Percutaneous closure of an iatrogenic atrial septal defect

The use of the Tandem Heart? percutaneous ventricular assist device (Tandem Heart pVAD, Cardiac Assist technologies, Pittsburgh, PA) as a bridge to recovery or to other cardiopulmonary support systems has been rising. One requirement for placement of this device is an intraatrial septostomy which is usually closed during the surgical insertion of more permanent ventricular assist devices. We present a case of a 62‐year‐old man with a residual acquired atrial septal defect (ASD) from Tandem Heart? placement, which could not be closed surgically during insertion of left and right ventricular assist devices. The patient remained intubated and hypoxemic after removal of his right ventricular assist device due to the presence of persistent right to left shunting. With closure of the ASD using an 8‐mm Amplatzer® septal occluder (ASO; AGA Medical Corp., Golden Valley, MN) the patient stabilized and was successfully extubated. © 2009 Wiley‐Liss, Inc.     

Echocardiographic Predictors of Hemodynamics in Patients Supported With Left Ventricular Assist Devices

Background

The assessment of hemodynamics in patients supported with left ventricular assist devices (LVADs) is often challenging. Physical examination maneuvers correlate poorly with true hemodynamics. We assessed the value of novel transthoracic echocardiography (TTE)–derived variables to reliably predict hemodynamics in patients supported with LVAD.

Echocardiographic assessment for ventricular assist device placement

While many factors depend on successful implantation and outcome of left ventricular assist devices (LVAD), echocardiography remains an integral part and is vital to the success of this process. Transesophageal echocardiography (TEE) allows interrogation of all the cardiac structures and great vessels. The pre-implantation TEE exam establishes a baseline and may identify potential problems that need palliation. Among these, most significant are aortic insufficiency (AI), intracardiac thrombi, poor right ventricular (RV) function, and intracardiac shunts. The post-implantation exam allows for adequate de-airing of the heart and successful LVAD initiation. The position and flow profiles of the inflow and outflow cannulas of the LVAD may be assessed. Finally, it assists in the astute management and vigilant identification and correction of a number of complications in the immediate post-implantation period. TEE will continue to remain vital to the successful outcomes LVAD patients.     

High Right Atrial Pressure and Low Pulse Pressure Predict Gastrointestinal Bleeding in Patients With Left Ventricular Assist Device

Background

Gastrointestinal bleeding (GIB) remains a major morbid event during continuous flow left ventricular assist device (LVAD) support. This study investigated whether a common hemodynamic profile is associated with GIB in patients with LVADs.

Apoptosis, Bcl-2, and proliferating cell nuclear antigen in the failing human heart: observations made after implantation of left ventricular assist device

BACKGROUND: Heart failure is characterized by progressive left ventricular remodeling, a complex process that results from cell growth and cell death. The quantitative contribution of apoptotic cells toward left ventricular remodeling has varied widely in tissue removed from cardiomyopathic hearts. Apoptosis has been responsive to angiotensin-converting enzyme inhibition in experimental heart failure, but the dynamics and responsiveness to chronic left ventricular unloading have not been studied. METHODS AND RESULTS: We studied 8 patients with severe heart failure before and after chronic left ventricular unloading with a left ventricular assist device (LVAD). Tissue from the left ventricular apex removed at the time of LVAD implantation was examined for apoptosis using the technique of terminal deoxynucleotidyl transferase deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) in 10 patients. These same hearts explanted at the time of cardiac transplantation were then examined for apoptosis after patients had been on the LVAD for 99 +/- 20 (SEM) days. An additional 10 patients with equally severe heart failure who underwent heart transplantation without the use of an LVAD served as controls. Eight hearts obtained at autopsy approximately 6 hours after death from patients who died of non-cardiovascular disease causes served as non-heart failure controls. Additionally, 6 hearts were examined by immunohistochemistry for the antiapoptotic protein, Bcl-2, and for the repair and/or proliferation marker, proliferating cell nuclear antigen (PCNA), before and after LVAD. Apoptosis was not detected in the tissue sections from the hearts of 8 patients at the time of LVAD implantation. Only 1 of these patients had limited apoptosis (< 1 apoptotic cell/1,000 myocytes) after LVAD insertion. Three of 10 patients with severe heart failure who did not receive an LVAD but underwent transplantation showed limited apoptosis (< 1 apoptotic cell/1,000 myocytes). Likewise, none of the control hearts from patients who died of noncardiovascular disease manifested apoptosis. Six of 6 patients overexpressed Bcl-2 at the time of LVAD insertion. In all these patients, Bcl-2 returned to negligible levels after chronic unloading of the heart. Likewise, PCNA was abundantly expressed in 5 of 6 failing hearts at the time of LVAD implantation and was reduced in 4 of 5 hearts after chronic unloading by LVAD. CONCLUSION: Apoptosis is a rare or inconsistent finding in the failing human heart. Overexpression of such indicators of cellular stress and DNA replication and/or repair as Bcl-2 and PNCA in heart failure may be altered by optimizing left ventricular loading conditions by such mechanical devices as the LVAD.     

