Right ventricular systolic and diastolic functions assessed by 81mKr scintigraphy and relation to ventricular septal ischemia

Right ventricular (RV) systolic and diastolic functions were assessed in patients with previous anteroseptal myocardial infarction to ascertain the influence of interventricular septal ischemia on RV function. Gated right ventriculography with continuous infusion of krypton-81 m was performed in 12 normal subjects and 28 patients with infarction but without significant stenosis of the right coronary artery. Furthermore, RV contractile reserve by postextrasystolic potentiation was evaluated by gated radionuclide ventriculography with 99mTc-HSA. The patients with anteroseptal infarction were divided into two groups by the presence or absence of three hours' redistribution in the septal region on exercise thallium-201 myocardial scintigraphy. Two indices of systolic function (ejection fraction and the peak ejection rate) and three indices of diastolic function (1/3 diastolic filling rate, the peak filling rate and time to the peak filling rate) were derived from the right ventricular time-activity curve and its derivative curve. There was no difference in systolic function among normal subjects and patients with or without redistribution. However, diastolic function was impaired only in the patients without redistribution. The RV contractile reserve in the patients without redistribution was less than in those with it. Thus, RV systolic function was maintained in the patients with anteroseptal infarction, but contractile reserve deteriorated only in severe septal ischemia. Similarly, diastolic function was maintained in mild septal ischemia, but impaired in severe septal ischemia. We concluded that RV systolic and diastolic functions are closely related to interventricular septal ischemia.     

The impact of right atrial ischemia on inferior myocardial infarction with extension to right ventricle: transesophageal echocardiographic examination

BACKGROUND: The role of the right atrium in adaptation to the hemodynamic changes produced by extension of myocardial infarction (MI) of the left ventricular inferior wall to the right ventricle is fundamental. HYPOTHESIS: The aim of this study was analyze a group of patients with MI with extension of right chambers, and particularly right atrial alterations, by transesophageal echocardiography and to correlate it with clinical and angiographic variables. METHODS: Thirty patients with right ventricular (RV) MI involving obstruction of the right coronary artery without stenosis of the left coronary artery were included; 18 underwent early reperfusion. Transesophageal echocardiography was performed on all within 5 days of coronary angiography. Follow-up was continued from hospitalization to the present. RESULTS: When patients with right atrial ischemia were compared with those with normal right atrium, the RV wall movement score was significantly greater in the group with right atrial ischemia, severe RV dilatation was more frequent, and association with proximal occlusion of the artery responsible for the MI, as well as absence of right atrial branches and poor collateral circulation, were significant. Hospitalization was more prolonged in this group, and there was a higher incidence of arrhythmias, complete atrioventricular block, and mortality. CONCLUSIONS: Right atrial ischemia associated with RV infarction leads to a higher incidence of complications and higher mortality. Transesophageal echocardiography is a safe, reproducible technique that provides detailed anatomic information about right chambers and aids in the determination of prognosis and therapeutic decisions.     

抗心肌肌凝蛋白抗体亲大鼠梗塞心肌特性的研究

目的　探讨抗心肌肌凝蛋白单克隆抗体 (antimyosinantibody ,AMA)亲梗塞心肌的特点。方法　心肌梗死大鼠静脉注射放射性锝 99m标记的抗心肌肌凝蛋白单克隆抗体 (99mTc AMA) ,观察注射时间 ,梗死时间和梗塞区对梗塞心肌摄取AMA的影响。结果　注射后 2h梗塞心肌开始摄取AMA ,以后摄取逐渐增加 ,2 4h达到高峰。心肌梗死后 2 0d ,梗塞心肌持续摄取AMA ,期间心肌梗死后 1～ 5d摄取最强 ,梗塞中央区以及梗塞区内层摄取强于其他梗塞区域。结论　急性心肌梗死大鼠梗塞心肌特异性地摄取AMA ,注射AMA后摄取迅速、持久 ,受心肌梗死时间影响较小 ,梗塞中央区内层心肌摄取最强 ,AMA具有亲梗塞心肌的特性。     

