Case Report

Hyperacute T wave, the early sign of myocardial infarction

Acute myocardial infarction (AMI) is a life-threatening disease that needs accurate and rapid diagnosis followed by appropriate treatment. Electrocardiogram is an inexpensive and commonly used tool in the diagnostic work up of AMI which provide diagnostic and prognostic information. Among other electrocardiographi signs of cardiac ischemia, tall and broad-base T waves, especially in the anterior precordial leads of 12 lead ECG may be the earliest and the only electrocardiographic sign of AMI. In this case, they are called Hyperacute T waves (HATWs). The three main differential diagnoses of HATW on electrocardiogram are left ventricular hypertrophy, hyperkalemia, and early repo- larization variant. This article presents cases and elctrocar- diograms of HATW and its three main differential diagnoses with a review of the electrocardiographic diagnostic criteria for these conditions based on the available literature.

A 57-year-old male patient presented to the emergency department (ED) approximately 2 hours after experiencing a severe crushing Retrosternal chest pain with no radiation to his arms or neck. The pain was not pleuritic or positional and had started suddenly while he was at rest. His past medical history and family history were not significant for any cardiovascular disease, and he did not take any medication on a regular basis. He had a 20 packs-year history of cigarette smoking approximately. He appeared pale and in distress with moderate shortness of breath. His vital signs were as follows: blood pressure of 98/58 mm Hg, pulse rate of 58 beats/min, respiratory rate of 24 breaths/min, and temperature of 98.18F. His oxygen saturation was 96% on 3 L of oxygen through nasal cannula. On physical examination, there was no jugular venous distention, carotid upstrokes were full and brisk, there were no rales on lung auscultation, and no Pitting edema in the lower extremities. First and second heart sounds were audible with no murmur. Intravenous normal saline was given and administration of Intravenous morphine

reduced the severity of the chest pain in the patient.

The patient’s basic metabolic panel and complete blood count did not show any significant abnormalities, and the cardiac biomarker levels were within normal limits. The electrocardiogram (ECG) (Fig. 1) showed sinus rhythm with a ventricular rate of 47 beats/min, T-wave inversion in lead III, QS pattern in leads V₁ and V₂, and tall and broad T waves in V₁ to V₅.

Oral aspirin and subcutaneous heparin were given to the patient, and because the chest pain was not completely resolved, he was taken to the cardiac catheterization laboratory. Left cardiac catheterization (Fig. 2) showed a total occlusion of the middle part of the left anterior descending artery with thrombolysis in myocardial infarc- tion antegrade flow of 0. It was successfully recannulated, and a stent was placed. A left ventriculogram showed significant apical hypokinesia with a low-normal left ventricular ejection fraction of 40%.

After the procedure, metoprolol, simvastatin, lisinopril, and clopidogrel were added to his medications, and he had an uneventful course of hospitalization for 2 days; then the patient was discharged home.

Acute myocardial infarction (AMI) is a life-threatening disease that needs accurate and rapid diagnosis followed by appropriate treatment. The ECG has remained the mainstay in the diagnostic workup for this condition. The ECG is an inexpensive tool, which can provide significant diagnostic and prognostic information about coronary artery disease and associated electrolyte disturbances. The classic ECG patterns for AMI are as follows: an ST-segment elevation of more than 2 mm in 2 or more contiguous leads, which is defined as ST-segment elevation myocardial infarction (STEMI); an ST-segment depression of more than 1 mm or a new deep (N3 mm) T-wave inversion in 2 or more contiguous leads, both of which are defined as non- ST-segment elevation myocardial infarctionwhen associated with elevated cardiac biomarkers; otherwise the conditions are called unstable anginawhen there is no permanent damage to the myocardium. T-wave inversion is not considered as specific as ST-segment changes.

T waves represent a ventricular repolarization period. A normal T wave usually has an amplitude of less than 0.5 mV in precordial leads and less than 1.0 mV in limb leads. T- wave amplitude (T amp) is greater in men than in women in leads II and V₄, and it decreases with age [1].

