Uncommon Causes of acute coronary syndrome

Uncommon Causes of ACS

1. Uncommon Causes of ACSUncommon Causes of ACS
Dr Kumar Gunawardane
Director of Cardiology
The Townsville Hospital
Associate Professor of Medicine
James Cook University
Townsville Qld

2. Case Study 1Case Study 1
M.A.R
53 yr old Female
transferred for management of Post
AMI angina.

3. Day 1Day 1
Presented at Atherton Hospital
–Diagnosed with Anterior STEMI
–Tenecteplase 3 hours after pain onset
–Good response
–Complete resolution of ST segments
–Reperfusion Arrhythmias - NS-VT

4. Day 1 continuedDay 1 continued
Medications:
–Enoxaparin
–Atenolol
–Lisinopril
–ASA
–Atorvastatin
Enzymes:
Peak CK 2240
TnT 3.95
Post Infarct Angina
GTN Infusion commenced
Transferred to Mater Misericordiae Hospital,
Townsville

5. Risk FactorsRisk Factors
Mother had MI at age 47
Dyslipidaemia – on statin therapy
Depression
Also past history of migraine

6. Day 1 - Coronary AngiogramDay 1 - Coronary Angiogram
Findings:
–Mid LAD segment plaque rupture
Dissection
The rest of the coronary circulation was
free of significant stenosis or
atherosclerotic disease
Anterior hypokinesia

8. Day 1 - AngioplastyDay 1 - Angioplasty
Immediate PCI with stenting
ReoPro cover
2 Drug eluting stents successfully deployed
Uneventful recovery

9. Day 5 - EchocardiographyDay 5 - Echocardiography
Findings
–Ejection Fraction > 50%
–Hypokinesis of distal anterior wall and
apex as well as distal septum and apex
–Small Patent Foramen Ovale

10. Day 7 - DischargedDay 7 - Discharged
Well
–Medications
•ASA
•Clopidogrel
•Atorvastatin
•Lisinopril
•Metoprolol

11. Spontaneous Coronary Artery Spontaneous Coronary Artery
DissectionDissection
Primary spontaneous coronary artery dissection is a
rare cause of acute coronary syndrome (ACS) and
sudden cardiac death.
The presentation of ACS due to spontaneous dissection
is indistinguishable from those due to plaque rupture.
Historically, most cases ~ 30% were diagnosed via
angiography, ~ 70% post-mortem, reflecting the poor
prognosis associated with this condition.
Sudden cardiac death is a common manifestation.

12. Spontaneous dissection is extremely uncommon with
only about 150 cases reported in the literature since
1931 (Yonglin Pu et al. 2003).
3 Main categories
 Young females in puerperium
 People with atherosclerosis
 Idiopathic

13. Coronary dissections are more common following:
•percutaneous intervention (less significant now with
intracoronary stenting),
•coronary bypass grafting,
•and extension from proximal aortic dissection.

14. EpidemiologyEpidemiology
Average age 40 years
– Females affected 3-4:1 compared to males
80% Single Vessel Disease cases involve
LAD
When LMCA involved multivessel
involvement possible
80% females LAD,
60% males Isolated RCA

15. AetiologyAetiology
Post-partum (25%) haemodynamic and hormonal
changes in the puerperium implicated in weakening
vessel media collagen.
For pregnancy related coronary dissection the mean age
is 33 with mean time span of 20 days post partum.
OCP implicated through same mechanism as post-
partum dissection
Spontaneous dissection should always be suspected
when patients present with AMI in the post partum state.

16. Aetiology cont’dAetiology cont’d
Connective Tissue Disorders: SLE,
Marfan’s, Ehlers Danlos (especially Type IV)
Inflammatory: Kawasaki Disease
Cocaine and intense physical exertion
Idiopathic
Atheromatosis with plaque rupture and dissection,
involves the intima media junction.

17. Pathophysiology and HistologyPathophysiology and Histology
Possible mechanisms:
–weakened collagen in vessel wall
–haemorrhage of vasa vasorum into tunica media resulting
in intramural haematoma and dissection
In spontaneous cases the plane of dissection is in the outer
1/3 of tunica media or between media and adventitia
Expansion of subadventitial haematoma (false lumen) causes
compression of true lumen
Intravascular ultrasound (IVUS) can best characterize lumen,
thrombus, and presence of associated atheroma
Diffuse inflammatory infiltrate throughout adventitia thought to
be 2nd to dissection rather than primary mechanism

18. TreatmentTreatment
No established guidelines though:
Conservative management with complete healing of dissection
without intervention has been well documented.
This is an acceptable approach in the patient who remains
asymptomatic following initial presentation, but without Left main
involvement.
“early clinical suspicion and diagnosis with urgent coronary
angiography and aggressive treatment that includes
percutaneous angioplasty with stent implantation and cardiac
surgery could improve the prognosis of these patients”
Extreme care should be taken during cardiac cath +/-
angioplasty when engaging the artery.

