Effect of stents coated with a combination of sirolimus and alpha-lipoic acid in a porcine coronary restenosis model.

The aim of this study was to evaluate antiproliferative sirolimus- and antioxidative alpha-lipoic acid (ALA)-eluting stents using biodegradable polymer [poly-L-lactic acid (PLA)] in a porcine coronary overstretch restenosis model. Forty coronary arteries of 20 pigs were randomized into four groups in which the coronary arteries had a bare metal stent (BMS, n = 10), ALA-eluting stent with PLA (AES, n = 10), sirolimus-eluting stent with PLA (SES, n = 10), or sirolimus- and ALA-eluting stent with PLA (SAS, n = 10). A histopathological analysis was performed 28 days after the stenting. The ALA and sirolimus released slowly over 30 days. There were no significant differences between groups in the injury or inflammation score; however, there were significant differences in the percent area of stenosis (56.2 ± 11.78% in BMS vs. 51.5 ± 12.20% in AES vs. 34.7 ± 7.23% in SES vs. 28.7 ± 7.30% in SAS, P < 0.0001) and fibrin score [1.0 (range 1.0-1.0) in BMS vs. 1.0 (range 1.0-1.0) in AES vs. 2.0 (range 2.0-2.0) in SES vs. 2.0 (range 2.0-2.0) in SAS, P < 0.0001] between the four groups. The percent area of stenosis based on micro-computed tomography corresponded with the restenosis rates based on histopathological stenosis in different proportions in the four groups (54.8 ± 7.88% in BMS vs. 50.4 ± 14.87% in AES vs. 34.5 ± 7.22% in SES vs. 28.9 ± 7.22% in SAS, P < 0.05). SAS showed a better neointimal inhibitory effect than BMS, AES, and SES at 1 month after stenting in a porcine coronary restenosis model. Therefore, SAS with PLA can be a useful drug combination for coronary stent coating to suppress neointimal hyperplasia.

Reliable femoral chronic total occlusion model using a thin biodegradable polymer coated copper stent in a porcine model.

Chronic total occlusions (CTOs) are common in patients with peripheral arterial disease (PAD). This study aimed to examine the feasibility and reliability of a CTO induced by a thin biodegradable polymer (polyglycolic acid) coated copper stent in a porcine femoral artery. Novel thin biodegradable polymer coated copper stents (9 mm long) were crimped on an angioplasty balloon (4.5 mm diameter × 12 mm length) and inserted into the femoral artery. Histopathologic analysis was performed 35 days after stenting. In five of six stented femoral arteries, severe in-stent restenosis and total occlusion with collateral circulation were observed without adverse effects such as acute stent thrombosis, leg necrosis, or death at 5 weeks. Fibrous tissue deposition, small vascular channels, calcification, and inflammatory cells were observed in hematoxylin-eosin, Carstair's, and von Kossa tissue stains; these characteristics were similar to pathological findings associated with CTOs in humans. The neointima volume measured by micro-computed tomography was 93.9 ± 4.04 % in the stented femoral arteries. CTOs were reliably induced by novel thin biodegradable polymer coated copper stents in porcine femoral arteries. Successful induction of CTOs may provide a practical understanding of their formation and application of an interventional device for CTO treatment.

Cardioprotective effect of fimasartan, a new angiotensin receptor blocker, in a porcine model of acute myocardial infarction.