The differential diagnosis of prominent T waves includes: hyperkalemia, noninfarction myocardial ischemia, left ventricular hypertrophy (LVH), benign early repolari- zation (BER), bundle-branch block, pericarditis, valvular heart disease, mitral stenosis, hemopericardium, ectopic ventricular rhythms, pacemaker rhythms, Hypertrophic cardiomyopathy, mitral valve prolapse, the sequela of Stokes-Adams episodes, cor pulmonale, central nervous system disease, hyperthyroidism, exercise, anemia, acidosis,

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Fig. 1 The ECG was taken in a 57-year-old male patient who presented with angina to the ED. It shows broad and tall T waves in V₁ to V₅ that are taller than 75% of QRS amp.

and tranylcypromine overdose [2-4]. However, conditions that most closely resemble the prominent T waves of AMI include LVH, hyperkalemia, and early repolarization.

Left ventricular hypertrophy (Fig. 3) is identified on the ECG by voltage criteria (cumulative voltage of the S wave in lead V₁ and the R wave in leads V₅ or V₆ of N35 mm), characteristic strain pattern (down-sloping ST-segment de- pression with asymmetric, biphasic, or inverted T waves in the lateral leads), and/or ST-segment/T-wave changes result- ing from altered repolarization of the hypertrophied myocar- dium. Repolarization ST-segment/T-wave abnormalities are noted in approximately 70% of patients with LVH [5].

Electrocardiographic LVH is associated with poor R wave progression and loss of the septal R wave in the right to midprecordial leads, most commonly producing a QS pattern. In general, these QS complexes are located in leads V₁ and V₂, rarely extending beyond lead V₃. ST-segment elevation is encountered in this distribution along with prominent T waves. The STE seen in this distribution may be greater than 5 mm in height and is difficult to distinguish from that associated with AMI. The initial, up-sloping

portion of the ST-segment/T-wave complex is frequently concave in LVH compared with either the flattened or the convex pattern observed in the patient with AMI. This morphological feature is imperfect; early AMI may reveal such a concave feature. The prominent T waves associated with ECG LVH may be misinterpreted as hyperacute T waves (HATWs) of early AMI, particularly when the T- wave changes are not accompanied by pronounced STE (ie, when the predominant ECG manifestation of the altered repolarization is the prominent T wave) [6].

Hyperkalemia (Fig. 4) presents with T waves of large magnitude that is also described as tall and peaked and may be confused with the HATW of early STEMI. The T waves associated with hyperkalemia tend to be tall, narrow, and peaked with a prominent or sharp apex. It is commonly mentioned that these T waves resemble the tall vaulting appearance of a church steeple. Also, these T waves tend to be symmetric in morphology; if split down the middle, the resulting portions would be mirror images. As the serum potassium level increases, the T waves tend to become taller, peaked, and narrowed in a symmetric fashion in the anterior

Fig. 2 Cardiac catheterization in the same patient showed complete occlusion of the left anterior descending artery.

distribution. With further progression of the metabolic abnormality, the QRS complex widens, advancing to the sinoventricular rhythm and, ultimately, to ventricular fibril-

lation. Hyperkalemic T waves may be misinterpreted as HATWs associated with AMI. In general, prominent T waves associated with AMI are often broad and asymmet- ric-in significant contrast to the narrow, peaked, symmetric HATWs of early AMI. In fact, moderate to severe hyper- kalemia with QRS-complex widening occasionally produ- ces STE in the Right precordial leads and simulates an infarction pattern [7,8]. Still, there are recognizable differ- ences between hyperkalemic T waves and the HATWs of STE AMI. Braun et al [13] found that a terminal slur in the QRS complex or an S wave in leads I or V₆ without gross QRS-complex widening was frequently associated with hyperkalemic T waves. These phenomena are not associated with the ECG changes accompanying AMI. Furthermore, the T-wave inversion noted in AMI is not associated with hyperkalemia. Hyperkalemia is most often secondary to renal failure. Renal failure manifests electrocardiographi- cally as a triad of prominent T waves from hyperkalemia, QT-interval prolongation from hypocalcemia, and LVH from hypertension [7].

