Hostname: page-component-76fb5796d-25wd4 Total loading time: 0 Render date: 2024-04-30T01:29:52.687Z Has data issue: false hasContentIssue false
  • English
  • Français

Myocardial Infarction Following t-PA for Acute Stroke

Published online by Cambridge University Press:  02 December 2014

M. Mehdiratta ,
C. Murphy ,
A. Al-Harthi  and
P. A. Teal
M. Mehdiratta
Affiliation:
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
C. Murphy
Affiliation:
Vancouver General Hospital, University of British Columbia, Vancouver, B.C., Canada
A. Al-Harthi
Affiliation:
Vancouver General Hospital, University of British Columbia, Vancouver, B.C., Canada
P. A. Teal
Affiliation:
Vancouver General Hospital, University of British Columbia, Vancouver, B.C., Canada
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background and Purpose:

Complications of intravenous (IV) thrombolysis with tissue plasminogen activator (t-PA) for acute stroke are commonly related to hemorrhage, anaphylaxis, or arterial re-occlusion. Embolic complications of t-PA are beginning to be recognized with increased use of t-PA for acute ischemic stroke. We hypothesize that disruption of intra-cardiac thrombus may result in myocardial infarction (MI) after use of t-PA for acute ischemic stroke.

Summary of Cases:

We describe three cases of acute MI immediately following IV t-PA infusion for acute stroke. In patient #1 apical thrombus was visualized on cardiac echocardiogram accounting for the MI after t-PA for acute stroke. Patient #2 had fresh thrombus seen on cardiac catherization after use of t-PA for acute stroke. Patient #3 developed a significant troponin rise 15 hours after the t-PA for stroke infusion with an echocardiogram revealing new wall motion abnormalities. Patient # 1 and #2 died secondary to multi-organ failure.

Discussion:

Acute MI immediately following t-PA treatment for stroke is a rare but serious complication. The disruption of intra-cardiac thrombus and subsequent embolization to the coronary arteries may be an important mechanism in the development of MI after t-PA treatment for acute ischemic stroke.

Résumé:

RÉSUMÉ:<span class='italic'><span class='bold'>Contexte et objectif</span></span>:

Les complications de la thrombolyse intaveineuse au moyen de l’activateur du plasminogène tissulaire (tPA) dans l’accident vasculaire cérébral aigu (AVCA) sont généralement reliées à l’hémorragie, à l’anaphylaxie ou à la réocclusion artérielle. Les complications emboliques de l’administration de tPA commencent à être reconnues depuis que le tPA est utilisé plus fréquemment pour traiter l’AVCA. Nous avons émis l’hypothèse que la perturbation d’un caillot intracardiaque peut provoquer un infarctus du myocarde (IM) suite à l’administration de tPA pour le traitement d’un AVCA ischémique.

<span class='italic'><span class='bold'>Sommaire des observations</span></span>:

Nous décrivons trois patients qui ont subi un IM immédiatement après l’administration IV de tPA pour le traitement d’un AVCA. Chez le patient #1, l’échocardiogramme a démontré la présence d’un thrombus apical expliquant l’IM après l’administration de tPA pour traiter un AVCA. Le cathétérisme cardiaque a montré que le patient #2 était porteur d’un thrombus frais suite à l’administration de tPA pour un AVCA. Le patient #3 a présenté une élévation significative de la troponine 15 heures après l’infusion de tPA pour un AVCA et l’échocardiogramme a révélé de nouvelles anomalies de la motilité de la paroi cardiaque. Les patients #1 et #2 sont décédés de défaillance multiviscérale.

<span class='italic'><span class='bold'>Discussion</span></span>:

L’IM immédiatement après l’administration de tPA pour un AVC est une complication rare, mais grave. La perturbation d’un thrombus intracardiaque et son embolisation subséquente à une artère coronaire peut jouer un rôle important dans la genèse d’un IM après l’administration de tPApour traiter unAVCA ischémique.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 34 , Issue 4 , November 2007 , pp. 417 - 420
Copyright
Copyright © The Canadian Journal of Neurological 2007

References

1. Compendium of Pharmaceuticals and Specialties, 2004. Canadian Pharmacists Association. 2004.Google Scholar
2. National Institute of Neurological Disorders and Stroke rt-PA Study Group. Tissue Plasminogen Activator for Acute Ischemic Stroke. N Eng J Med. 1995;333(24): 1581–7.Google Scholar
3. Hill, MD, Lye, T, Moss, H, Barber, PA, Demchuk, AM, Newcommon, NJ, et al. Hemi-orolingual angioedema and ACE inhibition after alteplase treatment of stroke. Neurology. 2003;60(9): 1525–7.Google Scholar
4. Stafford, PJ, Strachan, CJ, Vincent, R, Chamberlain DA: Multiple microemboli after disintegration of clot during thrombolyis for acute myocardial infarction. Br Med J. 1989; 299:1310–12.Google Scholar
5. Chang, GY. An ischemic stroke during intravenous recombinant tissue plasminogen activator infusion for evolving myocardial infarction. Eur J Neurology. 2001; 8: 267–8.Google Scholar
6. Meissner, W, Lempert, T, Saeuberlich-Knigge, S, Bocksch, W, Pape, U-F. Fatal Embolic Myocardial Infarction after Systemic Thrombolysis for Stroke. Cerebrovasc Dis. 2006;22:213–14.Google Scholar
7. Yasaka, M, Yamaguchi, T, Yonehara, T, Moriyasu, H. Recurrent embolization during intravenous administration of tissue plasminogen activator in acute cardioembolic stroke. A case report. Angiology. 1994;45(6):481–4.Google Scholar
8. Derex, L, Nighoghossian, N, Perinetti, M, Honnorat, J, Trouillas, P. Thrombolytic therapy in acute ischemic stroke patients with cardiac thrombus. Neurology. 2001;57:2122–5.Google Scholar
9. Sen, S, Laowatana, S, Lima, J, Oppenheimer SM: Risk factors for intracardiac thrombus in patients with recent ischaemic cerebrovascular events. J Neuol Neurosurg Psychiatry. 2004;75: 1421–5.Google Scholar
10. Abboud, H, Berroir, S, Labreuche, J, Orjuela, K. Amarenco P, GENIC Investigators. Insular involvement in brain infarction increases risk for cardiac arrhythmia and death. Ann Neurol. 2006 Apr;59(4):691–9.CrossRefGoogle ScholarPubMed