It is presentation about myocardial infarction in young patients

1. MYOCARDIAL INFARCTION
IN YOUNG

2.  A 19 years old married female homemaker by profession
came with complains of chest pain since morning 6.30 am ( 10
august 2022)- window period – 2 hrs
 HOPI- Patient had sudden onset severe retrosternal chest
pain associated with ghabrahat and sweating not radiating to
any site, since morning 6.30 am. Pain was present even at
rest, not decreasing by change in position, and it persisted till
she sought medical assistance. She had 1 episode of
vomiting containing food particles , non projectile.
 No h/o trauma
 No h/o palpitations
 No h/o any limb weakness
 No h/o bleeding from any site
 No h/o similar complains in past
 No family history of CAD
 She visited a private clinic nearby and was reffered to SMS
hospital for further management

3.  No history of diabetes mellitus/ hypertension/ CAD/
CVA/ COPD/ Koch’s
 She denies any addiction
 Past history- She is married since 6 months , had 6
weeks of amenorrhea – primi gravida . Her LMP
was- 10/ 06/ 2022. She had early failure of
pregnancy 10 days back, i.e on 1st august 2022.
She was admitted in Janana hospital for the same .
She had severe anemia with Hb – 4.7 gm%, 2 pints
of PRBC were transfused.
 She was treated with antibiotics and NSAIDS for 3
days , discharged on day 3.
 She developed chest pain after 10 days of early
failure of pregnancy.

4. ON 10TH AUGUST 2022
 O/E-
 Afebrile
 P- 120/min
 Bp- 70 mm Hg systolic
 Spo2- 94 %
 Cold extremities with persistant sweating +
 Pallor +
 No – cyanosis/ clubbing/ pedal edema
 CVS- S1, S2 normal , no murmur
 RS- air entry bilateral equal, no added sounds.

5. ECG – SUGGESTIVE OF INFERIOR WALL + RIGHT
VENTRICLE MYOCARDIAL INFARCTION

8. INVESTIGATIONS
Date 10/8/22 12/8/22 14/8/22
Hb 5.6 8.8 9.4
WBC 21,000 17,600 10,700
Platelet 2.4 lac 2.7 lac 2.5 lac
Creatinine 0.67 0.8 0.7
urea 18 14 21
Sodium/
potassium
141/ 3.5 139/ 4.2 142/ 4.0
PT (INR) 17.6 (1.52)
HHH Negative
TROPONIN
I
0.16
2D ECHO – RWMA+ , MID BASAL INFERIOR WALL AND IVS
AKINETIC, APEX- HYOKINETIC
NO E/O PFO/ ASD/ VSD
NORMAL LV SYSTOLIC FUNCTION , LVEF- 35%

9. MANAGEMENT
 Inj noradrenaline infusion started
 Loading done with tab aspirin 300 mg and tab
clopidogrel 600 mg
 Patient was posted for primary PCI
 Coronary angiography suggestive of-
- DVD/ DISTAL LCX-OM2 – 100% occlusion /
DISTAL LAD- 100% occlusion
 Intracoronary streptokinase 1 lac IU given
 2 pint PRBC was transfused i/v/o severe anemia
and Hb 5.6
 Recheck angiography done after 2 days –
suggestive of normal coronaries

10. CORONARY ANGIOGRAPHY

11. SPECIAL INVESTIGATIONS
 CRP- NEGATIVE
 ESR- 58 mm/hour
 ANA- Awaited
 RA FACTOR – negative
 APLA PROFILE-
-anticardiolipin Ab- IgG- 8.9/IgM- 3.0 (negative)
-lupus anticoagulant- negative
-anti beta 2 glyoprotein I Ab- negative
 ANCA: c- anca /p- anca- negative
 COAGULATION Profile – planned to be sent after 3
months

12. RECHECK ANGIOGRAPHY AFTER 2 DAYS OF
INTRACORONARY STK

13. DEFINITION
 Myocardial infarction is irreversible necrosis of
heart muscle secondary to prolonged ischemia
 YOUNG

14. CAUSES OF MYOCARDIAL INFARCTION IN
YOUNG
Normal coronaries Abnormal coronaries
Coronary artery spasm Accelerated atherosclerosis-
smoking, Diabetes, familial
hypercholesterolemia, combined
hyperlipidemia
Cocaine and amphetamine abuse Anomalous coronary arteries
Hypercoagulable states Myocardial bridging
Apla syndrome Spontaneous coronary artery
dissection
Peripartum, hypertension
Nephrotic syndrome Coronary artery aneurysm –
Kawasaki disease
Embolic phenomenon

