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ACUTE MYOCARDIAL INFARCTION FOLLOWING INTRAVENOUS
TISSUE PLASMINOGEN ACTIVATOR FOR ACUTE ISCHEMIC
STROKE : AN UNKNOWN DANGER
A CASE REPORT
DR. ASHOK KUMAR MISHRA
EMERGENCY MEDICINE CONSULTANT
AMRI HOSPITALS DHAKURIA, KOLKATA
AT 1.10PM PATIENT ARRIVED IN EMERGENCY
CNS ---- GCS -- E4V5M6
PUPIL NORMAL SIZE REACTING TO LIGHT
PLANTAR -- B /L FLEXOR
NO NEUROLOGICAL DEFECIT
POWER IN ALL LIMB 5/5
CVS --- S1S2 AUDIBLE
CHEST --- B/L VBS
P/A --- SOFT, IPS+
VITALS --- H.R. --- 78 BPM, B.P.-- 140/90MMHG, SAO2 -- 99% RA, CBG 202MG/DL
• PLAN --- CT SCAN BRAIN ( NCCT)
BLOOD FOR CBC, S.ELECTROLYTES, LIPID PROFILE
UREA, CREATININE, PT,APTT,INR,LFT
ECG 12 LEADS
CXR
CAROTID DOPPLER STUDY
TREATMENT -------------- IV ACCESS DONE
BLOOD SAMPLE SEND
ECG -------- SINUS RHYTM, REGULAR
CT SCAN BRAIN ( NCCT) AT 2.35PM ------
- NORMAL STUDY
• AT 3.20PM IN EMERGENCY DEPARTMENT
PATIENT SUDDENLY DEVELOPS
1) SLURRING OF SPEECH
2) FACIAL DEVIATION TO LEFT
3) RIGHT SIDE WEAKNESS OF
UPPER AND LOWER LIMB
• ON EXAMINATION-
• GCS-E3M6V4
• PLANTAR- RT-EXTENSOR, LT-FLEXOR
• POWER- RT-0/5 IN BOTH U&L
LIMBS,LT-5/5 IN BOTH U&L LIMBS
• BP-150/80
• HR-78/MIN
• RR-20/MIN
• SPO2-98% AT R.A
• CBG-202 MG%
NEUROLOGIST ATTENDED THE PATIENT AT
4PM
• AS ADVISED BY NEUROPHYSICIAN,PT.IS
BEING TREATED FOR ACUTE ISCHAEMIC
STROKE WITH THROMBOLYTIC THERAPY.
• THERE IS NO ABSOLUTE & RELATIVE
CONTRAINDICATIONS AGAINST
THROMBOLYSIS
• NIH STROKE SCALE - 13
• PT. SHIFTED TO ITU
• THROMBOLYSIS WAS DONE WITH
rTPA AS PER PROTOCOL
• ALL VITALS & NEUROLOGICAL
PARAMETERS ARE CHECKED
REGULARLY - NO ADVERSE EVENT
WAS DOCUMENTED DURING OR
IMMEDIATE AFTER THROMBOLYSIS.
• NEXT DAY -NEUROLOGICAL STATUS
SAME,REPEAT CT BRAIN
DONE,ANTIPLATELET & STATIN
STARTED AFTER 24HRS.
• AFTER 24 HRS ON 30/07/14 AT 6PM
CT SCAN BRAIN WAS REPEATED
SHOWS --- SUBACUTE INFARCT IN LEFT
BASAL GANGLIA - EXTERNAL CAPSULE
REGION
• ECHO - CONCENTRIC LVH,INFERO-
POSTERIOR WALL MILDLY
HYPOKINETIC,GRADE 2 DIASTOLIC
DYSFUNCTION,LVEF – 51%
• AT DAY3 OF ADMISSION,PT SHIFTED TO
HDU
• AT THAT NIGHT,PT DEVELOPED
PROGRESSIVE SOB,PROFUSE
SWEATING,TACHYCARDIA,
TACHYPNOEA,DESATURATION &
HYPOTENSION.
