AIM： To assess the validity of our selection criteria for hepatectomy procedures based on indocyanine green disappearance rate （KICG）, and to unveil the factors affecting posthepatectomy mortality in patients with ...AIM： To assess the validity of our selection criteria for hepatectomy procedures based on indocyanine green disappearance rate （KICG）, and to unveil the factors affecting posthepatectomy mortality in patients with hepatocellular carcinoma （HCC）. METHODS： A retrospective analysis of 198 consecutive patients with HCC who underwent partial hepatectomies in the past 14 years was conducted. The selection criteria for hepatectomy procedures during the study period were KICG≥0.12 for hemihepatectomy, KICG≥0.10 for bisegmentectomy, KCG≥0.08 for monosegmentectomy, and KICG≥ 0.06 for nonanatomic hepatectomy. The hepatectomies were categorized into three types： major hepatectomy （hemihepatectomy or a more extensive procedure）, bisegmentectomy, and limited hepatectomy. Univariate （Fishers exact test） and multivariate （the logistic regression model） analyses were used. RESULTS： Postoperative mortality was 5% after major hepatectomy, 3% after bisegmentectomy, and 3% after limited hepatectomy. The bhree percentages were comparable （P = 0.876）. The platelet count of ≤ 10× 10^4/μL was the strongest independent factor for postoperative mortality on univariate （P = 0.001） and multivariate （risk ratio, 12.5; P= 0.029） analyses. No patient with a platelet count of 〉7.3× 10^4/μL died of postoperative morbidity, whereas 25% （6/24 patients） of patients with a platelet count of ≤7.3×10^4/μL died （P〈0.001）. CONCLUSION： The selection criteria for hepatectomy procedures based on KICG are generally considered valid, because of the acceptable morbidity and mortality with these criteria. The preoperative platelet count independently affects morbidity and mortality after hepatectomy, suggesting that a combination of KICG and platelet count would further reduce postoperative mortality.展开更多
Background Aspirin and clopidogrel can improve myocardial reperfusion and alleviate myocardial injury during percutaneous coronary intervention （PCI）. Whether the addition of intravenous tirofiban during this proced...Background Aspirin and clopidogrel can improve myocardial reperfusion and alleviate myocardial injury during percutaneous coronary intervention （PCI）. Whether the addition of intravenous tirofiban during this procedure produces further benefit has not been clarified in ST segment elevation myocardial infarction （STEMI） patients. We evaluated this on STEMI patients who underwent primary PCI （p-PCI） via transradial artery approach. Methods Consecutive patients were randomized into tirofiban group （n=-72） or placebo group （n=-78）. Angiographic analysis included initial and final thrombolysis in myocardial infarction （TIMI） flow grade （TFG）, corrected TIMI frame count （CTFC） and TIMI myocardial perfusion grade （TMPG） of the thrombotic vessel. Platelet aggregation rate （PAR）, creatine phosphokinase （CPK）, CPK isoenzyme MB （CPK-MB） and troponin I levels were measured and TIMI definitions were used to assess bleeding complications. Left ventricular performance parameters were investigated with equilibrium radionuclide ventriculography. Major adverse cardiac events （MACE） were followed up for 6 months. Results The cases of TFG 0 and 1 before PCI, TFG 0 when first crossing of guide wire were less, and the cases of TFG 3 after PCI was more in tirofiban group than those in placebo group. The final CTFC was fewer and the incidence of no reflow phenomenon was lower, as well the percentage of final TFG 3 was higher in tirofiban group than those in placebo group （all P 〈0.05）. Mean peak CPK-MB was significantly lower, while the left ventricular performance parameters 1 week after PCI were much more improved in tirofiban group than those in the placebo group. PAR was significantly decreased shortly after tirofiban infusion. The incidence of 6-month MACE in tirofiban group was obviously lower than that in the placebo group. No statistical difference was noted between the two groups with regard to bleeding complications. Conclusions Intravenous tirofiban infusion, in addition to aspirin and clopidogrel in STEMI patients with p-PCI via transradial artery access, can quickly inhibit platelet aggregation, loosen occlusive thrombus, improve myocardial reperfusion and reduce incidence of MACE with few complications of vessel access and bleeding.展开更多
Acute aortic dissection(AAD) is a life-threatening cardiovascular disease caused by progressive medial degeneration of the aortic wall. A disintegrin and metalloproteinase with thrombospondin motifs 1(ADAMTS1) is a re...Acute aortic dissection(AAD) is a life-threatening cardiovascular disease caused by progressive medial degeneration of the aortic wall. A disintegrin and metalloproteinase with thrombospondin motifs 1(ADAMTS1) is a recently identified extracellular metalloproteinase participating in the development of vascular disease, such as atherosclerosis. In the present study, we found that ADAMTS1 was significantly elevated in blood samples from AAD patients compared with patients with acute myocardial infarction and healthy volunteers. Based on these findings, we established an AAD model by infusing angiotensin II in older mice. AAD was successfully developed in aorta tissues, with an incidence of 42% after 14 days in the angiotensin II group. Macrophage and neutrophil infiltration was observed in the media of the aorta, and ADAMTS1 overexpression was found in the aorta by Western blot and immunohistochemistry. Double immunofluorescence staining showed the expression of ADAMTS1 in macrophages and neutrophils. Consistent with the upregulation of ADAMTS1 in aortic dissection tissues, versican(a proteoglycan substrate of ADAMTS1) was degraded significantly more in these tissues than in control aortic tissues. These data suggest that the increased expression of ADAMTS1 protein in macrophages and neutrophils that infiltrated aortic tissues may promote the progression of AAD by degrading versican.展开更多