Cardioprotective effect of fimasartan, a new angiotensin receptor blocker (ARB), was evaluated in a porcine model of acute myocardial infarction (MI). Fifty swine were randomized to group 1 (sham, n=10), group 2 (no angiotensin-converting enzyme inhibitor [ACEI] or ARB, n=10), group 3 (perindopril 2 mg daily, n=10), group 4 (valsartan 40 mg daily, n=10), or group 5 (fimasartan 30 mg daily, n=10). Acute MI was induced by occlusion of the left anterior descending artery for 50 min. Echocardiography, single photon emission computed tomography (SPECT), and F-18 fluorodeoxyglucose cardiac positron emission tomography (PET) were performed at baseline, 1 week, and 4 weeks. Iodine-123 meta-iodobenzylguanidine (MIBG) scan was done at 6 weeks for visualization of cardiac sympathetic activity. Left ventricular function and volumes at 4 weeks were similar between the 5 groups. No difference was observed in groups 2 to 5 in SPECT perfusion defect, matched and mismatched segments between SPECT and PET at 1 week and 4 weeks. MIBG scan showed similar uptake between the 5 groups. Pathologic analysis showed similar infarct size in groups 2 to 5. Infarct size reduction was not observed with use of fimasartan as well as other ACEI and ARB in a porcine model of acute MI.

Priming of mesenchymal stem cells with oxytocin enhances the cardiac repair in ischemia/reperfusion injury.

Oxytocin stimulates the cardiomyogenesis of embryonic stem cells and adult cardiac stem cells. We previously reported that oxytocin has a promigratory effect on umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs). In this study, UCB-MSCs were cultured with oxytocin and examined for their therapeutic effect in an infarcted heart. UCB-MSCs were pretreated with 100 nM oxytocin and cardiac markers were assessed by immunofluorescence staining. Next, oxytocin-supplemented USC-MSCs (OT-USCs) were cocultured with hypoxia/reoxygenated neonatal rat cardiomyocytes and cardiac markers and dye transfer were then examined. For the in vivo study, ischemia/reperfusion was induced in rats, and phosphate-buffered saline (group 1), 1-day OT-USCs (group 2), or 7-day OT-USCs (group 3) were injected into the infarcted myocardium. Two weeks after injection, histological changes and cardiac function were examined. UCB-MSCs expressed connexin 43 (Cnx43), cardiac troponin I (cTnI), and α-sarcomeric actin (α-SA) after oxytocin supplementation and coculture with cardiomyocytes. Functional gap junction formation was greater in group 3 than in groups 1 and 2. Cardiac fibrosis and macrophage infiltration were lower in group 3 than in group 2. Restoration of Cnx43 expression was greater in group 3 than in group 2. Cnx43- and cTnI-positive OT-USCs in the peri-infarct zone were observed in group 2 and more frequently in group 3. The ejection fraction (EF) was increased in groups 2 and 3 in 2 weeks. The improved EF was sustained for 4 weeks only in group 3. Our findings suggest that the supplementation of UCB-MSCs with oxytocin can contribute to the cardiogenic potential for cardiac repair.

Percutaneous coronary intervention with drug-eluting stent implantation vs. coronary artery bypass grafting for multivessel coronary artery disease in metabolic syndrome patients with acute myocardial infarction.

BACKGROUND: Coronary artery bypass grafting (CABG) has been the treatment of choice for management of multivessel coronary artery disease, but percutaneous coronary intervention (PCI) with drug-eluting stents (DES) is increasingly being preferred. The aim of the present study was to compare outcomes of PCI with DES implantation (PCI-DES) and CABG for treating multivessel disease in metabolic syndrome patients with acute myocardial infarction (AMI). METHODS AND RESULTS: A total of 1,839 consecutive metabolic syndrome patients with AMI who underwent PCI-DES (n=1,715) and CABG (n=124) for treatment of multivessel disease were selected from Korea Acute Myocardial Infarction Registry from November 2005 through December 2006. Primary endpoint was 12-month all-cause mortality. The mortality rate at 12 months was significantly lower in the PCI-DES group (4.8% vs. 12.2% in CABG, P=0.014) on univariate analysis. According to a Cox model, 12-month mortality was similar between the 2 groups (P=0.603), which remained the same despite propensity score adjustment (P=0.485). Rate of repeat revascularization was significantly higher in the PCI-DES group compared to the CABG group (P<0.001). At 12 months, major adverse cardiovascular and cerebrovascular event (MACCE)-free survival was higher in ST-elevation MI (STEMI) patients in the CABG group. CONCLUSIONS: PCI-DES had an equivalent 12-month mortality risk to CABG for the treatment of multivessel disease in metabolic syndrome patients with AMI. CABG is more favorable for STEMI patients in terms of MACCE.