15. MYOCARDIAL INFARCTION IN YOUNG
PATIENT
 MI in young is defined as patient suffering from MI
at athe age < 45 years
 Myocardial infarction in young individuals can be
grouped into 5 categories:
(1) MI related to traditional cardiovascular risk factors
similar to those in older individuals,
(2) use of recreational drugs such as cocaine and
methamphetamine,
(3)MI due to SCAD, myocarditis, or coronary
embolism(CE)
(4) MI due to atheromatous coronary artery disease
(CAD) but without critical coronary stenosis
(5) coronary vasospasm

17. Hematological causes-
1 polycythemia vera
2 thrombocytosis
3 DIC
4 Hypercoagulablility
Miscellaneous –
1 Cocaine abuse
2 Complication of
cardiac catheterisation
3 pregnancy related
MI
4 myocardial bridging

18. PREGNANCY AND MYOCARDIAL INFARCTION
Pregnancy is a risk factor for cardiac ischemic events,
relating to –
 Elevated LDL
 Hypercoagulable state
 Inflammatory changes associated with
preeclampsia and infection
 Hormonal weakening of arterial wall
 Increased vascular reactivity
 Use of prostaglandin analogues in postpartum
period
 Increased maternal age with increased risk factor
for atherosclerosis

19.  Incidence of MI in pregnancy- 3 per 1lac
 Case fatality rate- 5%
 Causes of case fatality are as follows
Sales
SCAD- 43%
CORONARY
ATHEROSCLERO
SIS- 40%
INTRACORONAR
Y THROMBUS-
17%
ICORONARY
SPASM - 2%

20.  STEMI is more common in pregnancy as compared
to NSTEMI
 SCAD-
- SCAD leads to formation of intramural hematoma
which encroaches on the true coronary lumen
- Types of SCAD-

21.  Diagnosis of SCAD is made with the help of IVUS or
OCT
 As SCAD is most common cause of STEMI I pregnant
female – thrombolysis is not recommended
 Thrombolytic agents do not cross placenta but can
cause maternal and placental bleeding
 Risk of iatrogenic catheter induced SCAD is 3% more in
pregnant women as compared to normal population
 Extended medical management is considered best for
SCAD as extension of SCAD occurs most probably after
7 days.
 PCI should be avoided as it can lead to further increase
in iatrogenic dissection
 Dual antiplatelet and beta blocker are prescribed
-Aspirin and clopidogrel are considered safe.
-3 year risk of upcoming coronary event in patient with
SCAD is about 30%

22. APLA SYNDROME
 Autoimmune thrombotic disease
 It is characterised by recurrent arterial or venous
thrombosis, recurrent first trimester fetal loss or in –
utero death and / or thrombocytopenia
 CVD most frequent thromboembolic manifestations
 MI with normal coronary arteries seen
 Coronary thrombosis and myocardial infarction can
complicate primary APS in 0.5% to 6%of patients , and
intracardiac thrombi can also occur
 Other cardiovascular diseases in APS are-
-Valvular abnormalities( libman sacks ensocarditis)
-Congestive cardiac failure- develops in 5% patients.

23. DIAGNOSTIC CRITERIA FOR APAS
Clinical criteria Laboratory criteria
1- vascular thrombosis- one or
more episodes of arterial or
venous thrombosis in any tissue or
organ
( determined by imaging , doppler
studies or histopathology)
2- recurrent first trimester
pregnancy loss
1- Anticardiolipin antibody of Ig G
or Ig M on 2 or more occasions 12
weeks apart
2- lupus anticoagulant in plasma
on 2 occasions at least 12 weeks
apart
3- anti b2 glycoprotein I Ab od Ig G
or Ig M isotype in serum or plasma
present on 2 occasions at least 12
weeks apart

24. APLA SYNDROME PATHOGENSIS

25. APLA SYNDROME APPROACH TO DIAGNOSIS

26. TREATMENT OF APLA SYNDROME
 Confirmed thrombosis in patients with APS requires
anticoagulation
 Target INR- 2.5 to 3.5
 Low dose aspirin – 81 mg/ day
 Aspirin alone does not provide protection against
deep venous thrombosis .
 Direct oral anticoagulants DOAC’s are to be
avoided in patient with high risk of thrombosis ( all
three abtibody positive)
 Instead of DOAC’s vitamin K antagonist are
preferred.
 Low dose steroids / IVIG or Rituximab