Prescription at discharge of recommended treatments for secondary prevention in patients with ST-segment elevation myocardial infarction according to reperfusion strategies. Results from the IN-ACS outcome study

Since its first clinical application in patients with cardiogenic shock (CS) in 1968, the intra aortic balloon pump (IABP) increasingly has been used for several clinical conditions requiring mechanical cardiac assistance. In current practice, IABP therapy is still the most accessible and most frequently used method of mechanical cardiac assistance. It is primarily being used as a therapeutic instrument for hemodynamic stabilization in left ventricular failure and cardiogenic shock, mainly in patients with myocardial infarction. Although IABP therapy showed to be effective for stabilization of hemodynamically compromised patients, it has failed to show any long‐term survival benefit in any setting of acute myocardial infarction. The rapid developments in ventricular assist device technology have led to the availability of several percutaneous implantable left ventricular assist devices (LVADs). These more potent percutaneous LVADs herald a promising alternative therapeutic approach for mechanical cardiac assistance other than IABP therapy. This article reviews the current status, capabilities, limitations, and future perspectives of currently available percutaneous treatment options for mechanical cardiac assistance in acute myocardial infarction.     

Gastrointestinal Bleeding After Continuous-flow Left Ventricular Device Implantation: Review of Pathophysiology and Management

Gastrointestinal bleeding is one of the most common complications in patients with continuous-flow left ventricular assist devices. Though the exact pathophysiology is still unclear, continuous-flow physiology, acquired Von Willebrand disease, and formation of arteriovenous malformations in the gastrointestinal tract are implicated. An individualized plan of endoscopic therapy and anticoagulation management is required when caring for these patients.     

Transcatheter aortic valve replacement thrombosis in patient supported with durable left ventricular assist device

Aortic insufficiency (AI) is a frequent problem after continuous‐flow left ventricular assist device (LVAD) implantation and results in increased morbidity and mortality. Advances in transcatheter aortic valve replacement (TAVR) technology have resulted in this being discussed as a potential option for LVAD patients with AI. While small case series have been published, we report the first case of TAVR thrombosis in an LVAD patient. This case highlights a major diagnostic and management dilemma that should become more present if this strategy becomes more widespread.     

Right ventricular failure after left ventricular assist device implantation: a review of the literature

Right ventricular failure (RVF) following left ventricular assist device (LVAD) implantation remains a major complication which may significantly impair patient outcome. The genesis of RVF is, however, multifactorial, and the mechanisms underlying such a condition have not been fully elucidated, making its prevention challenging and the course not always predictable. Although preoperative risks factors can be associated with RV impairment, the physiologic changes after the LV support, can still hamper the function of the RV. Current medical treatment options are limited and sometimes, patients with a severe post-LVAD RVF may be unresponsive to pharmacological therapy and require more aggressive treatment, such as temporary RV support. We retrieved 11 publications which we assessed and divided in groups based on the RV support [extracorporeal membrane oxygenation (ECMO), right ventricular assist device (RVAD), TandemHeart with ProtekDuo cannula]. The current review comprehensively summarizes the main studies of the literature with particular attention to the RV physiology and its changes after the LVAD implantation, the predictors and prognostic score as well as the different modalities of temporary mechanical cardio-circulatory support, and its effects on patient prognosis for RVF in such a setting. In addition, it provides a decision making of the pre-, intra and post-operative management in high- and moderate- risk patients.     

Bridge to recovery: what remains to be discovered?

The use of left ventricular assist devices to induce substantial myocardial recovery with explantation of the device, bridge to recovery (BTR), is an exciting but currently grossly underused application. Recently acquired knowledge relating to BTR and its mechanisms offers unprecedented opportunities to streamline its use and unravel some of the secrets of heart failure with much wider implications. This article reviews the status, challenges, and future of cardiac recovery.     

