Atherosclerotic heart disease part ii myocardial infarction
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Atherosclerotic Heart Disease Part II: Myocardial Infarction. Humayun J. Chaudhry, D.O., M.S., S.M., FACP, FACOI Chairman, Department of Medicine and Assistant Dean for Health Policy New York College of Osteopathic Medicine of NYIT September 21, 2005. Acute Myocardial Infarction.

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Atherosclerotic Heart Disease Part II: Myocardial Infarction

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Atherosclerotic Heart DiseasePart II: Myocardial Infarction

Humayun J. Chaudhry, D.O., M.S., S.M., FACP, FACOI

Chairman, Department of Medicine and

Assistant Dean for Health Policy

New York College of Osteopathic Medicine of NYIT

September 21, 2005

Acute Myocardial Infarction

  • When it happens…

    • Usually caused by sudden thrombotic occlusion of a coronary artery at the site of an atherosclerotic plaque that has become unstable due to a combination of ulceration, fissuring and rupture

    • CHF ensues if 25% or more of the left ventricle is infarcted

    • Cardiogenic shock ensues if 40% or more of the left ventricle is infarcted

    • Right ventricular ischemia or infarction occurs in up to ½ of inferior wall infarctions

EKG Findings

  • EKG Patterns for Localization of Infarct

    • Inferior wall MI: see changes in leads II, III and aVF

    • Anterior septal MI: see changes in leads V1, V2 and V3

    • Anterior wall MI: see changes in leads V2, V3 and V4

    • Lateral wall MI: see changes in leads V5, V6, I and aVL

  • ST segment elevation and T wave changes occur first, then Q waves form

Coronary syndromes have exploded since the early 1920’s

Trends in the Leading Causes of Death in the U.S., 1970-2002

  • Absolute # of deaths and age at death continue to increase

  • There have been decreases in death rates from stroke (63%), ASHD (52%) and accidents (41%)

  • There have been increases in death rates from COPD (200%) and DM (45%) since 1987

  • Source: Ahmedin Jemal et al, JAMA, 294(10): 1255-1259, September 14, 2005


  • Atherosclerotic plaques rich in foam cells that are susceptible to sudden plaque will rupture and hemorrhage into the vessel wall. This may result in the sudden partial or total occlusion of the coronary artery

  • After total occlusion, myocardial necrosis is complete in 4-6 hours. Flow to ischemic area must remain above 40% of pre-occlusion levels for that area to survive

  • Myocardial infarctions can be divided into Q-wave and non Q-wave, with the former being transmural and associated with totally obstructed infarct-related artery and the latter being non-transmural (subendocardial) and associated with patent vessels

  • Total occlusion of the left main coronary artery, which usually supplies 70% of the LV mass, is catastrophic and results in death in minutes.

Common Signs/Symptoms


- Arm, back, jaw, epigastrium, neck, chest


Lightheadedness, pallor, weakness, syncope

Nausea, vomiting, diaphoresis

Chest heaviness, tightness

Cough, diaphoresis, dyspnea, crackles, and wheezing

Hypercholesterolemia (increased LDL; decreased HDL)

Premature (<55) familial onset of coronary disease


Diabetes mellitus


Sedentary life style


Hostile, frustrated personality



Pertinent Risk Factors

Estimating future ASHD, developed by Framingham Heart Study Group, stratifies patients by their age, number and severity of their risk factors

S4/S3 heart sounds


Hypertension, hypotension

Levine’s sign

Jugular venous distention (JVD)



Bradycardia, tachycardia, or irregular pulses

Physical Exam

Serum Cardiac Markers

  • Troponin I

    • Becomes positive in 3-12 hours

    • Peaks at 24 hours

    • Remains elevated for 4-10 days

    • Highly sensitive in early detection of cardiac injury

    • Can be used to help decide whether it is safe to discharge patients who present to the emergency department with acute chest pain

    • Patients without ST segment elevations during pain and 2 negative troponin I determinations (one at least 6 hours after the onset of symptoms) have a low risk of death or fatal acute MI (0.3%) during the next 30 days.

