Percutaneous transluminal coronary recanalization: Procedure, results, and acute complications

Rutsch, Wolfgang; Schartl, M.; Mathey, D; Kück, Karl‐Heinz; Merx, W; Dörr, R.; Rentrop, P.; Blanke, H.

doi:10.1016/0002-8703(81)90649-9

Cited by 76 publications

(11 citation statements)

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“…Lysis time was found to increase when therapy was initiated Ͼ6 hours after onset of infarction. 69 This finding may be related not only to cross linking of fibrin 70 but also to appositional thrombus growth. Full resistance to fibrinolytic therapy in 20% of patients corresponds to the observation of occlusive platelet thrombi in the same percentage of autopsy cases.…”

Section: Coronary Angioscopic Findingsmentioning

confidence: 94%

Thrombi in Acute Coronary Syndromes

2000

Circulation

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O ver the past 35 years, the view has evolved that the acute coronary syndromes, ie, unstable angina pectoris, myocardial infarction, and sudden death, are caused by plaque rupture and formation of a platelet thrombus. There is at least a transient total or subtotal coronary occlusion in all cases of acute myocardial infarction. Q-wave infarcts are thought to differ from non-Q-wave infarcts by more stable platelet thrombi causing more prolonged and/or severe ischemia, leading to more extensive infarction. The greater platelet stability in transmural infarction is attributed to more severe or extensive plaque rupture. 1-3 Unstable angina and non-Qwave infarction, in the present view, are due to less extensive, less stable platelet thrombi that cause less severe, less extensive ischemia and/or infarction.However, autopsy data and more recent clinical findings require significant refinement of this viewpoint on the basis of the following observations. The occlusive thrombi causing Q-wave myocardial infarction contain more fibrin than the thrombi found in the other acute coronary syndromes that are characterized by more platelets and less fibrin. The higher fibrin content of thrombi causing Q-wave infarction explains their greater stability. Furthermore, this higher fibrin content suggests that the coagulation cascade is activated to a greater degree during Q-wave infarction than during non-Q-wave infarction in which platelets play a more dominant role. This review analyzes our evolving concepts focusing on the growing divergence of the different mechanisms underlying the different acute coronary syndromes and their clinical and therapeutic implications. Morphological Basis for the Current Concept of Acute Coronary SyndromesBy the mid-1930s, acute myocardial infarction was shown to be caused by coronary thrombosis resulting from intimal fissuring, which is often associated with dissecting hemorrhage into the underlying plaque. 4 -7 In the late 1930s, however, intimal fissuring was questioned and subendothelial hemorrhages were ascribed to rupture of capillaries within the plaque. 8,9 The causative role of coronary thrombosis became controversial in 1956 when pathologists first reported a low prevalence of thrombi in fatal infarction. 10 -16 The pendulum began to swing back in the mid-1960s because of improved autopsy techniques. Coronary thrombi were found in Ͼ90% of fatal infarcts, most being occlusive.Plaque hemorrhages, which were usually traceable to an intimal tear within the thrombosed segment, were found in most cases. [17][18][19][20][21] These observations reaffirmed that intimal rupture was the essential mechanism causing both subendothelial hemorrhage and intraluminal thrombosis. 22 Having found that three quarters of occlusive coronary thrombi were composed of layers of different ages, Sinapius 17,21 concluded that these thrombi developed in a protracted, recurring course. The oldest portion of thrombus usually sealed the intimal fissure and was rich in platelets. The finding that mural thrombus forma...

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Section: Coronary Angioscopic Findingsmentioning

confidence: 94%

Thrombi in Acute Coronary Syndromes

2000

Circulation

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“…In general, local streptokinase infusions (30-294 x 10 3 RJ/60 min) have been followed by heparin anticoagulation or antiplatelet (ASA/dipyridamole) therapy. A single patient (0.4%) suffered an intracranial hemorrhage following intracoronary artery streptokinase in a series of 232 consecutive patients reported by Rutsch et al 7 In contrast, no cerebral events occurred in combined retrospective series of 183 patients,^8 a case controlled series of 95 patients, 9 or among 289 patients receiving intracoronary therapy in 5 prospective double blind studies (against placebo, anticoagulation, or standard therapy).…”

Section: Acute Myocardia] Infarctionmentioning

confidence: 96%

Thrombolytic therapy in stroke: possibilities and hazards.