急性心肌缺血大鼠诱生型一氧化氮合酶的检测

目的 观察诱生型一氧化氮合酶(inducible nitric oxide sythase,iNOS)蛋白在心肌梗死后早期大鼠心脏的表达变化.方法 将12只大鼠随机分为心肌梗死组和假手术组.采用开胸结扎冠状动脉左前降支的方法建立心肌缺血模型,用免疫组织化学方法检测大鼠心肌梗死后24 h缺血心脏iNOS蛋白颗粒的表达.结果 在大鼠冠状动脉结扎后24h,梗死周围区心肌组织细胞出现大量iNOS蛋白表达,与假手术组相比差异有统计学意义(P＜0.01)假手术组未见iNOS蛋白表达.结论 正常心肌组织无iNOS蛋白表达,心肌梗死后早期缺血心肌组织检测到大量iNOS蛋白表达.     

Assessment of myocardial ischemia and infarction by contrast enhanced magnetic resonance imaging

Although magnetic resonance imaging (MRI) has proven to be a useful technique in assessing cardiac anatomy and function, the identification of ischemic and infarcted myocardium has been greatly aided by the use of paramagnetic contrast agents. This article discusses the advantages of using contrast enhanced MRI for the identification of myocardial ischemia and infarction.     

An ECG marker of underlying right ventricular conduction delay in the hyperacute phase of right ventricular infarction or ischemia

Patients with extensive right ventricular (RV) infarction or ischemia often have an accompanying RV conduction delay. Such patients frequently show precordial ST-T wave elevation, which hides the late r' wave in lead V1, making it difficult to recognize the RV conduction delay during the hyperacute phase. We noted that such patients occasionally exhibited a "cove"-shaped ST-T elevation in lead V1, which strongly suggested the presence of this complication even in the hyperacute stage. This report describes three instances of RV infarction or ischemia with this characteristic electrocardiographic sign. This sign appears to be a marker of RV conduction delay during the hyperacute stage of RV infarction or ischemia.     

Pathophysiology and clinical management of right heart ischemia.

Right ventricular (RV) ischemia occurs in 50% of patients with acute inferior myocardial infarction, and may result in severe hemodynamic compromise associated with poor clinical outcome. Right coronary artery occlusion proximal to the RV branches results in RV systolic dysfunction, which decreases transpulmonary delivery of left ventricular (LV) preload and diminishes cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction. Under these conditions, RV pressure generation and output depend on LV-septal contractile contributions. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling and performance, leading to more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with RV ischemia and hemodynamic compromise often respond to volume resuscitation and restoration of a physiologic rhythm. In some patients, parenteral inotropic stimulation may be required. The ischemic right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover. The term RV infarction appears to be a misnomer, as RV performance improves spontaneously even in the absence of reperfusion. Reperfusion, however, enhances the recovery of RV performance and improves the clinical course.     

Silent inferior myocardial infarction with extensive right ventricular scarring

Right ventricular infarction (RVI) occurs in approximately 50% of patients with inferior myocardial infarction (MI). The assessment of RVI is important for identifying patients being at increased risk of in hospital mortality and poorer prognosis if impaired right ventricular (RV) systolic function is present. We report the case of an asymptomatic 38-year-old male who sustained a silent inferior myocardial infarction with extensive RV involvement. There was no history of myocardial ischemia and cardiovascular risk factors. Therefore, first cardiac magnetic resonance (CMR) imaging using delayed enhancement (DE) was performed and revealed a transmural inferior wall myocardial infarction of LV with extensive involvement of RV. This case illustrates the difficulties of conventional imaging modalities and invasive coronary angiography to depict an inferior myocardial infarction with RV involvement.     

S-T segment depression in right-sided precordial leads during acute inferior wall infarction.