Serum Cardiac Markers

  • CK-MB Fraction

    • CK-MB1 (plasma) and CK-MB2 (tissue)-myocardial necrosis can be detected earlier with subform analysis then with traditional CK-MB measurement

    • Within 6 hours CK-MB2 greater than 1.0 U/L with a ratio of CK-MB2/CK-MB1 greater than 1.5 is more sensitive and specific than CK-MB alone for diagnosis of MI

    • If a patient presents more than 24 hours after a presumed MI, and the CK isoenzymes are inconclusive, troponin I is now preferred over LDH

Early Assessment of Infarct Size

  • Currently, 2-D echocardiography is the technique used most frequently in the hospital course to evaluate acute MI infarction size

  • 2-D Echo reveals

    • Extent and location of ventricular wall abnormalities

    • Provides an assessment of overall ventricular function

    • Demonstrates left ventricular thrombus

    • Color flow doppler provides information about the extent of valvular disease and mechanical complications of acute MI

Approach to the patient with Acute MI

  • A. HistoryI. Aspirin

  • B. PhysicalJ. Oxygen

  • C. EKGK. Thrombolytic Therapy

  • D. EnzymesL. Heparin

  • E. Chest X-RayM. Angiography

  • F. NitratesN. PTCA with stenting

  • G. Beta-blockersO. CABG

  • H. Morphine sulfate P. GPIIB/IIIA inhibitors

Acute Reperfusion Therapy

  • Rapid reperfusion of the infarct related artery with IV thrombolytic therapy or primary PTCA is the main treatment strategy for acute MI

  • The main goal is to improve survival and outcome (decrease incidence of CHF)

  • The benefits of reperfusion therapy are time dependent: the sooner the blood flow is restored to the ischemic zone the greater the advantage in terms of survival and functional recovery









% ofPatients







Reperfusion of

Patency at

90 minutes

occluded arteries


Primary Outcome

Comparison of t-PA and Streptokinase

TIMI Study Group, N Engl J Med, 1985 (312): 397-401

Acute Reperfusion Therapy

  • Risk of hemorrhage

    • Age greater than 65

    • Weight less than 70 kg

    • Female

    • Hypertension

  • Although patients greater than 75 years have a greater risk of hemorrhage and stroke with thrombolytic therapy, they have a net benefit in overall outcome because of a significant mortality reduction with thrombolytic therapy

Thrombolytic therapy within the first six hours of a coronary event

After the first 10 hrs the mortality benefits decrease

Pt presents to ED s/p chest heaviness X3hrs

30 min post-arrival, terminal inverted T waves are noted septally

1 hr post-arrival the patient develops ST segment elevation in the anteroseptal walls

The lack of ST segment elevation decreases the mortality of a coronary event

Those with new LBBB (left bundle branch block) have worst prognosis

Management Protocol

No one thrombolytic has been shown to be superior, they differ really only by the Bolus and infusion rates…as well as price

Most important factor in treatment success with thrombolytics is time


Monitoring Reperfusion

TIMI Grade Flow Scoring System

Mortality at 42 Days

TIMI 0 Complete occlusion

TIMI 1 Penetration of obstruction by contrast but no distal perfusion

TIMI 2 Perfusion of entire artery but delayed flow

TIMI 3 Full perfusion, normal flow

P < 0.005

Flygenring BP et al. JACC 1991 (17): 275

GUSTO trial shows that the higher the TIMI grade for flow rate, the lower the mortality

2004 ACC/AHA STEMI Guidelines

  • 3 Major Areas of Revision

    • Preference for PCI over fibrinolysis in patients who present less than or equal to 12 hrs after symptoms and…

      • If PCI can be performed within 90 minutes of presentation by experienced personnel

    • Aggressive treatment of cardiogenic shock

    • Greater clarity regarding adjuvant therapy

Those patients Tx with frontloaded t-Pa as compared to streptokinase had achieved TIMI grade 3 in 54% of the time as compared to 33%

Meta-analysis shows the benefits of ß-blockade

Pt’s treated with B-blockers post infarction are seen to have a significant reduction in re-infraction

Adding an ACE-I dramatically reduces mortality

What about Nitrates?

