BACKGROUND AND OBJECTIVES: Percutaneuous transvenous mitral commissurotomy(PTMC) has been performed as an effective non-surgical treatment modality of rheumatic mitral stenosis. Mitral regurgitation(MR) as a complication of the procedure occur in 20-53% of the patients. The moderate to severe mitral reguargitation, created by the PTMC, sometimes leads to the requirement for mitral valve replacement, but most of the MR limits the optimal dilation of mitral commissure due to the worry about the progression of the MR. This study was designed to evaluate the occurrence of mitral regurgitation and predictive factors for the moderate to severe mitral regurgitation(grade> or =2) induced by PTMC. METHODS: This study enrolled 46 patients(female 42, mean age 45 years) who have performed PTMC in Yeungnam University Hospital from May 1996 to May 1999. We analyzed the occurrence rate of mitral regurgitation(MR) and predictive factors for MR grade> or =2 after procedure. RESULTS: MR was detected in 35% of the patients prior PTMC, and in 56% after the procedure(grade 1, 30%; grade 2, 15%; grade 3, 11%). 21 cases of the MR was commissure MR as a grade< or =2. MR grade 3, occured in 5 patients, was non-commissure MR caused by the unilateral rupture of the lateral commissure in 4 patients and tearing of the annulus in one patient. On the univariate analysis, patients with MR grade> or =2 showed more frequent atrial fibrillation, mitral regurgitation and fluoroscopic calcification, and had more severe symptoms than patients with MR grade<2 before the procedure. On the analysis of the calcification, there was no significant difference of the leaflet calcification score, but the commissure calcification score was significantly higher in MR> or =2 group than MR<2 group(1.5+/-0.54 vs 2.5+/-0.96, p=.02). On the multivariate logistic regression analysis, independent predictor of MR grade> or =2 was fluoroscopic mitral calcification(OR 6.38, p=.048). CONCLUSION: Mild to moderate commissure MR was observed in most of the patients after PTMC. Commissure calcification have more influence on the development of MR grade> or =2 than valvular calcification, and the fluoroscopic mitral calcification can predict the occurrence of MR grade> or =2 mitral regurgitation after PTMC.
Atrial Fibrillation ; Humans ; Logistic Models ; Mitral Valve ; Mitral Valve Insufficiency* ; Mitral Valve Stenosis ; Rupture

The 8 cases of left ventricular thrombus detected by the 2 D echocardiography or left ventriculography, after acute transmural anterior myocardial infarction were effectively lysed by the thrombolytic agents and heparin therapy. The thrombolytic agents were either urokinase or tissue plasminogen activator. Urokinase was infused intravenously at a dose of 1.0 million unit for three days. And tissue plasminogen activator was infused at a dose of 100mg for a day. In all cases, the thrombi were completely lysed. At follow up, no recurrence of left ventricular thrombus was found. We have experienced 2 cases of peripheral embolization in which, left ventricular thrombi were protruding nonmobile type. The one was the embolic cerebral infarction, the other was transient hoarseness and paresthesia on the left foot, which may be transient ischemic attack. These results show that left ventricular thrombi can be treated by intravenous thrombolytic agents without life-threatening complication. However, for the better establishment of the risk and benefit of therapy further investigation is needed.
Cerebral Infarction ; Echocardiography ; Fibrinolytic Agents ; Follow-Up Studies ; Foot ; Heparin ; Hoarseness ; Ischemic Attack, Transient ; Myocardial Infarction* ; Paresthesia ; Recurrence ; Thrombolytic Therapy* ; Thrombosis* ; Tissue Plasminogen Activator ; Urokinase-Type Plasminogen Activator

BACKGROUND: It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Recent laboratory data indicate that the adenosine during the ischemic period may trigger protection via A1 or A3 adenosine receptor and also protein kinase C(PKC) plays a central role. This study was designed to determine the role of adenosine receptor subtypes and PKC in the preconditioning protection. METHODS: All cat heart groups were subjected to 40min ischemia and 30min reperfusion. The preconditioning protocol consists of 4min ischemia and then 10min of reperfusion 4 times. The effects of ischemic preconditioning, nonselective adenosine receptor blocker(SPT), an A1 specific antagonist(DPCPX) and protein kinase C inhibitor(Polymyxin B), on ischemic preconditioning were determined by infarction size. There were 5 groups : (1) control group (Group 1, n=10)(2) Ischemic preconditioned group(Group 2, n=9)(3) DPCPX pretreatment group(Group 3, n=6)(4) SPT preteatment group(Group 3, n=6)(5) Polymyxin B pretreatment group(Group 5, n=6). SPT and DPCPX were given intravenously 5 min before ischemic preconditioning. Polymyxin B was administered to cats for 30min during ischemic preconditioning period. RESULTS: Ischemic preconditioning only or pretreatment with DPCPX prior to preconditioning demonstrated a significant reduction in infarct size(22.6+/-1.5, 25.4+/-0.9% infarction of the risk zone, respectively, p<0.05) with respect to control, SPT-pretreatment, and polymyxin B-pretreatment groups(44.0+/-1.7, 43.0+/-2.0 and 40.3+/-0.4% infarction of the risk zone, respectively). CONCLUSIONS: Ischemic preconditioning protects heart from subsequent ischemia. Protection was blocked by SPT and protein kinase C inhibitor(polymyxin B), but not by A1 antagonist DPCPX. The cardioprotective effects by ischemic preconditioning in the in vivo cat heart appear to be dependent on A3 adenosine receptors and activation of protein kinase C.
Adenosine* ; Animals ; Arrhythmias, Cardiac ; Cats* ; Heart* ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Polymyxin B ; Polymyxins ; Protein Kinase C* ; Protein Kinases* ; Receptors, Purinergic P1* ; Reperfusion