Safety and efficacy of overlapping homogenous drug-eluting stents in patients with acute myocardial infarction: results from Korea Acute Myocardial Infarction Registry.

The aim of this study was to compare safety and efficacy of 4 homogenous overlapping drug-eluting stents (DES) in acute myocardial infarction (AMI) patients. We selected 1,349 consecutive patients (62.1 ± 14.9 yr, 69.4% male) who received homogenous overlapping DESs in diffuse de novo coronary lesions from Korea Acute Myocardial Infarction Registry from April 2006 through September 2010. They were divided into 4 groups based on type of DES implanted - Paclitaxel (PES), Sirolimus (SES), Zotarolimus (ZES) and Everolimus (EES)-eluting stents. Primary endpoint was 12-month MACE. We also studied EES versus other DESs (PES + SES + ZES). Mean stent length was 26.2 ± 7.5 mm and mean stent diameter was 3.1 ± 0.4 mm. Average number of stents used per vessel was 2.2 ± 0.5. Incidence of major adverse cardiac events (MACE) in PES, SES, ZES, and EES groups were 9.5%, 9.2%, 7.5%, and 3.8%, respectively (P = 0.013). In EES group, overall MACE and repeat revascularization were lowest, and no incidence of stent thrombosis was observed. Non-fatal MI was highest in PES, almost similar in SES and EES with no incidence in ZES group (P = 0.044). Cox proportional hazard analysis revealed no differences in the incidence of primary endpoint (P = 0.409). This study shows no significant differences in 12-month MACE among 4 groups.

Endothelial dysfunction and increased carotid intima-media thickness in the patients with slow coronary flow.

Flow mediated brachial dilatation (FMD) and carotid intima-media thickness (IMT) have been a surrogate for early atherosclerosis. Slow coronary flow in a normal coronary angiogram is not a rare condition, but its pathogenesis remains unclear. A total of 85 patients with angina were evaluated of their brachial artery FMD, carotid IMT and conventional coronary angiography. Coronary flow was quantified using the corrected thrombosis in myocardial infarction (TIMI) frame count method. Group I was a control with normal coronary angiography (n = 41, 56.1 ± 8.0 yr) and group II was no significant coronary stenosis with slow flow (n = 44, 56.3 ± 10.0 yr). Diabetes was rare but dyslipidemia and family history were frequent in group II. Heart rate was higher in group II than in group I. White blood cells, especially monocytes and homocysteine were higher in group II. The FMD was significantly lower in group II than in group I. Elevated heart rate, dyslipidemia and low FMD were independently related with slow coronary flow in regression analysis. Therefore, endothelial dysfunction may be an earlier vascular phenomenon than increased carotid IMT in the patients with slow coronary flow.

Relation between anemia and vulnerable coronary plaque components in patients with acute coronary syndrome: virtual histology-intravascular ultrasound analysis.

The aim of the present study was to evaluate the plaque components and the predictors of thin-cap fibroatheroma (TCFA) in anemic patients with acute coronary syndrome using virtual histology-intravascular ultrasound (VH-IVUS). Anemia was defined according to criteria of the World Health Organization, (i.e. , hemoglobin levels < 13 g/dL in men and < 12 g/dL in women) and we compared VH-IVUS findings between anemia group (171 patients, 260 lesions) and non-anemia group (569 patients, 881 lesions). Anemia group had greater % necrotic core (NC) volume (21% ± 9% vs 19% ± 9%, P = 0.001) compared with non-anemia group. Hemoglobin level correlated negatively with absolute NC volume (r = -0.235, P < 0.001) and %NC volume (r = -0.209, P < 0.001). Independent predictors of TCFA by multivariate analysis were diabetes mellitus (odds ratio [OR], 2.213; 95% confidence interval [CI], 1.403-3.612, P = 0.006), high-sensitivity C-reactive protein (OR, 1.143; 95% CI, 1.058-1.304, P = 0.012), microalbuminuria (albumin levels of 30 to 300 mg/g of creatinine) (OR, 2.124; 95% CI, 1.041-3.214, P = 0.018), and anemia (OR: 2.112; 95% CI 1.022-3.208, P = 0.028). VH-IVUS analysis demonstrates that anemia at the time of clinical presentation is associated with vulnerable plaque component in patients with acute coronary syndrome.