The hyperkalemic T waves of renal failure are thus also readily distinguishable from the HATWs of STE AMI. Although there is no exact correlation between serum potassium levels and the onset of ECG changes, 80% of patients exhibit ECG changes with serum potassium of

6.8 mEq [4].

Fig. 3 The patient was a 71-year-old woman who presented to the ED with focal weakness and Seizure activity secondary to an ischemic stroke. The ECG shows sinus rhythm with premature supraventricular complexes. The T waves are prominent in precordial leads. The ECG meets the voltage criteria for LVH (Sokolow criteria: SV₁ + RV₅/V₆ of N35 mm; Cornell criteria: SV₃ + RaVL of N20 mm in female and N24 mm in male). In addition to voltage criteria for LVH, the T amp is not high compared with QRS amp. This criterion of HATW (T amp of N75% of QRS amp) is particularly useful to differentiate HATW from prominent T waves in LVH because of usually high QRS voltage in LVH.

Fig. 4 A 55-year-old woman with chronic kidney disease presented to the ED with serum potassium level of 7.2 mmol/L. Her ECG showed tall and narrow T waves especially in V₂ and V₃. Prominent T waves in hyperkalemia are narrow, usually symmetric, and resemble the tall vaulting appearance of church steeples. In contrast with HATW, hyperkalemic T waves are not broad. In addition, their amplitude is not greater than 75% of QRS amp in this ECG.

Fig. 5 A 41-year-old African American male patient with no known coronary artery disease or the risk factors presented to the ED with Atypical chest pain. His ECG shows mild STE with prominent T waves. The STE is concave, the end of QRS complexes has a notch (J wave) especially in leads V₄ and V₅, and prominent T waves are concordant with QRS complexes. These are characteristic features of BER.

Benign early repolarization (Fig. 5) is a variant of the normal ECG. This syndrome, first described by Shipley and Hallaran [9], has been reported in men and women of all age groups and varying ethnicities. It occurs in approximately 1% of the general population [10] and with increased frequency in young military recruits [11], athletes [12], and black men [13] to 40 years old [14]. Although BER is strictly an ECG syndrome, BER may present in the patient with chest pain. Benign early repolarization is found in 13% of adult patients with chest pain in the ED [15].

The ST segment of the cardiac electrical cycle represents the period between depolarization and repolarization of the left ventricle. In the normal state, the ST segment is isoelectric, which means it is neither elevated nor depressed relative to the TP segment. The ECG definition of BER includes the following characteristics: (1) STE; (2) upward concavity of the initial portion of the ST segment; (3) notching or slurring of the terminal QRS complex; (4) symmetric, concordant T waves of large amplitude; (5) widespread or diffuse distribution of STE on the ECG; and

(6) relative temporal stability [16,17]. This STE morpho- logically appears as if the ST segment has been evenly

lifted upward from the isoelectric baseline at the J point. This elevation results in a preservation of the normal concavity of the initial, up-sloping portion of the ST-segment/T-wave complex which is a very important ECG feature used to distinguish BER-related STE from STE associated with AMI.

Prominent T waves of large amplitude and slightly asymmetric morphology are also encountered; the T waves may appear peaked, suggestive of the HATW encountered in patients with AMI. The T waves are concordant with the QRS complex and are usually found in the precordial leads. The height of the T waves in BER ranges from approxi- mately 6.5 mm in the precordial distribution to 5 mm in the limb leads [8,10,14,17].

