PurposeTo investigate the effect of pretreatment with intravenous nicorandil on the incidence of contrast-induced nephropathy (CIN) in patients with renal dysfunction undergoing coronary angiography.Materials and MethodsThis randomized controlled multicenter study enrolled a total of 166 patients (nicorandil n=81; control n=85) with an estimated glomerular filtration rate <60 mL/min. Nicorandil 12 mg dissolved in 100 mL of 0.9% saline was administered intravenously for 30 minutes just prior to coronary angiography in the nicorandil group. The same volume of only saline was given to the control group. The primary end-point was the incidence of CIN, defined as >0.5 mg/dL increase or >25% rise in serum creatinine (SCr) concentration within 48 hours of contrast exposure compared to baseline.ResultsThe final analysis included 149 patients (nicorandil n=73; control n=76). The baseline characteristics and the total volume of the used contrast (Iodixanol, 125.6±69.1 mL vs. 126.9±74.6 mL, p=0.916) were similar between the two groups. The incidence of CIN also did not differ between the nicorandil and control groups (6.8% vs. 6.6%, p=0.794). There was no difference between the two groups in the relative change in SCr from baseline to peak level within 48 hours after coronary angiography (-1.58±24.07% vs. 0.96±17.49%, p=0.464), although the nicorandil group showed less absolute change in SCr than the control group (-0.01±0.43 mg/mL vs. 0.02±0.31 mg/mL, p=0.005).ConclusionProphylactic intravenous infusion of nicorandil did not decrease the incidence of CIN in patients with renal dysfunction undergoing coronary angiography.

Small non‑coding microRNAs (miRNAs) are not only important for heart and vascular development but are also important in cardiovascular pathophysiology and diseases, such as ischemia and atherosclerosis‑related diseases. However, the effect of miR‑146a, miR‑149, miR‑196a2 and miR‑499 polymorphisms on coronary artery disease (CAD) susceptibility remain unknown. The aim of the present study was to examine the genotype frequencies of miR‑146a, miR‑149, miR‑196a2 and miR‑499 polymorphisms in patients with CAD, and assess their clinical applications for diagnosing and monitoring CAD. Using polymerase chain reaction‑amplified DNA, microRNA polymorphisms were analyzed in 522 patients with CAD and 535 control subjects. The miR‑149 rs2292832 C>T and miR‑196a2 rs11614913 T>C polymorphisms were shown to be significantly associated with CAD prevalence. In subgroup analyses according to disease severity, the miR‑146a rs2910164GG genotype was significantly associated with CAD risk in the stent ≥2 group. In addition, miR‑146aG/‑149T/‑196a2C/‑499 G allele combination was significantly associated with CAD prevalence (G‑T‑C‑G and G‑C‑C‑G of miR‑146a/‑149/‑196a2/‑499). The combination genotypes of miR‑146aGG/149TC+CC and miR‑149CC/196a2TC were significantly associated with CAD incidence. In subgroup analyses, miR‑146a rs2910164 C>G increased the risk of developing CAD in non‑smoking, hypertensive and nondiabetic subgroups. Furthermore, miR‑149 rs2292832 C>T and miR‑196a2 rs11614913 T>C was shown to increase CAD risk in females and patients aged >63 years old. The miR‑149T allele, miR‑196a2C allele and miR‑146aG/‑149T/‑196a2C/‑499 G allele combination were associated with CAD pathogenesis. The combined effects of environmental factor and genotype combination of miRNA polymorphisms may contribute to CAD prevalence.

