U Wave Variability in the Surface ECG

Abstract

A 72‐year‐old man with heart failure, left ventricular dysfunction (ejection fraction 20%), prior ischemic stroke, COPD, and exacerbation of chronic renal failure was admitted in our unit. Serum potassium was 6.1 mmol/L, calcium concentration was at the lower normal range 2.15 mmol/L, and NT‐pro‐BNP was 28,900 pg/mL. The surface 12‐lead electrocardiogram (ECG) showed sinus rhythm at 60 bpm, PR interval 160 ms, QRS duration 115 ms, QT interval 460 ms, and left ventricular hypertrophy criteria. Negative T waves in leads I, II, aVL, and V₄–V₆ were also seen. In leads V₄–V₆, negative U waves were observed in concordance with negative T waves. In all precordial leads, beat‐to‐beat U‐wave polarity variability was observed as a polarity variation from negative to positive with associated and stable negative T waves, in a beat‐to‐beat alternate morphology.

The U wave is the last deflection of the cardiac cycle in the surface electrocardiogram (ECG). Many hypotheses have been proposed to explain its genesis; however, the origin of the U wave remains controversial.1, 2, 3 There are clinical situations in which abnormal U waves can be observed: (1) Negative U waves can be seen during myocardial ischemia in patients with significant coronary artery stenosis (mainly obstructions in the left anterior descending coronary artery), (2) in patients with left ventricular hypertrophy (LVH), (3) in patients with pheochromocytoma, (4) in patients with acute cerebrovascular diseases,4, 5, 6, 7 (5) in patients with Andersen Tawil syndrome,8, 9 and (6) in patients with multiple electrolyte disorders including marked hypomagnesemia.10, 11 In patients with LVH, the U wave is concordant with the T wave and it can be negative if the T wave is negative. Very rarely, U waves can be also seen in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) or in some patients with right ventricular outflow tract (RVOT) arrhythmia.12, 13

The aim of this presentation is to report an unusual ECG phenomenon: U‐wave polarity variability in a patient with heart failure and left ventricular dysfunction.

CASE PRESENTATION

A 72 year‐old man with heart failure New York Heart Association (NYHA) class II/III, left ventricular dysfunction (ejection fraction 20%), prior ischemic stroke, chronic obstructive pulmonary disease, and exacerbation of chronic renal failure (estimated glomerular filtration rate—19 mL/min) was admitted in our unit. Serum potassium was 6.1 mmol/L, calcium concentration was at the lower normal range 2.15 mmol/L, and NT‐pro‐BNP was 28,900 pg/mL (normal value: less than 200 pg/mL).

The surface 12‐lead ECG showed sinus rhythm at 60 bpm, PR interval of 160 ms, QRS duration of 115 ms, QT interval at 460 ms, and LVH criteria determined by Sokolow‐Lyon index. Negative T waves in leads I, II, aVL, and V₄–V₆ were detected. In leads V₄–V₆, negative U waves were observed in concordance with negative T waves.

An unusual ECG phenomenon was recorded in all precordial leads consisting in beat‐to‐beat U‐wave polarity variability (Fig. 1) manifested as a polarity variation from negative to positive with associated and stable negative T waves in a beat‐to‐beat alternate morphology (Fig. 2). U‐wave variability was better seen in leads V₅–V₆ and with double amplitude amplification (20 mm/mV).

Figure 1.

Precordial leads (V₁–V₆). U‐wave polarity variability seen in all leads. Stable polarity and amplitude of the T wave.

Figure 2.

ECG lead V₅, continuous recording of six consecutive beats, beat‐to‐beat variability of the U wave manifested as a variation of polarity, shape, and amplitude.

What are possible explanations and importance of this observation?

DISCUSSION

In heart failure patients, macroscopic T‐wave alternans is often observed14 and it has been linked to a poor prognosis and increased arrhythmogenic risk. However, patients with beat‐to‐beat U‐wave variability were occasionally reported in the literature. Aizawa et al. reported three patients with CPVT and “U‐wave alternans.”13 They documented U‐wave alternans in two patients and changes in the polarity of an inverted U wave after a pause, in one patient. The pause‐dependent change in U‐wave polarity was associated with a polarity change in the T wave. In our patient, the U‐wave variability was not related to sudden changes in cycle length or pause‐dependent phenomenon. The T‐wave polarity remained stable, thus, our case reflects pure variations of the U wave. We chose not to call it “alternans” because that refers to beat‐to‐beat alternating polarity, and that criteria was not met in our case.

Kataoka and Yano15 examined the relationships between the polarity of the U wave on intracoronary ECG and the status of myocardial ischemia during angioplasty. This study revealed two types (“acute” and “chronic”) of ischemia‐related negative U waves and one type (“pseudo‐normal”) of ischemia‐related positive U waves, each of which appeared at a different stage of myocardial ischemia. Based on the observations of Kataoka and Yano, it would be tempting to apply their observations to our case. Our patient presented with ischemic dilated cardiomyopathy, and dynamic U‐wave polarity changes from negative to positive could be a reflection of silent ischemia in a patient with heart failure.

However, other potential confounders may play a role in the explanation of this phenomenon. Multiple electrolyte disorders, as a cause of giant U waves has been previously reported by our group.11 In the presented case, moderate hyperkalemia and borderline hypocalcemia may contribute to U‐wave variability. Unfortunately, magnesium was not measured at the time of admission. Prior stroke may also play a role in the genesis of this phenomenon, as prior reports have linked depolarization and repolarization abnormalities in patients with cerebrovascular events; but we are uncertain to what extent.16 Pérez Riera et al. suggested that U‐wave alternans is an electrocardiographic sign of left ventricular heart failure or increased ventricular irritability due to concomitant hypomagnesemia and/or hypocalcemia.17 Our patient presented several of the aforementioned recognized causes of U‐wave alterations (advanced heart failure with severe systolic dysfunction, exacerbation of chronic renal failure with hyperkalemia and secondary hypocalcemia, possible silent ischemia and prior stroke). To what extent each one of the “U‐wave offenders” has contributed to the beat‐to‐beat variability remains speculative.

The clinical significance of this peculiar phenomenon remains uncertain but it deserves further investigation, as a possible noninvasive test to evaluate outcomes in this group of patients.