Estimation of right ventricular volume with two dimensional echocardiography

To evaluate the applicability of two dimensional echocardiography to right ventricular volume determination, a study was made of 33 consecutive patients separated into three groups (control, right ventricular volume overload and right ventricular pressure overload). Biplane two dimensional echocardiograms that were perpendicular to each other were obtained from the apical approach. The echocardiographic right ventricular volume, calculated by applying Simpson's rule, was considered to be right ventricular body volume without right ventricular outflow tract volume. The echocardiographic dimensions of the right ventricular long, short and maximal short axes were also measured in each view. These volumes and dimensions were compared with both the angiographic right ventricular body volumes calculated by applying Simpson's rule and with the values in each group. Correlation between the echocardiographic and the angiographic right ventricular body volumes (r = 0.94 at end-diastole, r = 0.84 at end-systole) was good and much better than that between echocardiographic right ventricular dimensions and angiographic right ventricular body volumes. Echocardiographic calculation of right ventricular body volume was useful in distinguishing the control group from the group with right ventricular volume overload (p < 0.005).

The correlation between the echocardiographic dimensions of the right ventricular long axis and angiographic right ventricular volumes was poor, whereas that between the echocardiographic dimensions of the right ventricular short or maximal short axis and the angiographic right ventricular volumes was fairly good. It was therefore suspected that during right ventricular enlargement, the increase in size is more extensive in the direction of the short than in the direction of the long axis. It is concluded that estimation of right ventricular volume and morphology with two dimensional echocardiography may be of value in clinical practice.     

超声心动图对先天性心脏病右心室功能的评价

目的以右心室造影为对照,使用超声心动图常规的四腔心切面和全新的右心室全显示切面定量评价右心室射血分数（right ventricular ejection fraction,RVEF）,探讨右心室全显示切面在右心功能评价中的应用价值。方法2011年4月至2011年11月通过临床和超声心动图检查选择伴有右心室形态或血流动力学改变的先天性心脏病患者22例（男13例,女9例,年龄16～67岁）为研究对象。除对人选患者行常规的超声心动图检查外,还使用四腔心切面和右心室全显示切面测量RVEF。在心导管实验室使用右心室造影测量RVEF。将四腔心和右心室全显示切面RVEF与右心室造影RVEF行随机区组设计方差分析及Pearson相关性分析,右心室全显示切面RVEF与其余右心功能指标行Pearson相关分析,并采用Bland—Ahman法评价右心室全显示切面与右心室造影的一致性。结果3种方法测得的RVEF分别为右心室全显示切面48．O％±11．3％、四腔心切面49．5％±13．1％、右心室造影48．7％±12．1％。3种方法测量结果比较,差异无统计学意义（F=0．327,P=0．723）。右心室全显示切面RVEF与右心室造影RVEF呈高度相关（r=0．908,P〈0．001）,四腔心切面RVEF与右心室造影RVEF呈中度相关（r=0．659,P=0．001）。右心室全显示切面RVEF与肺动脉收缩压及主肺动脉宽度负相关（P〈0．05）,与右心室每搏输出量正相关（P〈0．05）,与其他右心功能评价指标则无明显相关性。结论与常规的四腔心测量方法相比。超声心动图右心室全显示切面测量的RVEF与右心室造影的相关性更好,可能是一种准确和可靠的评价右心室收缩功能的方法。     

Myocardial histological changes in dilated cardiomyopathy during a long-term left ventricular assist device support

Summary As the myocardium in patients with dilated cardiomyopathy (DCM) is deteriorating progressively, resulting in a decrease in left ventricular function, patients with end-stage DCM may require implantation of a left ventricular assist device (LVAD) unless they undergo heart transplantation. Although LVAD has been reported to provide excellent hemodynamic support, no data are currently available about the effects of long-term LVAD support on the myocardium in patients with DCM. We describe two patients with end-stage DCM who underwent LVAD implantation and were supported with LVAD for 524 and 245 days, respectively. Serial myocardial biopsies showed increases in myocardial cell diameter and intercellular fibrosis, despite excellent hemodynamic support by LVAD. These data suggest that the myocardium in patients with end-stage DCM deteriorates progressively, even if the preload of the left ventricle is reduced by LVAD.     

