Safety of exercise-based cardiac rehabilitation and exercise testing for cardiac patients in Japan: a nationwide survey.

BACKGROUND: The safety of exercise-based cardiac rehabilitation (CR) has not been investigated in Japan, so a nationwide survey was conducted to investigate the incidence of adverse events (AEs) associated with CR and exercise testing. METHODS AND RESULTS: In total, 136 hospitals reported operating recovery-phase CR programs, amounting to 383,096 patient-hours of exercise training. The incidence rates of all AEs and life-threatening AEs (LAE: death, cardiac arrest, acute myocardial infarction, cardiac rupture) during exercise sessions were 12 and 1 event/383,096 patient-hours (3.13 and 0.26 events/100,000patient-hours), respectively. When CR programs were categorized as "Formal" in which an exercise prescription based on exercise testing was issued to individual patients or "Non-formal" without exercise prescription, the incidence of AEs during and within the 24 h after an exercise session was significantly lower in the Formal than the Non-formal CR programs (P<0.001), despite similar hospital size and coronary intervention volumes between the 2 category hospitals. Moreover, LAEs did not occur in 277,721 patient-hours in Formal CR, whereas 2 LAEs occurred in 105,375 patient-hours in Non-formal CR (P<0.05). During 469,215 exercise testing sessions, 3 LAEs (0.64 event/100,000tests) and 31 non-LAEs (6.61 events/100,000tests) occurred. CONCLUSIONS: This first nationwide survey in Japan revealed that both exercise-based CR and exercise testing are generally safe, and that Formal CR, in which an individual exercise prescription is determined by exercise testing, is particularly safe.

Diabetes mellitus as a predictor of retinopathy associated with acute myocardial infarction.

BACKGROUND: A unique transient retinopathy characterized by soft exudates around the optic disc after percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) has been reported, so in the present study the risk factors for retinopathy associated with AMI (RAMI) were investigated. METHODS AND RESULTS: The study group comprised 62 patients with their first AMI who underwent successful PCI within 24 h of onset (48 men, 14 women; age 63 +/-10 years). The fundus of each eye was assessed on days 3-5, and again at 4 weeks after AMI onset. New soft exudates developed in 29 patients (47%) at 4 weeks. The frequency of diabetes mellitus (DM), and the hemoglobin A(1c) and peak creatine kinase concentrations were higher in patients with than in those without RAMI (55% vs 21%, P=0.008; 7.0 +/-2.0% vs 5.9 +/-1.4%, P=0.013; and 3,428 +/-2,210 IU/L vs 2,352 +/-1,652 IU/L, P=0.036, respectively). Multivariate analysis identified DM as an independent predictive factor for the occurrence of RAMI (odds ratio, 6.60; 95% confidence interval, 1.68-25.90; P=0.007). CONCLUSIONS: DM might be a risk factor for RAMI.

Daily exercise and bone marrow-derived CD34+/133+ cells after myocardial infarction treated by bare metal stent implantation.

BACKGROUND: The aims of the present study were to explore the mobilization of bone marrow-derived CD34(+)/133(+) cells in patients with acute myocardial infarction (AMI) and bare metal stent implantation who participated in daily exercise training, and associations with exercise capacity and restenosis. METHODS AND RESULTS: Participants comprised 23 Japanese men with AMI (Killip 1) who had been treated with a bare metal stent. All patients were advised to walk for 30-60 min/day, at least 4 times per week starting at 11 days after AMI, and were instructed to record the amount of time spent walking each day. At 10 days and then at 3 months after onset of AMI, symptom-limited cardiopulmonary exercise tests were performed and the number of CD34(+)/133(+) cells in the peripheral blood were measured by fluorescence-activated cell sorter analysis. At 3 months after AMI, the number of CD34(+)/133(+) cells and oxygen consumption at anaerobic threshold were higher in the high exercise group (ie, exercise duration >4 h/week) than the low exercise group (ie, exercise duration <2 h/week). At 3 months after AMI, the number of CD34(+)/133(+) cells significantly correlated with oxygen consumption at the anaerobic threshold (p=0.002). CONCLUSION: Moderate daily exercise of >4 h/week increases exercise capacity and the number of circulating CD34(+)/133(+) cells at 3 months after AMI.

