CardiologyDr. Rohit GoelIschemic Heart Disease

Part 2 of 3 in Diagnosis and Management of Ischemic Heart Disease

Heart Attack Diagnosis: ECG, Troponin, CK-MB and Echo

Written by Jivo Healthcare from the transcript of a Jivo Masterclass by Dr. Rohit Goel, Principal Consultant, Cardiology, Max Hospital, Gurugram, India, on . Drafted with AI assistance and edited by the Jivo team. Watch the recording.

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Heart attack diagnosis rests on two investigations: a 12-lead ECG (electrocardiogram) and cardiac biomarkers, troponin I or T and CK-MB. The ECG is the most urgent test, because ST elevation or a new left bundle branch block demands immediate treatment without waiting for blood results. Biomarkers then separate non-ST-elevation heart attack from unstable angina, a chest X-ray helps exclude dangerous mimics, and an echocardiogram adds early evidence of heart damage.

That is the diagnostic logic Dr. Rohit Goel, Principal Consultant, Cardiology at Max Hospital, Gurugram, India, at the time of the session (currently Associate Director - Cardiology at Max Hospital, Gurugram, India), set out for referring doctors. Each test answers a specific question, and the order in which the questions are asked matters as much as the tests themselves. This article follows that order, from the symptoms that should start the work-up to the angiogram that confirms the blockage. For how the diagnosis translates into treatment, see the complete guide to ischaemic heart disease.

Heart attack symptoms that should start the work-up

The classical presentation of acute coronary syndrome (ACS) is retrosternal chest pain, felt behind the breastbone, that radiates to the left side of the body: to the arms, the shoulder, the neck or the upper abdomen (epigastrium). Dr. Goel listed the accompanying features that complete the picture:

  • excessive sweating (diaphoresis)
  • a sense of impending doom
  • restlessness
  • nausea and vomiting
  • breathing difficulty

Women and people with diabetes often present differently. For these groups, Dr. Goel listed the atypical symptoms to watch for: dizziness, light-headedness, fainting (syncope), fatigue, jaw pain, neck pain, upper back pain, palpitations or epigastric discomfort. A patient with diabetes who reports only fatigue and upper abdominal discomfort may be having a heart attack. His instruction was simply to be careful with all of these symptoms. Dr. Biswarup Purkayastha's article on heart attack symptoms in women and diabetics explores this atypical presentation further.

Heart attack diagnosis: the first investigations

Every patient with chest pain needs an ECG and cardiac markers. Once a patient arrives with chest pain or an equivalent symptom, Dr. Goel's immediate investigations are:

  1. A 12-lead ECG, the most urgent test of all.
  2. Cardiac biomarkers: troponin I or troponin T, depending on availability, and CK-MB.
  3. A chest X-ray.

The ECG and cardiac markers are the two investigations recommended in every patient who presents with chest pain. Depending on the findings, the patient then needs an echocardiogram followed by coronary angiography where it is available.

ECG changes in a heart attack: the STEMI criteria

The diagnosis of ST-elevation myocardial infarction (STEMI) is made on the ECG, a recording of the heart's electrical activity. It rests on one of two findings:

  • ST-segment elevation: the segment between the QRS complex and the T wave sits above the baseline, the electrical signature of heart muscle injured by a completely blocked artery.
  • New-onset left bundle branch block (LBBB): a block in the conduction pathway to the left ventricle that widens the QRS complex. Under current ESC guidance, a patient with ongoing ischaemic symptoms and left bundle branch block is managed as STEMI whether or not the block is known to be new; a previous ECG for comparison remains valuable.

Cardiac biomarkers, both troponin I and CK-MB, are also raised in STEMI. But Dr. Goel was clear that the ECG alone triggers treatment: presence of ST elevation or new LBBB "mandates immediate action".

Locating the infarct: inferior and anterior wall MI

The leads that show ST elevation identify the territory of the blocked artery, and so the site of the infarct (the area of heart muscle that is dying; MI stands for myocardial infarction, the medical term for a heart attack). Dr. Goel illustrated two common patterns:

  • Inferior wall MI: marked ST elevation in leads II, III and aVF, with reciprocal ST depression in leads I and aVL. ST depression in V1, V2 and V3, as in the example Dr. Goel showed, signals that the infarct extends to the posterior wall.
  • Anterior wall MI: ST elevation in V1 to V4, with ST depression in II, III and aVF.

The ST depression in the opposite leads is called a reciprocal change: the same injury viewed from the other side of the heart. Its presence strengthens the diagnosis of a true infarct.

How quickly ST elevation appears, and how long it lasts

Answering a question from a doctor in the session, Dr. Goel explained that the earliest ST elevation appears within 15 to 30 minutes of the onset of symptoms. It persists for as long as the artery remains completely blocked, and it can still be present up to 48 hours later. If blood flow returns spontaneously, whether because of medicines or for reasons that are not always clear, the ST elevation settles; otherwise it persists until the artery is opened. A normal ECG in the first minutes of chest pain therefore does not exclude an evolving heart attack, and the ECG should be repeated if symptoms continue.

Cardiac biomarkers: troponin and CK-MB

Cardiac biomarkers are proteins released into the blood when heart muscle cells are damaged. Several have been used: troponin I or T, creatine kinase (specifically its MB fraction, CK-MB), lactate dehydrogenase and aspartate aminotransferase. Routinely, Dr. Goel advises troponin I or T, or CK-MB.

