1.43±0.87、2.15±0.96、3.27±1.02、5.46±1.43,各组具有统计学差异(P<0.05);门诊体检者、心功能I、II、III、IV级的慢性心力衰竭患者的NT-ProBNP水平、左室射血分数、左房内径、左室舒张末径均具有统计学差异(P<0.05);纽约心功能分级越严重,心衰超声指数越大(P<0.05)。结论：心衰超声指数与氨基末端脑钠肽前体水平、左室射血分数、左房内径、左室舒张末径、纽约心功能分级具有相关性,心衰超声指数可用于评价与诊断慢性心力衰竭患者的心功能。     

全磁悬浮左心室辅助装置的研究进展

心脏移植是终末期心力衰竭治疗的金标准,但面临着供体短缺的问题。左心室辅助装置已成为目前终末期心力衰竭患者的重要治疗手段。出血、泵血栓形成、卒中、右心衰竭和溶血是限制左心室辅助装置治疗的关键因素,第三代全磁悬浮离心式连续流左心室辅助装置的研发,旨在克服这些并发症。近年来我国心室辅助装置发展迅速,多款设备已进入临床试验阶段。本文结合国际前沿研究进展,介绍国内外以磁悬浮为技术特点的左心室辅助装置的研究与应用现状。     

美托洛尔对舒张性心力衰竭兔治疗作用的研究

目的研究美托洛尔对舒张性心力衰竭兔的治疗作用。方法雄性新西兰兔30只随机分为手术组(12只,在兔右侧肾动脉上1 cm处行腹主动脉缩窄术)、治疗组(12只,从术后第1天起口服美托洛尔25mg,2次/d)和假手术组(6只,只穿线不结扎)。术后观察兔心力衰竭的临床表现,监测血流动力学变化并定期复查超声心动图。结果与手术组比较,治疗组兔心力衰竭发生率明显降低,室壁肥厚和心腔扩大得到抑制,左心室舒张末压和等容舒张期松弛时间指数以及二尖瓣舒张早期血流峰值运动速度(Em)、二尖瓣舒张早期血流峰值/Em比值显著改善(P0.05,P0.01)。结论美托洛尔可有效减轻舒张性心力衰竭兔的心室肥厚、心腔扩大和舒张功能损伤。     

Sudden onset congestive heart failure with a continuous murmur: ruptured sinus of Valsalva aneurysm complicated by anomalous origin of the left coronary artery

Ruptured sinus of Valsalva aneurysm is an unusual cause for congestive heart failure, and anomalous coronary arteries have rarely been found in association. A 47-year-old man developed sudden onset heart failure due to a ruptured noncoronary sinus of Valsalva fistula to the right atrium. Coronary angiography revealed an anomalous left coronary artery arising from the right coronary sinus, limiting percutaneous options for repair. We review the incidence, complications, and management of sinus of Valsalva aneurysms and anomalous left coronary arteries.     

Right heart dysfunction and failure in heart failure with preserved ejection fraction: mechanisms and management. Position statement on behalf of the Heart Failure Association of the European Society of Cardiology

There is an unmet need for effective treatment strategies to reduce morbidity and mortality in patients with heart failure with preserved ejection fraction (HFpEF). Until recently, attention in patients with HFpEF was almost exclusively focused on the left side. However, it is now increasingly recognized that right heart dysfunction is common and contributes importantly to poor prognosis in HFpEF. More insights into the development of right heart dysfunction in HFpEF may aid to our knowledge about this complex disease and may eventually lead to better treatments to improve outcomes in these patients. In this position paper from the Heart Failure Association of the European Society of Cardiology, the Committee on Heart Failure with Preserved Ejection Fraction reviews the prevalence, diagnosis, and pathophysiology of right heart dysfunction and failure in patients with HFpEF. Finally, potential treatment strategies, important knowledge gaps and future directions regarding the right side in HFpEF are discussed.     

