Branch segment occlusion with acute myocardial infarction is a risk for left ventricular free wall rupture.

BACKGROUND: Patients with acute myocardial infarction (AMI) whose culprit lesion lies in a branch of the 3 major coronary arteries have well-preserved cardiac function. A first MI with preserved cardiac function is a risk factor for left ventricular free wall rupture (LVFWR), so the aim of this study was to investigate the possible relationship between AMI with branch segment occlusion and LVFWR. METHODS AND RESULTS: The 439 patients with AMI were retrospectively studied. They were divided into 2 groups: group B (n=70; segments 4 atrioventricular node artery, 4 posterior descending coronary artery, 8, 9, 10, 12, 14, or 15 according to the AHA classification), and group P (n=369; segments 1, 2, 3, 5, 6, 7, 11, or 13). Primary percutaneous coronary intervention (PCI) was more often performed in group P (75% vs 57%; P=0.0018). In-hospital mortality tended to be lower in group B (1.4% vs 6.2%; P=0.105). The incidence of LVFWR was significantly higher in group B (10.0% vs 1.6%; P=0.0002).By multivariate logistic regression analysis, 1-vessel disease, absence of primary PCI, branch segment occlusion, and age were identified as independent predictors of LVFWR. CONCLUSIONS: The incidence of LVFWR was higher in group B and branch segment occlusion was identified as an independent predictor of LVFWR.

Myocardial salvage for ST-elevation myocardial infarction with terminal QRS distortion and restoration of brisk epicardial coronary flow.

Recently, it has been reported that large infarcts associated with terminal QRS distortion (QRSDIS) on the admission electrocardiograms of patients with ST-elevation myocardial infarctions (STEMIs) may be caused by a failure to achieve thrombolysis in myocardial infarction (TIMI) grade 3 flow after primary percutaneous coronary intervention (PCI). However, the relationship between QRSDIS and final infarct size when TIMI grade 3 flow could be achieved by primary PCI is still unclear. Sixty-two consecutive patients with first anterior STEMI and who achieved TIMI grade 3 flow by primary PCI were classified into two groups according to the presence (Group A, n = 18) or absence (Group B, n = 44) of QRSDIS. Two weeks after the onset of acute myocardial infarction, Group A had a larger left ventricular (LV) end-systolic volume index (LVESVI) and a lower LV ejection fraction (LVEF) than Group B (LVESVI: 38 +/- 13 vs 31 +/- 12 ml/m(2), P = 0.025: LVEF: 42% +/- 10% vs 51% +/- 10%, P = 0.004). Through multivariate analysis, independent predictors of poor LV systolic function (LVEF < 40%) were determined to be the presence of QRSDIS (odds ratio 21.04, P = 0.021) and proximal left anterior descending artery occlusion (odds ratio 16.15, P = 0.033). Myocardial damage could not be reduced in patients experiencing STEMI with QRSDIS, even when TIMI grade 3 flow could be achieved by primary PCI, as much as in patients experiencing STEMI without QRSDIS.

The effect of endothelial progenitor cells on the development of collateral formation in patients with coronary artery disease.

OBJECTIVE: Unlike arteriogenesis, little is known about the effects of vasculogenesis and its major effector cells, endothelial progenitor cells (EPCs) on collateral formation. In this study, we investigated whether or not the number and function of EPCs were associated with the development of collateral formation in patients with single-vessel coronary artery disease of chronic total occlusion (CTO). METHODS AND RESULTS: The subjects were patients (n=35) undergoing coronary angiography (CAG) who had CTO in one major coronary artery. EPCs were isolated from peripheral blood samples and cultured. Their phenotypes were confirmed by uptake of acetylated LDL and binding of fluorescein isothiocyanate (FITC)-labeled Ulex europaeus agglutinin 1 (UEA-1) lectin. The numbers of colony-forming units (CFUs) and the senescent cells, determined by acidic beta-galactosidase staining, were counted. The angiogenic growth factors from the culture medium were also measured by ELISA. Patients with good collaterals (n=22, Rentrop class 2 and 3) exhibited an increased number of CFUs (p=0.023), reduced number of senescent cells (p=0.010), and higher concentration of b-FGF (0.036) in the culture medium, compared with subjects with poor collaterals (n=13, Rentrop class 0 and 1). CONCLUSION: Our findings suggested that EPC-mediated angiogenesis might be associated with coronary collateral formation in humans.

Implication of plaque color classification for assessing plaque vulnerability: a coronary angioscopy and optical coherence tomography investigation.

