Downsloping TP Segment in the Precordial Leads on a Standard 12-lead Electrocardiogram: Suspected Cardiac Impulse-tapping Artifact

Abstract

We herein report an 80-year-old man showing a downsloping TP segment together with an increase in the height of the T wave in the precordial leads on a standard 12-lead electrocardiogram (ECG). Separately, an 87-year-old woman showed only a downsloping TP segment in the precordial leads on a standard 12-lead ECG. Neither patient reported chest pain or dyspnea when ECGs was obtained. This downsloping TP segment in the precordial leads on the standard 12-lead ECG is thought to be due to a cardiac impulse-tapping artifact. Differential diagnoses are also discussed.

Introduction

An electromechanical association artifact is a heart-made electrocardiogram (ECG) artifact caused by the pulsation of arteries or the heart at the site where the limb or chest leads are placed (1). It occurs in every cardiac cycle with a fixed coupling interval between the QRS complex and artifact.

Arterial pulse-tapping artifacts, known as Aslanger's signs (2-4), have recently garnered attention in cardiology and emergency medicine (1,5-7). However, there are few reports on artifacts caused by cardiac impulse tapping (7).

We herein report two cases of downsloping TP segments in the precordial leads on a standard 12-lead ECG due to suspected cardiac impulse-tapping artifacts. In one patient, ECG findings were associated with an increase in T-wave height.

Case Reports

Case 1

An 80-year-old Japanese man underwent mitral valve repair with chordal reconstruction and prosthetic ring support via minimally invasive cardiac surgery for chordal rupture of the mitral valve, which resulted in acute heart failure one month prior to presentation. Coronary angiography findings were normal. Postoperatively, the patient experienced no dyspnea or chest pain. At the request of the cardiovascular surgeon for a postoperative follow-up, the patient was referred to our cardiology department. The patient was prescribed bisoprolol fumarate (0.625 mg, once daily) and spironolactone (25 mg, once daily).

His body mass index, blood pressure, and pulse rate were 21.0 kg/m², 110/64 mmHg, and 94 beats/min, respectively. No significant heart murmurs or rales were noted. Blood tests revealed normal high-sensitivity cardiac troponin I (4.5 pg/mL; reference range, ≤18.4 pg/mL) and elevated brain natriuretic peptide (314.5 pg/mL; reference range, ≤18.4 pg/mL) levels. Serum potassium was 4.0 mEq/L (reference range, 3.5-5.0 mEq/L). Chest radiography did not reveal pulmonary congestion. A standard 12-lead ECG revealed a tall T wave with a downsloping TP segment in the lateral chest leads (Fig. 1A, 2A), which was not observed on the second ECG (Fig. 1B) obtained 1 h after the first ECG. Transthoracic echocardiography performed between the two ECG recordings revealed a normal left ventricular (LV) ejection fraction (EF) of 61.2% and mild mitral regurgitation. Pericardial effusion was not observed.

Figure 1.

Standard 12-lead electrocardiograms (ECGs) of Case 1 obtained at the first presentation. The initial ECG, obtained shortly after blood was drawn from a vein for blood tests, revealed left-axis deviation and tall T waves with downsloping TP segments, P waves, and PQ segments in the lateral chest leads (A). Because of the abnormalities detected on the first ECG, a second ECG was obtained without repositioning the electrodes 1 h after the initial ECG and shortly after the transthoracic echocardiography, and demonstrated the disappearance of tall T waves with downslopes spanning from the TP to PQ segments (B).

Figure 2.

Standard 12-lead electrocardiograms (ECGs) of Case 1 recorded 1 (B), 4 (C), and 7 (D) months after the first presentation (A). Downsloping TP segments in the lateral chest leads were observed to varying degrees.

Subsequently, the patient was healthy with no cardiac events. During the 1-, 4-, and 7-month follow-up visits, standard 12-lead ECGs were recorded (Fig. 2B-D, 3A, D). Downsloping TP segments in the lateral chest leads were often observed to varying degrees (Fig. 2); however, they were not observed following V4-6 lead repositioning (Fig. 3).

Figure 3.

Twelve-lead electrocardiograms (ECGs) of Case 1 recorded 7 months after the first presentation (A-D) and a schematic illustration of the thoracic skeleton showing the sites where chest electrodes were positioned (E). The initial ECG with standard lead positions (A) showed downsloping TP segments in the lateral chest leads. The improvement of downsloping TP segments is shown on the ECGs with the placement of the lateral chest leads (V4-6) in more cranial positions, the V4 electrode placed on the fifth rib and fourth intercostal space at the mid-clavicular line (B and C, respectively), and the V5 and V6 electrodes positioned on the same horizontal line as the V4 electrode in the anterior and midaxillary lines, respectively (E). The distortion of the TP segments is most pronounced in Panel A, followed by Panels B and C in descending order. Finally, an ECG re-recorded with standard lead positions (D) showed distortion of the TP segments similar to that of Panel B. The duration of Panels A-D is approximately 6 min. A schematic illustration of the thoracic skeleton showed chest electrodes positioned at the sites where V1-V6 are labeled in black with a yellow background in Panels A and D, recorded as standard 12-lead ECGs, and depicted chest electrodes positioned at the sites where V4-V6 are labeled in black with an orange background in Panel B and in white with a brown background in Panel C (E).

