• Proceedings of the KTCVS Conference
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• 1998.10a
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• pp.139-139
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• 1998

• Proceedings of the KTCVS Conference
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• 1998.10a
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• pp.185-185
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• 1998

• Investigative Magnetic Resonance Imaging
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• v.16 no.2
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• pp.189-194
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• 2012

We report a case of cardiac lymphoma in a 40-year-old man, who had a mediastinal mass which was diagnosed as sclerosing mediastinitis pathologically. The mediastinal mass caused right pulmonary arterial stenosis. The patient developed myocardial hypertrophy and echocardiography showed restrictive physiology and severely decreased left ventricle ejection fraction, 6 months later. MRI showed global left ventricular myocardial hypertrophy and diffuse late gadolinium hyperenhancement after administration of contrast material. Thus, non-ischemic cardiomyopathy was suspected on MRI. However, pathology confirmed the myocardial abnormality as lymphoma after myocardial biopsy. Because a basal part of the left ventricle and global subendocardial myocardium were not involved on contrast-enhanced delayed MRI, the MRI abnormalities could be differentiated from amyloidosis and other myocardial diseases. The peculiar non-mass forming diffuse hypertrophy pattern of cardiac lymphoma has not been known in the MRI literature.

• 대한핵의학회:학술대회논문집
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• 1990.04a
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• pp.195.1-195.1
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• 1990

• 대한핵의학회:학술대회논문집
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• 1991.05a
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• pp.154.2-155
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• 1991

• Journal of Chest Surgery
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• v.31 no.12
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• pp.1238-1242
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• 1998

Myocardial bridges as an anatomical arrangement in which an epicardial coronary artery becomes engulfed, for a limited segment, by myocardial fibers. These diseases are recognized primarily because of their systolic narrowing or milking effect as seen on coronary angiography. The most frequent site of myocardial bridging is the middle segment of left anterior descending artery. Myocardial bridges have an ischemic effect capable of causing : angina pectoris, myocardial infarction, ventricular fibrillation, or even sudden death in athletes. We report 2 patients having a milking effect of the middle segment of left anterior descending artery who were suffered from angina. The operation procedure was a simple supraarterial myotomy over the embedded segment of the LAD under cardiopulmonary bypass. Angina and milking effect were disappeared after the operation.

• Journal of Chest Surgery
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• v.30 no.8
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• pp.823-826
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• 1997

Myocardial abscess usually occurs as a complication of infective endocarditis or overwhelming septicemia. Coronary artery occlusion caused by myocardial abscess has been rarely reported. A 61-year-old man presented with fever and chill that developed 6 weeks prior to admission. He had a history of cardiopulmonary resuscitation for ventricular fibrillation and cardiac arrest 4 weeks prior to admission. Echocardiography showed a 3xfcm sized mass in the area of the right atrioventricular groove and coronary angiography showed complete occlusion of the proximal right coronary artery. Under the diagnosis of myocardial infarction complicating myocardial abscess, debridement of abscess and coronary artery bypass grafting with right internal mammary artery to distal right coronary artery was performed. Culture from the abscess cavity demonstrated Salmonella arizona.

• Journal of Chest Surgery
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• v.34 no.11
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• pp.823-830
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• 2001

Background: Paraplegia is a serious complication of thoracic or thoracoabdominal aortic operations, which is related to ischemic injury of the spinal cord induced by low perfusion pressure during cross clamping of the aorta. Ischemic preconditioning of heart or brain with reversible sublethal ischemic injury induces resistance to subsequent lethal ischemia. The aim of this study is to investigate whether ischemic tolerance could be induced by the preconditioning of the spinal cord using swine model. Material and Method: The animals were randomly assigned to three groups: sham group(n=3), control group(n=6) and pre-conditioning group(n=8). In the sham group, we performed the left thoracotomy only without any ischemic injury. In the preconditioning group, the swine received reversible spinal cord ischemic injury by aortic clamping for 20 minutes, whereas control group had no previous aortic cross- clamping. Forty-eight hours later, the aorta was clamped for 30 minutes in both groups. Neurological examination was done 24 hours later, then the animals were euthanized for histopathology and malonedialdehyde(MDA) spectrophotometry assay of the spinal cord. Result: Statistically significant difference in neurological outcome was observed between the control and preconditioning groups at 24 hours after ischemic injury. The incidence of paraplegia and severe paresis was 100% in the control group, and 62.5% in the preconditing group(p=0.028). There was no statistically significant difference in histopathology and MDA assay of the ischemic spinal cord between these two groups with borderline statistical difference in MDA assay(p=0.0745). Conclusion: In the present swine study, ischemic preconditioning could induce tolerance against 30 minute ischemic insult of the spinal cord, although the animals did not completely recover(stand-up or walk). We expect that combining this preconditioning with other currently existing protection methods might lead to a synergistic effect, which warrants further investigation.

