Bicuspid aortic valve is the most common form of congenital valvular disease, and its presence may predispose the patients to development of true aortic or dissecting aortic aneurysms. An intrinsic aortic weakness may underlie a bicuspid aortic valve, aortic aneurysm or aortic dissection. We experienced a case of an ascending aortic aneurysm associated with a functionally normal bicuspid aortic valve. A screening echocardiograph was performed due to atypical chest pain, which detected a large ascending aortic aneurysm and a bicuspid aortic valve. The patient underwent an operation for an ascending aortic aneurysm and, is living one year later, and is asymptomatic. To the best of our knowledge, this may be the first case of an ascending aortic aneurysm associated with a bicuspid aortic valve in Korea.
Aortic Aneurysm* ; Aortic Valve* ; Bicuspid* ; Chest Pain ; Humans ; Korea ; Mass Screening

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*

The clinical significance of myocardial bridges (MBs) is variable, and most patients are asymptomatic. However, angina, myocardial infarction and sudden death, associated with MBs, have been reported. Intracoronary stents offer a novel, and potentially definitive, treatment for myocardial ischemia associated with clinically significant MBs. We describe the use of intracoronary stenting for primary angioplasty in a patient with an anterior myocardial infarction associated with MBs.
Angioplasty ; Death, Sudden ; Humans ; Myocardial Infarction* ; Myocardial Ischemia ; Stents*

BACKGROUND AND OBJECTIVES: Radiofrequency (RF) catheter ablation of the pulmonary vein (PV) can treat drug refractory focal atrial fibrillation (AF). However, high RF energy (RFE) can cause severe PV damage, and the lower limits of effective RFE in PV have not yet been elucidated. This study attempts to evaluate the changes of PV structure after various modes of RFE delivery. MATERIALS AND METHODS: Right heart and transseptal catheterization were performed in 5 anesthetized mongrel dogs. RFE was delivered at the right superior pulmonary vein (RSPV) with 50 watts and 70degreesC and at the left superior pulmonary vein (LSPV) with 20 watts and 50degreesC. After the procedures, the endocardiums of the left atrium and both superior PVs were examined. RESULTS: Total applied RFE in both PVs was 14.2+/-.2 vs. 13.5+/-.6 watts, 46.6+/-.1 vs. 64.5+/-.2degreesC (p<0.05), in LSPV vs. RSPV, respectively. Follow up pulmonary venograms showed that total occlusions of PV branches and severe stenosis of proximal PV (>70% luminal narrowing) developed in 4 dogs with high RFE. Mild stenosis (<50% luminal narrowing) of PV developed in 1 dog with low RFE. Histological examination of the 5 dogs revealed coagulation necrosis over the whole PV layer, including the adventitia and some portion of the myocardial sleeve, and severe hemorrhage and destruction of PVs from high energy treatment, in contrast to intimal damage and swelling of subintimal PV layers in low energy treatment. CONCLUSION: High RF current may result in severe damage of pulmonary veins and sub-structures whereas low RF current may cause suboptimal pulmonary vein damage such as intimal only damage.
Adventitia ; Animals ; Atrial Fibrillation ; Catheter Ablation ; Catheterization ; Catheters ; Constriction, Pathologic ; Dogs ; Endocardium ; Follow-Up Studies ; Heart ; Heart Atria ; Hemorrhage ; Necrosis ; Phenobarbital ; Pulmonary Veins*

BACKGROUND AND OBJECTIVES: The diagnostic and prognostic importance of exaggerated blood pressure response to exercise is controversial. Endothelial dysfunction has been demonstrated in patients with atherosclerosis and risk factors for coronary artery disease, but there is a lack of information in patients with exercise hypertension. Thus, we designed this study to evaluate the endothelial function in patients with exaggerated blood pressure response during exercise. SUBJECTS AND METHODS: Exercise hypertension is defined as a systolic blood pressure >or= 210 mmHg in men, and >or=190 mmHg in female, during Treadmill tests. Using a high resolution ultrasound technique, the endothelial function of the brachial artery, in patients with exercise hypertension (n=25), and control subjects (n=25), were investigated. RESULTS: Endothelial-dependent vasodilation were impaired in patients with exercise hypertension (7.77+/-5.14 vs. 2.81+/-2.29%, p<0.05). On univariate analysis, the extent of vasodilation was significantly correlated with age (r=0.43, p<0.05) and systolic blood pressure (r=0.39, p<0.05). CONCLUSION: We conclude that patients with exercise hypertension have impaired endothelium-dependent vasodilation. Exercise hypertension is a finding, which may, by itself, raise concern when interpreted as an exercise test. This study also supports the concept that endothelial dysfunction may play a role in exercise hypertension.
Atherosclerosis ; Blood Pressure* ; Brachial Artery ; Coronary Artery Disease ; Endothelium ; Exercise Test* ; Female ; Humans ; Hypertension ; Male ; Risk Factors ; Ultrasonography ; Vasodilation

