ECG as Evidence of Heart Disease

Dr. Minhaj Rahim Choudhury

Acute Coronary Syndrome

Causes of ACS:

• ST elevation (Q-wave) MI (STEMI)

• Non-ST elevation (non-Q wave) MI (NSTEMI)

• Unstable angina (UA)

Acute MI

Diagnosis of ac MI relied on revised criteria of WHO (1979):• Chest discomfort characteristic of

ischemia • Typical ECG pattern including

development of Q waves • Typical elevations in serum markers of

myocardial injury, usually creatine kinase (CK)-MB

• Patients with typical chest pain, no evidence of ST elevation or Q waves, and elevated CK-MB would have an NSTEMI.

• In comparison, patients with an unstable pattern of chest pain, possible ECG changes of ischemia but no ST elevation or Q waves, and normal CK-MB would have UA.

• This definition of MI is too restrictive. Many pts with ac MI have no recognizable symptoms, a substantial number have ECG with nonspecific changes or may even be normal, & some pts have normal serum CK-MB but ↑ troponins.

• According to WHO criteria, pt with ischemic symp, no ST elevation, & normal serum CK-MB but ↑ serum troponins would be considered to have UA.

As a result of these limitations, joint European Society of Cardiology (ESC) & American College of Cardiology (ACC) committee proposed following definition of an acute, evolving, or recent MI in 2000:

• Typical rise & gradual fall (troponin) or more rapid rise & fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following:

•     a.  Ischemic symptoms     b.  Development of pathologic Q waves on the ECG     c.  ECG changes of ischemia (ST segment ↑ or ↓)     d.  Coronary artery intervention (eg, angioplasty)

• Pathologic findings of an ac MI

• According to this definition & guidelines published by the ACC & American Heart Association (AHA) in 2002, UA & NSTEMI differ primarily in whether ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury.

• UA is present in pts with ischemic symptoms suggestive of an ACS & no ↑ in troponins or CK-MB, with or without ECG changes indicative of ischemia (eg, ST segment ↓ or transient ↑ or new T wave ↓).

• Since an ↑ in troponins &/or CK-MB may not be detectable for hrs after presentation, UA & NSTEMI are frequently indistinguishable at initial evaluation.

• ST segment &/or T wave changes are often persistent in NSTEMI while, if they occur in UA, they are usually transient.

Established MIAny one of following 2 criteria satisfies diagnosis

for an established MI:• Development of pathologic Q waves (0.04 sec)

on serial ECGs. • The pt may or may not remember previous

symp. • Biochemical markers of myocardial necrosis

may have normalized, depending upon the length of time that has passed since the MI occurred.

• Pathologic findings of a healed or healing MI

Definitions: anginaDefinite angina

Substernal discomfort precipitated by exertion, with a typical radiation to the shoulder, jaw or inner aspect of the arm relieved by rest or nitroglycerin in less than 10 minutes

Probable angina

Has most of the features of definite angina but may not be entirely typical in some aspects

"Probably not" angina

Defined as an atypical overall pattern of chest pain that does not fit the description of definite angina

"Definitely not" angina

Chest pain is unrelated to activity, appears to be clearly of non-cardiac origin and is not relieved by nitroglycerin

Non-ischemic cardiovascular:

Aortic dissection*

Myocarditis

Pericarditis

Chest wall:

Cervical disc disease

Costochondritis

Fibrositis

Herpes zoster (before the rash)

Neuropathic pain

Rib fracture

Sternoclavicular arthritis

* Potentially life-threatening conditions.

Alternative diagnoses to cardiac ischemia for patients with chest pain

Gastrointestinal:

Biliary

Cholangitis

Cholecystitis

Choledocholithiasis

Colic

Esophageal

Esophagitis

Spasm

Reflux

Rupture*

Pancreatitis

Peptic ulcer disease

Nonperforating

Perforating*

Pulmonary:

Pleuritis

Pneumonia

Pulmonary embolus*

Tension pneumothorax*

Psychiatric:

Affective disorders (eg, depression)

Anxiety disorders

Hyperventilation

Panic disorder

Primary anxiety

Somatiform disorders

Thought disorders (eg, fixed delusions)

* Potentially life-threatening conditions.Adapted with permission from: ACC/AHA/ACP Guidelines for the Management of Patients with Chronic Stable Angina. J Am Coll Cardiol 1999; 33:2092. Copyright ©1999 American College of Cardiology.

ACS without chest pain• Some pts with an ACS present with

atypical symptoms rather than chest pain.