Case 2

An 87-year-old Japanese woman was admitted to our hospital with heart failure. Due to Alzheimer's disease, her Clinical Frailty Scale level was 7. She had a body mass index of 18.3 kg/m², blood pressure of 133/102 mmHg, and pulse rate of 80 beats/min. Blood test results showed an elevated C-reactive protein level of 1.91 mg/dL (reference range, 0.7 pg/mL), high-sensitivity cardiac troponin I concentration of 129.5 pg/mL, and brain natriuretic peptide level of 784.3 pg/mL. The patient's serum potassium level was 4.3 mEq/L. Chest radiography revealed pulmonary congestion with pleural effusion. An ECG revealed tachycardiac atrial fibrillation (Fig. 4A). Transthoracic echocardiography revealed diffusely reduced LV wall motion with an EF of 27.5% and severe aortic valve stenosis with an aortic valve area of 0.34 cm², peak aortic velocity of 4.14 m/s, and mean pressure gradient of 34.8 mmHg. Pericardial effusion was not observed.

Figure 4.

Twelve-lead electrocardiograms (ECGs) of Case 2. The admission ECG taken with standard lead positions showed tachycardiac atrial fibrillation with low voltage in the limb leads, poor R-wave progression, and ST-segment abnormality but no downsloping TP segment (A). A follow-up standard 12-lead ECG, which was obtained in a slightly left lateral position on day 42 of hospitalization, showed left axis deviation, ST-segment abnormality, and downsloping TP segments in the precordial leads (B). Downsloping TP segments almost disappeared on the ECG taken after repositioning the chest leads, but not the limb leads (C). Positive U waves in the precordial leads became less distinct in Panel B than in Panel C, indicating that waveform distortion of the TP segment in the precordial leads had developed.

The patient was prescribed loop diuretics, edoxaban tosylate hydrate, imidapril hydrochloride, bisoprolol fumarate, and amiodarone hydrochloride. In addition, the patient underwent balloon aortic valvuloplasty for severe aortic valve stenosis and electrical cardioversion for atrial fibrillation via synchronous direct current discharge on days 17 and 24 of hospitalization, respectively. Coronary angiography findings were normal. Finally, the sinus rhythm was restored.

Follow-up blood tests, ECGs, chest radiography, and echocardiography were performed on day 43 following hospitalization. Blood test results showed a normal C-reactive protein concentration of 0.24 mg/dL and a potassium level of 4.3 mEq/L. Despite their decline from the earlier noted values, high-sensitivity cardiac troponin I (41.2 pg/mL) and brain natriuretic peptide (231.8 pg/mL) levels remained elevated. Pulmonary congestion improved, and pleural effusion disappeared. The patient refused to lie supine; therefore, an ECG was performed in a slightly left lateral position and revealed sinus rhythm with a downsloping TP segment in the precordial leads (Fig. 4B). Following precordial lead repositioning (Fig. 4C), the ECG finding almost disappeared. Echocardiography revealed an improved LVEF of 52.0% and aortic valve area of 0.65 cm², although the peak aortic velocity and mean pressure gradient increased to 4.40 m/s and 46.2 mmHg, respectively. Pericardial effusion was absent. The patient was not readmitted for heart failure over the follow-up period of one year.

Discussion

A prominent ECG finding, a downsloping TP segment in the precordial leads, was observed in our two patients. In Case 1, the T-wave height increased, and the P wave and PQ segment were also involved. Distorted waveforms were not observed after precordial lead repositioning or patient rest, suggesting cardiac impulse-tapping artifacts.

During electric diastole, from the end of repolarization to the onset of the next depolarization, only a small voltage gradient develops (8). This corresponds to the TP segment on the ECG. The TP segment is typically nearly flat and isoelectric. Therefore, the downsloping TP segment is considered abnormal, although no definition is provided. Cardiac diseases that cause abnormalities in the TP segment are rare. In patients with acute pericarditis, a downsloping TP segment called Spodick's sign, observed in lead II and lateral chest leads, occurs together with ST-segment elevation and PR-segment depression (9). However, neither of the present patients developed acute pericarditis. The U-wave present in the TP segment is most evident in leads V2 and V3, where its amplitude has been suggested to be approximately 0.33 mV or 11.0% of the T-wave (8). Various cardioactive drugs with quinidine-like effects and hypokalemia may cause an increase in the U-wave amplitude. Transient prominent U waves, generally associated with ST-segment deviation, develop due to myocardial ischemia in the posterior/lateral LV wall perfused by the left circumflex coronary artery. In particular, a prominent U wave merges with the next P wave when the heart rate increases and presents as a downsloping TP segment (10). Furthermore, the prolonged T wave merging with the next P wave may mimic the downsloping TP segment in long QT syndrome. However, because the distorted waveform almost disappeared with precordial lead repositioning or after patient rest, it is unlikely that the downsloping TP segment was caused by a prominent U-wave and QT prolongation.