And if Mg++ was added…

Discharge treatment after MI

  • Beta-blocker

  • ACE-Inhibitor or, if not tolerated, ARB

  • Aspirin

  • Lipid lowering drug - Statin

  • Folic Acid, Vit B6, Vit B12?

  • Clopidogrel

Hemodynamic Compromise

  • Patients who develop hemodynamic compromise (CHF, Hypotension, Cardiogenic shock) following AMI have a worse prognosis than those with little or no hemodynamic impairment

  • Management of hemodynamic compromise is aided by balloon flotation Swan-Ganz catheter. This catheter makes it possible to measure cardiac output and PCWP that reflect LVEDP and helps the physician adjust therapy according to the patient’s hemodynamic subset

Right Ventricular Infarction

  • Nearly 50% of patients with inferior wall MI have some evidence of right ventricular ischemia or infarction (it is hemodynamically significant in only about 10% of these patients)

  • Should be suspected with inferior MI when patient presents with a triad of hypotension, clear lung fields, and jugular venous distention (right atrial pressure greater than 10 mmHg)

Right Ventricular Infarction

  • Right sided EKG should be done in patients with inferior wall myocardial infarction

  • Treatment

    • Reperfusion therapy

    • Increasing preload by volume expansion (1 or more Liters of normal saline)

    • Cautious administration of Dobutamine

    • Diuretics and Vasodilators should be avoided

Papillary Muscle Rupture

  • Has a mortality of 80-90% with medical therapy

  • Prompt surgical therapy is indicated

  • Intra-aortic balloon pump may be needed prior to surgery

Ventricular Septal Defect

  • Has a mortality of 50% with surgical treatment and at least 90% with medical treatment

  • Surgical repair and CABG

  • Intra-aortic balloon pump prior to surgery

Rupture of LV free wall

  • Occurs in 10% of patients who die of an AMI

  • Sudden hemodynamic collapse often accompanied by severe chest pain suggests possibility of rupture of free wall

  • Echocardiogram is diagnostic

  • Emergency pericardiocentesis and use of intra aortic balloon pump to stabilize

  • Emergency surgery is definitive therapeutic approach

  • Event is almost always fatal even when emergency surgery attempted

LV Aneurysm and Mural Thrombus

  • Occurs in 10% of AMI patients

  • 80% located in anterior apical segment and result from occlusion of LAD coronary artery

  • Mural thrombus develops in about 50% of patients with anterior apical Q wave MI usually during the first week after infarction

  • Thrombi are uncommon in inferior wall AMI and rare in non-Q wave infarctions

LV Aneurysm and Mural Thrombus

  • Echocardiography is useful for identifying LV aneurysm and mural thrombi

  • 4% of AMI patients have embolic events during the first week after infarction

  • There is a 5-fold increase in embolic events in patients with anterior apical MI’s found to have a mural thrombus by echo

LV Aneurysm and Mural Thrombus

  • Other complications of LV aneurysms are CHF and ventricular aneurysms

  • Treatment - anticoagulation with Heparin followed by Warfarin for 3-6 months significantly decreases the frequency of embolic events

Assessment of Resting LV function

  • Prognosis following AMI is related to degree of LV dysfunction

  • Evaluation is done by echocardiogram, radionuclide imaging (MUGA study) or positron emission tomography.

  • Identify stunned and hibernating myocardium

Non-Invasive Strategies for Identifying Risk of Sudden Death

  • Holter moniter - PVC’s, nonsustained ventricular tachycardia

  • Signal averaged EKG

  • Heart rate variability

  • In patients at high risk of non-sustained V-tach and low LVEF (less than 40%), consider electrophysiologic testing and implantable cardioverter defibrillator (AICD)

Non-Invasive Strategies for Identifying Risk of Sudden Death

  • Multi-center automatic defibrillator implantation trial revealed (MADIT trial)

    • LV dysfunction less than 35%

    • Asymptomatic non-sustained V-tach (3 beats-30 beats)

    • Inducible, sustained, non-supressible V-tach

  • Patients with these criteria had improved survival with AICD.

ASHD really is worth preventing!

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