• Review of over 430,000 pts with confirmed ac MI from National Registry of MI 2, 1/3 had no chest pain on presentation to the hospital. These pts may present with dyspnea alone, nausea &/or vomiting, palpitations, syncope, or cardiac arrest. They are more likely to be older, diabetic, & women.

ECG CHANGES

The ECG is mainstay in initial diagnosis of

ac MI. It allows initial categorization of pt.

• STEMI or new LBBB

• NSTEMI or UA (ST-depression, T-wave inversions, or transient ST-elevation)

• Undifferentiated chest pain syndrome (non-diagnostic ECG)

ECG Changes in STEMI• Initially, there is elevation of the J point & ST segment

retains its concave configuration.

• Over time, the ST segment elevation becomes more pronounced & ST segment becomes more convex or rounded upward.

• The ST segment may eventually become indistinguishable from the T wave; the QRS-T complex can actually resemble a monophasic action potential.

• An initial Q wave (typically 0.04 sec in duration) develops over a period of several hours to days and there is a loss of R wave amplitude. The joint ESC/ACC committee for the redefinition of myocardial infarction also redefined abnormal Q waves.

• According to the previous criteria, an abnormal Q wave was defined as a duration 40 msec and/or a depth 25 percent of the R wave in the same lead or the presence of Q wave equivalent (an initial R wave 0.1 mV) in any two contiguous leads.

• According to the new criteria, an abnormal Q wave was any Q wave in leads V1 to V3 or a Q wave 30 msec in leads I, II, aVL, aVF, or V4 to V6; the Q wave must be present in any two contiguous leads and 1 mm in depth.

Absence of Q waves• A subset of pts with an ACS present with

initial ST segment elevation but no Q waves.

• These pts are treated for an ST elevation MI & some never develop Q waves. Such pts have a better prognosis than those who develop Q waves because of more frequent reperfusion, a less severe infarction, &, at follow-up, better left ventricular function and improved survival.

Localization

• The ECG leads can also localize the MI. ST elevation and/or increased T wave positivity are seen in:

• One or more of the precordial leads (V1-V6) and in leads I and aVL with acute transmural anterior wall ischemia

• Leads V1 to V3 with anteroseptal ischemia • Leads V4 to V6 with apical or lateral ischemia • Leads II, III, and aVF with inferior wall ischemia • Right-sided precordial leads with right ventricular

ischemia

Other causes of ST elevation Myocardial ischemia or infarction

Noninfarction, transmural ischemia (Prinzmetal's angina pattern or acute takotsubo cardiomyopathy)

Acute myocardial infarction (MI)

Post-MI (ventricular aneurysm pattern)

Previous MI with recurrent ischemia in the same area

Acute pericarditis

Normal "early repolarization variants"

Left ventricular hypertrophy or left bundle branch block (only V1-V2 or V3)

Others

Myocarditis (may look like myocardial infarction or pericarditis)

Brugada patterns (V1-V3 with right bundle branch block-appearing morphology)

Myocardial tumor

Myocardial trauma

Hyperkalemia (only leads V1 and V2)

Hypothermia (J wave/Osborn wave)

Causes of Q waves

Physiologic or positional factors

Normal variant "septal" q waves

Normal variant Q waves in leads V1,V2, aVL, III, and aVF

Left pneumothorax or dextrocardia: loss of lateral precordial R wave progression

Myocardial injury or infiltration

Acute processes: myocardial ischemia or infarction, myocarditis, hyperkalemia

Chronic processes: myocardial infarction, idiopathic cardiomyopathy, myocarditis, amyloidosis, tumor, sarcoid, scleroderma, Chagas' disease, echinococcus cyst

Ventricular hypertrophy or enlargement

Left ventricle: slow R wave progression in which there are small or absent R waves in the mid-precordial leads

Right ventricle: reversed R wave progression in which there is a progressive decrease in R wave amplitude from V1 to the mid-lateral precordial leads, or slow R wave progression, particularly with chronic obstructive lung disease or acute pulmonary embolism

Hypertrophic cardiomyopathy - may simulate anterior, inferior, posterior, or lateral infarcts

Conduction abnormalities

Left bundle branch block - slow R wave progression in which there are small or absent R waves in the mid-precordial leads

Wolff-Parkinson-White patterns

Time course of markers for MITest Onset Peak Duration

Creatine kinase - total and MB (Hrs)

3-12 18-24 36-48

Troponins (Hrs) 3-12 18-24 Up to 10 days

Myoglobin (Hrs) 1-4 6-7 24

Lactate dehydrogenase (Hrs)

6-12 24-48 6 to 8 days