Background: The pathophysiological role and metabolic pathway of Lp(a) have not been clearly defined. An association between Lp(a) and oxidative low-density lipoprotein (LDL) were recently reported. And small dense LDL (sd-LDL) were associated with circulating malondialdehyde-modified LDL. We investigated the relationships between serum Lp(a) level and LDL particle size in coronary artery disease (CAD) patients. Further, we investigated the relationships of sd-LDL and Lp(a) with the extent and severity of CAD. Methods: A total of 490 patients (mean: 60.5 ± 11.5 years old) who underwent coronary angiography to evaluate chest pain were investigated. Patients were classified into two groups, a CAD group (n = 256), who had significant stenosis observed by coronary angiogram, and a control group (n = 234), who had normal, or minimal coronary arteries. CAD severity was measured by Gensini scores. The distribution of the LDL subfraction was analyzed using a Quantimetrix Lipoprint LDL System. Results: The serum Lp(a) concentration was correlated with the fraction of sd-LDL (r = 0.193, p < 0.001) and mean LDL size (r = 0.160, p = 0.003). The Lp(a) level and mean LDL particle size were significantly correlated with a high Gensini score. LDL particle size in the CAD group was smaller than in the control group (26.74 ± 0.64 vs. 26.43 ± 0.93 nm, p < 0.001). The Gensini score was significantly higher in small LDL with high Lp(a) level groups. Conclusion: The positive correlation of the level of Lp(a) and sd-LDL fraction were demonstrated. The mechanism of this association is not clearly defined; we can suggest that it may stem from the individual atherogenic condition that linked to increased oxidative stress. Both increased Lp(a) and sd-LDL fraction were correlated with the severity of CAD.

mong the many markers used to assess successful myocardial reperfusion after primary percutaneous coronary intervention (PCI) or thrombolysis therapy, the extent of resolution of ST-segment elevation is a simple noninvasive indicator of the outcome of infarcted myocardium. 1 Previous studies using myocardial contrast echocardiography 2,3 or radioisotope scintigraphy [4][5][6] have demonstrated that early ST-segment elevation resolution (STR) after primary PCI or thrombolysis is associated with better salvage of reperfused myocardium. However, both the pathologic correlates and the mechanisms of early STR are relatively unknown. Recent advances in cardiac magnetic resonance imaging (CMRI) allow relatively precise assessments of myocardial perfusion, infarct size, left ventricular (LV) remodeling and function, with excellent correlation with histology in animal models of acute and chronic myocardial infarction (MI). 7,8 However, there are little data on the CMRI findings related to early STR after successful Circulation Journal Vol.72, October 2008 primary PCI. Therefore, we performed CMRI serially in the early and late phases after successful revascularization by primary PCI for treatment of MI. We sought to determine whether the morphologic and functional parameters of CMRI correlated with early STR after primary PCI for ST-elevation myocardial infarction (STEMI). Method SubjectsWe investigated 45 patients with acute STEMI in whom primary PCI was performed successfully within 12 h of symptom onset. Diagnosis of acute MI (AMI) was based on the presence of acute ischemic chest pain, electrocardiogram (ECG) findings (ST-segment elevation ≥0.1 mV in 2 or more contiguous leads), elevated serum cardiac biomarkers (cardiac troponin T >0.1 g/L, creatine kinase-MB (CK-MB) fraction enzyme level >10 g/L), and angiographic significant stenosis (≥50%) of a coronary artery. Exclusion criteria were unstable hemodynamic status, any history of previous MI, or contraindications to CMRI (eg, pacemaker implantation or claustrophobia). We also excluded patients with recurrent chest pain or anginal equivalent associated with ST-segment changes during the time period between primary angioplasty and second CMRI. All participants gave written informed consent to the study protocol. ECG AnalysisA 12-lead ECG was performed before and 90 min after primary PCI. The sum of ST-segment elevation was mea- Correlation of Serial Cardiac Magnetic Resonance Imaging Parameters With Early Resolution of ST-Segment Elevation After Primary Percutaneous Coronary InterventionJung-Sun Kim, MD, PhD; Young-Guk Ko, MD; Se-Jung Yoon, MD, PhD*; Jae-Youn Moon, MD; Young Jin Kim, MD, PhD**; Byoung Wook Choi, MD, PhD**; Donghoon Choi, MD, PhD; Yangsoo Jang, MD, PhDBackground The aim of the present study was to determine whether the parameters of cardiac magnetic resonance imaging (CMRI) might correlate with early ST-segment resolution (STR) after primary percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI