Thrombin generation in human coronary arteries after percutaneous transluminal balloon angioplasty

Marmur, Jonathan D.; Sharma, Sanjeev; Khaghan, Neda; Torre, Sabino R.; Israel, Douglas H.; Merlini, Piera Angelica; Ardissino, Diego; Ambrose, John A.

doi:10.1016/0735-1097(94)90144-9

Cited by 67 publications

(36 citation statements)

References 27 publications

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“…This leads to the generation of large amounts of the serine protease thrombin through activation of the coagulation cascade by the tissue factor pathway (Marmur et al, 1994). By binding the subendothelial extracellular matrix, thrombin remains functionally active, localized, and protected from inactivation by circulating inhibitors (Schrör et al, 2010).…”

Section: (␣S)-n-[(1s)-3-amino-1-[[(phenylmethyl)-amino]carbonyl]propymentioning

confidence: 99%

Protease-Activated Receptor-1 Antagonist F 16618 Reduces Arterial Restenosis by Down-Regulation of Tumor Necrosis Factor α and Matrix Metalloproteinase 7 Expression, Migration, and Proliferation of Vascular Smooth Muscle Cells

Chieng-Yane¹,

Bocquet²,

Létienne³

et al. 2010

J Pharmacol Exp Ther

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Section: (␣S)-n-[(1s)-3-amino-1-[[(phenylmethyl)-amino]carbonyl]propymentioning

confidence: 99%

Protease-Activated Receptor-1 Antagonist F 16618 Reduces Arterial Restenosis by Down-Regulation of Tumor Necrosis Factor α and Matrix Metalloproteinase 7 Expression, Migration, and Proliferation of Vascular Smooth Muscle Cells

Chieng-Yane¹,

Bocquet²,

Létienne³

et al. 2010

J Pharmacol Exp Ther

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“…1,2 Thrombin is generated in large amounts at the site of injury after balloon angioplasty and is amplified by formation of the prothrombinase complex both in humans and animals. [3][4][5] Exposure of tissue factor in the atherosclerotic plaque to flowing blood leads to increased thrombin generation, resulting in platelet-and fibrin-rich thrombus formation. 3,6,7 The important role of thrombin in generating acute platelet-rich thrombus and vascular healing after arterial injury is well documented.…”

mentioning

confidence: 99%

“…[3][4][5] Exposure of tissue factor in the atherosclerotic plaque to flowing blood leads to increased thrombin generation, resulting in platelet-and fibrin-rich thrombus formation. 3,6,7 The important role of thrombin in generating acute platelet-rich thrombus and vascular healing after arterial injury is well documented. 8 -11 Thrombin is also the most potent activator of platelets, and its expression is upregulated in smooth muscle cells after severe arterial injury.…”

mentioning

confidence: 99%

Prolonged Thrombin Inhibition Reduces Restenosis After Balloon Angioplasty in Porcine Coronary Arteries

et al. 1998

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Background-Arterial injury after percutaneous transluminal coronary angioplasty (PTCA) triggers acute thrombus formation and thrombin generation. Hirudin, a potent and direct thrombin inhibitor, prevents thrombus formation after arterial injury. Two large clinical trials showed marked reduction in acute clinical events but no long-term benefits in reducing restenosis during short-term administration of thrombin inhibitors. Our hypothesis is that adequate, maintained thrombin inhibition, by inhibiting all the thrombin-dependent mechanisms, will reduce neointima formation after PTCA. Methods and Results-Thirty-six pigs received three different regimens of hirudin: bolus (1 mg/kg), short-term (bolusϩ0.7 mg/kg per day for 2 days), and long-term (bolusϩ0.7 mg/kg per day for 14 days). The results on neointima formation at 4 weeks after coronary angioplasty were compared with the control group (100 IU heparin/kg bolus). Hirudin was continuously administered for 2 weeks through an infusion pump. In vivo thrombin generation was persistently increased up to 2 weeks after angioplasty. Inhibition of thrombin activity for 14 days reduced luminal narrowing by 40% (58Ϯ3% versus 35Ϯ3%; PϽ.001). No differences were observed among the bolus and short-term hirudin groups and the control group. Conclusions-Our results indicate that there is a continued, marked thrombin generation that lasts for at least 2 weeks after PTCA. Administration of r-hirudin for 2 weeks significantly reduces neointima formation after PTCA. This observation, if extrapolated to humans, could explain the lack of effect on restenosis observed in the clinical trials with antithrombin agents despite the clear benefits on reducing acute thrombotic complications after PTCA. Therefore an adequate and prolonged administration of thrombin inhibitors is needed to "passivate" the thrombogenic substrate (disrupted arterial wall) and achieve full benefit of this therapeutic approach. (Circulation. 1998;97:581-588.)