• CONSERVATIVE MANAGEMENT
FAILED,PATIENT WAS INTUBATED &
VENTILATED,PUT ON VASOPRESSOR &
IONOTROPIC SUPPORT.
• ECG REVEALED ACUTE INFERIOR WALL MI.
• CARDIAC BIOMARKERS ARE ALL ELEVATED.
• URGENT PCI DONE - REVEALED LCX
THROMBOTIC OCCLUSION,RCA TOTAL
OCCLUSION WITH RETROGRADE FLOW &
D1 ORIGIN STENOSIS.
ECG ON IST DAY ( 29/07/14)
ECG ON 31/07/14 AT 10.40PM
• PRIMARY PTCA TO LCX DONE.
• WITHIN 24HRS OF PTCA,CARDIOGENIC
SHOCK WAS STARTED TO IMPROVE -
IONOTROPIC & VASOPRESSOR SUPPORT
STOPPED,URINE OUTPUT IMPROVED
WITHIN NEXT 2DAYS.
• POST PTCA ECHO - EVIDENCE OF STUNNED
MYOCARDIUM POSTERO-INFERIOR WALL
GROSSLY HYPOKINETIC,LVEF 38%.
• THOUGH PULMONARY OEDEMA WAS
PERSISTING,BUT IMPROVED WITH
PHARMACOTHERAPY & MECHANICAL
VENTILATION SUPPORT IN NEXT 4DAYS.
• PT WAS EXTUBATED AT D5 OF PRIMARY
PCI.
• ENDOCRINOLOGICAL OPINION WAS TAKEN
- GLYCAEMIC CONTROL WAS DONE WITH
BOTH OHA & INSULIN THERAPY.
• PT WAS DISCHARGED ON D5 AFTER
EXTUBATION WITH
ANTIPLATELET,STATIN,DIURETIC,OHA
& INSULIN.
• THERE ARE ONLY FEW ARTICLES ON
Acute myocardial infarction after thrombolytic treatment of acute ischemic
stroke.
1) [Article in English, Portuguese]
Santos N1, Serrão M, Silva B, Pereira A, Faria P, Oliveira R, Caires G,
Pereira D, Freitas D, Araújo J.
• Thrombolytic treatment in patients with acute ischemic stroke improves their
clinical prognosis when administered within three hours of symptom onset.
We report the case of a 57-year-old patient with a history of paroxysmal atrial
fibrillation and hypertension who developed an anterior acute myocardial
infarction after systemic thrombolytic treatment for acute ischemic stroke.
Embolization of a pre-existing cardiac thrombus or in situ formation of a
thrombus in a coronary artery has to be considered as a potential adverse
effect of thrombolytic therapy in stroke patients.
2) Acute myocardial infarction following intravenous
tissue plasminogen activator for acute ischemic
stroke: An unknown danger
• Adatia Sweta, Sanghani Sejal, Sanzgiri Prakash,1 Chauhan Vinay, and
Hastak Shirish
• Department of Neurology, Lilavati Hospital and Research Center, Bandra
(West), Mumbai-400 050, India
• 1Department of Cardiology, Lilavati Hospital and Research Center,
Bandra (West), Mumbai-400 050, India
.
• Abstract
• Thrombolysis with intravenous tissue (IV) plasminogen activator (tPA) is
considered for patients with acute ischemic stroke falling within the described
inclusion criteria defined by The National Institute of Neurological Disorders and
Stroke (NINDS) rtPA trial. Complications of IV thrombolysis with tPA are
commonly related to hemorrhage, anaphylaxis, or arterial occlusion. We
describe two cases of acute myocardial infarction (MI) following IV tPA
infusion for acute stroke. One of the patients had underlying ischemic
heart disease (IHD) while the other did not have any prior IHD. Both had
presented with acute ischemic stroke within the window period of
thrombolysis and had no contraindications for thrombolysis. Both the
patients succumbed due to myocardial infarction and cardiovascular
collapse due to new onset arrhythmias. Acute MI immediately following IV
tPA for stroke is a rare but serious complication. The disruption of intracardiac
thrombus and subsequent embolization to coronary arteries may be an
important mechanism in the occurrence of MI after administration of tPA for
acute ischemic stroke. As both the patients succumbed before the
arrangement for coronary angiography, the demonstration of intracardiac
or intracoronary thrombus was not possible. But clinically, the presence
of chest pain with elevated troponin levels and ST segment elevation
pointed to MI. We suspect that fragmentation and lysis of intracardiac
thrombus may result in MI after use of tPA for acute ischemic stroke, though the
remote possibility of simultaneous occurrence of two atherosclerotic events MI
and stroke exists.