C-reactive protein induces endothelial cell apoptosis and matrix metalloproteinase-9 production in human mononuclear cells: Implications for the destabilization of atherosclerotic plaque.

C-reactive protein (CRP) has been suggested to directly induce the inflammatory response leading to the progression of atherosclerosis. However, recent in vitro studies raised the possibility that the effects of CRP are caused by biologically active contaminants such as sodium azide and endotoxin. In this study, we tested whether azide- and endotoxin-free CRP induces endothelial cell apoptosis and production of proinflammatory mediators. In human endothelial cells, CRP significantly inhibited cell proliferation and increased endothelial cell apoptosis evaluated by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and caspase-3 activity assay, which is reversed by a function-blocking antibody to Fc gamma RIIIB by 78%. Western blot analysis showed that CRP significantly attenuated flow-mediated activation of Akt, a key molecule for endothelial cell survival pathways. In human mononuclear cells, CRP-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and matrix metalloproteinase-9 (MMP-9) in a concentration-dependent manner. This CRP-induced MMP-9 production was significantly inhibited by function-blocking antibodies to TNF-alpha, IL-1 beta, and Fc gamma RIIA. These findings suggest that CRP itself induces endothelial cell apoptosis and production of proinflammatory mediators. Because endothelial cell apoptosis and MMP-9 production are critical for the destabilization of atherosclerotic plaque, this study may provide insight into a role of CRP in the development of plaque rupture.

Subcutaneous injection of heparin calcium controls chronic disseminated intravascular coagulation associated with inoperable dissecting aortic aneurysm in an outpatient clinic.

BACKGROUND: Chronic disseminated intravascular coagulation (DIC) is a rare but critical complication of aortic aneurysm, and can represent a difficult long-term management problem. Although surgical correction is the treatment of choice, alternative therapy is required for inoperable patients. RESULTS: We report herein a case of acute exacerbation of chronic DIC with inoperable dissecting aortic aneurysm, which was recurrent and resistant to regular treatment. Intermittent subcutaneous self-injection of heparin calcium 15,000 units per day achieved stabilization of coagulation and fibrinolytic parameters and relief of the bleeding tendency. CONCLUSION: Subcutaneous heparin injection can be an alternative treatment for long-term management of chronic DIC associated with inoperable aortic dissection, beneficial for providing good symptomatic control on an outpatient basis.

Reduction of neointimal hyperplasia after coronary stenting by pioglitazone in nondiabetic patients with metabolic syndrome.

BACKGROUND: This study investigates whether pioglitazone reduces neointimal hyperplasia after coronary stenting in nondiabetic patients with metabolic syndrome (MS) using intravascular ultrasound (IVUS). Pioglitazone, a novel insulin-sensitizing thiazolidinedione, has been shown to reduce neointimal hyperplasia after coronary stenting in patients with type 2 diabetes. However, the effect of pioglitazone on in-stent restenosis in nondiabetic patients with MS remains unknown. METHODS AND RESULTS: Twenty-eight nondiabetic patients with MS after bare-metal stent implantation were randomized to 6-month treatment with or without 30 mg/d of pioglitazone (pioglitazone group [PIO] of 14 patients with 16 lesions and control group [CONT] of 14 patients with 16 lesions). At baseline and at 6-month follow-up, assessment of insulin resistance and visceral fat accumulation, quantitative coronary angiographic analysis, and IVUS measurements were performed. Pioglitazone treatment improved insulin resistance and decreased visceral fat accumulation without significant changes in plasma glucose levels, glycosylated hemoglobin A1c levels, and lipid profiles. Intimal index (intimal area/stent area) and intimal area were reduced in PIO compared with CONT (13% +/- 7% vs 21% +/- 13%, P = .033; 1.28 +/- 0.76 mm2 vs 1.90 +/- 1.16 mm2, P = .084; respectively). Binary restenosis rate was 0% in PIO versus 31% in CONT (P = .043). CONCLUSIONS: This is the first randomized, prospective IVUS study demonstrating that pioglitazone reduces neointimal hyperplasia after coronary stenting in nondiabetic patients with MS. Our data suggest that pioglitazone treatment may represent a novel therapeutic tool to target in-stent restenosis in nondiabetic patients with MS.

N-terminal pro-atrial natriuretic peptide and exercise prescription in patients with myocardial infarction.