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“…It is unknown which is the most reliable marker of thrombin generation after PCI. The serum F1+2 concentration exceeds the normal only in severe hypercoagulable states, 4,6) and Haude, et al 7) showed that the F1+2 concentration is the most specific and useful predictor of subacute stent thrombosis. FPA is very sensitive and indicates coagulation activity in real time because of its short 29.5 ± 6.9 § POBA = plain old balloon angioplasty; STENT = stenting; CB = cutting balloon angioplasty; CAG = coronary angiography; PAI-1 = plasminogen activator inhibitor-1.…”

Section: Discussionmentioning

confidence: 99%

Hemostatic and Fibrinolytic Activation Is Less Following Cutting Balloon Angioplasty of the Coronary Arteries

et al. 2004

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SUMMARYRecent studies have shown that percutaneous coronary intervention (PCI) activates systemic hemostatic activity, reflecting platelet activation and thrombin formation in the coronary arteries. The present study compared systemic levels of hemostatic markers induced by plain old balloon angioplasty (POBA), coronary stenting (STENT), and cutting balloon (CB) angioplasty.Sixty-one patients with stable angina pectoris, who underwent elective PCI or diagnostic coronary angiography (CAG) alone, were investigated. Patients who underwent PCI were divided into the POBA group (n = 11), the STENT group (n = 27), and the CB group (n = 11). Patients who underwent CAG alone were assigned to the CAG group (n = 12). Blood samples were collected before, 24 hours after, and 3 days after PCI or CAG. Plasma concentrations of prothrombin fragment 1+2 (F1+2), fibrinopeptide A (FPA), thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor-1 (PAI-1) were measured.In the CB group, the F1+2 (1.23 ± 0.4 nmol/L) level 3 days after PCI was significantly smaller than that of the POBA group (2.37 ± 0.5 nmol/L) (P < 0.05). The FPA (1.81 ± 0.9 ng/mL), TAT (3.36 ± 1.2 ng/mL) and PAI-1 (23.0 ± 4.1 ng/mL) levels in the CB group 3 days after PCI were significantly smaller than those of the POBA group (P < 0.05, respectively) and STENT group (P < 0.05, respectively), but similar to the CAG group.Systemic hemostasis is activated to a greater extent after POBA and stenting than it is after CB angioplasty of the coronary arteries. This may contribute to the favorable longterm outcome of CB angioplasty. (Jpn Heart J 2004; 45: 409-417)

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Thrombin generation in human coronary arteries after percutaneous transluminal balloon angioplasty

Cited by 67 publications

References 27 publications

Protease-Activated Receptor-1 Antagonist F 16618 Reduces Arterial Restenosis by Down-Regulation of Tumor Necrosis Factor α and Matrix Metalloproteinase 7 Expression, Migration, and Proliferation of Vascular Smooth Muscle Cells

Protease-Activated Receptor-1 Antagonist F 16618 Reduces Arterial Restenosis by Down-Regulation of Tumor Necrosis Factor α and Matrix Metalloproteinase 7 Expression, Migration, and Proliferation of Vascular Smooth Muscle Cells

Prolonged Thrombin Inhibition Reduces Restenosis After Balloon Angioplasty in Porcine Coronary Arteries

Hemostatic and Fibrinolytic Activation Is Less Following Cutting Balloon Angioplasty of the Coronary Arteries

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