Respiratory T-Wave Inversion in a Patient With Chest Pain.

T-wave inversion on electrocardiogram (ECG) is always a concerning finding as it is often associated with myocardial ischemia or ventricular strain. Respiratory variation in the T-wave morphology has been reported in the literature; however, the frequency of this observation remains unknown as this is not routinely evaluated. Although the exact physiological mechanisms underlying this ECG change are unclear, it is proposed to be due to the respiratory variation of the heart position resulting in an alteration in T-wave polarity. We describe a case of a patient who presented with chest pain with T-wave inversions in inferior and lateral ECG leads. On repeating ECG with breath held in end inspiration, the T waves became positive. The pain was found to be musculoskeletal in origin. This case is a reminder of an under-recognized physiological phenomenon involving the cardiac conduction. Variation of T-wave morphology with respiration may suggest a noncardiac cause of chest pain.

Background

There are several variations in the morphology of resting electrocardiogram (ECG) with breathing cycle. It is well known that frontal QRS axis varies with respiration as there is displacement of heart anatomically with diaphragmatic movement.[1] T-wave inversion can also be seen due to variation in T-wave polarity with the respiratory cycle.[1] Here, we describe a case of a patient with a history of coronary artery disease (CAD) who presented with chest pain. He had a coronary angiogram done 2 weeks before this episode, which revealed nonocclusive CAD. In the emergency department (ED), he was found to have T-wave inversions in inferior and lateral ECG leads. However, on repeating ECG with breath held in end inspiration, the T waves became positive.

Case Presentation

A 55-year-old patient with a history of CAD status after proximal circumflex artery stent placed in 2007 presented to the ED with acute onset sharp, nonradiating left-sided, nonexertional chest pain of 24 hours’ duration. He also had a history of well-controlled hypertension. His medications included the following: aspirin 81 mg, atorvastatin 40 mg, metoprolol tartrate 25 mg twice a day, and amlodipine 10 mg. He had a coronary angiogram done 2 weeks before current ED visit for a similar episode of sharp chest pain, which revealed 40% stenosis of the distal left anterior descending artery. The previously placed stent was patent. On examination, blood pressure was 130/90 mm Hg, heart rate 70 beats/min, respiratory rate 18/min, and temperature 98.7 F. Other than mild chest wall tenderness, the pulmonary and cardiovascular examination was unremarkable. Chest X-ray was normal. Electrocardiogram revealed T-wave inversion in the inferior and lateral leads, which was concerning for cardiac ischemia. However, it was reassuring that the patient had an angiographic evidence of nonocclusive coronary anatomy. Previous ECGs were inconsistent in T-wave morphology, as some had positive, whereas others had negative T-wave deflection (Figures 1 and 2).

Figure 1.

Electrocardiogram of the patient with breath held in end expiration, showing T-wave inversion in inferior leads (black arrows) and lateral leads precordial leads (gray arrows).

Figure 2.

Electrocardiogram of the patient with breath held in end inspiration, showing positive T waves in inferior leads (black arrows) and alteration in T-wave morphology in lateral leads precordial leads (gray arrows).

Laboratory studies including complete blood count, electrolytes, and d-dimer were normal. Troponin T was <0.01 ng/mL. It was noted on the cardiac monitor that there was a cyclic variation in T-wave morphology, corresponding with the respiratory cycle. Hence, the patient was asked to hold his breath in deep inspiration and ECG was obtained, which showed that T-wave inversions immediately became positive. The patient was admitted, and after his pain had resolved, he underwent a myocardial perfusion scintigraphy, which was negative, and his chest pain was thought to be musculoskeletal in origin. The next day, he was discharged home.

Discussion

Nonspecific T-wave changes including T-wave flattening and T-wave inversion without any other characteristic finding are the most common variations found in the routine ECG. These T-wave changes are often labeled as nonspecific T-wave changes and are difficult to interpret in the absence of appropriate clinical setting. This finding is very common and occurs as often as 11.5 per 1000 subjects.[2] T wave indicates ventricular repolarization, which can be influenced by body position, ingestion of food, medications, electrolyte imbalance, and exercise.[1] T-wave changes including low-amplitude T waves and abnormally inverted T waves may be the result of many cardiac conditions such as myocardial ischemia, myocarditis, mitral valve prolapse, or ventricular strain. Nonspecific T-wave changes, at many times, lead to erroneous diagnosis resulting in frequently unnecessary and invasive workup. Our patient presented with sharp chest pain, which is not typical for cardiac angina. However, history of CAD coupled with evidence of T-wave inversion on ECG added to the dilemma in deciding further management. However, recent coronary angiography revealing nonobstructive coronary anatomy was reassuring. His ECG demonstrated T-wave inversion which instantaneously became positive (180° change) on deep inspiration without any notable change in the QRS complex. However, these T waves inverted again at the end of expiration. A similar phenomenon was also observed by Joulia et al, in 1992,[3] in a 43-year-old man who demonstrated T-wave inversion with Valsalva maneuver and erection of T waves with deep inspiration.[4] This patient had normal coronary circulation on angiography. He also reported a case of a young black male student who had an elevation of the ST segments in leads I, II, aVR, V5, and V6, with nonspecific T-wave inversion in leads V1-5. In lead V1, inspiration caused T waves to become positive and tall. Joulia et al (1992) also reported similar phenomenon in 3 healthy divers who had no evidence of organic heart disease.[3] T-wave inversion was demonstrated in the precordial leads which disappeared on deep inspiration.[3] Simonson et al[4] observed that respiration causes a change of QRS and T vectors in different directions and also suspected that vagal tone might also influence this effect. It is a well-known fact that respiration causes variation in the heart position, namely, clockwise rotation in deep inspiration and counterclockwise rotation in deep expiration.[4,5] Oscillographic loop projection of vectorcardiogram has shown that inspiration causes downward rotation of the T and QRS axes along with increasing left axis deviation.[4] However, it is also possible that variation in heart position associated with movement of the diaphragm during respiration could produce T-wave inversion without a significant change in the QRS axis.[6]

In summary, whenever there is a T-wave abnormality on ECG in the setting of low probability of cardiac ischemia, the test should be repeated with breath held in end inspiration and expiration. Change in polarity of T waves with respiration is a physiological response, which points toward a noncardiac cause.