Right-sided chest leads (V3-V4R) were recorded in the early stages of first inferior wall acute myocardial infarction (AMI) in 100 consecutive patients. Nine patients (9%) presenting with S-T segment depression (greater than 1 mm) in these leads were subsequently studied by echocardiography and radionuclear angiography. In this group, there were 5 patients with intact right ventricular (RV) function and 4 other patients with clinical findings compatible with RV infarction. We suggest that one should not rule out RV involvement when S-T segment depression rather than elevation is seen in the right precordial leads in the presence of inferior wall AMI. An individual assessment for RV infarction is recommended when this pattern is apparent on the ECG.     

Pathophysiology and management of right heart ischemia

Acute right coronary artery occlusion proximal to the right ventricular (RV) branches results in right ventricular free wall dysfunction, exerting mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function decreases transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling and performance, resulting in more severe hemodynamic compromise. Bradyarrhythmias limit output generated by the rate-dependent noncompliant ventricles. Hemodynamic compromise may respond to volume resuscitation and restoration of physiologic rhythm. Vasodilators and diuretics should generally be avoided. In some patients, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and recovers even after prolonged occlusion. The term RV "infarction" appears to be somewhat of a misnomer, for in most patients acute RV dysfunction represents ischemic but predominantly viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances recovery of RV performance and improves the clinical course and survival.     

Imaging and modern assessment of the right ventricle

The right ventricular function is difficult to assess owing to its complex morphology, structure and function. The right ventricle (RV) comprises three compartments, the inlet, the apex, and the outlet contracting with a peristaltic motion from the inflow to the outflow chamber and is tightly linked to left ventricular (LV) function through the pulmonary circulation, the interventricular septum and the myocardium inside the pericardial envelop. The relation of RV function to symptom occurrence, exercise capacity and prognosis in a wide variety of cardiac diseases emphasizes the usefulness of its routine assessment. The evaluation of the RV is largely carried out by echocardiography in daily clinical practice despite important limitations inherent to two-dimensional imaging. Multiple views and numerous parameters allow clinicians to integrate the RV function in the clinical decision-making process. Recent modalities of echocardiography such as myocardial deformation and three-dimensional imaging or exercise echocardiography are promising tools for the assessment of the RV. Cardiac magnetic resonance imaging provides the unique opportunity to image the RV in motion and in three dimensions without the limitation of echogenicity. Therefore, cardiac magnetic resonance imaging is taking a growing place in the assessment of the RV in a wide variety of cardio-pulmonary diseases as pulmonary hypertension, ischemia, arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy, heart failure or congenital heart diseases. Integrating the complex interplay between both ventricles and the pulmonary circulation, this review will discuss the latest results of standard and novel techniques allowing the assessment of RV function by echocardiography and cardiac magnetic resonance imaging, and will provide to the clinicians, facing therapeutic challenges, a comprehensive overview of right heart function.     

Greater impairment of right ventricular systolic function in patients with anterior myocardial infarction because of the extent of proximal lesions.

The present study examined the influence of the extent of the ischemic area on right ventricular (RV) systolic function and the relation between the RV global and regional systolic function in patients with anteroseptal myocardial infarction (MI). Biplane right ventriculography was performed in 15 subjects as the control group, and 46 patients with anteroseptal MI as the MI group. Three dimensions of the RV (the long axis dimension [LA], the anterior-posterior dimension [AP] and the septum-free wall dimension [SF]) were examined to assess regional function The MI group had a larger right ventricular end-systolic volume index and lower right ventricular ejection fraction than the control group. The more proximal the coronary lesion, the lower was the ejection fraction of the RV in the MI group. The MI group had lower percent shortening (% shortening) of the SF than the control group, but there were no significant change in the % shortening of AP and LA between the groups. The results suggest that the degree of impairment of RV systolic function depends on the extent of the infarcted area, and that the impairment is mainly from a reduction in the %shortening of the SF.     

