Acute Myocardial Infarction:

Pathophysiology and Presentation

Thomas C. Smitherman University of Pittsburgh Medical Center

Acute Myocardial Infarction

750,000 documented acute MIs/year in USA Similar number of UAP Half of all deaths occur pre-hospital Up to 10% die during hospitalization 10% of survivors of initial MI die in year post MI, most suddenly, rest with re-MI

Acute MI Demographics and Statistics

3:1 to 4:1 male:female ratio in middle age. Equalizes with aging-in general women have MI about 20 years later First MI (men) in 50s, earlier with prominent risk factors Accounts for about 50% of all deaths in US

Thrombus Formation

Lesions

Necrosis

Evolution of Infarction

Acute Coronary Syndromes (ACS, Syndromes of Acute Myocardial Ischemia)

Terminology for Use after the first 24-48 h
Q wave MI Non-Q wave MI Unstable angina

Terminology for use in the first 24-48 h

SAMI with persistent ST-segment elevation SAMI without persistent ST-segment elevation

Acute MI
Electrical Consequences Ventricular Tachyarrhythmias VPBs
Simple Complex (frequent, multiform, couplets, R on T)

Ventricular Tachycardia
Polymorphic (ischemia) Monomorphic (re-entrant)

Ventricular Fibrillation Accelerated Idioventricular Rhythm

Acute MI
Electrical consequences
Bradycardia Sinus bradycardia AV block

Acute Myocardial Infarction

Electrical Consequences Bradycardia AV Block At the AV node
Usually with inferior/posterior MI Increased vagal tone (common) from Neurocardiac reflex or AV node damage (rare) 2o block of Mobitz I (Wenckebach) type 3o block usually slow in onset and heralded by 1o or 2o block Usually transient (hours or days)

Acute MI
Electrical consequences
Bradycardia
AV block Below AV Node
Damage to His-Purkinje system Usually with Anterior MI Often a/w prolonged QRS, BBB, Fasicular blocks 2nd degree block usually Mobitz II type 3rd degree block may occur suddenly

Acute MI
Electrical consequences
Atrial tachyarrhythmias
About 10% of cases Atrial fibrillation, atrial flutter, supraventricular tachycardia Usually due to atrial hypertension a/w higher mortality, because of association with atrial hypertension, larger MIs, more LV dysfunction

Acute MI
Functional consequences
Size of MI important because of effects on LV function Global systolic performance (LVEF and C.O.) are the most easily measured variables Diastolic LV dysfunction is universal but harder to measure and usually must be inferred The larger the MI, the greater the likelihood of CHF and shock Regional contraction patterns: hypokinesia, akinesia, dyskinesia Stunned myocardium

Acute MI
Mechanical complications
Myocardial rupture
Free wall, papillary muscle, IV septum

Cardiogenic shock RV Involvement with inferior MI LV aneursysm and thrombus

SHOCK IN ACUTE CORONARY SYNDROMES

Hypovolemic
Neurocardiac Reflex RV Involvement with IMI Typical Cardiogenic Shock

SHOCK IN ACUTE CORONARY SYNDROMES

Typical Cardiogenic Shock
> 35-40% of LV involved Low BP, high PCW, low CO, poor perfusion RA usually also elevated Historic death rate ca. 90%, now perhaps 40-60%

SHOCK IN ACUTE CORONARY SYNDROMES

RV Involvement with IMI
Proximal RCA occlusion High RA, CVP Underfilled LV causes LV stroke volume to drop

Acute MI
Mechanical complications
Left ventricular aneurysm and thrombus
12-15% of MIs Almost always with Q-wave MI True aneurysm never ruptures Soaks up LV contractile energy: worsens CHF Contributes to stagnant flow: increases risk of LV thrombus and thromboembolism, especially stroke. Risk highest in early days, lasts ca. 12 weeks

Acute MI
Mechanical complications
Ventricular ruptue
Ca. 10% of all MIs Risk factors: age, female, hypertension, first MI Dissection at infarct/viable muscle junction Ca. 90% free wall: hemopericardium, pericardial tamponade, pulseless electrical activity, worsening bradycardia, death within minutes. Rare case is subacute and may become a pseudoaneurysm, which almost always ruptures eventually.

