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증례 : 순환기 ; 관상동맥 전산화단층촬영으로 확진한 좌주간지 동맥류 혈전증에 의한 급성심근경색증
박종관 ( Jong Kwan Park ),윤세정 ( Se Jung Yoon ),오성진 ( Seung Jin Oh ),전동운 ( Dong Woon Jeon ),양주영 ( Joo Young Yang ) 대한내과학회 2014 대한내과학회지 Vol.86 No.2
관상동맥류는 드물게 보고되는 질환이나 이로 인한 증상이 발생하였을 경우 빠른 진단 및 치료 방침의 결정은 매우 중요하다. 이에 본 저자들은 국내에서 매우 드문 좌주간지 관상동맥류 혈전증에 의한 비 ST분절 상승 심근경색증을 관상동맥 전산화단층촬영을 통해 정확하게 진단하고 성공적으로 치료하였기에 이를 보고하는 바이다. Aneurysms of the left main coronary artery are very rare in patients with acute coronary syndrome. The increased accuracy of computed tomography permits the detection of coronary artery anatomic structures after one peripheral injection of contrast agent. We report a 42-year-old man with a left main coronary aneurysm, with a thrombus presenting as non-ST elevation myocardial infarction, detected by coronary computed tomographic angiography. (Korean J Med 2014;86:224-227)
증례 : 순환기 ; 우 관상동맥 기형과 동반된 운동 중 급성 심장사 1예
차민섭 ( Min Seob Cha ),윤세정 ( Se Jung Yoon ),홍석민 ( Seok Min Hong ),곽민섭 ( Min Seob Kwak ),최유리 ( Yu Ri Choi ),정상완 ( Sang Wan Chung ),김진배 ( Jin Bae Kim ) 대한내과학회 2011 대한내과학회지 Vol.80 No.2S
35세 이하에서 급성 심장사를 일으키는 원인 중 하나인 관상동맥 기형의 진단에 있어 관상동맥 조영술, 심장초음파 등이 이용되어 왔고 최근 MDCT의 도입으로 대혈관과의 관계, 주행 방향 등을 더 정확하게 진단할 수 있게 되었다. 저자들은 운동 후 발생한 급성 심정지를 주소로 내원한 환자를 MDCT를 이용하여 우 관상동맥 기시 이상을 진단하고 수술적 치료를 한 1예를 경험하였기에 문헌고찰과 함께 보고하는 바이다. There are many causes of sudden cardiac arrest. The main cause of sudden cardiac death (SCD) is coronary heart disease. However, the frequency of coronary heart disease is much lower in sudden cardiac arrest occurring below the age of 30-40. Congenital anomalous origin of the coronary arteries is a rare, but well-described, cause of myocardial ischemia and sudden death in young adults. Here, we report the case of a 23-year-old man with sudden cardiac arrest due to ventricular fibrillation associated with an anomalous origin of the right coronary artery. The patient was diagnosed using multi-detector computed tomography and successfully treated with surgical correction. (Korean J Med 2011;80:S178-S182)
Torsades de pointes을 동반한 Liddle 증후군 1예
박홍수,강신욱,한대석,이호영,하성규,신재호,윤세정,강태수,최규헌,황학진 대한신장학회 1999 Kidney Research and Clinical Practice Vol.18 No.6
Liddle syndrome is a rare cause of hypokalemic hypertension and caused by renal tubular sodiurn channel defect resulting in excessive sodium absorption, potassium wasting and metabolic alkalosis. Clinically this syndrome resembles the primary aldosteronism, however, aldosterone and renin secretion are markedly suppressed due to chronic state of volume expansion. This syndrome is transmitted in an autosomal dominant pattern. We have experienced a case of Liddle syndrome, a 74 years old female accompanying severe hypokalemia, long-standing hypertension, metabolic alkalosis and suppressed aldosterone and renin level in serum and urine. She had a history of arrhythmia, torsades de pointes, of unknown cause. We believe that the arrhythmia resulted from severe hypokalemia secondary to this syndrome. Two of her siblings died suddenly, probably from cardio-, cerebrovascular accidents. Five her offspring needed to be evaluated for this syndrome due to its autosomal dominant inheritance. Endocrinologically there was no clue for us to seek other diseases of enzyme deficiency needed in aldosterone synthesis. Once the diagnosis of Liddle syndrome was suspecti, we treated her with amiloride 5mg/day for several days. Thereafter metabolic abnormalities including persistent hypertension, not responded to conventional parenteral potassium replacement and antihypertensive drugs, were reversed and normalized until now. We believe that in some of patients of secondary hypertension of unknown cause, Liddle syndrome should be ruled out, and that the incidence of this syndrome has been underes- timated due to lack of suspicion.