BACKGROUND: Left ventricular end-diastolic pressure (LVEDP) during exercise workload is an important parameter to guide an exercise prescription for patients with cardiovascular disease. Plasma levels of neuro-hormonal factors can be used as a reflection of real-time LVEDP, but its utility is limited by its short half-life. By contrast, the N-terminal fragment of pro-ANP (NT-ANP) has a longer half-life of 1 h. OBJECTIVE: To determine whether plasma NT-ANP levels at 30 min after exercise can be used as a marker of LVEDP during peak exercise workload in patients with previous myocardial infarction. PATIENTS: Twenty patients with a previous history of myocardial infarction. INTERVENTIONS: Cardiopulmonary exercise test was performed to determine peak VO(2) and anaerobic threshold. Plasma levels of ANP, BNP, NT-ANP, vasopressin and plasma catecholamine were measured at rest, maximum exercise, and 30 min after exercise (recovery). RESULTS: With the exception of NT-ANP, the levels of each of neuro-hormonal factors peaked at maximum exercise and returned to baseline at recovery. By contrast, NT-ANP levels also increased at peak exercise but remained elevated at 30 min after exercise. Furthermore, NT-ANP levels at recovery correlated with ANP levels at maximum exercise (p<0.01, R=0.75), left ventricular ejection fraction (p<0.02, R=-0.54) and left ventricular systolic dimension (p<0.015, R=0.50). CONCLUSION: Plasma NT-ANP levels at 30 min after exercise reflect ANP levels at maximum exercise and left ventricular overload during exercise. These data indicate that plasma NT-ANP after exercise may be a useful parameter to guide prescription of cardiac rehabilitation.

Poor implementation of cardiac rehabilitation despite broad dissemination of coronary interventions for acute myocardial infarction in Japan: a nationwide survey.

BACKGROUND: The implementation of cardiac rehabilitation (CR) after acute myocardial infarction (AMI) has not been fully investigated in Japan, so a nationwide survey of hospitals was conducted. METHODS AND RESULTS: Questionnaires were sent in 2004 to a total of 1,875 hospitals in Japan, including all the 859 Japanese Circulation Society (JCS)-authorized cardiology-training hospitals (THs), 311 JCS-associated hospitals (AH), and 705 randomly sampled non-THs (NTHs). The response rate was 59% (1,106/1,875). The percentages of hospitals treating hospitalized AMI patients were 97% in 526 TH, 85% in 194 AH, and 20% in 339 NTH. Although the rates of implementation of emergency percutaneous coronary intervention were very high (92%, 56%, and 4%, respectively), the rates of implementation of recovery phase CR were low (20%, 8%, and 2%, respectively). In addition, patient education programs (23%, 13% and 2%) and formulated exercise prescriptions based on exercise testing (16%, 7% and 1%) were poorly implemented. More importantly, only 9%, 2% and 0% of these hospitals had outpatient CR programs. From these data, the nationwide participation rate in outpatient CR after AMI in Japan was estimated to be only 3.8-7.6%. CONCLUSION: This first nationwide survey demonstrated that, in contrast to the broad dissemination of acute phase invasive treatment for AMI, the implementation of recovery phase CR, especially outpatient CR, is extremely poor in Japan. In addition, patient education programs and exercise prescription based on exercise testing are only poorly implemented.

Association of hyperadiponectinemia with severity of ventricular dysfunction in congestive heart failure.

BACKGROUND: Adiponectin, which is a collagen-like plasma protein produced by adipose tissue, has anti-atherogenic and anti-inflammatory effects. Plasma adiponectin levels in patients with congestive heart failure (CHF) were determined, as well as relationships between the plasma levels of adiponectin and other hormones. METHODS AND RESULTS: The study group comprised 90 patients with CHF and 20 control subjects, who were divided into 4 subgroups according to New York Heart Association (NYHA) functional class. Plasma levels of adiponectin, tumor necrosis factor (TNF)-alpha and brain natriuretic peptide (BNP) and cardiac hemodynamics were determined. Plasma adiponectin levels were significantly increased according to the severity of NYHA class in the patients with CHF; control: 6.2+/-1.0; NYHA I: 8.5+/-1.9, NYHA II: 12.0+/-2.2, NYHA III: 13.0+/-2.7, NYHA IV: 14.9+/-2.7 microg/ml (p=0.0008). Similarly, plasma BNP levels were significantly increased in accordance with the NYHA class. Plasma adiponectin levels correlated positively with BNP (r=0.40, p=0.0002) and TNF-alpha (r=0.49, p=0.0001), and correlated negatively with cardiac index (r=-0.27, p=0.05). In 24 of 46 patients in the NYHA III and IV subgroups, according to the prompt improvement in cardiac function, levels of both plasma adiponectin and BNP were significantly reduced (p<0.0001). CONCLUSION: Plasma adiponectin levels increased according to the severity of CHF and, moreover, they correlated with the plasma levels of BNP and TNF-alpha. These results indicate that augmented release of adiponectin is involved in the pathogenesis of CHF and further study is needed to elucidate its exact role.