心力衰竭患者心脏机械运动周期时间变化的临床研究

目的应用超声组织多普勒的方法研究心力衰竭(简称心衰)患者心动周期各个间期的比例变化。方法对18例心衰患者(心衰组)及30例健康志愿者(对照组),在静息下标准四腔切面,测量左右心室基底段,同一心动周期中等容收缩期、快速射血期、减速射血期、等容舒张期、快速充盈期、舒张后期及心房收缩期,并换算成在收缩期和舒张期的比例。结果对照组左右心室收缩期和舒张期在心动周期的比例相同,心衰组左室收缩期和舒张期比例无明显变化,右室收缩期比例减小(43.29%±6.64%vs 38.98%±7.05%,P<0.05);在收缩期内,左室等容收缩期和快速射血期比例增加而慢速射血期比例减少,右室等容收缩期比例增加,快速射血期比例减少,慢速射血期比例不变;在舒张期内,左右心室等容舒张期比例均增加,右室快速充盈时间比例显著下降,左室无明显下降,左室舒张后期时间比例下降而右室增加,右室心房收缩时间比例下降而左室增加。对照组左右心室之间各个间期均有非常显著的差异,心衰患者左右心室之间的差异明显减小。结论心衰时心动周期的各个间期的分布比例与正常对照相比存在显著差异。左右心室之间各个间期的差异在正常对照非常显著,心衰时减小。     

Echocardiographic Features of Right Heart Failure in Infancy and Childhood

In infants and children, right heart failure is most frequently a consequence of increased afterload (pulmonary hypertension). However, it is also observed as a sequela of congenital cardiovascular surgery. The purpose of this report is to present the causes of right heart dysfunction in children and to define the echo-Doppler methods used in the evaluation of right heart failure.     

Progression of left ventricular enlargement in patients with hypertrophic cardiomyopathy: Incidence and prognostic value–K. Hina ef al.: Ventricular enlargement in HCM

A total of 51 patients with hypertrophic cardiomyopathy (HCM) were followed for at least 3 years (mean follow-up period 6.5 years) by serial M-mode and two-dimensional echocardiography. An increase of the left ventricular diastolic dimension (LVDd) to ≥ 55 mm with a decrease in the left ventricular ejection fraction (LVEF) to < 55% was observed in eight (15.7%) patients (progressive disease group). In five of these eight patients, the LVDd was ≥ 60 mm and the LVEF was < 40%. Ventricular enlargement was closely related to mortality and death due to congestive heart failure occurred in three of these patients. No deaths occurred among the 37 patients without significant progression of ventricular enlargement (nonprogressive group). The annual changes of LVEF and LVDd in the progressive disease group were larger than in the nonprogressive group (LVEF – 0.18 ± 1.45 vs. – 2.46 ± 1.47 %/year; LVDd 0.22 ± 0.81 vs. 1.43 ± 0.77 mm/year). An increment in LVDs occurred earlier than the enlargement of the LVDd. Therefore, close attention to the LVDs seems to be important to detect early left ventricular morphological changes in HCM. In summary, this study indicates that HCM patients include a subgroup with symptoms resembling dilated cardiomyopathy, in whom the left ventricle enlarges with hypofunction and in whom there is high mortality due to congestive heart failure.     

Clinical Characteristics,Left and Right Ventricular Ejection Fraction,and Long-term Prognosis in Patients with Non-insulin-dependent Diabetes Surviving an Acute Myocardial Infarction

Patients with diabetes mellitus have a high morbidity and mortality from acute myocardial infarction, the reason for which is not fully understood. The relationship between congestive heart failure symptoms, left ventricular ejection fraction, and long-term mortality was examined in 578 hospital survivors of acute myocardial infarction, 47 of whom had Type 2 (non-insulin-dependent) diabetes mellitus. None of the patients were treated with insulin. The prevalence of congestive heart failure during hospitalization was similar in patients with and without diabetes, although mean diuretic dose was higher in the former patients. Left and right ventricular ejection fraction was measured with radionuclide ventriculography in the second week after acute myocardial infarction. At discharge from the coronary care unit, patients with and without diabetes had similar left ventricular ejection fraction (with diabetes: median 46% vs without diabetes: median 43%; p = 0.89). Median right ventricular ejection fraction (62 %) was within normal limits in both groups and did not differ statistically. Survival data were obtained for all patients. The 5-year mortality was increased in patients with diabetes compared with non-diabetic patients independent of left ventricular ejection fraction. Univariate analysis showed that the cumulative 5-year mortality rate was 53 % in the group with diabetes compared with 43% in the non-diabetic group (p = 0.007). Using multivariate regression analysis presence of diabetes was found to have a significant association with long-term mortality after myocardial infarction, that was independent of age, history of hypertension, congestive heart failure symptoms during hospitalization or of either left or right ventricular ejection fractions at discharge. We conclude that the excess mortality in patients with non-insulin-dependent diabetes mellitus is not explained by available risk markers after myocardial infarction. Even though left ventricular ejection fraction and serum creatinine did not differ significantly, the apparent higher dose of Frusemide in patients with than without non-insulin-dependent diabetes mellitus might indicate that heart failure, if present, is more severe in patients with than in those without diabetes. The importance of diastolic dysfunction in this context needs to be determined.