Acute Myocardial infarction in Young adult

Benny TM Togatorop

Critical Care and Clinical Cardiology Division

Department of Cardiology and Vascular Medicine
Faculty of Medicine University of Indonesia
 INTRODUCTION

 US annual death toll caused by CAD > 800.000.

 300.000 or more are estimated to die of acute
myocardial infarction before hospitalization
 Acute myocardial infarction occurs every 25 second and
the mortality of cardiovascular disease present every 36
seconds

Christofferson RD. Acute Miocardial Infarction. In : Griffin BP, Topol EJ, eds. Manual of cardiovascular
medicine. 3rd ed. Philadelphia: Lippincot Williams & Wilkins, 2009: 1-28.
 Indonesia ?

Kusmana D and Team : Jakarta Cardiovasculer Study; The city that promotes Indonesia Healthy Heart , Report I; 2006 *
Kusmana D : Pengaruh tidak/stop merokok disertai olah raga teratur dan/atau pengaruh kerja fisik terhadap daya survival penduduk di Jakarta ;
penelitian kohort selama 13 tahun. Disertasi, program studi Ilmu kedokteran S3 FK UI, Jakarta, 2002**
Incidence of MI and symptomatic CAD in
young adult about 3 % of all CAD
(Klein LW, J A m Coll Cardiol 2003, 41: 521)
 ACS in Young Adult in
NCVCHK*

2006: 10,1 % (92 among 962)

2007: 10,7% (117 among 1096)
2008: 10,1% (108 among 1065)

*Data from Medical Record Unit National Centre of Cardio Vascular

Harapan Kita, 2009
AIM OF PRESENTATION
The aim of this case presentation is to
present a case of a myocardial infarction in
young adult.
To elaborate some risk factors for
myocardial infarction in young adult
 CASE ILLUSTRATION

36 years old male Hospital Admission : Jan 14th, 2010

EMG NCCHK

Chief Complaint:
Shortness of breath since 2 weeks before
admission
 HISTORY OF PRESENT ILLNESS
24-12-2009 1-01-2010
Adam Malik Adam Malik Hospital
Hospital

•Chest pain • Shortness of breath (+)

•Shortness of breath (-) •Chest pain(-)
•Coronangiography:  Therapies:
Stenosis proximal RCA 70%, Farsorbid 3x 5 mg
mid RCA 60 %, mid LAD 85%, Aspilet 1x 80 mg
proximal LCX 100% Plavix 1x 75 mg
Sinvastatin1x 20 mg
Referred to NCCHK for CABG
PHYSICAL EXAMINATION
 Patient’s condition : looked moderately ill /CM
 Weight/height : 71 kg/ 163 cm
 BP : 103/67 mmHg
 HR : 94 bpm
 RR : 24/min
 Head : Conjunctiva was not pale and sclera was
not icteric
 Neck : JVP: 5-2 cmH2O
 Cardiac auscultation : normal S1 and S2, no murmur, no gallop
 pulmonary sound : vesicular with no rales, nor wheezing
 Abdomen : No ascites, no liver and spleen
enlargement, normal peristaltic sound.
 Extremities : warm, no oedema
 ECG
 

SR, QRS rate 94 x/i, axis + 900 , normal P wave, PR int 0,14 s, QRS dur 0,06 s, QS with inverted T
wave at V2 – V6, I, aVL
  