In AMI, the presence of broad-base T waves, especially in anterior precordial leads, may be significant for very early stages of this condition. In this case, they are called HATWs. The ability to identify early ECG changes in AMI would allow the physician to promptly initiate appropriate therapy, which can prevent further damage to the myocardium. In the best available study of HATWs, Collins et al [18] screened 13393 adult ECGs for T amp

Fig. 6 A 59-year-old man presented with acute onset of typical chest pain (angina) and his ECG shows STE with prominent T waves (HATW) in inferior leads consistent with inferior STEMI. The patient received thrombolytic therapy and then was transferred to our facility where he underwent a rescue percutaneous coronary intervention because of persistent chest pain and STE. Angiography showed 100% occlusion of the proximal right coronary artery, and a stent was placed. In this case, the presence of STE on the ECG makes the recognition of the myocardial infarction easier. However, it is important to recognize the prominent T waves (broad T waves with T amp of N75% of QRS amp, ST on of N0.3 mV, ST on/T amp of N25%) because they may be the only ECG sign of ischemia with no ST-segment deviation similar to the patient with his ECG in Fig. 1.

greater than 0.5 mV in limb leads and greater than 1.0 mV in precordial leads. They then excluded patients with second- ary etiologies of tall T waves (eg, bundle-branch block, paced or escape beats, ventricular hypertrophy) and those with known causes of primary tall T waves (hyperkalemia, acute central nervous system events including intracranial hemorrhage or massive Cerebrovascular accidents, acute pericarditis, valvular heart disease, idiopathic hypertrophic subaortic stenosis, acute hypertension, anemia, or acidosis). After exclusion, they divided the patients into 2 groups based on retrospective evidence of myocardial infarction:

(1) patients with HATWs and (2) patients with early Repolarization variant (ERV). Hyperacute T waves repre- sented 0.16% (21 patients) of all screened ECGs, and the time from onset of chest pain until the HATW changes were observed was 170.2 F 34.6 minutes. However, HATWs have been reported as early as 30 minutes after chest pain [1]. All patients with HATWs in the study by Collins et al had chest pain. After analyzing the data, they suggested the following criteria for HATWs with a specificity of 98.0% and a sensitivity of 69.1%:

1. ST on/T amp of greater than 25%
2. T amp/QRS amplitude (QRS amp) of greater than 75%
3. ST on of greater than 0.30 mV
4. Patients older than 45 years

Their study did not show any sex differences between the HATW and ERV groups. The mean age in the HATW group was 61.8 (F3.2) years, and it was 38.9 (F2.1) years in ERV group. The authors did not include J-point elevation as a criterion for the HATW group, when in fact some other authors have considered HATWs to be tall T waves associated with J-point changes [1,19] (Fig. 6). Also, they did not compare the changes with previous ECG data, which might have provided very valuable information for clini- cians. They excluded many secondary and primary causes of tall T waves retrospectively based on information in the patients’ charts. The ability to exclude some of these conditions, such as pericarditis and valvular disease, may be difficult to achieve in an acute setting. One of the advantages of the previously mentioned criteria is that they are based on relative rather than absolute values, which can allow for differences in patient body habitus or in the technicalities of ECG acquisition.

In our 57-year-old patient, T amp was greater than QRS amp; therefore, he met 2 of the 4 criteria for HATW.

In our opinion, a good and practical set of ECG criteria for HATW does not exist. However, we suggest that clinicians seriously consider the possibility of AMI in a patient older than 45 years who presents with angina and early high-amplitude and broad T waves with T amp/QRS amp of more than 75%. It is important to consider that occasionally, such as in our patient, HATW is not associated with ST-segment deviation. Acute myocardial infarction is even more likely the main diagnosis in this setting if both

secondary and other common primary causes of prominent T waves (as noted previously) can be excluded based on clinical or ECG findings or laboratory tests (eg, serum potassium). Because HATWs usually appear before eleva- tion in cardiac enzyme or ST changes in ECG, the ability to diagnose myocardial infarction by recognizing this ECG pattern can prevent further damage to the myocardium by appropriate and prompt treatment.

Ali A. Sovari MD

Department of Internal Medicine

University of Illinois COM-UC, Urbana, IL 61801, USA

E-mail address: [email protected]

Ramin Assadi MD Department of Internal Medicine Loma Linda University

Loma Linda, CA 92354, USA

Bataulatundu Lakshminarayanan MD, FACC Abraham G. Kocheril MD, FACC Department of Internal Medicine

Division of Cardiology University of Illinois

COM-UC Urbana, IL 61801, USA

doi:10.1016/j.ajem.2007.02.005

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