OBJECTIVES: The purpose of this study was to assess the relationship between plaque color evaluated by coronary angioscopy and fibrous cap thickness estimated by optical coherence tomography (OCT) in vivo. BACKGROUND: Yellow color intensity of coronary plaque evaluated by coronary angioscopy might be associated with plaque vulnerability. METHODS: Seventy-seven coronary artery plaques in patients with acute coronary syndrome were observed by angioscopy and OCT. Plaque color was graded as white, light yellow, yellow, or intensive yellow. RESULTS: There were significant differences among the groups classified by plaque color with respect to the fibrous cap thickness estimated by OCT: 389 +/- 74 mum in white plaques, 228 +/- 51 microm in light yellow plaques, 115 +/- 28 microm in yellow plaques, and 59 +/- 14 microm in intensive yellow plaques (p < 0.0001). In Spearman rank-order correlation analysis, there was a significant negative correlation between yellow color intensity and fibrous cap thickness (p < 0.0001). Furthermore, 80% of intensive yellow plaques were thin cap fibroatheroma with a cap thickness of < or =65 microm. CONCLUSIONS: The plaque color in coronary angioscopy was determined by the fibrous cap thickness, which was assessed by OCT. Although coronary angioscopy remains a specialized research tool, it might allow us to evaluate plaque vulnerability.

Comparison of vascular response after sirolimus-eluting stent implantation between patients with unstable and stable angina pectoris: a serial optical coherence tomography study.

OBJECTIVES: The aim of the present study was to compare lesion morphologies after sirolimus-eluting stent (SES) implantation between patients with unstable angina pectoris (UAP) and stable angina pectoris (SAP) with the use of optical coherence tomography (OCT). BACKGROUND: The lesion morphologies before and after coronary stenting have been proposed as important predictors of clinical outcome. The high resolution of OCT provides detailed information of coronary vessel wall. METHODS: We enrolled 55 patients (UAP: n = 24, SAP: n = 31), and examined lesion morphologies by using OCT at pre- and post-SES implantation and 9 months' follow-up. RESULTS: The incidence of plaque rupture (42% vs. 3%, p < 0.001), intracoronary thrombus (67% vs. 3%, p < or = 0.001) and thin-capped fibroatheroma (cap thickness <65 microm; 46% vs. 3%, p < 0.001) at pre-intervention was significantly greater in UAP than that in SAP. Although stent profiles and procedural characteristics were not different between the 2 groups, inadequate stent apposition (67% vs. 32%, p = 0.038) and tissue protrusion (79% vs. 42%, p = 0.005) after percutaneous coronary intervention were observed more frequently in patients with UAP. Plaque rupture was significantly increased after percutaneous coronary intervention in patients with UAP (42% to 75%, p = 0.018), and the persistence of core cavity after plaque rupture (28% vs. 4%, p = 0.031) at 9 months' follow-up was observed more frequently in UAP patients compared with SAP patients. At 9 months' follow-up, the incidence of inadequately apposed stent (33% vs. 4%, p = 0.012) and partially uncovered stent by neointima (72% vs. 37%, p = 0.019) was significantly greater in UAP patients than that in SAP patients. All patients took aspirin and ticlopidine during follow-up period, and no patients had stent thrombosis or adverse coronary events. CONCLUSIONS: Serial OCT examinations demonstrated markedly different vascular response up to 9 months after SES implantation between UAP and SAP patients. Although the inadequate lesion morphologies after stenting were observed more frequently in UAP patients, these findings were not associated with adverse outcomes in patients with antiplatelet therapy.

Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy.

OBJECTIVES: The aim of the present study was to evaluate the ability of optical coherence tomography (OCT) for assessment of the culprit lesion morphology in acute myocardial infarction (AMI) in comparison with intravascular ultrasound (IVUS) and coronary angioscopy (CAS). BACKGROUND: Optical coherence tomography is a new intravascular imaging method with a high resolution of approximately 10 microm. This may allow us to assess the vulnerable plaques in detail in vivo. METHODS: We enrolled 30 patients with AMI, and analyzed the culprit lesion by OCT, CAS, and IVUS. RESULTS: The average duration from the onset of symptom to OCT imaging was 3.8 +/- 1.0 h. The incidence of plaque rupture observed by OCT was 73%, and it was significantly higher than that by CAS (47%, p = 0.035) and IVUS (40%, p = 0.009). Furthermore, OCT (23%) was superior to CAS (3%, p = 0.022) and IVUS (0%, p = 0.005) in the detection of fibrous cap erosion. The intracoronary thrombus was observed in all cases by OCT and CAS, but it was identified in 33% by IVUS (vs. OCT, p < 0.001). Only OCT could estimate the fibrous cap thickness, and it was 49 +/- 21 microm. The incidence of thin cap fibroatheroma (TCFA) was 83% in this population by OCT. CONCLUSIONS: Optical coherence tomography is a feasible imaging modality in patients with AMI and allows us to identify not only plaque rupture, but also fibrous cap erosion, intracoronary thrombus, and TCFA in vivo more frequently compared with conventional imaging techniques.

