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Review
. 2022 Apr;26(4):249-257.
doi: 10.5152/AnatolJCardiol.2022.1083.

Low-Dose Slow Infusion Tissue Plasminogen Activator (tPA) in Treatment of Thrombotic Coronary Artery Occlusions: Case Series and Literature Review

Affiliations
Review

Low-Dose Slow Infusion Tissue Plasminogen Activator (tPA) in Treatment of Thrombotic Coronary Artery Occlusions: Case Series and Literature Review

Murat Akçay et al. Anatol J Cardiol. 2022 Apr.

Abstract

Thrombotic coronary artery occlusions usually manifest as acute coronary syndrome with cardiogenic shock, acute pulmonary edema, cardiac arrest, fatal arrhythmias, or sudden cardiac death. Although it usually occurs based on atherosclerosis, it can also occur without atherosclerosis. There is no predictor of coronary artery thrombosis clinically and no consensus regarding the optimal treatment. In the current literature, treatment options include emergency coronary artery bypass grafting, entrapment of thrombus in vessel wall with stent implantation, intracoronary thrombolysis, glycoprotein IIb/IIIa inhibitors, anticoagulation with heparin, and thrombus aspiration as reperfusion strategies. Here, we reviewed a new treatment strategy based on the literature, and a case series with successful results in hemodynamically stable patients with low-dose slow infusion tissue plasminogen activator (tPA) for thrombotic coronary artery occlusions that allow coronary flow was reported. Prospective randomized studies and common consensus are needed on low-dose, slow-infusion tissue plasminogen activator treatment regimen and optimal treatment management for thrombotic coronary artery occlusions.

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Figures

Figure 1.
Figure 1.
(A) A semi-mobile thrombus was observed in the left main coronary artery in coronary angiography. (B) Imaging the left main coronary artery, after tirofiban infusion. (C) Imaging the left main coronary artery, 24 hours after tPA therapy. (D) A nonobstructing plaque was observed in the left main coronary artery in intravascular ultrasound imaging. tPA, tissue-type plasminogen activator.
Figure 2.
Figure 2.
(A) A semi-mobile thrombus in the left main coronary artery in coronary angiography. (B) Imaging the left main coronary artery, after tirofiban infusion. (C-D) Right anterior oblique cranial and left anterior oblique caudal view of the left main coronary artery, 24 hours after tPA therapy. tPA, tissue-type plasminogen activator.
Figure 3.
Figure 3.
(A-B). Right anterior oblique caudal and anteroposterior cranial view of the left anterior descending artery with a semi-mobile thrombus. (C) Imaging the left anterior descending artery, after tirofiban infusion. (D) Imaging the left anterior descending artery, after tPA therapy. tPA, tissue-type plasminogen activator.
Figure 4.
Figure 4.
(A) Left anterior oblique caudal view of the left anterior descending artery with a semi-mobile thrombus. (B) Imaging the left anterior descending artery, after tirofiban infusion. (C-D) Left anterior oblique caudal and anteroposterior cranial view of the left anterior descending artery, after tPA therapy. tPA, tissue-type plasminogen activator.
Figure 5.
Figure 5.
(A) The electrocardiography showing the ST-segment elevation in DII, DIII, aVF, and V4-V6 leads. (B) Right anterior oblique caudal view during the diagnostic coronary angiography showing the proximal 80-90% occlusion of left anterior descending artery. (C) Right anterior oblique caudal view during control coronary angiography after tirofiban infusion, showing the proximal 50-60% occlusion of left anterior descending artery. (D) Right anterior oblique caudal view during control coronary angiography after low-dose ultraslow-infusion tPA, showing the patency of left anterior descending artery without thrombus. tPA, tissue-type plasminogen activator.

References

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