Hypertrophic Cardiomyopathy Complicated by Left Ventricular Apical Necrosis and Aneurysm in a Young Man: FDG-PET Findings

A 29-year old male was transferred to our hospital with an abnormal chest X-ray finding diagnosed as hypertrophic cardiomyopathy with apical necrosis and aneurysm formation. Four years after the initial hospitalization, we confirmed the aneurysm and necrosis using both integrated positron emission tomography (PET) and computed tomography (CT) scanning. The F-18 2-fluoro-2-deoxy-D-glucose (FDG) PET/CT enabled precise localization of the aneurysm, which was found to be composed of semi-lunar calcification of non-metabolic myocardium. A contrast-enhanced CT angiography showed an hour-glass appearance of the left ventricular cavity. The integrated PET/CT fusion scanner is a novel multimodality technology that allows for a comprehensive analysis of the anatomical and functional status of complex heart disease. Based on these findings, long standing mechanical and physiologic abnormalities may have led to chronic ischemia in the hypertrophied myocardium, induced necrosis and calcification at the cardiac apex.

Clinical and Angiographic Outcome of Sirolimus-Eluting Stent for the Treatment of Very Long Lesions

BACKGROUND AND OBJECTIVES: Compared to bare metal stent, drug-eluting stent has improved the clinical and angiographic outcomes for de novo, simple lesions. In real world clinical practice, we often encounter more complex, long lesions, which increase the rate of restenosis and cardiovascular events. The aim of this study was to evaluate the clinical and angiographic outcome of sirolimus-eluting stent (SES) for the treatment of very long lesions in real world clinical practice. SUBJECTS AND METHODS: We implanted multiple SESs (>40 mm in total length) in 113 de novo lesions in 113 patients. The average length of the implanted stents was 58+/-14 mm (range: 41-112 mm) and a mean of 2.2 stents were implanted in each lesion and the average stent diameter was 3.0+/-0.3 mm. RESULTS: Procedural and angiographic success were achieved in all the patients without death or coronary artery bypass surgery. Non-Q wave MI (CK-MB > or = 3 times the normal value) developed in 13 patients (11.5%). Two patients experienced late stent thrombosis after discharge (1.8%). The major adverse cardiac events (MACE)-free survival was 94% at 12 months. There were two sudden cardiac deaths. Six months follow up angiography was performed on 76 patients (67%) and angiographic binary restenosis developed in 7 patients (9.2%). All of them were the focal type in-stent restenosis and these were found to be located at the distal stents. CONCLUSIONS: In conclusion, long lesion coverage with SESs is feasible with a favorable mid-term outcome in real world clinical practice.

Successful Treatment of Ischemic Dysfunction of the Sinus Node with Thrombolytic Therapy: A Case Report

We report on a case of ischemic dysfunction of the sinus node as a complication after percutaneous transluminal coronary angioplasty of the distal left circumflex artery. After local thrombolytic therapy in the sinus node artery, sinus node arterial flow was re-established and sinus node function normalized over the period of a week. Our experience suggests that immediate reperfusion of a totally occluded nodal artery can be re-established. Ischemic dysfunction of the sinus node, as a complication of angioplasty, is generally transient and requires a prolonged period for recovery. Therefore the decision to implant a permanent pacemaker should be delayed for at least one week after the ischemic insult.

Treatment of Coronary Artery Perforation and Tamponade Complicating Balloon Angioplasty by PTFE-Covered Stent. A Case Report / 영남의대학술지

A coronary artery perforation is a rare but often fatal complication of angioplasty. We experienced a coronary artery perforation and cardiac tamponade during balloon angioplasty. A polytetrafluorethylene (PTFE) -covered stent was used to successfully close the perforation.

Expression and Regulation of Endothelial Nitric Oxide Synthase by Vascular Endothelial Growth Factor in ECV 304 Cells

Nitric oxide (NO) seems to play a pivotal role in the vascular endothelial growth factor (VEGF)-induced endothelial cell proliferation. This study was designed to investigate the role and intracellular signal pathway of endothelial nitric oxide synthase (eNOS) activation induced by VEGF. ECV 304 cells were treated with betaVEGF(165) and then cell proliferation, eNOS protein and mRNA expression levels were analyzed to elucidate the functional role of eNOS in cell proliferation induced by VEGF. After exposure of cells to betaVEGF(165) , eNOS activity and cell growth were increased by approximately two-fold in the betaVEGF(165) -treated cells compared to the untreated cells. In addition, VEGF stimulated eNOS expression at both the mRNA and protein levels in a dose-dependent manner. Phosphatidylinositol-3 kinase (PI-3K) inhibitors were used to assess PI-3K involvement in eNOS regulation. LY294002 was found to attenuate VEGF-stimulated eNOS expression. Wortmannin was not as effective as LY294002, but the reduction effect was detectable. Cells activated by VEGF showed increased ERK1/2 levels. Moreover, the VEGF-induced eNOS expression was reduced by the PD98059, MAPK pathway inhibitor. This suggests that eNOS expression might be regulated by PI-3K and the ERK1/2 signaling pathway. In conclusion, betaVEGF(165) induces ECV 304 cell proliferation via the NO produced by eNOS. In addition, eNOS may be regulated by the PI-3K or mitogen-activated protein kinase pathway.

Change of Serum Levels of C-Reactive Protein After Coronary Angioplasty and Its Effects on Clinical Restenosis / 영남의대학술지

BACKGROUND: There are many evidences that inflammation is an important determinant of the development of atherosclerosis and one of the systemic markers of inflammation, C-reactive protein(CRP), is associated with extent of coronary artery disease and risk of coronary events. We assessed the time response of CRP response after coronary angioplasty and it's influence on the clinical restenosis in angina patients. MATERIALS AND METHODS: Patients included 36 angina patients undergoing single vessel angioplasty. Levels of CRP were measured before and 12, 24, 48, and 72 hours after angioplasty. Clinical restenosis was assessed at 6 months after procedure. RESULTS: Baseline CRP level was 0.30+/-0.01 mg/dL in stable and 0.46+/-0.28 mg/dL in unstable angina patients(p<0.05). After angioplasty, CRP level was increased with peak at 24 hour and persisted to 72 hours after angioplasty. At 24 hour after angioplasty, the magnitude of CRP change was 0.32+/-0.31 mg/dL in stable and 0.79+/-0.73 mg/dL in unstable angina patient(p<0.05). The change of CRP level was not associated with troponin-T after angioplasty. In unstable angina patients, clinical restenosis was developed in 8% of patients with low baseline CRP levels and in 50% of those with high baseline CRP levels more than 0.6 mg/dL(p<0.05). CONCLUSION: In unstable angina patients, inflammatory response is more increased than stable angina patients, and increased inflammatory response effects on the restenosis after coronary angioplasty.