Right ventricular dysfunction after acute pulmonary embolism: Pathophysiologic factors, detection, and therapeutic implications

Acute PE may lead to right ventricular dilatation and failure. Through ventricular interdependence and decreased left ventricular filling, cardiac output and systemic circulation also may be compromised. The associated decrease in coronary perfusion pressure to the acutely overload right ventricle may produce ischemia and worsening right heart failure. This downward cycle of right ventricular failure and ischemia may ultimately progress to right ventricular infarction, circulatory arrest, and death. Certain clinical findings, hemodynamic values, and, particularly, echocardiographic signs can identify right ventricular dysfunction after PE. Detection of right ventricular hypokinesis helps to stratify patients' risk, because right ventricular dysfunction confers a worse prognosis than does normal right ventricular function after PE. The concept of “hemodynamic instability’ after PE should be expanded to include right ventricular dilatation and wall motion abnormalities, even among normotensive patients. Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcome.     

Measurements of conduction times with catheter electrodes during pacing from different ventricular sites.

Filtered bipolar catheter electodes, I mm apart, were used to pace and record from the high right atrium, right ventricular apex, right ventricular outflow tract, right ventricular inflow tract, middle cardiac vein, great cardiac vein, and endocardium of the left ventricular septal surface. Right ventricular apex to middle cardiac vein and the middle cardiac vein to right ventricular apex conduction intervals gave a rough estimate of anteroposterior and posteroanterior "transseptal plus free left ventricular wall" conduction times, respectively. On the other hand, the right ventricular apex to left ventricular septal surface and left ventricular septal surface to right ventricular apex intervals represented pure "transseptal" conduction times, since both sets of electrodes were in contact with the respective septal surface. During stimulation of the intermediately located right ventricular inflow tract propagation to the right ventricular apex and right ventricular outflow tract was longer than between these two sites. Moreover, conduction was almost as delayed to the right ventricular apex and right ventricular outflow tract as it was to the left ventricular septal surface. These findings were attributed to the peculiar electrophysiological behaviour of the right ventricular inflow tract muscle. Pacing from different segments of the great cardiac vein produced QRS morphologies and arrival of excitation patterns consistent with the relation between the anatomical location of this structure and the recording electrodes. However, from this study no inferences could be drawn regarding the conduction velocity or specific conduction pathways used by the stimulus in its journey from stimulating to recording areas.     

Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease: Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction

Right ventricular infarction associated with left ventricular infarction was identified by gross examination at necropsy in 33 (14 percent) of 236 patients with transmural myocardial infarction. Right ventricular infarction occurred exclusively as a complication of posterior left ventricular infarction. Associated right ventricular infarction occurred in none of the 97 patients with isolated anterior wall infarction of the left ventricle, but in 33 (24 percent) of the 139 patients with posterior left ventricular infarction. Transmural infarction of the posterior ventricular septum was an additional prerequisite for right ventricular infarction. Of the 139 patients with infarction of the posterior left ventricular wall, 74 had no transmural infarction of the ventricular septum and none of these 74 had associated right ventricular infarction. In contrast, of the 65 patients with infarction of the posterior left ventricular wall and transmural infarction of the ventricular septum, 33 (50 percent) had associated right ventricular infarction.

Among the 33 patients with right ventricular infarction, the infarct was limited to the posterior right ventricular free wall in 27 (82 percent); in the other 6 patients (18 percent) it extended to involve the anterolateral right ventricular free wall. Among patients with a posterior left ventricular infarct, those with a right ventricular infarct had right ventricular dilatation nearly three times (P < 0.05) more frequently than the patients without a right ventricular infarct. Comparison of the same two groups disclosed no differences in the patients' age, sex, extent of coronary arterial luminal narrowing, right ventricular hypertrophy, right ventricular thrombi or duration of symptoms of myocardial ischemia.

Hemodynamic data in four patients with a right ventricular infarct disclosed previously reported characteristic hemodynamics of right ventricular infarction in only one patient. Recognition of right ventricular infarction is important because it implies specific therapy, namely, aggressive volume administration. Clinical evidence of posterior left ventricular infarction and right ventricular dilatation should arouse strong suspicion of associated right ventricular infarction.     

Measurements of conduction times with catheter electrodes during pacing from different ventricular sites.