Echocardiographic evaluation of spontaneous recovery of right ventricular systolic and diastolic function in patients with acute right ventricular infarction associated with posterior wall left ventricular infarction

We evaluated right ventricular (RV) systolic and diastolic function in 30 patients with acute RV myocardial infarction on echocardiography. Systolic and diastolic function were impaired early in the setting of RV myocardial infarction, but improved significantly at 3 months.     

Assessment of denervated but viable myocardium in patients with myocardial infarction--by myocardial imaging with 201Tl and 123I-MIBG

The present study assessed sympathetic function in viable infarcted areas of the myocardium following the onset of myocardial infarction. The subjects were 19 patients with myocardial infarction. After exercise on a bicycle ergometer, simultaneous SPECT with Tl-201 and I-123 MIBG was performed. The behavior of MIBG following exercise remains to be clarified, but in the present study MIBG provided images different from those obtained with Tl. While the redistribution of Tl in the infarcted area was observed in 8 of 19 patients, MIBG was absent in the infarcted area in both the initial and delayed scans. In the patient undergoing CABG, the infarcted area showed no MIBG despite the normal perfusion of Tl. The previous proposal that the redistribution of Tl indicates myocardial viability to some extent suggests that the sympathetic function of the area of the myocardium showing the redistribution of Tl decreases even though the area is viable. These findings indicate that after the onset of myocardial infarction, there is a denervated but viable area in the myocardium, despite the viability demonstrated by Tl imaging. They also indicate that concurrent myocardial imaging with MIBG is useful for the detection of such a myocardium.     

Electrical Impedance Properties of Normal and Chronically Infarcted Left Ventricular Myocardium

Background: Previous reports have disclosed that a significant difference exists between the electrical impedance properties of healthy and chronically infarcted ventricular myocardium.Purpose: To assess the potential utility of electrical impedance as the basis for mapping in chronically infarcted left ventricular myocardium. Specifically: (1) to delineate electrical impedance properties of healthy and chronically infarcted ventricular myocardium, with special emphasis on the infarction border zone; (2) to correlate impedance properties with tissue histology; (3) to correlate impedance properties with electrogram amplitude and duration; (4) To demonstrate that endocardial impedance can be measured effectively in vivo using an electrode mounted on a catheter inserted percutaneously.Methods: An ovine model of chronic left ventricular infarction was utilized. Sites of healthy myocardium, densely infarcted myocardium and the infarction border zone were investigated. Bulk impedance was measured in vitro using capacitor cell, four-electrode and unipolar techniques. Epicardial and endocardial impedances were measured in vivo using four-electrode and unipolar techniques. Impedance was measured at multiple frequencies. Electrographic amplitude, duration and amplitude/duration ratio were measured using bipolar electrograms during sinus rhythm. Quantitation of tissue content of myocytes, collagen, elastin and neurovascular elements was performed.Results: Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the border zone transitioning between healthy myocardium and dense infarction. Decreasing impedance correlated with a decrease in tissue myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as the measurement frequency decreased. Healthy myocardium exhibited a marked frequency dependence in its impedance properties; this phenomenon was not observed in densely infarcted myocardium. There was a direct association between impedance and both electrogram amplitude and amplitude/duration ratio. There was an inverse association between impedance and electrogram duration. Endocardial impedance, measured in vivo using a electrode catheter inserted percutaneously, was demonstrated to distinguish between healthy and infarcted myocardium.Conclusions: The electrical impedance properties of healthy and infarcted left ventricular myocardium differ markedly. The properties of the infarction border zone are intermediate between healthy and infarcted myocardium. Impedance may be a useful assay of cardiac tissue content and adaptable for cardiac mapping in vivo.Condensed Abstract. To delineate the electrical impedance properties of healthy and chronically infarcted left ventricular myocardium emphasizing the infarction border zone, impedance was measured in chronically infarcted ovine hearts. Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the infarction border zone in transition between healthy myocardium and dense infarction. This correlated with a decreasing myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as measurement frequency decreased. There was a direct association between impedance and electrogram characteristics. Endocardial impedance, measured in vivo using an electrode catheter inserted percutaneously, distinguished between healthy and infarcted myocardium     