Impact of plaque components on no-reflow phenomenon after stent deployment in patients with acute coronary syndrome: a virtual histology-intravascular ultrasound analysis.

AIMS: We used virtual histology-intravascular ultrasound (VH-IVUS) to evaluate the relation between coronary plaque characteristics and no-reflow in acute coronary syndrome (ACS) patients. METHODS AND RESULTS: A total of 190 consecutive ACS patients were imaged using VH-IVUS and analysed retrospectively. Angiographic no-reflow was defined as TIMI flow grade 0, 1, and 2 after stenting. Virtual histology-intravascular ultrasound classified the colour-coded tissue into four major components: fibrotic, fibro-fatty, dense calcium, and necrotic core (NC). Thin-cap fibroatheroma (TCFA) was defined as focal, NC-rich (≥10% of the cross-sectional area) plaques being in contact with the lumen in a plaque burden≥40%. Of the 190 patients studied at pre-stenting, no-reflow was observed in 24 patients (12.6%) at post-stenting. The absolute and %NC areas at the minimum lumen sites (1.6±1.2 vs. 0.9±0.8 mm2, P<0.001, and 24.5±14.3 vs. 16.1±10.6%, P=0.001, respectively) and the absolute and %NC volumes (30±24 vs. 16±17 mm3, P=0.001, and 22±11 vs. 14±8%, P<0.001, respectively) were significantly greater, and the presence of at least one TCFA and multiple TCFAs within culprit lesions (71 vs. 36%, P=0.001, and 38 vs. 15%, P=0.005, respectively) was significantly more common in the no-reflow group compared with the normal-reflow group. In the multivariable analysis, %NC volume was the only independent predictor of no-reflow (odds ratio=1.126; 95% CI 1.045-1.214, P=0.002). CONCLUSION: In ACS patients, post-stenting no-reflow is associated with plaque components defined by VH-IVUS analysis with larger NC and more TCFAs.

The novel role of mast cells in the microenvironment of acute myocardial infarction.

Mast cells are multifunctional cells containing various mediators, such as cytokines, tryptase, and histamine, and they have been identified in infarct myocardium. Here, we elucidated the roles of mast cells in a myocardial infarction (MI) rat model. We studied the physiological and functional roles of mast cell granules (MCGs), isolated from rat peritoneal fluid, on endothelial cells, neonatal cardiomyocytes, and infarct heart (1-hour occlusion of left coronary artery followed by reperfusion). The number of mast cells had two peak time points of appearance in the infarct region at 1day and 21days after MI induction in rats (p<0.05 in each compared with sham-operated heart). Simultaneous injection of an optimal dose of MCGs modulated the microenvironment and resulted in the increased infiltration of macrophages and decreased apoptosis of cardiomyocytes without change in the mast cell number in infarct myocardium. Moreover, MCG injection attenuated the progression of MI through angiogenesis and preserved left ventricular function after MI. MCG-treated cardiomyocytes were more resistant to hypoxic injury through phosphorylation of Akt, and MCG-treated endothelial cells showed enhanced migration and tube formation. We have shown that MCGs have novel cardioprotective roles in MI via the prolonged survival of cardiomyocytes and the induction of angiogenesis.