19. Treatment continuedTreatment continued
Thrombolytics often administered in centers without primary
angioplasty - controversial
–may dissolve clot in false lumen and relieve the obstruction
–may increase intramural haematoma and compound an otherwise
self-limited dissection
–Therefore it is generally not recommended.
CABG for Left Main or multivessel involvement
–Marked survival benefit - some recommend CABG for all.
Intracoronary Stenting when technically appropriate

20. Treatment continuedTreatment continued
Intracoronary Stenting when technically appropriate
Ideal for single vessel and no Left main involvement.
Proven to be of mortality benefit
No reports of extension of dissection with antiplatelet therapy

21. MortalityMortality
Beyond initial mortality, there is a 20%
3-year mortality that is directly related to
infarct size and severity of LV
dysfunction.

22. ReferencesReferences
[Online] www.medicine.northwestern.edu/residentnet/Dan's%20stuff/
Spontaneous_Coronary_Artery_Dissection.doc [Accessed 01/06/2004]
Roig S, Gomez JA, Fiol M, Guindo J, Perez J, Carrillo A, Esplugas E, Bayes de Luna A.
Spontaneous coronary artery dissection causing acute coronary syndrome: an early
diagnosis implies a good prognosis. Am J Emerg Med. 2003 Nov;21(7):549-51.
Yonglin Pu, M.D., Ph.D., Tom R. Miller, M.D., Ph.D. , 03/22/03 Diagnosis: Spontaneous
Coronary Artery Dissection [Online] http://gamma.wustl.edu/mi023te15 .html
[Accessed 15/06/2004]
http://www.acc.org/education/online/cath%5Fmonth/0103/jan02%5F03.htm#1
http://www.acc.org/education/online/cath%5Fmonth/0604/june02%5F04.htm
FOR MORE INFO...

23. Case Study 2Case Study 2Day 1 Day 1 W.P. 58 years W.P. 58 years
chest pain
20:30QAS ASA + GTN
22.10TTH arrival
22:30Pain resolved
–AF - likely chronic, Rate 70, BP 180/105
–NonSTEMI, widespread minor ST -T changes
–TnT 20.9
Treatment:IVI GTN, ASA Clexane/Atorvastatin
Irbesartan and sotalol

24. BackgroundBackground
MI 1995
coronary angiogram - no significant stenosis, medical
management recommended.
Hypertension,Dyslipidaemia,Ex smoker of 20 years
Echo - Mild MR, moderate inferior and lateral
hypokinesia
Ulcerative colitis
Primary sclerosing cholangitis with persistently
abnormal LFT’s

25. Day 4 - Angiography FindingsDay 4 - Angiography Findings
Markedly abnormal ectatic arteries with
proximal aneurysms in the Cx and LAD.
Severe multiple stenoses in RCA with
thrombus
Possible vasculitis, but exhaustive antibody
screening was negative.

28. Day 9 - CABG x 3Day 9 - CABG x 3
SVG - acute marginal branch of RCA
Skip SVG graft to PDA & PL branches of RCA
Ligation of RCA and embolectomy
RCA biopsy - chronic adventitial inflammation.
No evidence of primary small vessel vasculitis

29. Uneventful recovery
remains in AF, otherwise well.
Declined cardioversion
Wishes to continue with medical treatment, which
includes standard therapy plus warfarin.

30. Coronary Artery Ectasia (CAE)Coronary Artery Ectasia (CAE)
Abnormal dilatation of coronary artery
wall

31. EpidemiologyEpidemiology
Incidence 2-3% of consecutive angiograms
Some evidence that incidence is increasing
No consensus regarding aetiology, prognostic
significance and morbidity

32. AetiologyAetiology
Primary or idiopathic CAE main cause: atherosclerosis
Secondary:
 ? Chronic exposure to vasodilatory substances
Angioplastic procedures
Possible other aetiologies:
– over stimulation of endogenous nitric oxide
– also can be associated with annuloaortic ectasia

33. Aetiology CAEAetiology CAE
Maybe related to chronic elevation of
acetylcholine
A cluster of cases observed in Australian
farmers exposed to herbicide spray containing an
acetyl cholinesterase inhibitor

34. Associated with increased coronary morbidity
eg. Vasospasm, spontaneous dissection and
thrombus formation
Not clear whether “iatrogenic’ ectatic arteries
are subject to same complications as
“idiopathic” CAE

35. ReferencesReferences
Pagel A, Horovitz M, Michovich Y, Rapoprt M. Coronary artery ectasia: a therapeutic
dilemma. Harefuah. 2002 Dec 141(12):1055-8.
Sorrell VL, Davis MJ, Bove AA. Current knowledge and significane of coronary artery
ectasi: a chronlogic review of the literature, reccomendations for treatment, possible
etiologies, and future considerations. Clinical Cardiology 1998 Mar 21(3): 157-60.
Hoshio A, Shirota K, DoiT, Sawada Y, Fukuki M, Kotake H, Mashiba H, Kasahara T, Endo
S. Coroanry artery ectasia with annuloaortic ectasia. Japanese Heart Journal 1994
May 35(3):389-94.
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36. TownsvilleTownsville
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