Zoppo¹,

Zeumer²,

Harker³

1986

Stroke

202

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patients with various thrombolytic agents, and to weigh the relative risk of intracerebral hemorrhage in patients treated with fibrinolytic agents for stroke and for other thrombotic disorders. Mechanism of ThrombolysisArterial thrombosis and thrombus extension involve to varying degrees the processes of endothelial injury, platelet aggregation and release, and thrombin generation. Thrombin-mediated fibrinogen cleavage results in fibrin formation which is required for thrombus stabilization.80 Thrombin-mediated fibrin formation occurs in direct relation to platelet activation by several mechanisms. Platelets promote activation of the early stages of intrinsic coagulation by a process that involves a factor XI receptor and high molecular weight kininogen.81 Also, factors V and VHI interact with platelet membrane phospholipids to facilitate the activation of factor X to Xa and the conversion of prothrombin to thrombin.82 Platelet-bound thrombinmodified factor V (factor Va) serves as a high affinity platelet receptor for factor Xa. 83 Consequently, the rate of thrombin generation is accelerated 10 3 fold, providing a potent positive feedback mechanism for initiation of thrombin formation on the platelet surface, fibrin network formation in the thrombus, and indirectly, fibrinolysis.Thrombus dissolution is, in large part, mediated by fibrinolysis localized within the thrombus.84 " 86 Fibrin (and fibrinogen) degradation is catalyzed by plasmin, the product of plasminogen activation. 87 In the consolidating thrombus plasminogen binds to fibrin and to platelets, allowing local release of plasmin within the thrombus. The circulating plasminogen activators, tissue plasminogen activator (tPA) and single chain urokinase plasminogen activator (scuPA), catalyze plasby guest on

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“…Even among clinical studies, varied incidence of reperfusion arrhythmias has been demonstrated. 2,[27][28][29][30][31] These results suggest that mechanisms responsible for AIVR and VT in clinical cases might be somewhat different from those observed in experimental models. In the present study, we clinically demonstrated for the first time that AIVR and VT that occur after reperfusion are probably cAMP-mediated arrhythmias and are therefore likely to be triggered arrhythmias.…”

Section: Electrophysiological Mechanisms Of Reperfusion Arrhythmiasmentioning

confidence: 83%

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

et al. 2000

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Background-Intracellular calcium overload is believed to play an important role in development of reperfusion arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusion arrhythmias by reducing intracellular calcium overload. Methods and Results-First, we tested for a preventive effect of dipyridamole. Sixty-one patients who underwent primary PTCA for treatment of acute anterior wall myocardial infarction were enrolled in this prospective study. Patients were divided into dipyridamole (DP) and nondipyridamole (non-DP) groups. The 2 groups had similar baseline characteristics. In the DP group, dipyridamole 0.5 mg/kg was infused intravenously for 3 minutes immediately before reperfusion during primary PTCA. Arrhythmias after reperfusion were analyzed from continuous ECG recordings. None of the patients in the DP group (nϭ23) had accelerated idioventricular rhythms (AIVR) or ventricular tachycardia (VT). In contrast, 7 (18.4%) had AIVR and 3 (7.9%) had VT in the non-DP group (nϭ38; PϽ0.01). Second, we tested for a termination effect of dipyridamole. Dipyridamole 0.5 mg/kg was infused intravenously while continuous ECG recordings were obtained in 9 patients who had either sustained AIVR (nϭ7) or sustained VT (nϭ2) after reperfusion of occluded coronary artery. Arrhythmias were terminated in all patients. Conclusions-These results indicate that administration of dipyridamole can prevent and terminate reperfusion arrhythmias such as AIVR and VT. cAMP-mediated triggered activity may, at least in part, be responsible for reperfusioninduced AIVR and VT. (Circulation. 2000;101:624-630.)

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Percutaneous transluminal coronary recanalization: Procedure, results, and acute complications

Cited by 76 publications

References 0 publications

Thrombi in Acute Coronary Syndromes

Thrombi in Acute Coronary Syndromes

Thrombolytic therapy in stroke: possibilities and hazards.

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

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