PURPOSE: The aim of this study was to review the outcome of local control after the local excision for T1/T2 rectal cancers and, thus, to assess its effectiveness as an alternative to a more radical resection. METHODS: This retrospective study analyzed 23 patients with T1/T2 rectal cancer treated by local excision (LE), and their results were compared with the results for 22 patients with rectal cancer of the same stage treated by a radical resection (RR). All patients with pT2 lesions in the LE group received postoperative adjuvant chemoradiation. The outcomes were defined as 5-year local-recurrence-free survival (LRFS). The median follow-up was 72 (range, 40~92) months. RESULTS: Recurrence occurred in 4 patients (pT1, 1; pT2, 3) in the LE group and in 3 patients (all pT2) in the the RR group. One patient with vascular invasion (T2N1M0) in the RR group showed multiple liver metastases at 23 months postoperatively. The difference in 5-year LRFS was not statistically significant between the two groups. In the LE group, the 5-year LRFS for pT2 lesions was significantly less favorable than that for pT1 lesions (40% vs. 94%; P= 0.005). The 5-year LRFS for pT2 in the RR group was more favorable than that in the LE group, although the difference was not statistically significant (76.9% vs. 40%, P=0.138). CONSLUSIONS: Local excision provides a favorable local control for pT1 rectal cancers. A more radical resection, however, remains an effective surgical option for pT2 lesions because local excision, even combined with adjuvant chemoradiation, showed substantial local recurrences.
Follow-Up Studies ; Humans ; Liver ; Neoplasm Metastasis ; Rectal Neoplasms* ; Recurrence ; Retrospective Studies

BACKGROUND: It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Two phases of the effect of preconditioning has been explored, early protection and second window of protection at 24 hours. The late protection was seen in some animal model, but the precise mechanism is controversal. This study was designed to evaluate the late cardioprotective effect and role of HSP70 in ischemic preconditioning of cat heart. METHODS: Two groups of cats were studied. Control animals were subjected to an episode of 40-min coronary artery occlusion followed by 30-min reperfusion. Experimental animals were subjected to ischemic preconditioning before the 40-min ishcemia/reperfusion. The preconditioning protocol was comprised of three 5-min episodes of ischemia interspersed by 10-min episodes of reperfusion. After sustained ischemia and reperfusion, left ventricular risk area and infart area were measured by injection of Evans blue bye and triphenyltetrazolium staining, and myocardial HSP70 mRNA was examined in risk(left ventricular anterior wall) and nonrisk(left ventricular posterior wall) area using northern blot hybridization. HSP70 mRNA expression was quantified as a percent of GAPDH. The late cardioprotective effects of ischemic preconditioning were determined by infarct size (% area at risk). RESULTS: Infarct size was markedly limited by ischemic preconditioning when compared with the control group (18.5+/-6.9% vs 38.5+/-11.1%; p<0.001). HSP70 mRNA expression in risk area was much higher in preconditioning group than control group(78+/-12% vs 41+/-11%; p<0.01). But, there was no significant difference of HSP70 mRNA expression in the posterior wall between control and ischemic preconditioning group. CONCLUSIONS: These data suggest that ischemic preconditioning have delayed myocardial protective effect from ischemia. The increase in myocardial HSP70 mRNA may be one of the contributing factors to the delayed cardioprotective effects of ischemic preconditioning in cats.
Animals ; Arrhythmias, Cardiac ; Blotting, Northern ; Cats* ; Coronary Vessels ; Evans Blue ; Heart* ; Heat-Shock Proteins* ; Hot Temperature* ; HSP70 Heat-Shock Proteins ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Models, Animal ; Reperfusion ; RNA, Messenger

No abstract available.

No abstract available.
Cellulitis* ; Dermatitis, Allergic Contact*

No abstract available.
Bowen's Disease ; Foot

No abstract available.
Echocardiography, Transesophageal*

No abstract available.