A variety of clinical conditions are known to result in a giant T wave and a marked QT prolongation. We report a case of a giant T wave and a QT prolongation after the resolution of an acute cardiogenic but nonischemic pulmonary edema.
Heart Failure ; Pulmonary Edema*

BACKGROUND: In patients with myocardial infarction (MI) and chronic stable angina, the coronary flow reserve (CFR) is reduced not only in the region of myocardium perfused by the ischemia-related artery but also in the regions supplied by angiographically normal coronary arteries. The effect of myocardial stunning on the remote CFR is unknown, however. METHODS: In ten open-chest anesthetized dogs, left circumflex coronary artery was occluded for 15 minutes (myocardial stunning group, n=5) or for 30 minutes (MI group, n=5) and was followed by a reperfusion for 60 minutes. Before coronary occlusion and at 30 minutes and at 60 minutes after reperfusion, resting coronary blood flow (CBF) and maximal CBF after IV injection of each of adenosine (ADE) and acetylcholine (Ach) was measured with electromagnetic flow probe located in the proximal left anterior descending coronary artery. CFR was calculated as the ratio of maximal and resting CBF. RESULTS: At 30 minutes and 60 minutes after reperfusion, the remote resting CBF were significantly increased in both groups and the remote CFR was significantly decreased in both groups. The CFR of the MI group was lower than myocardial stunning group. The coronary vasodilator response to Ach was significantly lower than the response to ADE in both groups. CONCLUSION: After MI and myocardial stunning, there was severe coronary vasodilator abnormality in the remote myocardium and that was more marked after MI. The coronary vasodilator response to Ach was significantly lower than the response to ADE in both groups, suggesting endothelial dysfunction in remote myocardium.
Acetylcholine ; Adenosine ; Angina, Stable ; Animals ; Arteries ; Coronary Occlusion ; Coronary Vessels ; Dogs ; Humans ; Magnets ; Myocardial Infarction ; Myocardial Stunning* ; Myocardium ; Reperfusion

No abstract available.
Choriocarcinoma* ; Female ; Lung Neoplasms* ; Lung* ; Pregnancy

No abstract available.
Foreign Bodies* ; Pulmonary Artery*

Background and Objectives: The objective of this study was to estimate the supply and demand for cardiologists in Korea and provide evidence for healthcare policy to ensure a stable and adequate workforce for optimal cardiovascular disease management. Methods: Past trends of inflow and outflow of cardiologists were used to make crude projections, which were then adjusted based on demands of services to obtain final projections. Inflow of cardiologists was estimated using second-order polynomial regression and demand for cardiology care was estimated using linear regression. Results: There were 1,139 active cardiologists who were under the age of 65 in clinical practice in Korea. The estimated number of cardiologists from 2022 to 2040 showed that the number of cardiologists would peak at 1,344 in 2032 and gradually decrease thereafter. We also estimated an increase of 947,811 cases of heart-related procedures annually from 2023 to 2032. The number of heart-related procedures per cardiologist would increase 1.4 times from 12,964 in 2023 to 17,862 in 2032. The estimated number of emergency patients per cardiologist under 50 years old would almost double from 544 in 2022 to 987 in 2032. Conclusions We expect significant shortage of cardiologists in Korea within the next 10 years. The number of emergency patients per cardiologist will increase by nearly 50%, leading to high individual workload for cardiologists. To prevent this imbalance between supply and demand, an organized and collective approach by the specialty of cardiology is imperative to produce a balanced workforce.

One of the authors' names was misprinted.

The Noonan syndrome is a rate clinical syndrome associated with similar congenital abnormalities, that is characteristics of Turner syndrome, such as short stature, webbed neck, low posterior hairline, cubitus valgus, shield chest or funnel chest, congenital features similar to Turner syndrome but with a normal karyotype, and Opitz et al. proposed the name "Noonan syndrome" for this condition in 1965. We experienced a 31-year old man with Noonan syndrome combined with valvular and infundibular pulmonic stenosis who had short stature, webbed neck and normal karyotype. So we report a case Noonan syndrome with a review of literature.
Adult ; Congenital Abnormalities ; Funnel Chest ; Humans ; Karyotype ; Neck ; Noonan Syndrome* ; Pulmonary Valve Stenosis* ; Thorax ; Turner Syndrome

No abstract available.
Cardiomyopathy, Hypertrophic

Eosinophilic gastroenteritis is a rare disorder of the stomach, small intestine and colon, characterized by variable eosinophilic infiltration of the bowel wall and peripheral blood eosinophilia, abnormal gastrointestinal symptoms and signs. The pathogenesis of this disease still remains unknown, but several studies support allergic or immunologic etiology. Considerable variability in clinical presentation depends on the site of the gastrointestinal tract and the depth of bowel wall involvement. Herein we experienced a case of eosinophilic gastroenteritis confined to small intestine presenting progressive weight loss, abdominal pain and diarrhea. Enteroscopic findings showed diffuse multiple nodularity of mucosal folds in small bowel, especially duodenum and proximal jejunum. Jejunal and duodenal biopsy specimen demonstrated marked eosinophilic infiltration. These symptoms and signs were improved within 3 weeks after short course of prednisone therapy.
Abdominal Pain ; Biopsy ; Colon ; Diarrhea ; Duodenum ; Enteritis* ; Eosinophilia ; Eosinophils* ; Gastroenteritis ; Gastrointestinal Tract ; Intestine, Small ; Jejunum ; Prednisone ; Stomach ; Weight Loss

Antithrombin III deficiency is an autosomal dominant disorder, which is manifested by recurrent venous thromboembolisms, such as: deep vein thrombosis and/or pulmonary embolism, but arterial embolisms are very rare. We report a case of a patient with hereditary antithrombin III deficiency, manifested by myocardial infarction and deep vein thrombosis.
Antithrombin III Deficiency* ; Antithrombin III* ; Embolism ; Humans ; Myocardial Infarction* ; Pulmonary Embolism ; Thromboembolism ; Venous Thrombosis*