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Chapter: Medicine Study Notes : Cardiovascular

Myocardial Infarction (MI)

Old WHO definition: two out of three of: chest discomfort for > 30 minutes, enzyme rise and typical pattern of ECG involving the development of Q waves (ie normal ECG does not rule out infarction)

Myocardial Infarction (MI)


Definition and Classification


·         Old WHO definition: two out of three of: chest discomfort for > 30 minutes, enzyme rise and typical pattern of ECG involving the development of Q waves (ie normal ECG does not rule out infarction)

·        New definition: Blood levels of sensitive and specific markers are raised in the clinical setting of acute ischaemia (ie ­importance of biochemical tests). See Laboratory Diagnosis(Topic)


·        2 classifications:


o  ST elevation MI verses none (ie STEMI and non-STEMI). Often ST elevation progresses to Q wave


o  Q wave verses none (older classification) Þ transmural or not




·        Same risk factors as for atherosclerosis

·        5% occur under age 40, 45% over age 65

·        Oestrogen protective in women pre-menopause

·        30% mortality with 20% dying before admission




·        Crushing chest pain (absent in 15% of cases).  But < 25% with chest pain have an MI

·        Can also present as epigastric, arm, wrist, or jaw discomfort with exertion or at rest

·        May be associated with dyspnoea, sweating, nausea, vomiting, weakness, dizziness, fainting




·        Irreversible damage in 20 – 40 minutes

·        Occlusive intracoronary thrombus, overlying ulcerated or stenotic plaque:

o  Causes 90% of transmural acute MIs.

o  For blood to clot need: abnormal flow, damage to vessel wall and clotting factors.

o  Thrombis formation: activated platelets adhere to exposed collagen of damaged endothelium ® release thromboxane A2 ® expanding platelet mass + coagulation


·        Vasospasm: with or without atherosclerosis. Postulate where no findings at post-mortem (10%) – but many of these will be thrombi that have lysed

·        Emboli: from left sided mural thrombosis, vegetative endocarditis

·        Arteritis: polyarteritis nordosa, Kawasaki disease

·        Other: dissecting aneurysm occluding coronary ostia, ¯O2 supply (anaemia, CO, cyanide), ­O2 demand (hyperthyroidism, fever)


Gross Morphology


·        Transmural infarct: entire thickness of wall from endocardium to epicardium. Usually Anterior wall (50%) or posterior free wall/septum in 15 – 30%. Q wave


·        Subendocardial infarct: multifocal necrosis confined to inner 1/3 to ½ of left ventricle wall. More commonly associated with temporary hypoperfusion (eg shock). No Q wave


·        Occlusion:

o  LAD: 40 – 50%

o  RCA: 30 – 40%

o  LCA: 15 – 20%

·        Gross changes over time:


o   18 – 24 hours    Pallor of myocardium – anaemic, grey brown (cf normal brown-red)

o   24 – 72 hours    Pallor (yellow/brown) with increasingly defined hyperaemia border

o   3 – 7 days           Hyperaemic border (darker brick red) with central yellowing,

·        haemorrhagic areas

o   10 – 21 days      Maximally yellow and soft with vascular margins (red edge – granulation

·        tissues moves in)

o   7 weeks   White fibrosis


Microscopic Appearance


o   C    – 3 hours      Wavy myocardial fibres

o   2    – 3 hours      Staining defect with tetrazolium

o   4    – 12 hours    Coagulative necrosis with loss of cross striations, oedema, haemorrhage,

·        early neutrophil infiltrate (WBCs with multilobed nuclei), loss of

·        myocardial striations


Laboratory Diagnosis


·        Troponins:


o   Increases highly specific for MI injury – but not synonymous with MI or ischaemia, but probably indicates irreversible injury

o   Increases above the 99th percentile are significant (lower than previously)

o   Prognosis related to degree of elevation

o   Rises no faster than CK (ie starts to rise within 3 – 12 hours) and more expensive but substantial rise after MI (400 fold)

o   Causes besides MI:

§  Subendocardial injury from wall stress in left ventricular hypertrophy (eg heart failure)

§  Right ventricular injury in severe PE

§  Direct trauma (eg contusion)

§  Toxic injury by drugs or in septic shock

§  Myocarditis

§  Cardioversion

o   Troponin T

§  = Cardiac troponin T, cTnT, TnT: only available from Boehringer Mannheim

§  Normal < 0.03 mg/l

§  Increases in renal failure due to ¯clearance (Þ false positive)

o   Troponin I:

§  Everyone else‟s test.  Normal value depends on which assay is used

§  I remains elevated for 5 – 9 days and T for 2 weeks. Better marker for recent MI than LDH. Harder to interpret in re-infarct – don‟t know whether it‟s the 1st or 2nd infarct

o   Test on admission to either see if already raised (poor prognosis) or to establish baseline

·        CK – total: not specific to myocardial injury. Do baseline and use to check for reinfarction (Troponins not so good for this)

·        Older tests:

o   CK – MB fraction:

§  MM fraction is in both skeletal and myocardial muscle. But 15 – 40% of cardiac CK is MB, compared with 2% skeletal. BB found in brain, bowel and bladder. The MB fraction is therefore very specific


§  MB fraction rises within 2 – 8 hours. Dissipates within 1 – 3 days. So also a good marker of reinfarction

§  CK – MB isoforms: Ratio of isoform 2 to isoform 1 > 1.5 Þ early acute MI (changes before CK- MB elevated). Requires electrophoresis, so labour intensive. False positives with heart failure


o   Myoglobin: Oxygen binding protein in skeletal and cardiac muscle. Elevated before CK-MB, but is not specific to cardiac muscle. Negative myoglobin can help rule out MI


o   LDH: supplanted by other tests. Rises later (24 – 48 hours) and elevated for 7 – 14 days. Isoenzyme measurement of LDH 1 and 2 necessary for cardiac specificity


o   AST and ALT: intermediate timing but rather non-specific


·        Other Investigations: CXR, echo, ABG, FBC, ?perfusion scan, ?amylase  <



·        Exclude differentials:

o   Aortic dissection

o   Pericarditis

o   PE or other causes of pleuretic chest pain

o  Peptic ulcer

·        Investigations as for Unstable Angina(Topic)

·        They will be frightened.  Reassure.  > 90% survival if low risk (< 60, no diabetes, no past history, pulse <100)

·        High flow O2 (unless CO2 retaining)

·        Morphine 5 – 15 mg iv at < 1 mg/min (+ antiemetic eg metoclopramide 5 – 10 mg iv). Effects: analgesic, anxiolytic, anti-arrhythmic, venodilatory

·        Restoring/Maintaining vessel patency:

o  Aspirin 300 mg (unless contra-indicated)

o  Thrombolysis:

·        Indicated if with 12 hours of MI

·        Best within 60 mins

·        Contraindications:

o   General bleeding tendency: warfarin, haemophilia, severe liver disease, thrombocytopenia

o   Local bleeding risk: Past haemorrhagic stroke or recent surgery, prolonged resuscitation (® rib fractures, contusion, etc), peptic ulcer, GI bleeding, pregnancy, cavitating Tb

o   Severe hypertension (systolic > 200, diastolic > 120)

o   Pre-existing thrombis that might embolise (eg endocarditis, aortic aneurysm)

·        Options:

o   Streptokinase: restores perfusion in 30%

o   TPA: restores perfusion in 54%. Expensive. Use tPA if previous reaction to SK, or if SK has been used between 1 year and 5 days ago

·        Complications: 1% risk of stroke

·        Watch this space for platelet receptor blocking drugs (eg IIb/IIIa inhibitors)

o  Consider for primary angioplasty (acute stenting of an occluded coronary artery) if large anterior infarct refractory to thrombolysis

·        Management of preload, afterload and heart rate and rhythm:

o  Glyceryl trinitrate

o  ACE inhibitor + b-blocker (unless contra-indicated)

o  Bed rest

·        Monitor ECG, BP, cardiac enzymes, ABGs

·        Stop smoking

·        Early stress/treadmill test




·        Good prognostic indicators:

o  No pre-existing hypertension

o  Normal heart size

o  No post MI pulmonary oedema

o  No significant arrhythmias after day 1

o  No post-MI angina


·        If good prognosis, discharge on aspirin and b-blocker. Add an ACE inhibitor if ¯LVF. Consider a statin if ­lipids.




·        35% die within one year, 10% per year thereafter.  NZ overall hospital mortality 19%


·        Arrhythmias and conduction defects: eg premature ventricular beats, sinus bradycardia, VT, VF, heart block


·        Extension of infarction, re-infarction


·        Congestive heart failure (pulmonary oedema): everyone who‟s had a significant MI will have some degree of this


·        Cardiogenic shock: if more than 40% of the left ventricle is infarcted.  70 – 90% die


·        Pericarditis: fibrinous adhesions in the pericardium overlying the infarct (Dressler‟s syndrome – autoimmune adherent pericarditis – occurring 2 – 6 weeks post MI or cardiac surgery. Treatment - steroids)


·        Mural thrombosis ® embolisation


·        Myocardial rupture ® tamponade. Maximum incidence day 5 - 7. Can include rupture of interventricular septum


·        Papillary muscle rupture or infarct ® mitral incompetence


·        Ventricular aneurysm formation: 12 – 20% of cases


·        Ischaemic cardiomyopathy: severe atherosclerosis involving all major branches ® inadequate vascular supply ® myocyte loss and interstitial fibrosis ® ¯compliance & dilation ® compensation by myocyte hypertrophy ® slow progressive heart failure and enormous heart size (up to 2 to 3 times normal)


·        Time to complications:

o   1 – 3 days: arrhythmia, CHF, pericarditis

o   5 – 7 days: rupture

o   Later: recurrent MI, angina, embolism from mural thrombosis, mitral regurgitation, Dressler‟s syndrome (Post MI syndrome)


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