Acute MI
Mechanical complications
Ventricular rupture
Papillary muscle rupture (ca. 10% of all ruptures)
Acute mitral regurgitation (MR) Dramatic onset of CHF and new murmur

IV septal rupture (ca. 10% of all ruptures)

Acute ventricular septal defect (VSD) Dramatic onset of CHF and new murmur

Distinguishing acute MR vs. acute VSD

Oxygen run of right heart Echo/Doppler interrogation

SHOCK IN ACUTE CORONARY SYNDROMES

Hypovolemic
Look for cause LV post-MI functions best with a slightly overfilled state: PCW ca. 16-18, PAD ca. 1820

Acute MI
Determinants of mortality
LV function LV size Status of infarct-related artery Presence & severity of ventricular rhythm disorders Presence of spontaneous or provokable (stress test-induced) ischemia Age

KILLIP CLASS POST MI

I. II. Uncomplicated MI, no abnormalities. Rales limited to the lower half of the lung fields and/or S3. III. Severe ventricular failure and acute pulmonary edema. IV. Typical cardiogenic shock.

Acute MI
Clinical presentation Symptoms potentially indicative of MI
New onset of chest discomfort that is suggestive of myocardial ischemia occurring at rest or with ordinary day-to-day activities A change in the angina pattern such that angina has become more frequent, severe, prolonged or difficult to relieve, or the occurrence of angina at rest for the first time Chest discomfort suggestive of myocardial ischemia in patient with known CAD that is unrelieved by rest or nitroglycerin

Discomfort Associated with the Acute Coronary Syndromes

Nature of discomfort Location of discomfort Duration > 15 - 20 minutes Associated dyspnea, diaphoresis, palpitations, nausea/vomiting History of & risk factors for ASHD

The Pain of Syndromes of Acute Myocardial Ischemia

The seven most common categories
A Pressure Heaviness Weight B Ache Soreness C Tightness Constriction Compression Choking Strangulation Vise-like Squeezing D Oppression Uncomfortable Discomfort Hard E Bursting Fullness Swelling F G Heartburn Burning Indigestion Searing

Discomfort Associated with the Acute Coronary Syndromes

Nature of discomfort Location of discomfort Duration > 15 - 20 minutes Associated dyspnea, diaphoresis, palpitations, nausea/vomiting History of & risk factors for ASHD

Discomfort with ACS--Location

Central or substernal Radiation to neck, jaw, shoulders, arms, upper back

Discomfort Associated with the Acute Coronary Syndromes

Nature of discomfort Location of discomfort Duration > 15 - 20 minutes Associated dyspnea, diaphoresis, palpitations, nausea/vomiting History of & risk factors for ASHD

Acute MI
Clinical Presentation AHA recommends seeking emergency treatment:
History of angina, known CAD: typical symptoms not relieved by 3 TNGs within 10 minutes Unrecognized CAD: typical symptoms lasting more than 2 minutes

Acute MI
Clinical Presentation
Many are clinically silentca. 25% of all Qwave MIs Physician must be alert to possibility of silent MI Pulmonary edema and stroke in appropriate patients should always raise question of acute MI

Acute MI
Clinical Presentation and Diagnosis Electrocardiography
Transmural injury: ST-segment elevation with flattening or concave downwards appearance. Q-wave evolution often follows. Subendocardial injury: ST-segment depression with flat or downgoing appearance. T-wave inversion less specific. Q-wave evolution unlikely. Fair correlation of leads with LV segments: Anterior: V1-V4; Inferior: II, III, aVF; Lateral: I, avL, V5-V6.

Baseline ECG and Outcome

GUSTO IIb
Six-Month Mortality
10% 8% 6% 4% 2% 0% 0 30 60 90 120 150 180
T-wave inversion

T-wave inversion ST-segment depression ST-segment elevation

ST
ST

Days from Randomization

The 12 Lead ECG - Ischemia, injury and infarction

The 12 Lead ECG - Ischemia, injury and infarction

Inferior Injury

The 12 Lead ECG - Ischemia, injury and infarction

Anterior Septal Injury with Infarction

Time Course for Cardiac Markers

* Recommended for use Limited use

Not used any longer

Figure adapted and modified from Abbott

Non-ischemic Causes of Elevated Troponin

Direct trauma to the heart and mechanical injury (such as ablation, angioplasty, cardiac surgery, cardioversion (implantable cardioverter defibrillator discharges) Myocardial toxins such as adriamycin or 5fluorouracil In response to endogenous substances released in critically ill patients (e.g., patients with septic shock) Cardiotropic viral infections, pericarditis, myocarditis Subendocardial injury in patients with increased wall stress (pulmonary embolism, hypertension, congestive heart failure, acute heart failure with shock, tachycardia, strenuous and prolonged exercise).