Successfully treated massive pulmonary thromboembolism and thrombus in the right atrium due to diffuse malignant lymphoma: a case report.

A 40-year-old man presented with massive pulmonary embolism related to diffuse large B cell lymphoma. His hemodynamic state worsened rapidly to shock after sudden onset of dyspnea. Echocardiography and thoracic computed tomography indicated pulmonary thromboembolism due to deep venous thromboembolism, associated with a mass in the anterior mediastinum and a 5 x 8 cm mass in the left pelvis compressing the left femoral vein. He underwent emergent surgery to remove a huge thrombus from the right atrium through the bilateral pulmonary arteries. Soon after this surgery, his hemodynamic state recovered and excision of the left cervical lymph node revealed diffuse large B cell lymphoma. Venous compression by the lymphoma mass had caused hemostasis and thrombus formation in the present case.

Close association of regional interleukin-6 levels in the infarct-related culprit coronary artery with restenosis in acute myocardial infarction.

BACKGROUND: The involvement of interleukin (IL)-6 in restenosis of the recanalized coronary artery after the percutaneous coronary intervention (PCI) was examined. METHODS AND RESULTS: There were 40 patients enrolled in the study who had acute myocardial infarction and whose infarct-related coronary arteries were treated by new thrombectomy devices and stenting. Blood samples were collected from the culprit coronary artery before and immediately after the maneuver of the PCI. Restenosis was defined as residual stenosis because it accounted for more than 50% at the follow-up coronary angiography. Plasma IL-6 levels in the infarct-related coronary artery were 12.8 and 13.2 pg/ml before and after the initial maneuver of the PCI, respectively, values that were significantly greater than that of 7.2 pg/ml in the peripheral vein (p<0.0001). The levels of IL-6 in the pre- and the post-stage of PCI were significantly greater in the patients with restenosis than those without restenosis. The plasma IL-6 levels in the post-stage of PCI had significant correlations with late loss and loss index. CONCLUSIONS: The present study findings indicate that plasma IL-6 levels in the culprit coronary artery at the post-stage of PCI are closely associated with the future restenosis of the revasculized coronary artery in acute myocardial infarction.

Acute mitral regurgitation due to ruptured chordae tendineae in a patient with hypertrophic obstructive cardiomyopathy: a case report.

A 63-year-old woman had been followed up for hypertrophic obstructive cardiomyopathy with 85 mmHg of left ventricular outflow tract pressure gradient over 7 years. She was hospitalized because of acute dyspnea and syncope. On admission, echocardiography revealed severe mitral regurgitation with ruptured chordae tendineae at the medial scallop of the posterior mitral leaflet. Mitral valve replacement was successfully performed and her symptoms improved to 28 mmHg of left ventricular outflow tract pressure gradient. In patients with hypertrophic obstructive cardiomyopathy, elevated left ventricular systolic pressure and systolic anterior motion of the mitral leaflets may lead to mucoid degeneration in the chordae tendineae. Rupture of the mitral chordae tendineae should be considered in the differential diagnosis of acutely deteriorated mitral regurgitation in patients with hypertrophic obstructive cardiomyopathy, because this is a rare but critical complication.

Noninvasive tissue characterization of coronary arterial plaque by 16-slice computed tomography in acute coronary syndrome.