BACKGROUND AND OBJECTIVES: Peripartum cardiomyopathy (PPCM) is a rare form of heart failure affecting women between the last month of pregnancy and the first five months after delivery. The etiology and prognostic factors of PPCM remains poorly understood, although some risk factors have been described. SUBJECTS AND METHODS: In order to characterize the features of PPCM, clinical and echocardiographic data, obtained from 19 patients who fulfilled diagnostic criteria of PPCM, from January 1996 to march 2001, were retrospectively analyzed. We divided the sample into 2 groups, which were classified according to clinical and echocardiographic improvements. (Group I; patients who improved, Group II; patients who did not improved, or deteriorated). RESULTS: Patients with PPCM (n=19, age: 32+/-5 yrs, NYHA Class: II-IV, LVEF: 34.1+/-8.8%, follow-up period: 14.2+/-16.3 months) had a high frequencies of the following clinical factors: Anaemia (16/19, 84.2%); Pre-eclampsia (11/19, 57.9%); Multiparity (11/19, 57.9%); aged over 30 yrs old at delivery (11/19, 57.9%). During follow up, 10 patients improved to NYHA Class I, 8 patients failed to improve, or deteriorated, and 1 patient died due to ventricular fibrillation. Group II (n=9, age: 31+/-3 yrs, follow up LVEF: 38.8+/-12.9%), as compared to Group I (n=10, age: 33+/-6 yrs, follow up LVEF: 56.4+/-6.4%), had greater left ventricular end-systolic dimension (LVESD, 53.0+/-7.7 mm vs 45.9+/-4.8 mm; p<0.05). CONCLUSION: PPCM has a high rate of progression to dilated cardiomyopathy. Therefore, in pregnant women with common clinical findings of PPCM, including anemia, pre-eclampsia, multiparity and old age at delivery, the initial echocardiographic assessment for cardiac function is essential, and serial follow-up is required.
Anemia ; Cardiomyopathies* ; Cardiomyopathy, Dilated ; Echocardiography ; Female ; Follow-Up Studies ; Heart Failure ; Humans ; Parity ; Peripartum Period* ; Pre-Eclampsia ; Pregnancy ; Pregnant Women ; Retrospective Studies ; Risk Factors ; Ventricular Fibrillation

BACKGROUND AND OBJECTIVES: Cardiac troponin T (cTnT) has been used as a very sensitive marker of cardiac injury caused by ischaemia, myocarditis, and cardiomyopathy. After cardiac injury, the fetal cTnT isoform expression in the heart and serum cTnT increases. To investigate the increased levels of serum cTnT, and the expression of fetal cTnT isoform in the heart, that can predict myocardial injury, we measured serum cTnT levels and the fetal cTnT isoform expression at various time points during the early phase of myocardial toxicity induced by adriamycin (ADR) in rat. MATERIALS AND METHODS: Male Sprague-Dawley rats were injected, intraperitoneally, with ADR (5 mg/kg) twice a week for 2 weeks. Control rats were injected with saline. Serum cTnT levels were measured by ELISA. The ratio of fetal/adult (F/A) cTnT isoform expression (%) was semi-quantified by RT-PCR using total RNA from frozen hearts. RESULTS: Serum cTnT levels did not increase by 1 week after ADR injection, but increased significantly after 2 weeks. The ratio of F/A cTnT in the heart significantly increased from day 1, peaked at 1 week and persisted until the end of 2 week. CONCLUSION: The expression of the fetal cTnT isoform occurred from 1 day after ADR injection when the serum cTnT levels were still normal. Although the serum cTnT level is a very sensitive, and an early marker, of cardiac damages, the fetal cTnT isoform expression in the endomyocardial biopsy specimen may be a more sensitive and an earlier marker in the ADR-induced myocardial damage.
Animals ; Biopsy ; Cardiomyopathies ; Cardiomyopathy, Dilated ; Doxorubicin ; Enzyme-Linked Immunosorbent Assay ; Heart ; Humans ; Male ; Myocarditis ; Rats* ; Rats, Sprague-Dawley ; RNA ; Troponin T* ; Troponin*

