Jong-Shin Woo

Effect of myocardial protection of intracoronary adenosine and nicorandil injection in patients undergoing non-urgent percutaneous coronary intervention: A randomized controlled trial

BACKGROUND Several studies have demonstrated that adenosine and nicorandil protect the myocardium against angioplasty-related myocardial injury. We conducted a prospective study to investigate the myocardial protective effects of combination therapy with intracoronary adenosine and nicorandil. METHODS We enrolled 213 consecutive patients with stable or unstable angina who were scheduled for non-urgent PCI for de-novo coronary lesions. Patients were randomized into group I (control saline, n=55), group II (adenosine 50 μg, n=54), group III (nicorandil 4 mg, n=54), or group IV (adenosine-nicorandil combination, n=50). Serial assessments of CK-MB were used to assess myocardial necrosis before and after PCI. The primary endpoint was the incidence of myocardial necrosis (elevation of CK-MB), and the secondary endpoints were the changes in serum CK-MB and cTnI levels and the incidence of post-procedural myocardial infarction (MI). RESULTS No significant differences were observed among the four groups with regard to baseline or angiographic characteristics. No major adverse events related to adenosine and nicorandil were observed. There were no significant differences in the incidence of post-procedural myocardial necrosis among the four groups (10.9, 14.8, 14.8, and 14.0%, respectively, p=0.9). There were no significant differences in the incidence of post-procedural MI among groups (p=0.6). In multivariate regression analysis, multivessel stenting, median stent length, and the presence of a compromised side branch were independent predictors of myonecrosis. CONCLUSIONS Pretreatment with intracoronary adenosine, nicorandil, or the combination of the two drugs did not reduce the incidences of myocardial necrosis or MI after non-urgent PCI in patients with low-risk angina pectoris.

Effects of sildenafil on nanostructural and nanomechanical changes in mitochondria in an ischaemia-reperfusion rat model

Sildenafil exerts cardioprotective effects by activating the opening of mitochondrial ATP‐sensitive potassium channels to attenuate ischaemia–reperfusion (IR) injury. In the present study, we used atomic force microscopy (AFM) to investigate changes in mitochondrial morphology and properties to assess sildenafil‐mediated cardioprotection in a rat myocardial infarction model. To investigate the cardioprotective effects of sildenafil, we used an in vivo Sprague‐Dawley rat model of IR. Rats were randomly divided into three groups: (i) sham‐operated rats (control; n = 5); (ii) IR‐injured rats treated with vehicle (normal saline; IR; n = 10); and (iii) IR‐injured rats treated with 0.75 mg/kg, i.p., sildenafil (IR + Sil; n = 10). Morphological and mechanical changes to mitochondria were analysed by AFM. Infarct areas were significantly reduced in sildenafil‐treated rats (7.8 ± 3.9% vs 20.4 ± 7.0% in the sildenafil‐treated and untreated IR groups, respectively; relative reduction 62%; P < 0.001). Analysis of mitochondria by AFM showed that IR injury significantly increased the areas of isolated mitochondria compared with control (24 150 ± 18 289 vs 1495 ± 1139 nm2, respectively; P < 0.001), indicative of mitochondrial swelling. Pretreatment with sildenafil before IR injury reduced the mitochondrial areas (7428 ± 3682 nm2; P < 0.001; relative reduction 69.2% compared with the IR group) and ameliorated the adhesion force of mitochondrial surfaces. Together, these results suggest that sildenafil has cardioprotective effects against IR injury in a rat model by improving the morphological and mechanical characteristics of mitochondria.

Exenatide Prevents Morphological and Structural Changes of Mitochondria Following Ischaemia-Reperfusion Injury

BACKGROUND Exenatide exerts cardioprotective effects by attenuating ischaemic reperfusion (IR) injury, possibly through activating the opening of mitochondrial ATP-sensitive potassium channels. We used atomic force microscopy (AFM) to investigate changes in mitochondrial morphology and properties in order to assess exenatide-mediated cardioprotection in IR injury. METHODS We used an in vivo Sprague-Dawley rat IR model and ex vivo Langendorff injury model. In the left anterior descending artery (LAD) occlusion model, animals were randomly divided into three groups: sham-operated rats (Sham, n=5), IR-injured rats treated with placebo (IR, n=6), and IR-injured treated with exenatide (IR + EXE, n=6). For the Langendorff model, rats were randomly divided into two groups: IR injury with placebo (IR, n=4) and IR injury with exenatide (IR+EXE, n=4). Morphological and mechanical changes of mitochondria were analysed by AFM. RESULTS Exenatide pre-treatment improved cardiac function as evidenced by improvement in echocardiographic results. The ratio of infarct area (IA) to risk area (RA) was significantly reduced in exenatide-treated rats. According to AFM, IR significantly increased the area of isolated mitochondria, indicative of mitochondrial swelling. Treatment with exenatide reduced the mitochondrial area and ameliorated the adhesion force of mitochondrial surfaces. CONCLUSIONS Exenatide pre-treatment improves morphological and mechanical characteristics of mitochondria in response to IR injury in a rat model. These alterations in mitochondrial characteristics appear to play a cardioprotective role against IR injury.

THE PREDICTIVE VALUE OF AORTIC ARCH CALCIFICATION ON CHEST X-RAY FOR CARDIOVASCULAR EVENTS IN COMPARISON WITH THE CORONARY ARTERY CALCIUM SCORE AND THE FRAMINGHAM RISK SCORE

Background: The coronary artery calcium (CAC) and aortic arch calcification (AoAC) are individually associated with cardiovascular disease and outcome. Methods: A total of 2,018 stable angina patients who underwent chest X-ray and cardiac multi-detector computed tomography were followed up for 4

INCIDENCE OF SUBCLINICAL ATHEROSCLEROSIS IN PATIENTS WITH RESISTANT HYPERTENSION

Aim: The purpose of the study was to investigate the incidence of subclinical atherosclerosis by coronary artery calcium(CAC) score and atherosclerotic cardiovascular disease(ASCVD) risk score in patients with resistant hypertension. Methods: For 8823 subjects taking one or more antihypertensive