Noninvasive characterization of coronary plaques is challenging for cardiologists. The authors' goal was to explore the clinical feasibility of newly developed 16-slice computed tomography (CT) in tissue characterization of coronary arterial plaques in patients with acute coronary syndrome. Sixteen patients with acute coronary syndrome underwent 16-slice CT (Aquillion, Toshiba) and coronary arteriography with intravascular ultrasound (IVUS) within 7 days. Twenty-three plaques were classified by IVUS according to plaque echogenicity: 6 soft plaques, 11 intermediate plaques, and 6 calcified plaques. Mean (+/- SD) CT numbers (Hounsfield units [HU]) of these 3 types of plaques were 50.6 +/-14.8 HU, 131 +/-21.0 HU, and 721 +/-231 HU, respectively. Sixteen-slice CT facilitates noninvasive tissue characterization of coronary arterial plaques.

Relation of atherothrombosis burden and volume detected by intravascular ultrasound to angiographic no-reflow phenomenon during stent implantation in patients with acute myocardial infarction.

This study investigated the mechanism of occurrence of the no-reflow phenomenon during stent implantation in patients with acute myocardial infarction (AMI) using intravascular ultrasound (IVUS) with volumetric analysis. Of 70 patients with AMI who underwent IVUS-guided stent implantation within 24 hours of symptom onset, 12 developed decreased Thrombolysis In Myocardial Infarction flow grade during stent implantation and without subsequent restoration to Thrombolysis In Myocardial Infarction flow grade before stenting. External elastic membrane cross-sectional area and maximum diameter at the culprit lesion as measured by IVUS before stent implantation were significantly larger in the no-reflow group (n = 12) than in the normal reflow group (n = 58; 20.1 +/- 6.5 vs 16.4 +/- 4.3 mm2, p = 0.015 for cross-sectional area and 5.2 +/- 0.9 vs 4.8 +/- 0.6 mm, p = 0.049 for maximum diameter). Plaque volume, volumetric plaque burden (plaque volume/external elastic membrane volume), and change in plaque volume during stent implantation (plaque volume after vs before) were significantly greater in the no-reflow group than in the normal reflow group (239 +/- 142 vs 178 +/- 72 mm3, p = 0.030; 0.76 +/- 0.07 vs 0.71 +/- 0.06, p = 0.010; and -46 +/- 63 vs -11 +/- 37 mm3, p = 0.013, respectively). In conclusion, high atherothrombotic burden and decreased plaque volume as detected by IVUS may be risk factors for development of the no-reflow phenomenon during stent implantation in patients with AMI.

Transient mid-ventricular ballooning cardiomyopathy: a new entity of Takotsubo cardiomyopathy.

We present a case of a 64-year-old man with transient mid-ventricular ballooning cardiomyopathy. Left ventriculography showed morphological differences with ballooning around the whole mid-portion of the left ventricle, although precipitating factors and clinical courses were similar to Takotsubo cardiomyopathy. We suspect that transient mid-ventricular ballooning cardiomyopathy is a new pathological entity in Takotsubo cardiomyopathy.

Alteration in risk factor accumulations of acute myocardial infarction during the last one decade: analysis of patients admitted in Coronary Care Unit.

The present study was undertaken to determine accumulation of risk factors in acute myocardial infarction during two periods of 2002 and 1990-1991. We collected 173 and 153 patients with acute myocardial infarction in 2002 and 1990-1991, respectively, and analyzed the history of multiple risk factors, including diabetes mellitus, impaired glucose tolerance, hyperlipidemia, hypertension and obesity, and laboratory findings. The numbers and their percentages of all the risk factors increased in 2002 compared with 1990-1991. According to plasma glucose level, the patients who had type 2 diabetes mellitus, and impaired fasting glucose or impaired glucose tolerance had increased markedly from 41 to 65%. Multiple accumulation of risk factors had increased during the last one decade, and only one or no risk factor per se was not the case in the patients with acute myocardial infarction. Hyperlipidemia and hypertension became fairly controlled in the patients, but not hyperglycemia in type 2 diabetes mellitus in the period of 2002. These findings may indicate that increased multiple accumulation of risk factors accelerates the occurrence of acute myocardial infarction in 2002 as compared to 1990-1991.

Possible vascular role of increased plasma arginine vasopressin in congestive heart failure.