Usefulness of computed tomographic pulmonary angiography in the risk stratification of acute pulmonary thromboembolism. Comparison with cardiac biomarkers.

BACKGROUND: To evaluate the usefulness of computed tomographic pulmonary angiographic (CTPA) variables in the risk stratification of acute pulmonary thromboembolism (APE) and compare these variables with cardiac biomarkers. METHODS AND RESULTS: Eighty consecutive patients with APE were divided into patients with right ventricular (RV) dysfunction (n=49, 62.1±15.1 years, 31 females) vs. patients without RV dysfunction (n=31, 67.7±13.7 years, 18 females). CTPA variables were analyzed and compared with cardiac biomarkers. The ratio of right to left ventricular dimension (RVD/LVD), CT index of PA clot load, contrast reflux to the inferior vena cava (IVC), and ventricular septal bowing (VSB) were significantly different CTPA variables between the groups. These variables were also significantly associated with cardiac biomarkers. By receiver operation characteristic curve analysis, the area under the curve to predict RV dysfunction was 0.863 for RVD/LVD, 0.841 for PA clot load, 0.744 for contrast reflux to IVC, and 0.635 for VSB. The optimal cut-off value to predict RV dysfunction was 1.12 for RVD/LVD (sensitivity: 89.8%, specificity: 77.4%) and 19.5 for PA clot load (sensitivity: 81.6%, specificity: 77.4%). CONCLUSIONS: RVD/LVD, PA clot load, contrast reflux to IVC, and VSB on CTPA were significantly associated with RV dysfunction and cardiac biomarkers in APE. The present study demonstrated that CTPA is useful not only in the diagnosis, but also in the risk stratification of APE.

Comparison of effects of rosuvastatin and atorvastatin on plaque regression in Korean patients with untreated intermediate coronary stenosis.

BACKGROUND: Serial intravascular ultrasound (IVUS) was used to compare the effects of moderate doses of rosuvastatin and atorvastatin on plaque regression in patients with intermediate coronary stenosis. METHODS AND RESULTS: This was a prospective, randomized, and comparative study for lipid-lowering therapy with rosuvastatin 20mg (n=65) and atorvastatin 40mg (n=63) using serial IVUS (baseline and 11-month follow-up). Efficacy parameters included changes in total atheroma volume (TAV) and percent atheroma volume (PAV) from baseline to follow-up. Changes of TAV (-4.4±7.3 vs. -3.6±6.8mm(3), P=0.5) and PAV (-0.73±2.05 vs. -0.19±2.00%, P=0.14) from baseline to follow-up were not significantly different between the 2 groups. Plaque was increased in 15% in the rosuvastatin group and in 30% in the atorvastatin group at follow-up (P=0.064). The plaque increase group had higher baseline high-sensitivity C-reactive protein (hs-CRP; 1.28±2.70mg/dl vs. 0.54±1.16mg/dl, P=0.034) and higher follow-up low-density lipoprotein cholesterol (LDL-C) (78±24mg/dl vs. 63±21mg/dl, P=0.002) compared with the plaque non-increase group. Follow-up LDL-C (odds ratio [OR]=1.038, 95% confidence interval [CI]=1.003-1.060, P=0.036) and baseline hs-CRP (OR=1.025, 95%CI=1.001-1.059, P=0.046), not the type of statin, were the independent predictors of plaque increase at follow-up. CONCLUSIONS: Moderate doses of rosuvastatin and atorvastatin could contribute to effective plaque regression. Follow-up LDL-C and baseline hs-CRP are associated with plaque progression in patients with intermediate coronary stenosis.

Relationship between microalbuminuria and vulnerable plaque components in patients with acute coronary syndrome and with diabetes mellitus. Virtual histology-intravascular ultrasound.

