Abstract
In pulmonary hypertension (PH), T wave inversions (TWI) are typically observed in precordial leads V1–V3 but can also extend further to the left-sided leads. To date, the cause and prognostic significance of this extension have not yet been assessed. Therefore, we aimed to assess the relationship between heart morphology and precordial TWI range, and the role of TWI in monitoring treatment efficacy and predicting survival. We retrospectively analyzed patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) treated in a reference pulmonary hypertension center. Patients were enrolled if they had a cardiac magnetic resonance (cMR) and 12-lead surface ECG performed at the time of assessment. They were followed from October 2008 until March 2021. We enrolled 77 patients with PAH and 56 patients with inoperable CTEPH. They were followed for a mean of 51 ± 33.5 months, and during this time 47 patients died (35.3%). Precordial TWI in V1–V6 were present in 42 (31.6%) patients, while no precordial TWI were observed only in 9 (6.8%) patients. The precordial TWI range correlated with markers of PH severity, including right ventricle to left ventricle volume (R = 0.76, p < 0.0001). The presence of TWI in consecutive leads from V1 to at least V5 predicted severe RV dilatation ( ≥ 2.3) with a sensitivity of 88.9% and specificity of 84.1% (AUC of 0.90, 95% CI = 0.83–0.94, p < 0.0001). Presence of TWI from V1 to at least V5 was also a predictor of mortality in Kaplan–Meier estimation (p = 0.02). Presence of TWI from V1 to at least V5 had a specificity of 64.3%, sensitivity of 58.1%, negative predictive value of 75%, and positive predictive value of 45.5% as a mortality predictor. In patients showing a reduction in TWI range of at least one lead after treatment compared with patients without this reduction, we observed a significant improvement in RV-EDV and . We concluded that the extension of TWI to left-sided precordial leads reflects significant pathological alterations in heart geometry represented by an increase in RV/LV volume and predicts poor survival in patients with PAH and CTEPH. Additionally, we found that analysis of precordial TWI range can be used to monitor the effectiveness of hemodynamic response to treatment of pulmonary hypertension.
Highlights
In a surface electrocardiogram, the period of cardiac repolarization is represented by flat ST segments and positive T waves in most leads. 2 of ??In healthy subjects, the surface ECG signals originate mainly from the predominant left ventricle, and the electrical forces of the right ventricle (RV) are reduced or canceled.to be seen in ECG the RV dilatation must be severe enough to overcome the canceling effects of the left ventricle
In pulmonary hypertension (PH), precordial T wave inversions (TWI) are typically observed in precordial leads V1–V3 [? ], but they can extend beyond lead V3 to the left-sided leads, including V5 and V6 [? ? ]
We showed that most with pulmonary arterial hypertenIn the thecurrent current study, we showed that patients most patients with pulmonary arterial sion or chronic thromboembolic pulmonary hypertension were characterized by T wave hypertension or chronic thromboembolic pulmonary hypertension were characterized by inversion in one or more precordial leads of the resting ECG
Summary
The period of cardiac repolarization is represented by flat (isoelectric) ST segments and positive T waves in most leads. 2 of ??In healthy subjects, the surface ECG signals originate mainly from the predominant left ventricle, and the electrical forces of the right ventricle (RV) are reduced or canceled.to be seen in ECG the RV dilatation must be severe enough to overcome the canceling effects of the left ventricle. The period of cardiac repolarization is represented by flat (isoelectric) ST segments and positive T waves in most leads. The surface ECG signals originate mainly from the predominant left ventricle, and the electrical forces of the right ventricle (RV) are reduced or canceled. To be seen in ECG the RV dilatation must be severe enough to overcome the canceling effects of the left ventricle. Since V1 is close to the RV, it is the most sensitive to changes induced by RV abnormalities. Repolarization abnormalities originating from the RV are first present in V1, followed by V2 and V3. In pulmonary hypertension (PH), precordial T wave inversions (TWI) are typically observed in precordial leads V1–V3 [? ], but they can extend beyond lead V3 to the left-sided leads, including V5 and V6 [? The cause and prognostic significance of this extension have not been systematically assessed
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