Filtered bipolar catheter electodes, I mm apart, were used to pace and record from the high right atrium, right ventricular apex, right ventricular outflow tract, right ventricular inflow tract, middle cardiac vein, great cardiac vein, and endocardium of the left ventricular septal surface. Right ventricular apex to middle cardiac vein and the middle cardiac vein to right ventricular apex conduction intervals gave a rough estimate of anteroposterior and posteroanterior "transseptal plus free left ventricular wall" conduction times, respectively. On the other hand, the right ventricular apex to left ventricular septal surface and left ventricular septal surface to right ventricular apex intervals represented pure "transseptal" conduction times, since both sets of electrodes were in contact with the respective septal surface. During stimulation of the intermediately located right ventricular inflow tract propagation to the right ventricular apex and right ventricular outflow tract was longer than between these two sites. Moreover, conduction was almost as delayed to the right ventricular apex and right ventricular outflow tract as it was to the left ventricular septal surface. These findings were attributed to the peculiar electrophysiological behaviour of the right ventricular inflow tract muscle. Pacing from different segments of the great cardiac vein produced QRS morphologies and arrival of excitation patterns consistent with the relation between the anatomical location of this structure and the recording electrodes. However, from this study no inferences could be drawn regarding the conduction velocity or specific conduction pathways used by the stimulus in its journey from stimulating to recording areas.     

右心室流入道间隔部起搏血流动力学研究

目的本文旨在对右心室流入道间隔部起搏的血流动力学进行分析,以确立右心室流入道间隔部起搏的临床地位。方法本研究通过射频消融房室结建立Ⅲ°房室传导阻滞模型,结合影像学及心电图定位方法于右心室流入道间隔部置入螺旋电极导线,并分别比较右心室心尖部、右心室流出道及右心室流入道间隔部起搏后急性血流动力学指标变化,并随访右心室流入道间隔部起搏2周后的血流动力学指标。结果即刻血流动力学研究结果显示,右心室流入道间隔部较心尖部和右心室流出道起搏心排血量高(P<0.05),左心室舒张末期压力较低(P<0.05),而右心室流入道间隔部起搏前后各项血流动力学无显著变化。结论右心室流入道间隔部起搏具有良好的血流动力学效应,可作为右心室心尖部起搏的替代起搏部位。     

Two dimensional echocardiography and Doppler in the right ventricular infarction

Two dimensional and Doppler echocardiography provide reliable and valuable information in order to evaluate right ventricular function and associated complications in patients with right ventricular infarction. Right ventricular function in right ventricular infarction. There are a number of indirect findings that may support the noninvasive diagnosis of ischemic right ventricular dysfunction and right ventricular infarction: 1. Right ventricular dilatation: A right ventricular diastolic dimension greater than 8 mm/m2 is highly indicative of ischemic right ventricular dysfunction, provided that other causes of right ventricular dilatation, but the sensitivity of this findings is low (50%), the same is true for a RVDD/LVDD ratio greater than 0.63. 2. Right ventricular contraction abnormalities: Wall motion abnormalities constitute the most sensitive and specific echocardiographic findings in the right ventricular infarction. The most common site of involvement is the posterior wall, over 32 patients with right ventricular infarction, 60% present abnormalities confined to the posterior segment; in 30% there is also abnormal contraction of the lateral wall and 10% of the cases present asyneresys of the anterior, lateral and posterior segments. Those patients with the most severe right ventricular dysfunction presented a higher number of right ventricular wall segments with abnormal wall motion. Abnormalities in right ventricular contraction may still be present after evolution and normalization of the hemodynamic data of right ventricular infarction. These findings suggest that wall motion abnormalities can be more sensitive than the hemodynamic in detecting right ventricular infarction. 3. Paradoxical septal motion: Is a common findings after right ventricular infarction and has been attributed to volume overload and alterations in right ventricular compliance, near of 50% present abnormalities of septal motion and those patients with most severe ventricular dysfunction presented most frequently abnormal septal motion. Right ventricular infarction complications. Right ventricular aneurysm: In a series of 50 consecutive patients surviving an episode of right ventricular infarction, we could only find five (10%) with a true ventricular aneurysm. The segments included always the apex and in two cases a thrombus was identified inside its cavity. Functional right ventricular aneurysm may be found in a high percentage (10/50.20%) of patients with right ventricular infarction. Right ventricular thrombi: The identification of thrombi in the right heart is more difficult than in the left ventricle, due to the trabeculation of the right ventricular wall. We could only find 6 cases, in a series of 50 patients studied by two dimensional echocardiography. In all of the cases the ventricular wall adjacent to the thrombus presents contraction abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)