Effects of plasma adiponectin levels on the number and function of endothelial progenitor cells in patients with coronary artery disease.

BACKGROUND: It is not known whether plasma adiponectin levels are associated with the number and function of endothelial progenitor cells (EPCs) in patients with coronary artery disease (CAD). METHODS AND RESULTS: Plasma levels of adiponectin were measured in 70 patients undergoing coronary angiography. The numbers of colony-forming units (CFUs) of EPCs and senescent EPCs, determined by acidic beta-galactosidase staining, were counted. The angiogenic growth factors in the culture medium were also measured. There was a significant positive correlation between adiponectin level and CFUs (r=0.257, p<0.05) but not with the occurrence of senescent EPCs. Next, patients were divided into a high adiponectin group (high ADP: > or =6.17 microg/ml, n=36) and low adiponectin group (low ADP: <6.17 microg/ml, n=34). The number of diseased coronary arteries was less in the high ADP group than that in the low ADP patients (1.7+/-0.8 vs 2.1+/-0.7, p<0.05). No significant differences between the 2 groups were demonstrated in angiogenic growth factors secreted from EPCs. CONCLUSIONS: The results suggest that plasma adiponectin levels are associated with the number of EPCs in patients with CAD.

The effect of senescence of endothelial progenitor cells on in-stent restenosis in patients undergoing coronary stenting.

OBJECTIVE: Restenosis after stent implantation is caused by endothelial cell damage and subsequent neointimal formation. The objective of this study is to elucidate the relevance of endothelial progenitor cells (EPCs) in the development of in-stent restenosis in patients undergoing stent implantation. PATIENTS OR MATERIALS: The subjects were 46 patients who underwent coronary stenting. Blood samples were collected at the time of follow-up coronary angiography after coronary stenting. EPCs were isolated from blood samples and cultured. Their phenotypes were confirmed by uptake of acetylated low-density lipoprotein and binding of fluorescein isothiocyanate-labeled Ulex europaeus agglutinin 1 lectin. The number of colony-forming units (CFUs) and the senescent cells, determined by acidic beta-galactosidase staining, was counted. Angiogenic growth factors secreted by EPCs, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (b-FGF), hepatocyte growth factor (HGF), and macrophage chemoattractant protein (MCP-1) from the culture medium were also measured by enzyme-linked immunosorbent assay. RESULTS: Patients with in-stent restenosis (defined as >40% stenosis, n=16) had a decreased number of CFUs (p<0.05), and increased senescent cells (p<0.05), compared to patients without restenosis (n=30). There was no significant difference of angiogenic growth factors (VEGF, HGF, b-FGF, and MCP-1) secreted by EPCs between the two groups. On multivariate analysis, an increased number of senescent EPCs was the indepen-dent factor associated with in-stent restenosis (OR 1.10, 95% CI 1.01 to 1.20). CONCLUSION: These data suggested that EPCs might be involved in the development of in-stent restenosis.

["Stunned myocardium" on echo cardiogram in myotonic dystrophy: a case report].

A 56-year-old woman with a 23 year-history of myotonic dystrophy was admitted to our hospital because of dysphagia and aspiration pneumonia. On admission, patient's ECG showed Ist degree of atrioventricular block and elongation of QRS (133 msec.). On the third hospital day, abnormal Q wave abruptly appeared in aVL associated with elevation of ST segment in V2 and V3, reverse T wave in I, II, III, aVF and V 2-6 leads on ECG. Echo cardiogram demonstrated asynergy at the apex and septal wall. Coronary angiography was normal. Left ventricular ejection fraction determined by left ventriculography decreased to 47.4%. Based on these findings, we thought "stunned myocardium" had developed. Biopsied myocardium from the apex, septum, and free wall showed non-specific findings including mild fibrosis and lymphocytic infiltration. Although overt myocardial disease is rare in myotonic dystrophy, myocardiac disease such as "stunned myocardium" not due to arrhythmia or coronary angiopathy may develop under severe infection, stress, and/or respiratory distress.