3) The West London Medical Journal 2011 Vol 3 No 1 pp 7-13
ST-ELEVATION MYOCARDIAL INFARCTION FOLLOWING
THROMBOLYSIS FOR ACUTE STROKE: A CASE REPORT
Bo Wang
Hitesh Patel*
Tom Snow
Ed Leatham
• ABSTRACT
• Diseases of the coronary and cerebral vasculature share common
aetiologies and hence are often linked. Whereas ischaemic stroke
following an acute myocardial infarction is relatively common, the converse
is much rarer. We present a case of a 69 year old patient with a ST-
elevation myocardial infarction three days after systemic thrombolysis for
acute ischaemic stroke. We discuss the possible underlying aetiologies
and the necessary investigations, and highlight the possibility of
thrombosis as a paradoxical complication of thrombolysis.
• KEY POINTS
• ST elevation myocardial infarction following an
acute stroke is not commonly seen and an
underlying aetiology should be investigated for
from several possible differentials.
• A prothrombotic state exists after systemic
thrombolysis that can contribute to
complications and impacts upon management.
Glycoprotein IIb/IIIa inhibitor can be considered
in patients with ischaemic cardiac chest pain
despite recent thrombolysis for stroke.
THANKS
Dr. Ashok Kumar Mishra
M.D. FEM
AMRI HOSPITAL DHAKURIA

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Presentation1

  • 1. ACUTE MYOCARDIAL INFARCTION FOLLOWING INTRAVENOUS TISSUE PLASMINOGEN ACTIVATOR FOR ACUTE ISCHEMIC STROKE : AN UNKNOWN DANGER A CASE REPORT DR. ASHOK KUMAR MISHRA EMERGENCY MEDICINE CONSULTANT AMRI HOSPITALS DHAKURIA, KOLKATA
  • 2. AT 1.10PM PATIENT ARRIVED IN EMERGENCY CNS ---- GCS -- E4V5M6 PUPIL NORMAL SIZE REACTING TO LIGHT PLANTAR -- B /L FLEXOR NO NEUROLOGICAL DEFECIT POWER IN ALL LIMB 5/5 CVS --- S1S2 AUDIBLE CHEST --- B/L VBS P/A --- SOFT, IPS+ VITALS --- H.R. --- 78 BPM, B.P.-- 140/90MMHG, SAO2 -- 99% RA, CBG 202MG/DL
  • 3. • PLAN --- CT SCAN BRAIN ( NCCT) BLOOD FOR CBC, S.ELECTROLYTES, LIPID PROFILE UREA, CREATININE, PT,APTT,INR,LFT ECG 12 LEADS CXR CAROTID DOPPLER STUDY TREATMENT -------------- IV ACCESS DONE BLOOD SAMPLE SEND ECG -------- SINUS RHYTM, REGULAR
  • 4. CT SCAN BRAIN ( NCCT) AT 2.35PM ------ - NORMAL STUDY
  • 5.
  • 6.
  • 7.