CHEST X-RAY

CTR 60 %, Normal Aorta segment, Normal pulmonary segment , cardiac waist (-), downward lateral
apex, congestion (-), infiltrat (-)
Laboratory
 Hb 12,5 mg/dl • Chloride 105 mmol /l
 leucosit 6530/ul
• Magnesium 1,8 mmol/l
 Ht 37
 CKMB 10 U/l • total cholesterol 169 mg/dl
 Trop T 0,13 ng/ml • Lp(a) 3,6 mg/dl
 Ureum 26 mg/dl • HDL cholesterol 21 mg/dl
 BUN 12,15 mg/dl
• LDL cholesterol 99
 Creatinin 1,2 mg/dl
 random blood glucose 95 • trigliserida 241 mg/dl
mg/dl
•total cholesterol:HDL
 sodium 137 mmol/l
 potassium 4,7m mol/l cholesterol ratio 8,05mg/dl
 total Calcium 2 m mol/l, •hsCRP 3,1 mg/dl.
TTE
Catheterization
DIAGNOSIS
HeartFailure Fc III ec recent anterior
MCI onset 21 days ec CAD 3 VD
Therapy
Aspilet 1 x 80 mg
Plavix 1 x 75 mg
Fasorbid 3 x 5 mg
Simvastatin 1 x 20 mg
Captopril 3 x 6,25 mg
Laxadine 1 x C1
Diazepam 1 x 5 mg
Aldactone 1 x 12,5 mg,
Concor 1 x 1,25 mg
LITERATURE REVIEW
 Many differences between young and older patients are
described
 Except classical risk factors leading to ACS other cardiac
predictors are being searched in the group of younger sick
persons.
 It is worth considering the importance of defects of
coagulation:
◦ proportions’ disorders of tissue factor,
◦ tissue plasminogen activator
◦ Leiden factor, protein C
◦ lipoprotein (a)
◦ mutations of propter genes (the role of the polymorphism in the
fibrinogen beta-chain gene, prothrombin gene, thrombopoetin gene).

Debska A and Lelonek M, Defects of coagulation and antiphospholipid antibodies in patients up to 40 years
old with acute coronary syndrome, Index Copernicus Journal Abstract, Arc Med Sci 2005; 1 (1): 34 - 36
 Novell risk factors as a potential new
screening tools
hsCRP
markers of inflammation
◦ lipoprotein(a)
◦ homocysteine
markers of fibrinolytic and hemostatic function
◦ fibrinogen
◦ D-dimer
◦ tissue plasminogen activator (t-PA)
◦ plasminogen activator inhibitor 1 (PAI-1) antigens

Riedker PM and Libby P. Risk Factor for atherotrombotic Disease. In: Zipes DP, Libby P, Bonow RO,
Braunwald E. Braunwald Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed. Philadelphia: Elsevier
Saunders, 2008: 1012 - 023.
TABLE 1 -- Clinical Epidemiology of Proposed Plasma-Based Biomarkers for
Prediction of Future Cardiovascular Events

Prospective Standardized Additive to Additive to

Studies Commercial Lipid Framingham
Biomarker Convincing? Assay? Screening? Risk Score?
Inflammation
hsCRP ++++ +++ +++ +++
sICAM-1 ++ ± + -
SAA ++ - + -
IL-6/IL-18 ++ - + -
Myeloperoxidase + - ± -
sCD40L + - - -
Altered thrombosis
t-PA/PAI-1 ++ ± - -
Fibrinogen +++ ± ++ -
Homocysteine ++++ +++ ± -
D-dimer ++ + - -
Oxidative stress- ± - - -
oxidized LDL
Altered lipids
Lipoprotein(a) +++ ± ± -
LDL particle size ++ ± ± -
Modified from Ridker PM, Brown NJ, Vaughan DE, et al: Established and emerging plasma biomarkers in the prediction of
first atherothrombotic events. Circulation 109(25 Suppl 1):IV6, 2004.
hsCRP = high-sensitivity C-reactive protein; IL = interleukin; LDL = low-density lipoprotein; PAI-1 = plasminogen
activator inhibitor-1; sICAM-1 = intercellular adhesion molecule-1; SAA = serum amyloid A; sCD40L = soluble CD40
ligand; t-PA = tissue plasminogen activator. Plus signs indicate increasing strength of evidence.(from reference no 6)
Table 2 Optimal cut-off levels and associated specificity, sensitivity and diagnostic value of
concentration of biomarkers for the diagnosis of angiographically documented coronary
artery disease
This patient is man and smoker
His lipid profile were:
◦ total Cholesterol 169 mg/dl
◦ HDL cholesterol 21 mg/dl
◦ LDL cholesterol 99 mg/dl
◦ trigliserida 241 mg/dl
◦ total cholesterol:HDL cholesterol ratio 8,05.
HisLp(a): 3,6 mg/dl
hsCRP: 3,1 mg/dl.
The American Heart Association and the
Centers for Disease Control and Prevention
issued guidelines in 2003 for the use of
hsCRP in clinical practice.

