A 49-year-old man presented to the emergency department (ED) with substernal chest pain that had started an hour earlier. The pain radiated to the left arm, was constant, and was associated with diaphoresis, nausea, and dyspnea. A similar episode 4 days earlier had spontaneously resolved. He denied fever or chills, pleuritic chest pain, vomiting, and diarrhea.
The patient smoked but denied current use of alcohol(Drug information on alcohol) or illicit drugs; however, he had used heroin in the past. He had no history of hypertension, hyperlipidemia, diabetes mellitus, or coronary artery disease. Three of his second-degree relatives had died of myocardial infarction in their 60s.
He was in moderate distress and diaphoretic. Blood pressure was 138/94 mm Hg; heart rate, 72 beats per minute; respiration rate, 22 breaths per minute; and temperature, 36.8ºC (98.1ºF). Oxygen saturation was 100% on room air. Heart, lung, and abdominal findings were normal. Extremities had equal pulses with no edema or cyanosis.
Results of the initial bedside troponin test were negative; however, the creatine kinase-MB fraction was elevated at 155 ng/mL (normal, 0 to 5 ng/mL), or 9% (normal, 0% to 3.5%). The glucose level was slightly elevated; electrolyte levels were otherwise normal. A chest radiograph showed poor inspiratory effort with no cardiomegaly, focal infiltrate, pleu-ral effusion, or pneumothorax. The initial ECG revealed normal sinus rhythm with normal intervals and hyperacute T waves in the anteroseptal precordial leads (V1 to V3) (Figure 1). The patient was given aspirin, metoprolol(Drug information on metoprolol), heparin(Drug information on heparin) bolus, and heprin drip according to acute coronary syndrome protocol. After a cardiology consultation, he was transferred to the cardiac catheterization laboratory.
HYPERACUTE T WAVES: AN OVERVIEW
The T wave represents the period of ventricular repolarization on the surface ECG. Normal T waves are symmetric; however, the amplitudes vary with the electrode placement as well as with the patient’s age and sex.
T-wave amplitude is typically greatest in leads II and V4; it decreases with age and is relatively greater in men than in women. Despite these variations, T-wave amplitude tends to track with the QRS amplitude. It is always greater than the amplitude of the U wave, if the latter is present.1 T-wave amplitudes of 0.50 mV and 1.0 mV in the limb and precordial leads, respectively, are the generally accepted upper limits of normal.2
T waves may be tall, peaked, prominent, tented, or hyperacute, depending on the associated illness or event. Prominent T waves are classically associated with the early phase of an ST-segment elevation acute myocardial infarction (STEMI).2 These changes are usually present for only 5 to 30 minutes after the onset of the infarction and are rarely seen on the initial ECG in the ED.3
Causes. Although the differential diagnosis of hyperacute T waves is broad (Table), a thorough history and basic laboratory data can help differentiate the cause. For example, hyperkalemia is the likely cause in a patient who missed a dialysis session, whereas benign early repolarization (BER) is more likely in a young, healthy patient. Left ventricular hypertrophy (LVH) is also commonly associated with prominent T waves.
The earliest ECG finding associated with hyperkalemia is symmetric T waves described as tall, peaked, or tented. They are usually most prominent over the precordial leads. This is generally seen when the serum potassium level exceeds 6.5 mEq/L. If you suspect hyperkalemia as the cause of the T-wave abnormality, inspect the ECG for other signs of renal failure, such as prominent T waves, QT prolongation, and evidence of LVH.1,2
In BER, the ECG usually shows diffuse ST elevation with upward concavity that arises from a notched or slurred distal QRS complex and terminates in symmetric, tall T waves.2 Diffuse T-wave abnormalities are also seen in acute pericarditis. Both BER and pericarditis must be differentiated from an acute myocardial infarction (AMI), because the treatment is quite different. The ECG changes of pericarditis and BER tend to be static during the clinical encounter, whereas those seen in acute STEMI are dynamic as the clinical picture changes over time.
LVH is the presumed cause of prominent T waves in patients with a history of long-standing hypertension. Other ECG criteria of LVH should be obvious—prominent R-wave voltages across the left precordial leads (and prominent S waves or QS waves in the right precoridal leads), slight prolongation of the QRS duration, and a leftward shift in QRS axis. Left ventricular strain, in which the direction of the ST segment and T waves is opposite to that of the QRS complex, may be seen. The prominent T wave is asymmetric in these cases.1,2
ECG FINDINGS IN EARLY AMI
The earliest ECG changes associated with an AMI are increased amplitude of the R and T waves, followed by ST-segment elevation, loss of the R wave, and subsequent development of the Q wave. In other cases of AMI there is greater positive deviation of the T wave without an increase in the R wave—this description applies to the hyperacute T wave of early AMI.3
Although its origin is still unclear, the hyperacute T wave in AMI presumably arises from the same mechanisms that underlie the current of injury. Experiments in animals suggest there is increased activity of an adenosine(Drug information on adenosine) triphosphate–sensitive K+ channel.
The morphology of T waves in early AMI is variable. In most instances, the T waves are tall, asymmetric, broad-based, and associated with reciprocal ST-segment depression in other ECG leads. The R wave also increases in amplitude at this stage. The J point (or junction), which marks the end of the QRS complex and the beginning of the ST segment, may also be elevated. This progresses over time, and the ECG shows characteristic QRS complex and STsegment/ T-wave changes of AMI.2,4
Hyperacute T waves are not associated with elevated levels of cardiac serum markers.2 The initial ECG is diagnostic of AMI in about 50% of cases. About 1% to 21% of patients with AMI present with an initially normal ECG or nonspecific ST-segment/T-wave abnormalities, which include hyperacute T waves.5 Thus, it is important to keep in mind the early ECG changes associated with AMI in patients with chest pain.
In this patient, as the infarct progressed, the ECG findings evolved (Figure 2). As transmural injury occurs, ST elevation with hyperacute T-wave changes becomes marked. With necrosis of the cardiac muscle, pathological Q waves develop, with decreasing ST elevation and terminal T wave. In these cases, pathological Q waves are usually defined as greater than 0.04 second in duration or greater than 25% of R-wave amplitude. As necrosis continues into the fibrotic stage, pathological Q waves and T-wave inversion become upright in some cases.4
OUTCOME OF THIS CASE
This patient had 100% occlusion of the mid left anterior descending coronary artery. A stent was placed from the proximal to midsection of the artery with good results. Other vessels were normal. An echocardiogram showed an akinetic middle anterior wall and apex, an ejection fraction of 40%, normal pulmonary artery systolic pressure, and no significant valvular disease. The patient’s hospital course was uneventful. He was discharged after 3 days, and a daily regimen that included aspirin(Drug information on aspirin), metoprolol, atorvastatin(Drug information on atorvastatin), and clopidogrel(Drug information on clopidogrel) was prescribed.