  • 8. • AT 3.20PM IN EMERGENCY DEPARTMENT PATIENT SUDDENLY DEVELOPS 1) SLURRING OF SPEECH 2) FACIAL DEVIATION TO LEFT 3) RIGHT SIDE WEAKNESS OF UPPER AND LOWER LIMB
  • 9. • ON EXAMINATION- • GCS-E3M6V4 • PLANTAR- RT-EXTENSOR, LT-FLEXOR • POWER- RT-0/5 IN BOTH U&L LIMBS,LT-5/5 IN BOTH U&L LIMBS • BP-150/80 • HR-78/MIN • RR-20/MIN • SPO2-98% AT R.A • CBG-202 MG%
  • 10. NEUROLOGIST ATTENDED THE PATIENT AT 4PM • AS ADVISED BY NEUROPHYSICIAN,PT.IS BEING TREATED FOR ACUTE ISCHAEMIC STROKE WITH THROMBOLYTIC THERAPY. • THERE IS NO ABSOLUTE & RELATIVE CONTRAINDICATIONS AGAINST THROMBOLYSIS • NIH STROKE SCALE - 13 • PT. SHIFTED TO ITU
  • 11. • THROMBOLYSIS WAS DONE WITH rTPA AS PER PROTOCOL • ALL VITALS & NEUROLOGICAL PARAMETERS ARE CHECKED REGULARLY - NO ADVERSE EVENT WAS DOCUMENTED DURING OR IMMEDIATE AFTER THROMBOLYSIS. • NEXT DAY -NEUROLOGICAL STATUS SAME,REPEAT CT BRAIN DONE,ANTIPLATELET & STATIN STARTED AFTER 24HRS.
  • 12. • AFTER 24 HRS ON 30/07/14 AT 6PM CT SCAN BRAIN WAS REPEATED SHOWS --- SUBACUTE INFARCT IN LEFT BASAL GANGLIA - EXTERNAL CAPSULE REGION
  • 13.
  • 14.
  • 15. • ECHO - CONCENTRIC LVH,INFERO- POSTERIOR WALL MILDLY HYPOKINETIC,GRADE 2 DIASTOLIC DYSFUNCTION,LVEF – 51% • AT DAY3 OF ADMISSION,PT SHIFTED TO HDU • AT THAT NIGHT,PT DEVELOPED PROGRESSIVE SOB,PROFUSE SWEATING,TACHYCARDIA, TACHYPNOEA,DESATURATION & HYPOTENSION.
  • 16. • CONSERVATIVE MANAGEMENT FAILED,PATIENT WAS INTUBATED & VENTILATED,PUT ON VASOPRESSOR & IONOTROPIC SUPPORT. • ECG REVEALED ACUTE INFERIOR WALL MI. • CARDIAC BIOMARKERS ARE ALL ELEVATED. • URGENT PCI DONE - REVEALED LCX THROMBOTIC OCCLUSION,RCA TOTAL OCCLUSION WITH RETROGRADE FLOW & D1 ORIGIN STENOSIS.
  • 17. ECG ON IST DAY ( 29/07/14)
  • 18. ECG ON 31/07/14 AT 10.40PM
  • 19.
  • 20.
  • 21.
  • 22.
  • 23. • PRIMARY PTCA TO LCX DONE. • WITHIN 24HRS OF PTCA,CARDIOGENIC SHOCK WAS STARTED TO IMPROVE - IONOTROPIC & VASOPRESSOR SUPPORT STOPPED,URINE OUTPUT IMPROVED WITHIN NEXT 2DAYS. • POST PTCA ECHO - EVIDENCE OF STUNNED MYOCARDIUM POSTERO-INFERIOR WALL GROSSLY HYPOKINETIC,LVEF 38%.
  • 24. • THOUGH PULMONARY OEDEMA WAS PERSISTING,BUT IMPROVED WITH PHARMACOTHERAPY & MECHANICAL VENTILATION SUPPORT IN NEXT 4DAYS. • PT WAS EXTUBATED AT D5 OF PRIMARY PCI. • ENDOCRINOLOGICAL OPINION WAS TAKEN - GLYCAEMIC CONTROL WAS DONE WITH BOTH OHA & INSULIN THERAPY.
  • 25. • PT WAS DISCHARGED ON D5 AFTER EXTUBATION WITH ANTIPLATELET,STATIN,DIURETIC,OHA & INSULIN.
