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.

Progressive dilation of the left atrium and ventricle after acute myocardial infarction is associated with high mortality.

BACKGROUND AND OBJECTIVES: The purpose of this study is to identify the prevalence of progressive dilation in patients with acute myocardial infarction (AMI) combined with heart failure (HF) and determine the prognostic significance and associated factors with a geometric change of an infarcted heart. SUBJECTS AND METHODS: A total of 1310 AMI patients with HF (63.9±12.5 years, 70% male) between November 2005 and April 2011 underwent echocardiography at admission and one year later. Left ventricular (LV) remodeling is defined as 20% progression, and left atria (LA) remodeling is 10% compared with the initial volume index. RESULTS: The prevalence of both LA and LV remodeling was 13.9%; LV only was 9.3%, LA only 22.8% and non-remodeling was 55.1%, respectively. In the non-remodeling group, Killip class II was more frequent (83.9%, p<0.001) whereas in other remodeling groups, Killip class III was more frequent. Initial wall motion score index, ejection fraction, maximal cardiac enzyme, high sensitive C-reactive protein, B type natriuretic peptide, and triglyceride serum levels were significantly associated with heart remodeling. All causes of death occurred in 168 cases (12.8%) during the follow-up period. Mortality was the highest in the LV and LA remodeling group (20.9%) and the lowest in the non-remodeling group (11.4%). During the period of follow-up, the cumulative survival rate was significantly lower in the groups of LA and LV remodeling than in others (log rank p=0.006). CONCLUSION: Total mortality was significantly increased in patients AMI with geometrically progressive LA and LV dilatation.

Comparison of Coronary Plaque Components between Non-Culprit Lesions in Patients with Acute Coronary Syndrome and Target Lesions in Patients with Stable Angina: Virtual Histology-Intravascular Ultrasound Analysis.

BACKGROUND AND OBJECTIVES: The differences in plaque characteristics between non-culprit lesions (NCL) in acute coronary syndrome (ACS) patients (ACS-NCL) and target lesions (TL) in stable angina (SA) patients (SA-TL) are not well understood. We used a virtual histology-intravascular ultrasound (VH-IVUS) to compare the plaque components between ACS-NCL and SA-TL. SUBJECTS AND METHODS: We compared VH-IVUS findings between 290 ACS-NCL and 276 SA-TL. VH-IVUS classified the color-coded tissue into four major components: green (fibrotic); yellow-green (fibro-fatty); white {dense calcium (DC)}; and red {necrotic core (NC)}. Thin-cap fibroatheroma (TCFA) was defined as a NC ≥10% of the plaque area in at least 3 consecutive frames without overlying fibrous tissue in the presence of ≥40% plaque burden. RESULTS: Although the plaque burden was significantly smaller (52±13% vs. 54±14%, p=0.044), ACS-NCL had a greater %NC area (17.9±11.6% vs. 14.3±8.7%, p<0.001) and %DC area (9.7±9.8% vs. 8.1±8.0%, p=0.032) compared with SA-TL at the minimum lumen site. By volumetric analysis, ACS-NCL had a greater %NC volume (15.8±9.2% vs. 13.9±7.4%, p=0.006) compared with SA-TL. TCFA was observed more frequently in ACS-NCL compared with SA-TL (27.6% vs. 18.1%, p=0.032). Independent predictors of TCFA by multivariate analysis were ACS {odds ratio (OR): 2.204, 95% CI: 1.321-3.434, p=0.021} and high-sensitivity C-reactive protein (OR: 1.101; 95% CI 1.058-1.204, p=0.035). CONCLUSION: Although the plaque burden was significantly smaller, ACL-NCL had more vulnerable plaque components compared with SA-TL, and ACS and high-sensitivity C-reactive protein were the independent predictors of TCFA.

A patient with repeated catastrophic multi-vessel coronary spasm after zotarolimus-eluting stent implantation.

Drug-eluting stents (DES) have gained great popularity because of extraordinarily low rates of restenosis. Despite these superior clinical outcomes, several cases regarding the severe multi-vessel coronary spasm, although rare, after the placement of first generation DES have been reported. We report a case of severe, multi-vessel coronary spasm that occurred two occasions after placement of a zotarolimus-eluting stent, one of the second generation DES, in a 42-year-old man with unstable angina. The first incidence was relieved by intracoronary nitroglycerin alone, and second incident, which had combined fixed stenosis was treated with intracoronary nitroglycerin and everolimus-eluting stent.

Relation between poststenting peristent plaque components and late stent malapposition after drug-eluting stent implantation: virtual histology-intravascular ultrasound analysis.

