No abstract available.
Sarcoma, Synovial*

No abstract available.
Mitral Valve*

No abstract available.
Chylothorax*

BACKGROUND: Handgrip and cold pressor test may increase the afterload of the heart. And in left ventricular hypertrophy, it is known that mitral flow pattern is affected by decreased left ventricular compliance. We investigated the effects of handgrip and cold pressor test on mitral flow pattern in patients with left ventricular hypertrophy. METHODS: Handgrip and cold pressor test were performed in 12 subjects with left ventricular hypertrophy and in 14 healthy normal subjects. In supine position, blood pressure, heart rate and Doppler echocardiographic parameters(early peak flow velocity : E, atrial peak flow velocity : A) were obtained at rest, 1 and 3 minutes after the onset of tests respectively. RESULTS: In both groups, handgrip and cold pressor test increased blood pressure slightly without a statistical significance. In left ventricular hypertrophy group, there were significant increments in heart rates at 1 minute of handgrip (78+/-12min-1, p<0.001) and cold pressor test(77+/-7min-1, p<0.05) as compared to that at rest (73+/-12min-1). Mitral flow velocities did not show significant change after the tests in control group. A waves after 1 minute of handgrip(85.2+/-18.4cm/sec, p<0.05) and cold pressor test (87.3+/-17.8cm/sec, p<0.001) showed significant increases as compared to that at rest (79.1+/-14.9cm/sec) in left ventricular hypertrophy group whereas E waves did not. CONCLUSION: Although handgrip and cold pressor tests did not affect the mitral flow significantly in control group, each test raised A waves in left ventricular hypertrophy group. These results suggest that increased A waves may be due to a rise in afterload and decreased left ventricular compliance caused by handgrip and cold pressor test in left ventricular hypertrophy group.
Blood Pressure ; Compliance ; Echocardiography ; Heart ; Heart Rate ; Humans ; Hypertrophy, Left Ventricular* ; Supine Position

BACKGROUND: Tuberculous pleurisy is the leading cause of pleural effusion in Korea. And differential diagnosis of tuberculous pleurisy with other cause is clinically very important. Traditional diagnostic methods such as routine analysis of pleural fluid, staining for acid-fast bacilli or pleural biopsy have major inherent limitaion. This study was designed to evaluate the significance of pleural fluid polymerase chain reaction (PCR) and adenosine deaminase (ADA) activity in early diagnosis of tuberculous pleurisy. MATERIAL AND METHOD: Between March 1996 and July 1997, 198 patients with pleural effusion reviewed retrospectively. The study group included 112 cases with tuberculous effusion and 86 cases with non-tuberculous effusions, whose diagnoses were confirmed by pleural biopsy, microbiological methods, or cytology. We compared the results of PCR and pleural fluid levels of ADA between tuberculous and non-tuberculous effusions. Mean age was 47.54+/-19.52 years (range 2 to 85 years). The positive rate of PCR was significantly higher in tuberculous group than non-tuberculous group (p<0.05). The sensitivty, specificity, positive predictive value (PPV), and negative predictive value (NPV) for PCR were 31.7, 90.9, 83.0, and 48.8%, respectively. Mean ADA activity was significantly higher in tuberculous group than non-tuberculous group (83.2 U/L vs 49.8 U/L) (p<0.05). With diagnostic thresholds of 40 U/L, the sensitivity, specificity, PPV, and NPV of ADA for tuberculosis were 75.9, 70.9, 77.3, and 69.3% respectively. At a level of 70 U/L, the sensitivity, specificity, PPV, and NPV of ADA for tuberculosis were 70.1, 75.9, 82.9, and 60.3% respectively. CONCLUSION: PCR is very highly specific, but less sensitive methods in diagnosis of tuberculous pleurisy. But ADA level of pleural fluid has acceptable sensitivity and specificity in diagnosis of tuberculous pleurisy. ADA activity is more useful test in the evaluation of pleural effusions.
Adenosine Deaminase ; Biopsy ; Diagnosis* ; Diagnosis, Differential ; Early Diagnosis ; Humans ; Korea ; Pleural Effusion ; Polymerase Chain Reaction* ; Retrospective Studies ; Sensitivity and Specificity ; Tuberculosis ; Tuberculosis, Pleural*

No abstract available.
Coronary Artery Bypass* ; Coronary Vessels*

No abstract available.
Lymphocyte Subsets* ; Lymphocytes*

No abstract available.
Arteriovenous Fistula*

BACKGROUND: Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of 25 degrees C moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. MATERIAL AND METHOD: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups. All hearts were perfused at 37 degrees C for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained. Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37 degrees C, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4 degrees C) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at 25 degrees C, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minutes (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37 degrees C normothermic ischemia and 30 minutes of reperfusion (n=6). Group 4 served as ischemic controls for group 3 (group 3, 4: warm ischemia group). RESULT: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, improving the LVSP, LVEDP, RPP, and LVdp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). CONCLUSION: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.
Animals ; Blood Pressure ; Cardiac Surgical Procedures ; Heart Arrest, Induced* ; Heart* ; Hemodynamics ; Ischemia ; Ischemic Preconditioning* ; Myocardial Ischemia ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Warm Ischemia

No abstract available.
Carcinosarcoma* ; Lung*