Potential of an intracardiac electrogram for the rapid detection of coronary artery occlusion

BACKGROUND: Early identification of acute MI and prompt intervention can improve clinical outcomes. It would be valuable to identify a method that could allow the earliest possible detection of myocardial injury or ischemia. METHODS AND RESULTS: This article reports one of the first clinical investigations to examine the ability of an intracardiac right ventricular (RV) electrode to identify the early onset of myocardial ischemia/injury in a cohort of patients undergoing balloon occlusion of a coronary artery during percutaneous transluminal coronary angioplasty. The primary data set for analysis included observations from 14 patients with 17 lesions, with a matched comparison of a V6 surface lead and the RV to left upper chest, "intracardiac" lead. The intracardiac lead was sensitive in detecting myocardial injury current/ischemia. There was a 36.4+/-5.6% ST-segment shift, relative to the amplitude of the QRS complex, in the intracardiac lead at 2 min, compared with a 10.1+/-1.9% ST shift from a surface lead (P=.00011). The RV to left upper chest lead detected a >10% shift in ST segment within 2 min in 17 (100%) of 17 cases vs. 8 (47%) of 17 for a V6 surface lead. The intracardiac lead provided detection of ischemia in all three major epicardial coronary distributions. CONCLUSIONS: This study demonstrates the ability of an intracardiac (RV apex to left upper chest) lead to rapidly detect myocardial ischemia/injury during acute coronary occlusion in the setting of balloon angioplasty. The results of this study suggest that a simple implantable system resembling a ventricular pacemaker could be programmed to assist in the very early diagnosis of acute myocardial infarction.     

Bone-marrow-derived progenitor cell therapy in need of proof of concept: design of the REPAIR-AMI trial

Early reperfusion of occluded coronary arteries has significantly reduced early mortality and improved the long-term prognosis of patients with an acute myocardial infarction. However, the development of postinfarction heart failure remains a major challenge. Initial experimental studies indicated that mononuclear progenitor cells derived from the bone marrow may contribute to the functional regeneration of freshly infarcted myocardium and increase neovascularization of ischemic areas. A number of clinical pilot trials have now transferred the experimental approach into the clinical arena, aiming at regenerating myocardial function with infusion of bone-marrow-derived progenitor cells in patients after an acute myocardial infarction. While these initial trials using intracoronary infusion of bone-marrow-derived progenitor cells indeed suggested that such a strategy appears to be feasible and safe in patients with an acute myocardial infarction, there is definitely a pressing need for a proof-of-concept study documenting a potentially beneficial effect of progenitor cell therapy on cardiac function.     

Cardiovascular Magnetic Resonance: Myocardial Perfusion

There is growing evidence that the noninvasive assessment of myocardial perfusion with cardiovascular magnetic resonance is a valid and accurate tool for the assessment of ischemic heart disease and its introduction into routine clinical evaluation of patients is rapidly expected. Magnetic resonance measurements allow the evaluation of reversible and irreversible myocardial ischemia, the assessment of acute myocardial infarction, as well as the recognition and detection of viable myocardium. Magnetic resonance perfusion measurements are mainly performed with T1-shortening contrast agents such as gadolinium-DTPA either by visual analysis or based on the analyses of signal intensity time curves. For the detection of myocardial ischemia the first pass kinetics of a gadolinium-DTPA bolus and for the detection of myocardial necrosis and the definition of viable myocardium steady state distribution kinetics are assessed. Quantitative analysis of myocardial perfusion can be performed but requires complex modeling due to the characteristics of gadolinium-DTPA. Thus, semi-quantitative parameters are preferred. There is accumulating evidence in the literature that magnetic resonance imaging can be used for the detection of coronary artery stenosis with high diagnostic accuracy both with semi-quantitative or visual analysis. Myocardial infarction can be reliably detected and the infarcted area determined. Non-reperfused infarcted myocardium can be differentiated from reperfused myocardium by different enhancement patterns that correlates with viability. Cardiac magnetic resonance is a promising technique that can combine different functional studies during one examination, such as the assessment of wall motion and perfusion at rest and stress. With further improvements in analysis software magnetic resonance perfusion measurement may rapidly become a routine tool for the assessment of patients with coronary artery disease.     