제 2형 당뇨병 환자에서 알부민뇨와 심혈관계 질환의 유병율에 대한 연구
김영아,한대석,박홍수,강신욱,하성규,이호영,최소래,윤세정,강태수,황학진,신석균,최규헌,서정건,허애정 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.5
There are opinions that microalbuminuria acts as an independent risk factor for cardiovascular diseases, related to other risk factors such as endothelial cell dysfunction, hypertension, insulin resistance, obesity, hyperlipidemia and platelet aggregation dysfunction in diabetic and non-diabetic patients. We examined the prevalence of microalbuminuria and macroalbuminuria and the relationship of microalburninuria and macroalbuminuria to coronary heart. disease in type 2 diabetic patients. Out of 798 t 2 diabetic patients who were hospitalized at Yonsei medical center from Oct. 1997 to Feb. 1999, we studied 181 patients who had normal renal function and were examined 24 hour urine albumin excretion. According to the amount of urine albumin excretion, 181 patients were categorized into three groups; normoalbuminuria(less than 30mg/24hour), microalbuminuria(30-300mg/24hour) and macroalbuminxia (more than 300mg/24hour). Patients were tested using treadmill test, stress thallium scan, echocardiography, and coronary angiography for the evaluation of coronary heart disease. The freguency of normoalburninuria, microalbuminuria, and macroalbuminuria in our patients were 50.3%(91/181), 30.9%(56/181), and 18.3%(34/181), respectively. In each group, the prevalence of hypertension were 42.5%, 78.5%, and 82.3%, respectively and the prevalence of cardiovascular disease were 24.7%, 50.0%, and 46.0%, respectively. Microalbuminuria and macroalbuminuria groups showed statistically significant differences in the prevalence of hypertension and coronary heart disease compared with normoalbuminmia group(p$lt;0.05). In addition, the prevalence of diabetic retinopathy were 37.3%, 58.9%, and 55.8%, respectively and microalbuminuria and macroalbuminuria groups showed statistically significant differences in the prevalence of diabetic retinopathy compared with normoalbuminuria group(p$lt;0.05). We conclude that microalbuminuria and macroalbuminuria is a strong predictor of coronary heart disease in patients with type 2 diabetes.
지상원,허갑범,이현철,임승길,김경래,송영득,남수연,김경욱,윤세정 대한내분비학회 1999 Endocrinology and metabolism Vol.14 No.3
Background: As GHBP is believed to be derived from proteolytic cleavage of the extracellular domain of the GH receptor and may be regarded as an intrinsic part of the GH-IGF-1 axis, an effect of body composition on circulating GHBP levels may be expected. We investigated GHBP variations in obesity with varying glucose tolerance and its relationship to body fat distribution, sex hormones, insulin secretion, and the GH-IGF-1 axis. Methods: Bioelectrical impedence for measurement of total body fat and computed tomography for visceral fat and subcutaneous fat at umbilicus level were performed in 69 obese Koreans and 21 lean Koreans. Insulin secretion in response to an oral glucose tolerance test (OGTT) and a GH stimulation test by L-dopa, growth hormone-binding protein (GHBP), insulin-like growth factor (IGF)-1 and sex hormones (estrone, estradiol, total and free testosterone) were measured. Results: Obese type 2 DM group had the highest GHBP levels and the most visceral fat amount. GHBP levels were most strongly correlated with the ratio of visceral fat area to body weight (VWR) above other parameters (r=0.725, p$lt;0.001). Insulin- and free fatty acid-area under the curve (AUC) during OGTT and IGF-1 level were also positively correlated with GHBP levels (r=0.474, p$lt;0.005; r=0.572, p$lt;0.005; r=0.453, p$lt;0.005). GH-AUC to L-dopa stimulation test was negatively correlated with GHBP levels (r=0.432, p$lt;0.005). The GHBP level was slightly higher in females than in male in the same glucose tolerance category. In males, total and free testosterone levels were negatively correlated with GHBP levels (r=-0.516, p$lt;0.001;r=-0.653, p$lt;0.001). Stepwise multiple linear regression analysis showed that VWR, FFA-and insulin-AUC significantly contributed to the variability of GHBP (r=0.58). Conclusion: We demonstrated that 1) visceral fat amount was mainly determined GHBP levels in obese subjects with varying glucose tolerance; 2) hyperglycemia per se did not influence GHBP level, whereas insulin and FFA could play a role in regulation of GHBP level. 3) The constant concentration of IGF-1 despite GH hyposecretion suggests that increased GHBP level retlect GHBP hypersensitivity in order to compensate for decreased GH secretion in obesity; 5) the lower level of GHBP in males might be explained at least in part by a suppressive effect of androgen (J Kor Soc Endocrinol 14:531-540, 1999).