Publications (5)22.88 Total impact
-
Article: Effect of activated protein C on plasma plasminogen activator inhibitor activity in patients with acute myocardial infarction treated with alteplase: comparison with unfractionated heparin.
[show abstract] [hide abstract]
ABSTRACT: We examined whether activated protein C (APC) is an effective conjunctive therapy to thrombolysis in patients with ST-segment-elevated acute myocardial infarction (AMl). Activated protein C possesses both systemic anticoagulant and anti-inflammatory properties. It has been also shown to enhance fibrinolysis by inhibiting plasminogen activator inhibitor (PAI) activity in vitro. After successful thrombolysis with alteplase, study patients were assigned to receive one of the two conjunctive therapies for 48 h intravenously: human plasma-derived APC at 0.06 mg/kg per day (APC group, n = 9) or unfractionated heparin at 100 to 400 U/kg per day, adjusted to maintain an activated partial thromboplastin time at 1.5 to 2 times of the control level (heparin group, n = 10). Adverse events, including reocclusion of the recanalized infarct-related coronary artery and major or minor hemorrhagic complications, occurred more frequently in the heparin group (4 of 10 cases) than in the APC group (none of 9 cases) (p = 0.033). In the heparin group, plasma PAI activity (IU/ml, median value [range]) was increased continuously from 8 to 24 h after thrombolysis and peaked at 24 h (30.9 [11.3 to 38.5]); on the other hand, it was not increased in the APC group at 24 h after thrombolysis (11.3 [0.0 to 31.0], p < 0.01 vs. heparin group). Administration of APC suppressed increasing of plasma PAI activity observed after thrombolysis in patients with AMI. The effect of APC could be more eligible, compared with heparin, as a conjunctive regimen to thrombolysis in AMI patients.Journal of the American College of Cardiology 10/2003; 42(8):1389-94. · 14.16 Impact Factor -
Article: Challenging case of pulse infusion thrombolysis using a unique pump system for a patient with deep vein thrombosis: a case report.
[show abstract] [hide abstract]
ABSTRACT: A 69-year-old man presented with chronic deep vein thrombosis due to massive thrombi extending from the inferior vena cava to both femoral veins. He had undergone surgery for prostatic cancer in 1991, and since then he had been taking an artificial estrogen agent. He was successfully treated by pulse infusion thrombolysis using a unique pump system, which we have developed, without complication.Journal of Cardiology 03/2002; 39(2):115-9. · 1.28 Impact Factor -
Article: Increased expression of monocyte chemoattractant protein-1 in atherectomy specimens from patients with restenosis after percutaneous transluminal coronary angioplasty.
[show abstract] [hide abstract]
ABSTRACT: The plasma concentration of monocyte chemoattractant protein-1 (MCP-1) antigen is higher in patients with restenosis after coronary angioplasty than in those who do not restenose. In this study the MCP-1 expression of coronary atherectomy specimens was investigated by immunohistochemistry. Samples were obtained from 12 patients with restenosis and 15 with de novo lesions by directional coronary atherectomy. MCP-1 immunoreactivity was found in all patients in the restenosis group and in 8 of the de novo group. The frequency of macrophage expression was higher in the restenosis group than in de novo group. These results indicate that local expression of MCP-1 may be associated with the mechanisms of vascular remodeling after coronary angioplasty.Circulation Journal 02/2002; 66(1):114-6. · 3.77 Impact Factor -
Article: Association of Plasma Levels of Activated Protein C with Recanalization of the Infarct-Related Coronary Artery after Thrombolytic Therapy in Acute Myocardial Infarction
[show abstract] [hide abstract]
ABSTRACT: Protein C is one of the most important antithrombotic components. After activation by the thrombin-thrombomodulin complex on endothelial cells, activated protein C (APC) inactivates factors Va and VIIIa, which leads to the inhibition of thrombin formation. We examined the association of plasma levels of APC with the responsiveness to coronary thrombolytic therapy of the infarct-related coronary artery in patients with acute myocardial infarction (AMI). Plasma levels of APC, thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor (PAI) activity were measured in 32 consecutive AMI patients who underwent coronary angiography followed by thrombolytic therapy, and compared to the measurements in 23 control subjects. On admission, APC levels (ng/mL) were significantly elevated in patients with AMI, as compared with controls (2.5±0.4 vs. 1.2±0.2, 1.3±0.2, respectively, p<0.01). At discharge, plasma levels in AMI patients decline to values not significantly different from those in controls. (1.2±0.2, 1.3±0.2, respectively). TAT levels (ng/mL) were different among the groups in a fashion similar to that of APC (14.1±3.1 on admission vs. 3.3±0.4 at discharge, 1.8±0.1 in the control subjects, respectively, p<0.01). PAI activity levels (IU/mL) were higher on admission than at discharge and higher than the control subjects (19.7±1.8 vs. 10.5±1.0, 5.4±0.7, respectively, p<0.01). Thirty-two patients with AMI were classified into two groups according to the results of thrombolysis: the success group (24 patients) and the failure group (eight patients). APC levels were higher in the failure group than in the success group (5.1±0.7 vs. 1.6±0.2, p<0.01). TAT levels were also higher in the failure group than in the success group (30.8±9.6 vs. 8.6±1.7, p<0.01). PAI activity levels (IU/mL) were lower in the failure group than in the success group (13.5±3.1 vs. 21.7±2.1, p<0.05). There were correlations between APC and TAT levels both on admission and at discharge . Elevated APC was thought to correlate with increased thrombin generation in patients with AMI. This study demonstrated that there was a significant relation between plasma APC level and the responsiveness to thrombolytic therapy of the infarct artery. This study may also indicate that increased thrombin generation is a cause of the resistance to thrombolytic therapy.Thrombosis Research 08/1999; · 2.44 Impact Factor -
Article: Relationship between serum angiotensin-converting enzyme activity and plasma plasminogen activator inhibitor activity in patients with recent myocardial infarction
[show abstract] [hide abstract]
ABSTRACT: Background An elevated level of angiotensin-converting enzyme (ACE) has been demonstrated to increase the risk of myocardial infarction. Plasminogen activator inhibitor (PAI) is the most important physiological inhibitor of tissue plasminogen activator in plasma. An elevated level of PAI has been reported to be associated with decreased fibrinolytic capacity and to constitute a marker of the risk for recurrent coronary thrombosis. Methods We measured the serum ACE activity and plasma PAI activity in 34 patients with recent myocardial infarction, and evaluated the correlation between these two values by linear regression analysis. We also administered captopril (37.5 mg/day) to 17 of these patients and placebo to the other 17 patients at random, and compared the changes in PAI activity and ACE activity in these two groups over a 1-month period. Results There was a significant correlation between the serum ACE activity and the plasma PAI activity at baseline in the patients (r = 0.498, P < 0.01). The captopril-treated patients showed significantly reduced PAI activity (P < 0.01), and a concomitant decrease in ACE activity. Conclusion These results suggest that elevated ACE activity is associated with impaired fibrinolysis and that treatment with an ACE inhibitor improves the fibrinolytic function in patients with recent myocardial infarction. The results also suggest that the renin-angiotensin system plays a role in the increased risk of ischemic cardiovascular events when it is activated, and in the reduction of risk of recurrent myocardial infarction by ACE inhibition. (C) 1998 Lippincott Williams & Wilkins, Inc.Coronary Artery Disease 08/1998; 9(10). · 1.24 Impact Factor