Bone marrow-derived myocyte-like cells and regulation of repair-related cytokines after bone marrow cell transplantation

OBJECTIVE: Whether bone marrow cells injected following acute myocardial infarction (MI) transdifferentiate into cardiomyocytes remains controversial, and how these cells affect repair-related cytokines is not known. METHODS: Autologous bone marrow-derived mononuclear cells (BM-MNCs) labeled with DiI, 1,1'-dioctadecyl-1 to 3,3,3',3'-tetramethylindocarbocyanine perchlorate, or saline were intravenously injected into rabbits 5 h following a 30-min ischemia and reperfusion protocol, and cardiac function and the general pathology of the infarcted heart were followed up 1 and 3 months post-MI. To search for regenerated myocardium, electron microscopy as well as confocal microscopy were performed in the infarcted myocardium 7 days post-MI. Expression levels of repair-related cytokines were evaluated by immunohistochemistry and Western blotting. RESULTS: Improvements in cardiac function and reductions in infarct size were observed in the BM-MNC group 1 month and 3 months post-MI. Using electron microscopy 7 days after infarction, clusters of very immature (fetal) and relatively mature cardiomyocytes undergoing differentiation were identified in the infarcted anterior LV wall in the BM-MNC group, though their numbers were small. These cells contained many small and dense DiI particles (a BM-MNC marker), indicating that cardiomyocytes had regenerated from the injected BM-MNCs. The expression of both transforming growth factor-beta, which stimulates collagen synthesis and matrix metalloproteinase-1, a collagenase, were both down-regulated 7 days and 1 month post-MI in the BM-MNC group. Stromal cell-derived factor-1, which is known to recruit BM-MNCs into target tissues, was overexpressed in the infarcted areas of BM-MNC hearts 7 days post-MI. CONCLUSIONS: Intravenous transplantation of BM-MNCs leads to the development of BM-MNC-derived myocyte-like cells and regulates the expression of repair-related cytokines that facilitate repair following myocardial infarction.     

Studies on pathophysiological significance of sympathetic activity in myocardial infarction.

In an attempt to elucidate the pathophysiological significance of the sympathetic hyperactivity in the acute stage of myocardial infarction, the author observed changes in the urinary excretion of CA, the CA content in the myocardium and the hemodynamics in both clinical and experimental myocardial infarction, and the following were found: 1) In clinical myocardial infarction, the urinary excretion of CA was markedly increased immediately after an attack, and the assay of myocardial specimens form the autopsied patients of acute myocardial infarction revealed that the CA content in the non-infarcted area was lower than that in the infarcted area. 2) In the experiments on rabbits with ligated coronary artery, the increase in cardiac contractility and rise in blood pressure in response to CA was supressed after the ligation of coronary artery. In the early stage of experimental myocardial infarction, the decrease of myocardial CA content in the non-infarcted area was, as in autopsied patients, predominant over the decrease of that in the infarcted area. In the chronic stage (more than one week after the coronary ligation), the CA content in the infarcted area showed further decrease, but in the non-infarcted area it was recovered to the level in the control animals. The uptake of exogenous NA into the non-infarcted area decreased in the acute stage, and in the infarcted area it showed marked decreased in the chronic stage. The urinary excretion of CA was increased in the acute stage of myocardial infarction. 3) The administration of betamethasone suppressed the decrease in the CA content in the myocardium following the ligation of coronary artery. Based on these findings, the author came to a postulation that the sympathetic hyperactivity which is suggested by increased urinary excretion of CA and decreased CA content in the myocardium results from the reasonable biophylactic reaction so as to supplement the cardiac hypofunction derived from myocardial infarction.