BACKGROUND: The purpose of the present study was to use virtual histology-intravascular ultrasound (VH-IVUS) to evaluate the relationship between microalbuminuria and plaque components in 920 patients. METHODS AND RESULTS: Patients with albumin levels <30mg/g creatinine were defined as having normoalbuminuria (n=824), and those with albumin levels 30-300mg/g as having microalbuminuria (n=96). The microalbuminuria group contained more patients with acute coronary syndrome (ACS; 72% vs. 61%, P=0.018) and more patients with diabetes (53% vs. 26%, P<0.001). In ACS patients, %necrotic core (NC) volume was significantly greater in the microalbuminuria group compared with the normoalbuminuria group (19±10% vs. 15±9%, P=0.019), but not in patients with stable angina. In ACS patients, thin-cap fibroatheroma (TCFA) was observed more frequently in the microalbuminuria group (36% vs. 18%, P=0.008), and microalbuminuria was the independent predictor of TCFA (odds ratio [OR], 1.106; 95% confidence interval [CI]: 1.025-1.144, P=0.018). In diabetic patients, %NC volume was significantly greater in the microalbuminuria group compared with the normoalbuminuria group (20±9% vs. 16±10%, P=0.017), but not in non-diabetic patients. In diabetic patients, TCFA was observed more frequently in the microalbuminuria group (38% vs. 17%, P=0.002) and microalbuminuria was the independent predictor of TCFA (OR, 1.120; 95%CI: 1.038-1.204, P=0.012). CONCLUSIONS: Microalbuminuria was associated with a higher number of vulnerable plaque components in ACS and diabetic patients. More intensive medical therapy is needed to stabilize the vulnerable plaque if microalbuminuria is observed in diabetic ACS patients.

Comparison of paclitaxel-, sirolimus-, and zotarolimus-eluting stents in patients with acute ST-segment elevation myocardial infarction and metabolic syndrome.

BACKGROUND: The purpose of the present study was to compare the efficacy and safety of paclitaxel-eluting stent (PES), sirolimus-eluting stent (SES), and zotarolimus-eluting stent (ZES) in primary percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI) with metabolic syndrome (MS). METHODS AND RESULTS: Using data from Korea Acute Myocardial Infarction Registry (KAMIR; November 2005-December 2007), a total of 1,768 MS patients with STEMI who underwent primary PCI were enrolled: The PES group was 634, SES group, 906, and ZES group, 228. The primary endpoint was major adverse cardiac event (all-cause death, re-myocardial infarction, target lesion revascularization) during 12 months follow-up. At 12 months, the cumulative incidence of primary endpoint in the PES, SES, and ZES groups was 10.9%, 9.1%, and 11.0%, respectively (P=0.086). Incidence of death, recurrent myocardial infarction, or target lesion revascularization did not differ among the 3 groups. There were 7 episodes of acute (0.3% in PES group, 0.4% in SES group, and 0.4% in ZES group, respectively, P=0.773) and 18 episodes of cumulative stent thrombosis including late stent thrombosis (0.9% in PES group, 1.0% in SES group, and 1.3% in ZES group, respectively, P=0.448). CONCLUSIONS: Implantation of SES, PES, and ZES in MS patients with STEMI undergoing primary PCI provided comparable clinical outcomes in patients enrolled in KAMIR.

Unusual cause of acute right ventricular dysfunction: rapid progression of superior vena cava aneurysm complicated by thrombosis and pulmonary thromboembolism.

Aneurysms of the major thoracic veins are rare. They are usually asymptomatic and thus treated conservatively. We report an extremely rare case of rapidly progressing superior vena cava (SVC) aneurysm complicated by thrombosis and acute pulmonary thromboembolism (PTE) with right ventricular dysfunction. Thrombolytic therapy for hemodynamically significant acute PTE was harmful to the patient in the present case, because it induced further thrombosis and mobilization of the thrombi within the aneurysm, subsequently causing de novo PTE. Surgical aneurysmectomy combined with pulmonary artery embolectomy would be a treatment of choice in patients with SVC aneurysm complicated by acute PTE.