BACKGROUND: The present study was undertaken to determine the relation of cardiac dysfunction with hormonal release in patients with congestive heart failure. METHODS: Seventy-two patients with congestive heart failure were examined, who were divided into four subgroups classified by the criteria of the New York Heart Association (NYHA). Also, 10 age-matched subjects were served as a control. Plasma arginine vasopressin (AVP), norepinephrine, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were determined. Cardiac index and pulmonary capillary wedge pressure (PCWP) were measured in 51 of 72 patients. RESULTS: Plasma AVP levels were significantly increased according to the severity of NYHA classes; control: 1.7 +/- 0.2; NYHA I: 4.9 +/- 0.8, NYHA II: 5.5 +/- 0.9, NYHA III: 13.4 +/- 2.6 (p < 0.05), NYHA IV: 26.9 +/- 5.6 pmol/l (p < 0.001). Similar results were obtained with plasma norepinephrine, ANP and BNP. Plasma AVP levels had negative correlation with cardiac index (r = -0.36, p < 0.01), but did not with PCWP and plasma osmolality. Plasma BNP levels positively correlated with PCWP (r = 0.44, p < 0.001), but did not with cardiac index. There was no correlation between plasma AVP and BNP. Intensive therapy profoundly reduced all the hormones according to the improvement of cardiac index in the patients with NYHA class III and IV. The percent decrease in plasma AVP was 60.0%, a value greater than that in plasma BNP. CONCLUSION: The present study indicates that increased AVP may deteriorate cardiac function through V(1a) as well as V(2) action, and that plasma AVP level is also a proper marker for the presence and severity of congestive heart failure.

Glimepiride induces nitric oxide production in human coronary artery endothelial cells via a PI3-kinase-Akt dependent pathway.

Diabetes mellitus is one of the major risk factors for coronary artery disease (CAD). A recent study reported that glimepiride, a new third-generation sulfonylurea, inhibited the formation of atheromatous plaques in high-cholesterol fed rabbits. However, the mechanism by which glimepiride induces atheroprotection remains unknown. In the present study, we tested the hypothesis that glimepiride may stimulate NO production in vascular endothelial cells. Human coronary artery endothelial cells (HCAECs) were treated with glimepiride, glibenclamide or vehicle, and NO release was measured. Akt phosphorylation was evaluated by Western blot. The effects of LY294002, a specific PI3-kinase inhibitor, and antisense oligonucleotides directed to Akt, on glimepiride-induced NO production were examined. Glimepiride (0.1-10 microM), but not glibenclamide, induced NO production, significantly increasing it by 1.8-fold (n=6, p<0.05). LY294002 inhibited glimepiride-induced NO production by 68%. Akt was rapidly phosphorylated by glimepiride and antisense oligonucleotides directed to Akt completely inhibited glimepiride-induced NO production. These data demonstrate that glimepiride induces NO production in HCAECs by activating PI3-kinase and Akt, and also suggest that use of glimepiride in type 2 diabetes may show promise for preventing CAD in addition to lowering glucose levels.

Evaluation of transmural myocardial perfusion by ultra-harmonic myocardial contrast echocardiography in reperfused acute myocardial infarction.

BACKGROUND: The transmural distribution of myocardial perfusion is important for predicting the contractile reverse of an infarcted wall in reperfused acute myocardial infarction (AMI). Evaluating transmural myocardial perfusion by myocardial contrast echocardiography (MCE) could predict the long-term recovery of left ventricular (LV) function. METHODS AND RESULTS: The study group comprised 20 consecutive patients with a first-episode anterior AMI with total occlusion of the proximal left anterior descending artery, who underwent successful percutaneous coronary intervention within 24 h of onset. MCE was performed on the 15th day after the onset, using ultraharmonic gray-scale imaging with intermittent end-systolic triggering every 4 beats or every 6 beats. Regions of interest were placed over both the endocardial and epicardial region at the mid-septal level. Regional wall motion (RWM) of the infarcted anterior wall and global LV function were assessed by 2-dimensional echocardiography and left ventriculography in both the acute and chronic phase. The transmural distribution of myocardial perfusion by MCE demonstrated a significant relation with RWM score index (r = 0.75, p = 0.0004). Recovery of RWM and LV ejection fraction (LVEF) at 6 months after reperfusion was significantly greater in the group with good perfusion of the epicardium according to MCE than in the poor perfusion group [RWM (SD/cord); -1.23+/-0.91 vs -3.51+/-0.84, p = 0.001, LVEF (%); 63.8+/-10.4 vs 47.0+/-3.4, p = 0.04]. CONCLUSIONS: Assessing the transmural distribution of myocardial perfusion by MCE can predict the long-term recovery of LV function after a reperfused AMI.