• Journal of Chest Surgery
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• v.38 no.5 s.250
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• pp.323-334
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• 2005

Background: Gene therapy is a new and promising option for the treatment of severe myocardial ischemia by therapeutic angiogenesis. The goal of this study was to elucidate the efficacy of therapeutic angiogenesis by using VEGF165 in large animals. Material and Method: Twenty-one pigs that underwent ligation of the distal left anterior descending coronary artery were randomly allocated to one of two treatments: intramyocardial injection of pCK-VEGF (VEGF) or intramyocardial injection of pCK-Null (Control). Injections were administered 30 days after ligation. Seven pigs died during the trial, but eight pigs from VEGF and six from Control survived. Echo-cardiography was performed on day 0 (preoperative) and on days 30 and 60 following coronary ligation. Gated myocardial single photon emission computed tomography imaging (SPECT) with $^{99m}Tc-labeled$ sestamibi was performed on days 30 and 60. Myocardial perfusion was assessed from the uptake of $^{99m}Tc-labeled$ sestamibi at rest. Global and regional myocardial function as well as post-infarction left ventricular remodeling were assessed from segmental wall thickening; left ventricular ejection fraction (EF); end systolic volume (ESV); and end diastolic volume (EDV) using gated SPECT and echocardiography. Myocardium of the ischemic border zone into which pCK plasmid vector had been injected was also sampled to assess micro-capillary density. Result: Micro-capillary density was significantly higher in the VEGF than in Control ($386\pm110/mm^{2}\;vs.\;291\pm127/mm^{2};\;p<0.001$). Segmental perfusion increased significantly from day 30 to day 60 after intramyocardial injection of plasmid vector in VEGF ($48.4\pm15.2\%\;vs.\;53.8\pm19.6\%;\;p<0.001$), while no significant change was observed in the Control ($45.1\pm17.0\%\;vs.\;43.4\pm17.7\%;\;p=0.186$). This resulted in a significant difference in the percentage changes between the two groups ($11.4\pm27.0\%\;increase\;vs.\;2.7\pm19.0\%\;decrease;\;p=0.003$). Segmental wall thickening increased significantly from day 30 to day 60 in both groups; the increments did not differ between groups. ESV measured using echocardiography increased significantly from day 0 to day 30 in VEGF ($22.9\pm9.9\;mL\;vs.\;32.3\pm9.1\;mL;\; p=0.006$) and in Control ($26.3\pm12.0\;mL\;vs.\;36.8\pm9.7\;mL;\;p=0.046$). EF decreased significantly in VEGF ($52.0\pm7.7\%\;vs.\;46.5\pm7.4\%;\;p=0.004$) and in Control ($48.2\pm9.2\%\;vs.\;41.6\pm10.0\%;\;p=0.028$). There was no significant change in EDV. The interval changes (days $30\~60$) of EF, ESV, and EDV did not differ significantly between groups both by gated SPECT and by echocardiography. Conclusion: Intramyocardial injection of pCK-VEGF165 induced therapeutic angiogenesis and improved myocardial perfusion. However, post-infarction remodeling and global myocardial function were not improved.

• 대한핵의학회:학술대회논문집
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• 1998.11a
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• pp.28.2-28.2
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• 1998