hsCRP levels less than 1, 1 to 3, and higher

than 3 mg/liter should be interpreted as
lower, moderate, and higher relative
vascular risk, respectively, when considered
along with traditional markers of risk.
PROVE IT-TIMI 22 clinical trial conducted in
patients with acute coronary syndromes
treated with statin therapy

achieving levels of hsCRP less than 2 mg/liter

was as important for long-term event-free
survival as was achieving levels of LDL
cholesterol less than 70 mg/dl; in fact, the best
long-term outcomes were found in those who
achieved both these goals.
 Relative risks of future myocardial infarction among apparently healthy women according to baseline levels of
lipoprotein(a), homocysteine, interleukin-6, total cholesterol, low-density lipoprotein (LDL) cholesterol, soluble
intercellular adhesion molecule-1 (sICAM-1), serum amyloid A, apolipoprotein B, ratio of total cholesterol to high-density
lipoprotein cholesterol (TC:HDLC), high-sensitivity C-reactive protein (hsCRP), and the combination of hsCRP with the
TC:HDLC.  (From Ridker PM: Clinical application of C-reactive protein for cardiovascular disease detection and
prevention. Circulation 107:363, 2003
RESUME
A case report of a 35 years old male, came to
emergency
chief complain: shortness of breath.
The patient has conventional risk factor such
as smoking and lipid disorder.
He also had high level of hsCRP as novel
risk factors.
The patient underwent successful PCI
procedure with 1 drug eluting stent in mid
part of LAD and discharge properly.
Ashen MD, N Eng J Med 2005, 353 : 1253
Zimmerman FH, JACC 1995, 26 : 654 - 61
Zimmerman FH, JACC 1995, 26 : 654 - 61
Zimmerman FH, JACC 1995, 26 : 654 - 61
Tsimikas S, et al. J Am Coll Cardiol 2006, 47 : C 20
Interheart

www.INTERHEART Nine modifiable risk factors predict 90%25 of acute MI.htm

Hs-CRP
 Largely on the basis of these data, the American Heart Association and the
Centers for Disease Control and Prevention issued guidelines in 2003 for the use
of hsCRP in clinical practice.[119] Briefly, hsCRP levels less than 1, 1 to 3, and
higher than 3 mg/liter should be interpreted as lower, moderate, and higher
relative vascular risk, respectively, when considered along with traditional
markers of risk. This critical finding has corroborated studies conducted
worldwide; all studies of adequate sample size have found the risk of hsCRP to
be independent of and additive to traditional risk factors ( Fig. 39-11 ). [57] [116] [120]
[121] [122] [123] [124]

 Screening for hsCRP should be done at the discretion of the physician as part of global risk
evaluation, not as a replacement for LDL and HDL testing. Although hsCRP predicts risk
across the entire population spectrum, its greatest usefulness is likely to be for those at
intermediate risk—that is, individuals with anticipated 10-year event rates between 5 and
20 percent. In a recent analysis of the impact that CRP makes on clinical risk prediction,
global risk prediction models that included hsCRP reclassified approximately 20 percent of
those otherwise considered to be at intermediate risk; moreover, the impact of hsCRP on
risk prediction was at least as large as that of lipid screening.[
Homocystein
 With regard to clinical trials of homocysteine reduction, several major studies
have been completed and none have shown substantive benefit. In the Vitamin
Intervention for Stroke Prevention (VISP) trial conducted among 3680 patients
with prior stroke allocated to high-dose or low-dose vitamin regimens
containing folate and pyridoxine, there was no evidence of differential benefit in
the high-dose group, despite greater homocysteine level reduction

 Finally, in the Heart Outcomes Prevention Evaluation (HOPE-2) trial of 5522

patients with vascular disease or diabetes, 5 years of therapy with folate,
vitamin B6, and vitamin B12 resulted in no benefit compared with placebo for
total vascular events (HR, 0.95; 95 percent CI, 0.84 to 1.07), cardiovascular
mortality (HR, 0.96; 95 percent CI, 0.81 to 1.13), or any of several prespecified
secondary endpoints.[154] As a group, these sharply negative trial results conflict
with the supposition made from studies of mendelian randomization that had
previously argued for a clear causal role between homocysteine concentration
and vascular events.[155]