No abstract available.
Humans ; Infant, Newborn*

No abstract available.
Phototherapy*

BACKGROUND: renal artery stenosis (RAS) is a major cause of renovascular hypertension and renal function due to ischemic atrophy of kidney. There are several methods to treat the RAS, including are surgery, percutaneous transluminal renal angioplasty, and medical treatment. The purpose of this study is to evaluate the usefulness, safety, and efficacy of percutaneous transluminal stent deployment in RAS. METHOD: From January 1995 to July 1996, 17 patients underwent renal stent implantation due to renal artery stenosis (11 male, 6 female). the mean age was 49 years old, one patient had both renal artery stenosis and total lesions were 18. The causes of renal artery stenosis were atherosclerosis in 12, fibromuscular dysplasia in 2, Takayasu's disease in 2, and autoimmune disease (Bechet's) in one case. Renal artery stenting was performed via femoral artery in 12 lesions and brachial artery in 6 lesions. Follow up was performed by renogram, renal angiogram, and clinical examination. RESULT: the degree of renal artery stenosis was 83% (70-95%). the lesion sites were 12 ostial and 6 non-ostial lesions. The used renal stents were Palmaz-biliary stent in 17 lesions and Micro-2 stent in one lesions. All stents were implanted successfully and there was no residual stenosis in all patients except one case showed 20% residual stenosis due to huge renal artery size. The transstenotic pressure gradients after renal artery stenting was decreased markedly from 74mmHg to 2mmHg. There no serious complications such as a death, emergency surgery, or nephrectomy. There were two minor complications which were one case of pyelonephritis and one case of inguinal hematoma. After stenting, blood pressure was decreased partially in 13 patients and completely in 2 cases. CONCLUSION: Renal artery stenting appears to be safe and feasible and the alternative treatment modality to surgery for renal artery stenosis.
Angioplasty ; Atherosclerosis ; Atrophy ; Autoimmune Diseases ; Blood Pressure ; Brachial Artery ; Constriction, Pathologic ; Emergencies ; Femoral Artery ; Fibromuscular Dysplasia ; Follow-Up Studies ; Hematoma ; Humans ; Hypertension, Renovascular ; Kidney ; Male ; Middle Aged ; Nephrectomy ; Pyelonephritis ; Renal Artery Obstruction* ; Renal Artery* ; Stents*

No abstract available.
Drainage* ; Lung Abscess* ; Lung* ; Pneumothorax* ; Suppuration*

BACKGROUND: Plaque compression (and/or redistribution) and vessel expansion are important mechanisms of percutaneous coroanry balloon angioplasty. We investigated the mechanisms of balloon angioplasty according to plaque characteristics by intravascular ultrasound and assessed the time-sequencing morphometric changes of target vessel after balloon dilation without catheter change using intravascular ultrasound balloon catheter. METHOD: We studied balloon angioplasty in 10 patients (eight male, average age of 55.3 years). Quantitative coronary angiography and intravascular ultrasound images were attained at baseline and at timed intervals of 0sec, 60sec and 180sec post-balloon angioplasty. The following categories were attained : reference diameter, minimal lumen diameter, cross sectional area (CSA) of lumen (L), external elastic membrane (EEM), and plaque + media (P+M). We also assessed the plaque morphology of target lesion and classified them into two groups according to intravascular ultrasound imaging : a soft plaque group versus a group characterized by fibrous and/or mildly calcified plaque. RESULTS: The proportions of plaque compression in the total luminal gain were 80% in the soft plaque group and 70% in the other ; the absolute amount of plaque compression was 26.9% in soft plaque and 24.0% in the other group. The time sequencing changes of target lesion EEM CSA of both group were 14.4+/-2.9mm2, 14.3+/-3.8mm2 (baseline) 15.1+/-2.5mm2, 15.4+/-3.7mm2 (immediate) 15.0+/-2.8mm2, 14.5+/-3.9mm2 (180sec), those of P+M CSA (target lesion) were 10.4+/-3.3mm2, 10.7+/-2.4mm2 (baseline) 7.6+/-2.7mm2, 8.1+/-2.4mm2 (immediate) 7.9+/-2.9mm2, 8.5+/-3.4mm2 (180sec). Target lesion lumen CSA were 4.0+/-1.1mm2, 3.6+/-2.0mm2 (baseline) 7.5+/-1.1mm2, 7.3+/-3.2mm2 (immediate) 7.1+/-1.3mm2, 6.0+/-1.7mm2 (180sec) respectively. CONCLUSION: Plaque compression (and/or redistribution) is the predominant mechanism of luminal gain in both groups. The absolute amounts of P+M CSA changes and time sequencing increment of target lesion were similar in both groups. In the non-soft group, the immediate increment and time sequencing reduction of EEM CSA in target lesion were greater than those of the soft plaque group.
Angioplasty ; Angioplasty, Balloon ; Angioplasty, Balloon, Coronary* ; Catheters ; Coronary Angiography ; Humans ; Male ; Membranes ; Phenobarbital ; Ultrasonography

No abstract available.
Pyrazoles ; Sulfonamides ; Celecoxib

We evaluate the effects of diltiazem in 19 patients with ischemic heart disease (15 patients) of classical anginal pectoris & 4 patients of variant angina) by means of clinical status & electrocardiographic changes and obtain the results as follows: 1. The pulse rate & blood pressure were decreased by diltiazem slightly but these decreases were not significant in statistical meaning. 2. Diltiazem administration of 4 weeks duration normalized EKG completely in 4 patients & partially in 3 patients among the 13 patients who showed abnormal resting EKG initially. 3. All 19 patients who received diltiazem showed clinical improvement; 9 patients had excellent responses, 7 patients good responses & 3 patients fair responses. 4. Diltiazem had side effects in 3 patients, drowsiness, mild euphoria & possibly tolerance respectively in each patients.
Angina Pectoris* ; Blood Pressure ; Diltiazem ; Electrocardiography ; Euphoria ; Heart Rate ; Humans ; Myocardial Ischemia ; Sleep Stages

No abstract available.
Coronary Artery Disease* ; Coronary Vessels* ; Fibrinogen* ; Plasma*

No abstract available.
Coronary Artery Disease* ; Coronary Vessels* ; Fibrinogen* ; Plasma*

BACKGROUND: There are many reports about the correlation between cardiovascular disorders and estrogen deficiency in postmenopausal women. The purpose of current study is to know that postmenopausal estrogen therapy may affect the lipid metabolism and endogenous fibrinolytic system and exercise tolerance. METHOD: We investigated the relation of estrogen treatment (srogen 0.625 mg/day) to serum lipid levels, angiotensin converting enzyme activity, plasminogen activator inhibitor-1 and parameters of treadmill test in 22 postmenopausal women of normal coronary artery with abnormal exercise test complained with chest pain accompanied by postmenopausal symptoms. RESULTS: Estrogen treatment significantly elevated the serum HDL-cholesterol level (42.8 to 50.1 mg/dl, p<0.05) and reduced the PAI-1 level (16.2 to 10.4 ng/dl, p<0.01) without considerable side effects. During the exercise test, the positivity appearance time and total exercise duration is significantly increased after estrogen treatment. CONCLUSION: The postmenopausal use of estrogen favorably changed the lipid level, fibrinolytic system and might improve the microcirculation which may protect against the ischemic heart disease risk without significant side effects.
Chest Pain ; Coronary Vessels ; Estrogens* ; Exercise Test ; Exercise Tolerance ; Female ; Humans ; Lipid Metabolism ; Microcirculation ; Myocardial Ischemia ; Peptidyl-Dipeptidase A ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Postmenopause