27. HYPERCOAGULABLE STATES
PRIMARY SECONDARY
Antithrombin deficiency
Antiphospholipid syndrome
Protein C Deficiency
Protein S Deficiency
FactorV Leiden
Disorders of fibrinolytic system
-Hypoplasminogenemia
-Abnormal plasminogen
-Plasminogen activator deficiency
Factor XIIdeficiency
Dysfibrinogenemia
Factor VIII elevation
Abnormalities of coagulation and
fibrinolysis
-Trossen syndrome
Nephrotic syndrome
Abnormalities of blood vessels and
flow
-Venous stasis
Homocysteinuria
Thrombotic thrombocytopenic
purpura
Abnormalities of platelets
-Myeloproliferative disorders
-Paroxysmal hemoglobinuria
-Diabetes mellitus

28. COAGULATION CASCADE

29. FACTOR V LEIDEN MUTATION
 Activated protein C resistance
 It is most prevalent thrombophilic syndrome
 Characterised by resistance of plasma to the
anticoagulant effect of activated protein C
 Venous thrombosis and fetal death seen
 Loss of principal APC cleavage site on factor V
protein --- resistance to inactivation of factor Va by
APC
 Heterozygosity: increases risk of thrombosis by by
2- 3 * folds
 Homozygosity increases risk ofthrombosis by 80*
folds

30. VASCULITIS AND MI
 Medium vessel vasculitis most commonly causes
coronary vasculitis and can lead to development of
MI in young patients
-Eosinophilic granulomatosis with polyangitis
-Wegener’s granulomatosis
-Polyarteritis nodosa
-Microscopic polyangitis
-Kawasaki vasculitis –
It causes coronary artery aneurysm in children less
than 5 years of age- causisng MI in < 5 years of
age

31. TAKAYASU ARTERITIS
 Takayasu arteritis is a chronic inflammatory disease of aorta and
its main branches
 It is a large vessel vasculitis
 F: M ratio= 10:1
 Most common affects – subclavian arteries and carotid arteries-
90%
 Pulmonary artery is affected in 50% patient- leading to PAH
 It rarely affects coronary arteries – rarely causes AMI
 In patients < 40 years of age following are indications of
takayasu’s arteritis-
-Unexplained acute phase response- ESR/ CRP
-Carotidynia
-hypertension
-Discrepent BP between arms(>10 mm hg)
-absent or week peripheral pulses
-limb claudication
-arterial bruit
-angina

32. SUBSTANCE ABUSE LEADING TO MI
 Cocaine use is associated with various cardiac
complications including MI- due to coronary spasm
 48% of non traumatic chest pain in young patients
are associated with cocain abuse
 Amphetamine use can lead to myocardial infarction
 Smoking causes earlier atherosclerotic changes
leading to MI in young age
 Binge alcohol consumption can lead to coronary
spasm

33. MANAGEMENT OF ACUTE MYOCARDIAL
INFARCTION
 Prehospital management
1) Patient education about symptoms of acute MI and
appropriate action to be taken
2) Prehospital evaluation , treatment and transport
 Management in emergency department –
1) Initial evaluation of patient with 12 lead ecg should be
done within 10 min of arrival.
2) If STEMI is present- initiate reperfusion therapy
Door to needle time of <30 min forr fibrinolytic therapy
Door to ballon time < 90 min
3) General measures-

34. -Loading of patient with -Tab aspirin 325 mg
-To control cardiac pain by analgesiscs – to decrese
sympathetic activity
-Nitrates – s/l if SBP> 100 mm Hg
-Beta blockers – to decrease infarct size , but to avoid
IV beta blockers in patients with > killip II class.
-Oxygen administration- only if SaO2 <90%
 Reperfusion therapy:
- Reperfusion therapy should be given as so as
possible – either by fibrinolysis or by PTCA.
- Primary PTCA should be performed as an
alternative to thrombolytic therapy , provided it can
be accomplished in time

35. GOLDEN PERIOD OF REPERFUSION

36. INTRACORONARY STREPTOKINASE
 A study was carried out to see effect of
intracoronary STK in patients after primary PCI.
 Intracoronary streptokinase given at low dose of –
1,40,000 IU post PCI – can lead to better
myocardial perfusion.
 Intrcoronary stk was also associated with lower
TIMI frame count.
 At the end of 6 months – there was no improvement
in LV size or function in group of patient receiving
intracoronary STK as compared to group not
receiving it.

37. SECONDARY PREVENTION
 Control of modifiable risk factors-
-smoking
-weight loss
-exercise
-cholesterol levels
-Strict blood sugar level control
-anti coagulant for hypercoagulable states
Modifiable risk factors should be aggresively
controlled in young patients at risk of MI

38. PROGNOSIS OF MI IN YOUNG
 Younger patients have better outcome during
medium and short term follow up due to better
baseline characteristics , but may have long term
morbidity and mortality.
 Greater influence of modifiable risk factors in
prognosis is seen in younger patients.
 There is increased prevalence of smoking ,
hypertension and obesity in younger patients with
MI.

39. THANK YOU