Relationship between coronary artery calcium score by multidetector computed tomography and plaque components by virtual histology intravascular ultrasound.

The aim of this study was to evaluate the relationship between coronary artery calcium score (CACS) assessed by multidetector computed tomography (MDCT) and plaque components assessed by virtual histology-intravascular ultrasound (VH-IVUS) in 172 coronary artery disease (CAD) patients with 250 coronary lesions. CACS was assessed according to Agatston scoring method by MDCT and patients were divided into four groups: Group I (CACS = 0 [n = 52]); Group II (CACS = 1-100 [n = 99]); Group III (CACS = 101-400 [n = 84]); and Group IV (CACS > 400 [n = 15]). Total atheroma volume was greatest in Group IV (152 ± 132 µL vs 171 ± 114 µL vs 195 ± 149 µL vs 321±182 µL, P < 0.001). The absolute dense calcium (DC) and necrotic core (NC) volumes were greatest, and relative DC volume was greatest in Group IV (5.5 ± 6.6 µL vs 11.0 ± 10.3 µL vs 15.6 ± 13.6 µL vs 36.6 ± 18.2 µL, P < 0.001, and 14.8 ± 18.2 µL vs 19.5 ± 18.9 µL vs 22.5 ± 19.1 µL vs 41.7 ± 27.9 µL, P < 0.001, and 6.4 ± 5.3% vs 11.0 ± 6.2% vs 14.0 ± 6.5% vs 20.0 ± 7.8%, P < 0.001, respectively). The absolute plaque and DC and NC volumes and the relative DC volume correlated positively with calcium score. CAD patients with high calcium score have more vulnerable plaque components (greater DC and NC-containing plaques) than those with low calcium score.

Are drug-eluting stents safer and more effective than bare-metal stents in patients with acute myocardial infarction?

Questions about the long-term safety over the beneficial effects of drug-eluting stents (DES) have grown. We compared the long-term safety and efficacy of DES and bare-metal stents (BMS) in patients with acute myocardial infarction (AMI). A total of 1,017 AMI patients treated with stent implantation were followed for 3 years; 660 (64.9%) patients were treated with at least one DES and 357 (35.1%) patients were treated with at least one BMS. The primary endpoints were total mortality and the composite of major adverse cardiac events (MACE) including total mortality, re-MI, target lesion revascularization (TLR), and coronary artery bypass graft. At 3-years, the overall risks of cardiac and all-cause mortality were not different between the groups. However, the use of DES significantly decreased TLR (17.4% versus 7.1%, adjusted hazard ratio [HR] 0.44, 95% confidence interval [CI] 0.30 to 0.65) and the composite of MACEs (27.2% versus 19.5%, adjusted HR 0.65, 95% CI 0.48 to 0.87) with no differences in MI. The risk of MACE up to 1 year (HR 0.56, 95% CI 0.39 to 0.80) was higher in BMS patients, whereas from 1 year to 2 years (HR 0.55, 95% CI 0.27 to 1.10) and from 2 years to 3 years (HR 1.13, 95% CI 0.56 to 2.28), it was similar between the groups. The use of DES does not have a significant effect on overall long-term clinical survival compared with that of BMS in AMI patients. However, the use of DES reduced the need for re-intervention and the risk of MACE, mostly within 1 year.

Early statin therapy within 48 hours decreased one-year major adverse cardiac events in patients with acute myocardial infarction.