BACKGROUND AND OBJECTIVES: Vascular brachytherpy known to be an effective method in the prevention of restenosis following percutaneous coronary intervention (PCI). In this study we observed the effects of a radioisotope-loaded stent in a porcine model. MATERIALS AND METHODS: Holmium-166 ((166)Ho) was loaded onto the stent surface using impregnated polyurethane, and placed the stents into 7 porcine coronary arteries. Four weeks after stent overdilation injury, histopathological examination was performed. RESULTS: The absorbed dose of (166)Ho to the coronary artery, from the 158.5+/-140.9 microCi (166)Ho stent, was about 141 Gy at a depth of 0.5 mm, which was calculated by Monte Carlo EGS 4 Code. The mean external, and internal elastic lamina areas, the luminal and neointimal areas and the histopathological area stenosis in the 7 porcine coronary arteries were 7.6+/-2.8 mm2, 4.7+/-1.6 mm2, 2.4+/-1.4 mm2, 2.3+/-1.6 mm2 and 49.4+/-24.9%, respectively. The histopathological findings revealed remarkable inflammatory reactions and thrombosis in two of the porcine coronary arteries. CONCLUSION: (166)Ho radioactive loaded stents, using impregnated polyurethane, may inhibit neointimal hyperplasia, but the problems of stent thrombosis and inflammation should be solved.
Constriction, Pathologic ; Coronary Restenosis ; Coronary Vessels ; Hyperplasia ; Inflammation ; Percutaneous Coronary Intervention ; Phenobarbital ; Polyurethanes ; Radioisotopes ; Stents* ; Thrombosis

BACKGROUND AND OBJECTIVES: Recently many studies have confirmed positive identification of patients with posterior infarction through ST segment elevation in the electrocardiogram of posterior chest leads V7 through V9. However, the ECG patterns from posterior chest leads in normal adults have not been investigated, so this study was designed to examine such patterns. SUBJECTS AND METHODS: We studied 100 patients with normal conventional 12-lead ECG, normal physical examination and without any history of cardiovascular disease. Leads V7, V8 and V9 were recorded immediately after routine 12-lead ECG at the same horizontal level as that of V6 on the posterior axillary line (lead V7), the posterior scapular line (lead V8), and the left border of the spine (ead V9). RESULTS: The upright P waves in leads V7, V8 and V9 were 99%, 99% and 95% upright, respectively, while the other P waves were isoelectric and none were inverted. The T waves were all upright in leads V7 and V8, while in lead V9, 98% were upright, 2% were isoelectric and none were inverted. None of the subjects had a Q wave duration greater than 0.04 second in any of the 3 leads. At 0.08 second after the J point, only 2 subjects (2%) showed 0.5 to 1.0 mm ST segment elevation, but ST segment elevation was not greater than 1.0 mm in any of the subjects. CONCLUSION: P wave and T wave inversion were absent in all 3 leads. Q wave duration of greater than 0.04 second was also absent in all 3 leads. ST segment elevation was not greater than 1.0 mm in any of the subjects.
Adult* ; Cardiovascular Diseases ; Electrocardiography* ; Humans ; Infarction ; Physical Examination ; Spine ; Thorax*

BACKGROUND AND OBJECTIVES: Myocardial ruptures, including: ventricular free wall rupture (VFWR) and ventricular septal rupture (VSR), after acute myocardial infarction (AMI), are fatal complications. Recently, ubiquitous use of echocardiographs, and other imaging techniques, allows us to diagnose these complications in the antemortem period. Thus, this study retrospectively evaluated the clinical characteristics of patients with myocardial ruptures following AMI. SUBJECTS AND METHODS: 620 patients that had had AMIs, between January 1999 and June 2001, were analysed for the purpose of this study. Myocardial ruptures were diagnosed from their clinical symptoms, echocardiographs, and pericardiocenteses or cardiac catheterizations. The clinical characteristics of the patients with myocardial ruptures (n=15) were compared to those patients with myocardial infarction, without rupture (n=397), from their Q waves. RESULTS: The patients with myocardial ruptures were older than those without (67+/-9.7 years vs 60+/-11.7 years, p<0.05), and ruptures were more frequent in women (66.7% vs 25.2%, p<0.001). The frequency of systemic hypertension, DM, and the distribution of infarction sites were similar in both groups. Also, clinical characteristics between patients with VFWR, and those with VSR, were similar. Of the patients with VFWR (n=8), 7 suddenly died, and 1 was alive directly following surgery. Of the patients with VSR (n=7), 4 died. CONCLUSION: Myocardial rupture is a fatal complication of AMI, which is more frequent in women, and the patients with ruptures, in our study, were older than those without.
Cardiac Catheterization ; Cardiac Catheters ; Female ; Heart Rupture ; Humans ; Hypertension ; Infarction ; Myocardial Infarction* ; Pericardiocentesis ; Retrospective Studies ; Rupture* ; Ventricular Septal Rupture