When troponin and CK-MB rise after chest pain

Biomarkers take time to rise. In Dr. Goel's account, CK-MB becomes detectable about four hours after the onset of chest pain, and troponin I after six to eight hours. Contemporary troponin assays usually become positive within about three hours, no later than CK-MB, and troponin is the preferred biomarker; CK-MB is now used mainly where troponin is unavailable. A blood test taken too early may be normal even when a heart attack is under way, which is why a single early test can mislead.

His answer is serial testing: measure CK-MB and troponin I at four- to six-hour intervals and look for a rising level across the samples. A single normal value early in the course proves nothing; a rise between two samples confirms myocardial damage.

Laboratories that offer high-sensitivity troponin assays can shorten this process considerably. The ESC recommends high-sensitivity troponin with rapid rule-in and rule-out protocols that compare a sample on arrival with a second sample one or two hours later.

Why biomarkers must never delay thrombolysis

Cardiac biomarkers have no value in deciding whether to thrombolyse a STEMI patient. This was a central point Dr. Goel made about what biomarkers cannot do: the markers may still be undetectable in the first hours after symptoms begin. Their value lies in non-ST-elevation myocardial infarction (NSTEMI) and unstable angina, where the ECG is not diagnostic. If the ECG shows STEMI, the instruction is unambiguous: do not wait for the blood test, and treat immediately.

How to tell STEMI, NSTEMI and unstable angina apart

The ECG separates STEMI from the other two forms, and the troponin result separates NSTEMI from unstable angina. Dr. Goel summarised the classification as a short decision sequence:

  1. Take the clinical history and examine the patient.
  2. Chest pain with ST elevation or new LBBB means STEMI. Treatment is thrombolysis or primary angioplasty (primary PTCA, percutaneous transluminal coronary angioplasty).
  3. Chest pain without ST elevation, with ST depression, T-wave inversion or even a normal ECG, means either NSTEMI or unstable angina. The biomarkers decide:
  • Troponin positive: NSTEMI.
  • Troponin negative: unstable angina.
  1. NSTEMI and unstable angina are treated medically with heparin or low molecular weight heparin, with or without a glycoprotein IIb/IIIa inhibitor. They are never thrombolysed.

In unstable angina the ECG may show ischaemic changes or be entirely normal, and the biomarkers are normal by definition. The diagnosis therefore rests mainly on a good clinical history and a careful examination.

Chest X-ray: excluding the conditions that mimic a heart attack

A chest X-ray helps exclude conditions that look like a heart attack. Dr. Goel sometimes adds one because acute coronary syndrome can mimic, or be mimicked by, other conditions, such as aortic dissection and pulmonary oedema. The X-ray helps to tell them apart, for example by showing a widened mediastinum in dissection or fluid in the lungs in pulmonary oedema.

Aortic dissection or heart attack: why it must be excluded before thrombolysis

Aortic dissection is a tear in the inner wall of the aorta that lets blood track between its layers. It can extend into a coronary artery and produce ST elevation on the ECG. Dr. Goel's warning was direct: when dissection is suspected in a patient with apparent STEMI, do not thrombolyse. Thrombolysis in such patients can propagate the dissection and cause sudden cardiac arrest and collapse. The diagnosis of STEMI must be secure before a thrombolytic is given.

The management of a confirmed dissection depends on which part of the aorta is involved. When it involves the ascending aorta or the arch, management is surgical. When it involves the descending thoracic aorta or the abdominal aorta, Dr. Goel noted that percutaneous (endovascular) repair is possible.

Echocardiography in a suspected heart attack

Echocardiography, an ultrasound scan of the heart, is now a first-line test alongside the ECG and cardiac enzymes. Asked whether cardiac ultrasound has any role, Dr. Goel answered that echocardiography is very important. In tertiary care hospitals, echo is done routinely in every suspected heart attack. It looks for three findings:

  • A regional wall motion abnormality: a segment of heart muscle that moves poorly because its blood supply has failed.
  • Valvular leakage, such as new mitral regurgitation.
  • Poor overall heart function.

Any of these can indirectly confirm an ongoing acute coronary syndrome and point to the need for immediate intervention. In Dr. Goel's words, echo can also pick up early signs of heart damage.

Coronary angiography: confirming the blockage

Coronary angiography, in which contrast dye is injected into the coronary arteries under X-ray, is the definitive test. It shows the exact site and severity of the blockage and leads directly to treatment. Dr. Goel showed two examples: a right coronary artery that was completely blocked, opened with a stent so that blood flow was fully restored; and a left anterior descending artery with a tight 95% narrowing causing a heart attack, likewise opened with a stent. In STEMI, angiography is followed straight away by angioplasty, which is covered in Thrombolysis vs Primary Angioplasty for STEMI: When to Refer.

The questions referring doctors asked about ECG timing, echocardiography and dissection are answered in full in the session's Live Discussion, and Dr. Goel's clinical background is on his doctor profile. For a different perspective on reading the ECG, including localisation of the culprit artery, see Dr. Vikas Thakran's article on STEMI, NSTEMI and unstable angina on the ECG. More heart care articles are on the cardiology specialty page.

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In This Series: Diagnosis and Management of Ischemic Heart Disease

  1. 1.Ischaemic Heart Disease Management
  2. 2.Heart Attack Diagnosis: ECG, Troponin, CK-MB and Echo
  3. 3.Thrombolysis vs Primary Angioplasty for STEMI: When to Refer
  4. 4.Live Discussion: 8 questions from doctors, answered by Dr. Rohit Goel

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