HMG-CoA reductase inhibitors (statins) reduce major adverse cardiac events (MACE) and mortality in patients with acute coronary syndrome. We investigated whether early statin therapy would be effective at reducing MACE in patients with acute myocardial infarction (AMI).A total of 1,159 patients were analyzed. They were grouped by initiation time of statin administration after admission as follows: group I; n = 945, ≤ 48 hours, group II; n = 214, > 48 hours.Cardiovascular risk factors and noncardiac comorbidities were not different between the two groups. ST-elevation MI as initial diagnosis was more prevalent in group I (68.4% versus 59.3%, P = 0.013). In-hospital mortality was not different in the two groups (0.8% versus 0.5%, P = 0.483). In one-year clinical follow-up, MACE and repercutaneous coronary intervention were lower in group I (17.8% versus 24.6%, P = 0.016, 10.2% versus 15.5%, P = 0.021, respectively). However, there was no difference in mortality (3.8% versus 4.7%, P = 0.319). In multivariate analysis, statin initiation within 48 hours after admission was an independent predictor of one-year MACE (OR 1.49, 95% CI = 1.00-2.21, P = 0.045).Consequently, early statin therapy within 48 hours after admission reduced MACE at one-year follow-up in patients with AMI.

Relation between plaque components and plaque prolapse after drug-eluting stent implantation--virtual histology-intravascular ultrasound.

BACKGROUND: It is not well known which plaque components are associated with the development of plaque prolapse (PP) and what are the major components in prolapsed plaque. The relationship between pre-stenting plaque components and post-stenting PP was assessed and the plaque components of prolapsed plaque were evaluated in patients who underwent drug-eluting stent (DES) implantation using virtual histology-intravascular ultrasound (VH-IVUS). METHODS AND RESULTS: The study group consisted of 132 patients who underwent DES implantation and pre- and post-stenting VH-IVUS. Of these patients, 68 patients had 76 PP lesions and 64 patients had 76 non-PP lesions. Intra-stent PP volume was 3.6+/-1.5 mm(3). Plaque volume was significantly greater and absolute fibrotic (FT) and necrotic core (NC) volumes were significantly greater in PP lesions compared with non-PP lesions. On multivariate analysis, absolute NC (odds ratios [OR]=1.14, P<0.001) and FT volume (OR =1.09, P<0.001) were independently associated with the development of PP. In intra-stent prolapsed plaque the FT component was greatest, but the NC component was also large, and %NC volume correlated positively with Deltacreatine kinase-MB (r=0.489, P<0.001) and Deltatroponin-I (r=0.679, P<0.001), and %FT volume correlated negatively with DeltaCK-MB (r=-0.539, P<0.001) and Deltatroponin-I. CONCLUSIONS: NC and FT components were associated with development of PP; and NC and FT components in prolapsed plaque were associated with cardiac enzyme elevation after DES implantation.

Long-term clinical course of patients with isolated myocardial bridge.

BACKGROUND: Myocardial bridge (MB) is regarded as a common benign lesion on coronary angiography (CAG). It is known to be harmless but may cause several cardiac events and recurrent hospitalization, so in the present study the long-term clinical course of patients with isolated MB and predictors of readmission were investigated. METHODS AND RESULTS: Total 684 patients (343 males, 60.5+/-11.2 years) with persistent chest pain without critical stenosis on CAG were enrolled. The patients were divided into 2 groups according to the presence of MB. Clinical follow-up was performed with respect to readmission after baseline CAG. At a mean follow-up of 37 months, 92 patients (13.3%) were re-admitted because of 79 recurrent chest pain refractory to medication (11.5%), 8 myocardial infarctions (1.2%), 1 life-threatening arrhythmia (0.1%) and 4 deaths (0.6%). There was a significant higher incidence of readmission in the MB group (P=0.038). In multivariate analysis, long MB (hazard ratio (HR) 2.780; 95% confidence interval (CI) 1.070-7.218, P=0.036) and spontaneous vasospasm in CAG (HR 2.335; 95%CI 1.055-5.171, P=0.037) were the predictors of readmission. Moreover, additional use of aspirin or statin decreased the readmission rate. CONCLUSIONS: This study suggests that MB on non-occlusive CAG is not benign and may cause recurrent chest pain, myocardial infarction or life-threatening arrhythmia. Especially, patients with a long MB and vasospasm on CAG need intensive medical therapy, including antiplatelet treatment.