Comparison of coronary and myocardial morphologic findings in patients with and without thrombolytic therapy during fatal first acute myocardial infarction

Gertz, S. David; Kragel, Amy H.; Kalan, Jay M.; Braunwald, Eugene; Roberts, William C.; Investigators, The TIMI

doi:10.1016/0002-9149(90)90923-o

Cited by 55 publications

(12 citation statements)

References 25 publications

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“…Consistent with this is the observation of platelet-rich thrombi in the coronary arteries of patients who died after a first fatal myocardial infarction, despite having received thrombolytic therapy [41].…”

Section: Platelet Activation Associated With Fibrinolytic Therapysupporting

confidence: 55%

Platelet activation in acute myocardial infarction and the rationale for combination therapy

Conde-Pozzi

Kleiman

2000

Curr Cardiol Rep

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Current fibrinolytic regimens fail to fully restore coronary blood flow in slightly less than 50% of patients with acute myocardial infarction. Platelet activation and aggregation may be responsible for a large proportion of these therapeutic failures. Therefore, platelet inhibition may enhance thrombolysis. Experimental and early clinical evidence suggest that glycoprotein IIb/IIIa antagonists may enhance reperfusion when combined with reduced doses of thrombolytic agents. However, the clinical benefit of combination therapy will depend on the outcomes of a number large clinical trials that are currently being performed.

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Section: Platelet Activation Associated With Fibrinolytic Therapysupporting

confidence: 55%

Platelet activation in acute myocardial infarction and the rationale for combination therapy

Conde-Pozzi

Kleiman

2000

Curr Cardiol Rep

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“…21 Thrombolytic therapy increases the incidence of haemorrhagic infarct independently of vessel patency with the haemorrhagic area almost exclusively confined to the infarct area and not associated with infarct expansion. [34][35][36] Although thrombolytic therapy increases the number of infarcts with haemorrhage, the incidence of myocardial rupture, is probably not significantly affected as nearly all myocardial ruptures occur in the small percentage of infarcts that have extensive haemorrhage in any case. It is therefore unlikely that post-myocardial infarction VSD is a haemorrhagic complication of thrombolytic therapy.…”

Section: Discussionmentioning

confidence: 99%

Influence of thrombolytic therapy on the patterns of ventricular septal rupture after acute myocardial infarction

Rhydwen

Charman

Schofield

2002

Postgraduate Medical Journal

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Background Post-myocardial infarction ventricular septal defect (VSD) complicates ∼2% of myocardial infarctions. Thrombolytic therapy may accelerate the time from myocardial infarction to VSD formation. The effects of thrombolytic therapy in patients with a post-myocardial infarction VSD were investigated. Method Demographic, procedural, and event data were retrospectively analysed in patients transferred to a regional cardiothoracic centre with the diagnosis of post-myocardial infarction VSD over five years. Results Twenty nine patients were analysed; 15 received thrombolytic therapy: 10 (<12 hours) early and five (≥12 hours) late. The median time to post-myocardial infarction VSD was shorter with thrombolytic therapy at 1 v 5.5 days (p=0.01). The median time to post-myocardial infarction VSD was shorter with early compared with late thrombolytic therapy at 1 v 6 days (p<0.01). There was no difference between late and no thrombolytic therapy, 5.5 v 6 days. Patients treated with thrombolytic therapy had a trend towards higher mortality at 11/15 (73%) compared with 5/14 (36%) (p=0.066). Twenty five (86%) patients had surgery. All four not having surgery died. Surgical survival was 13/25 (52%) at discharge and six months of follow up. Within the surgical group survival with prior thrombolytic therapy was 4/25 (25%) and 9/13 (69%) without (p=0.07). Conclusion There appears to be an earlier presentation of post-myocardial infarction VSD when thrombolytic therapy has been used. An early presentation can carry a worse prognosis and may have implications for the identification and treatment of this life threatening complication.

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“…It has been suggested that early thrombolysis reduces the incidence of myocardial rupture [15,16]. However, there has been concern that reperfusion of necrotic myocardium may cause myocardial hemorrhage predisposing to wall rupture [12].…”

Section: Discussionmentioning

confidence: 99%

Ventricular rupture during coronary angioplasty for acute reinfarction

Kwong

Carere

Thompson

et al. 1998

Cathet. Cardiovasc. Diagn.

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Comparison of coronary and myocardial morphologic findings in patients with and without thrombolytic therapy during fatal first acute myocardial infarction

Cited by 55 publications

References 25 publications

Platelet activation in acute myocardial infarction and the rationale for combination therapy

Platelet activation in acute myocardial infarction and the rationale for combination therapy

Influence of thrombolytic therapy on the patterns of ventricular septal rupture after acute myocardial infarction

Ventricular rupture during coronary angioplasty for acute reinfarction

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