In Case 1, an increase in the height of the T-wave amplitude of over 10 mm in lead V4, together with a downsloping TP segment, was observed, as shown in Figure 1A, 2A. In healthy adults, the T-wave amplitude is most positive in leads V2 and V3. The reported normal standards for T wave vary to some extent by age, sex, and race. However, there is no universally accepted upper limit for the normal T-wave amplitude. The T-wave is generally no greater than 5 mm in amplitude in the limb leads and 10 mm in the precordial leads (11). Thus, the ECG in Case 1 revealed T waves with an increased height (or tall T waves). Tall T-waves can be a sign of acute ischemia or hyperkalemia; however, the patient did not have acute ischemia or hyperkalemia. We speculate that the presence or absence of an increase in T-wave height is related to the degree of waveform distortion of the TP segment as an artifact, similar to how the degree of waveform distortion due to arterial pulse-tapping artifacts depends on the magnitude of the affected artifacts (5,6).

There are a limited number of reports on artifacts caused by cardiac impulse tapping (7). Türer Cabbar reported that this ECG artifact is particularly prone to occur in lean individuals. In addition, Türer Cabbar's patient had a tiny undulation in the ST segment of lead V3 as an artifact, which was different from the waveform distortion observed in our patients. Chest computed tomography images of Cases 1 and 2, acquired during acute heart failure approximately one month prior, revealed that the skin and heart were close to each other around the left fifth to sixth intercostal space, where the lateral chest electrodes were placed (Fig. 5, 6). This may support Türer Cabbar's hypothesis. Because of the lungs, chest wall, pectoralis major muscle, serratus anterior muscle, and breasts between the chest electrodes and the heart, distortion of the ECG waveform as an artifact of the heartbeat is unlikely. However, an impulse from the heart is visible, particularly in thin-chested patients, even when lying flat (12). The normal point of the maximal impulse of the heart is usually located inside the mid-clavicular point at intercostal space 5, where the electrode of lead V4 is placed. Waveform distortion, a downslope of the TP segment in the chest leads, can be caused by a visible and palpable heartbeat. However, this is different from the superposition of two waveforms: the apex cardiogram and electrocardiogram. In the present study, the downsloping TP segment was not consistently observed under similar conditions. This suggests that this waveform is captured when various conditions predisposing the transmission of heartbeats to the chest electrode coincide. For instance, the resolution of a cardiac impulse-tapping artifact detected in the ECG obtained after rest, as shown in Fig. 1, indicates susceptibility to sympathetic stimulation, similar to arterial pulse-tapping artifacts (6,13). In addition, the ECG recorded in a slightly left lateral position exhibited a downsloping TP segment in the chest leads, as shown in Fig. 4B. This positioning brought the heart closer to the chest wall (14). Body positioning may influence waveform distortion due to cardiac impulse-tapping artifacts. However, the factors governing the number and distribution of affected leads, as well as the extent of waveform distortion attributable to cardiac impulse-tapping artifacts, cannot be determined based solely on the data derived from the two cases in this study.

Figure 5.

Chest computed tomography acquired during acute heart failure one month prior to first presentation while the arms were elevated over the head (Case 1). Around the left fifth and sixth intercostal spaces, where the lateral chest electrodes were placed, the skin and heart were close to each other. The horizontal lines in panel D indicate the level of the coronal slice shown in panels A-C. Asterisks indicate the pleural effusion. Roman numerals V, VI, and VII indicate the left fifth, sixth, and seventh ribs, respectively. LV: left ventricle, RV: right ventricle

Figure 6.

Chest computed tomography acquired on admission (Case 2). Around the left fourth and sixth intercostal spaces, where the precordial electrodes are placed, the skin and heart are close to each other. The horizontal lines in panel D indicate the level of the coronal slice shown in panels A-C. Asterisks indicate the pleural effusion. Roman numerals IV, V, VI, and VII indicate the left fourth, fifth, sixth, and seventh ribs, respectively. LV: left ventricle, RV: right ventricle

In conclusion, the ECG of the two cases showing a downsloping TP segment in the precordial leads was suspected to be due to cardiac impulse-tapping artifacts. This artifact may involve an increase in T-wave height and distortion of P wave and PQ segment. If this finding is observed on an ECG recorded using a standard lead placement, a repeat ECG is recommended after changing the position of the precordial electrodes or after patient rest, as this might be an artifact.

This study was approved by the Ethics Committee of Yawatahama City General Hospital (20240325-002) and conducted in accordance with the Declaration of Helsinki. Informed consent was obtained from the patients and their families for the publication of this case report. This case report was written while respecting patient confidentiality and privacy. The patients and their families had the opportunity to receive an explanation in Japanese regarding this report from the authors and had no objections to the final form.

The authors state that they have no Conflict of Interest (COI).