BACKGROUND: Impact of plaque composition on late stent malapposition (LSM) after drug-eluting stent (DES) implantation has not been evaluated. METHODS: We evaluated the relation between plaque components at poststenting peristent area (between external elastic membrane and stent areas) and LSM after DES implantation in 266 patients (314 native lesions; paclitaxel-eluting stent in 205 lesions, sirolimus-eluting stent in 66 lesions, zotarolimus-eluting stent in 32 lesions and everolimus-eluting stent in 11 lesions) in whom virtual-histology intravascular ultrasound was performed at index (poststenting) and follow-up (mean: 11.7 ± 4.8 months). RESULTS: LSM occurred in 24 patients with 30 lesions (9.6%) and there were no significant differences in the incidences of LSM among 4 DES groups [21/205 (10.2%) in paclitaxel-eluting stent, 6/66 (9.1%) in sirolimus-eluting stent, 2/32 (6.3%) in zotarolimus-eluting stent and 1/11 (9.1%) in everolimus-eluting stent, p=0.5)]. Patients with LSM were presented with more acute myocardial infarction (50% vs. 28%, p=0.026) and were more diabetics (50% vs. 30%, p=0.030) compared with those without LSM. Lesions with LSM had more poststenting peristent %necrotic core (NC) volume compared with those without LSM (25.8 ± 11.1% vs. 21.0 ± 5.7%, p<0.001). Independent predictors of LSM were poststenting peristent %NC volume [odds ratio (OR); 1.216, 95% CI; 1.053-1.405, p=0.008], acute myocardial infarction (OR; 2.897, 95% CI; 1.675-4.118, p=0.029), and diabetes mellitus (OR; 2.413, 95% CI; 1.543-3.996, p=0.038). CONCLUSIONS: Poststenting peristent NC component especially in patients with acute myocardial infarction and in those with diabetes mellitus is associated with the development of LSM after DES implantation.

Is Myocardial Infarction in Patients without Significant Stenosis on a Coronary Angiogram as Benign as Believed?

The present study aimed to investigate the clinical characteristics and 1-year outcomes of acute myocardial infarction (AMI) patients without significant stenosis on a coronary angiogram comparison with the clinical characteristics and outcomes of patients with significant coronary artery stenosis. A total of 1,220 patients with AMI were retrospectively classified into Group I (≥50% diameter stenosis, n=1,120) and Group II (<50%, n=100). Group II was further divided into two subgroups according to the underlying etiology: cryptogenic (Group II-a, n=54) and those with possible causative factors (Group II-b, n=46). Patients in Group II were younger, were more likely to be women, and were less likely to smoke and to have diabetes mellitus than were patients in Group I. The levels of cardiac enzymes, LDL-cholesterol levels, and the apo-B/A1 ratio were lower in Group II. However, 1-month and 12-month rates of major adverse cardiac events (MACE) were not significantly different between the two groups. The Group II-b subgroup comprised 29 patients with vasospasm, 11 with myocardial bridge, and 6 with spontaneous thrombolysis. Left ventricular ejection fraction and creatinine clearance were lower and levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity C-reactive protein (hs-CRP) were higher in Group II-a than in Group II-b. However, outcomes including MACE and mortality at 12 months were not significantly different between the two subgroups. The 1-year outcomes of patients in Group II were similar to those of patients in Group I. The clinical outcomes in Group II-a were also similar to those of Group II-b, although the former group showed higher levels of NT-proBNP and hs-CRP.

Comparison of clinical outcomes of hydrophilic and lipophilic statins in patients with acute myocardial infarction.

BACKGROUND/AIMS: A controversy exists about which statin is preferable for patients with acute myocardial infarction (AMI), and clinical impacts of different statins according to lipophilicity have not been established. METHODS: The 1,124 patients with AMI included in the present study were divided into hydrophilic- and lipophilic-statin groups. In-hospital complications (defined as death, cardiogenic shock, ventricular arrhythmia, infection, bleeding, and renal insufficiency, and other fatal arrhythmias), major adverse cardiac events (MACE), all-cause death, re-myocardial infarction, re-percutaneous coronary intervention (re-PCI), and surgical revascularization were analyzed during a 1-year clinical follow-up. RESULTS: Baseline characteristics were similar between the two groups, and in-hospital complication rates showed no between-group differences (11.7% vs. 12.8%, p = 0.688). Although MACE at the 1- and 6-month clinical follow-ups occurred more in hydrophilic statin group I (1 month: 10.0% vs. 4.4%, p = 0.001; 6 month: 19.9% vs. 14.2%, p = 0.022), no significant difference in MACE was observed at the 1-year follow-up (21.5% vs. 17.9%, p = 0.172). Both statin groups showed similar efficacy for reducing serum lipid concentrations. A Cox-regression analysis showed that the use of a hydrophilic statin did not predict 1-year MACE, all-cause death, AMI, or re-PCI. CONCLUSIONS: Although short-term cardiovascular outcomes were better in the lipophilic-statin group, 1-year outcomes were similar in patients with AMI who were administered hydrophilic and lipophilic statins. In other words, the type of statin did not influence 1-year outcomes in patients with AMI.