  • 26. • THERE ARE ONLY FEW ARTICLES ON Acute myocardial infarction after thrombolytic treatment of acute ischemic stroke. 1) [Article in English, Portuguese] Santos N1, Serrão M, Silva B, Pereira A, Faria P, Oliveira R, Caires G, Pereira D, Freitas D, Araújo J. • Thrombolytic treatment in patients with acute ischemic stroke improves their clinical prognosis when administered within three hours of symptom onset. We report the case of a 57-year-old patient with a history of paroxysmal atrial fibrillation and hypertension who developed an anterior acute myocardial infarction after systemic thrombolytic treatment for acute ischemic stroke. Embolization of a pre-existing cardiac thrombus or in situ formation of a thrombus in a coronary artery has to be considered as a potential adverse effect of thrombolytic therapy in stroke patients.
  • 27. 2) Acute myocardial infarction following intravenous tissue plasminogen activator for acute ischemic stroke: An unknown danger • Adatia Sweta, Sanghani Sejal, Sanzgiri Prakash,1 Chauhan Vinay, and Hastak Shirish • Department of Neurology, Lilavati Hospital and Research Center, Bandra (West), Mumbai-400 050, India • 1Department of Cardiology, Lilavati Hospital and Research Center, Bandra (West), Mumbai-400 050, India .
  • 28. • Abstract • Thrombolysis with intravenous tissue (IV) plasminogen activator (tPA) is considered for patients with acute ischemic stroke falling within the described inclusion criteria defined by The National Institute of Neurological Disorders and Stroke (NINDS) rtPA trial. Complications of IV thrombolysis with tPA are commonly related to hemorrhage, anaphylaxis, or arterial occlusion. We describe two cases of acute myocardial infarction (MI) following IV tPA infusion for acute stroke. One of the patients had underlying ischemic heart disease (IHD) while the other did not have any prior IHD. Both had presented with acute ischemic stroke within the window period of thrombolysis and had no contraindications for thrombolysis. Both the patients succumbed due to myocardial infarction and cardiovascular collapse due to new onset arrhythmias. Acute MI immediately following IV tPA for stroke is a rare but serious complication. The disruption of intracardiac thrombus and subsequent embolization to coronary arteries may be an important mechanism in the occurrence of MI after administration of tPA for acute ischemic stroke. As both the patients succumbed before the arrangement for coronary angiography, the demonstration of intracardiac or intracoronary thrombus was not possible. But clinically, the presence of chest pain with elevated troponin levels and ST segment elevation pointed to MI. We suspect that fragmentation and lysis of intracardiac thrombus may result in MI after use of tPA for acute ischemic stroke, though the remote possibility of simultaneous occurrence of two atherosclerotic events MI and stroke exists.
  • 29. 3) The West London Medical Journal 2011 Vol 3 No 1 pp 7-13 ST-ELEVATION MYOCARDIAL INFARCTION FOLLOWING THROMBOLYSIS FOR ACUTE STROKE: A CASE REPORT Bo Wang Hitesh Patel* Tom Snow Ed Leatham • ABSTRACT • Diseases of the coronary and cerebral vasculature share common aetiologies and hence are often linked. Whereas ischaemic stroke following an acute myocardial infarction is relatively common, the converse is much rarer. We present a case of a 69 year old patient with a ST- elevation myocardial infarction three days after systemic thrombolysis for acute ischaemic stroke. We discuss the possible underlying aetiologies and the necessary investigations, and highlight the possibility of thrombosis as a paradoxical complication of thrombolysis.
  • 30. • KEY POINTS • ST elevation myocardial infarction following an acute stroke is not commonly seen and an underlying aetiology should be investigated for from several possible differentials. • A prothrombotic state exists after systemic thrombolysis that can contribute to complications and impacts upon management. Glycoprotein IIb/IIIa inhibitor can be considered in patients with ischaemic cardiac chest pain despite recent thrombolysis for stroke.
  • 31. THANKS Dr. Ashok Kumar Mishra M.D. FEM AMRI HOSPITAL DHAKURIA