文摘AIM： To assess the validity of our selection criteria for hepatectomy procedures based on indocyanine green disappearance rate （KICG）, and to unveil the factors affecting posthepatectomy mortality in patients with hepatocellular carcinoma （HCC）. METHODS： A retrospective analysis of 198 consecutive patients with HCC who underwent partial hepatectomies in the past 14 years was conducted. The selection criteria for hepatectomy procedures during the study period were KICG≥0.12 for hemihepatectomy, KICG≥0.10 for bisegmentectomy, KCG≥0.08 for monosegmentectomy, and KICG≥ 0.06 for nonanatomic hepatectomy. The hepatectomies were categorized into three types： major hepatectomy （hemihepatectomy or a more extensive procedure）, bisegmentectomy, and limited hepatectomy. Univariate （Fishers exact test） and multivariate （the logistic regression model） analyses were used. RESULTS： Postoperative mortality was 5% after major hepatectomy, 3% after bisegmentectomy, and 3% after limited hepatectomy. The bhree percentages were comparable （P = 0.876）. The platelet count of ≤ 10× 10^4/μL was the strongest independent factor for postoperative mortality on univariate （P = 0.001） and multivariate （risk ratio, 12.5; P= 0.029） analyses. No patient with a platelet count of 〉7.3× 10^4/μL died of postoperative morbidity, whereas 25% （6/24 patients） of patients with a platelet count of ≤7.3×10^4/μL died （P〈0.001）. CONCLUSION： The selection criteria for hepatectomy procedures based on KICG are generally considered valid, because of the acceptable morbidity and mortality with these criteria. The preoperative platelet count independently affects morbidity and mortality after hepatectomy, suggesting that a combination of KICG and platelet count would further reduce postoperative mortality.
基金This project was supported by a grant from the Natural Science Foundation of Hebei Province （No. C2004000615）.
文摘Background Aspirin and clopidogrel can improve myocardial reperfusion and alleviate myocardial injury during percutaneous coronary intervention （PCI）. Whether the addition of intravenous tirofiban during this procedure produces further benefit has not been clarified in ST segment elevation myocardial infarction （STEMI） patients. We evaluated this on STEMI patients who underwent primary PCI （p-PCI） via transradial artery approach. Methods Consecutive patients were randomized into tirofiban group （n=-72） or placebo group （n=-78）. Angiographic analysis included initial and final thrombolysis in myocardial infarction （TIMI） flow grade （TFG）, corrected TIMI frame count （CTFC） and TIMI myocardial perfusion grade （TMPG） of the thrombotic vessel. Platelet aggregation rate （PAR）, creatine phosphokinase （CPK）, CPK isoenzyme MB （CPK-MB） and troponin I levels were measured and TIMI definitions were used to assess bleeding complications. Left ventricular performance parameters were investigated with equilibrium radionuclide ventriculography. Major adverse cardiac events （MACE） were followed up for 6 months. Results The cases of TFG 0 and 1 before PCI, TFG 0 when first crossing of guide wire were less, and the cases of TFG 3 after PCI was more in tirofiban group than those in placebo group. The final CTFC was fewer and the incidence of no reflow phenomenon was lower, as well the percentage of final TFG 3 was higher in tirofiban group than those in placebo group （all P 〈0.05）. Mean peak CPK-MB was significantly lower, while the left ventricular performance parameters 1 week after PCI were much more improved in tirofiban group than those in the placebo group. PAR was significantly decreased shortly after tirofiban infusion. The incidence of 6-month MACE in tirofiban group was obviously lower than that in the placebo group. No statistical difference was noted between the two groups with regard to bleeding complications. Conclusions Intravenous tirofiban infusion, in addition to aspirin and clopidogrel in STEMI patients with p-PCI via transradial artery access, can quickly inhibit platelet aggregation, loosen occlusive thrombus, improve myocardial reperfusion and reduce incidence of MACE with few complications of vessel access and bleeding.
基金supported by the National Natural Science Foundation of China(81170287)
文摘Acute aortic dissection(AAD) is a life-threatening cardiovascular disease caused by progressive medial degeneration of the aortic wall. A disintegrin and metalloproteinase with thrombospondin motifs 1(ADAMTS1) is a recently identified extracellular metalloproteinase participating in the development of vascular disease, such as atherosclerosis. In the present study, we found that ADAMTS1 was significantly elevated in blood samples from AAD patients compared with patients with acute myocardial infarction and healthy volunteers. Based on these findings, we established an AAD model by infusing angiotensin II in older mice. AAD was successfully developed in aorta tissues, with an incidence of 42% after 14 days in the angiotensin II group. Macrophage and neutrophil infiltration was observed in the media of the aorta, and ADAMTS1 overexpression was found in the aorta by Western blot and immunohistochemistry. Double immunofluorescence staining showed the expression of ADAMTS1 in macrophages and neutrophils. Consistent with the upregulation of ADAMTS1 in aortic dissection tissues, versican(a proteoglycan substrate of ADAMTS1) was degraded significantly more in these tissues than in control aortic tissues. These data suggest that the increased expression of ADAMTS1 protein in macrophages and neutrophils that infiltrated aortic tissues may promote the progression of AAD by degrading versican.
