Analysis of Electrocardiographic Criteria of Right Ventricular Hypertrophy in Patients with Chronic Thromboembolic Pulmonary Hypertension before and after Balloon Pulmonary Angioplasty

Background: Chronic thromboembolic pulmonary hypertension (CTEPH) may lead to typical electrocardiographic changes that can be reversed by balloon pulmonary angioplasty (BPA). The aim of this study was to investigate the significance of rarely used electrocardiogram (ECG) parameters, possible electrocardiographic differences between residual and significantly improved CTEPH and the role of electrocardiographic parameters in low mPAP (mean pulmonary arterial pressure) ranges since the mPAP threshold for the definition of pulmonary hypertension has recently been adjusted (& GE;25 mmHg to >20 mmHg). Material and Methods: Between March 2014 and October 2020, 140 patients with CTEPH and 10 with CTEPD (chronic thromboembolic pulmonary disease) without pulmonary hypertension (PH) were retrospectively enrolled (12-lead ECG and right heart catheterization before and 6 months after BPA). The ECG parameters of right heart strain validated by studies and clinical experience were evaluated. Special attention was paid to six specific ECG parameters. After BPA, the cohort was divided into subgroups to investigate possible electrocardiographic differences with regard to the haemodynamic result. Results: The present study confirmed that the typical electrocardiographic signs of CTEPH can be found on an ECG, can regress after BPA and partially correlate well with haemodynamic parameters. "R V1, V2 + S I, aVL - S V1" was a parameter of particular note. BPA reduced its frequency (47% vs. 29%) statistically significantly after Bonferroni correction (p < 0.001). Moreover, it showed a good correlation with mPAP and PVR (r-values: 0.372-0.519, p-values: < 0.001). Exceeding its cut-off value before therapy was associated with more severe CTEPH before therapy (higher mPAP, PVR, NT-pro-BNP and troponin and lower TAPSE) and an increased risk of death. Exceeding its cut-off value before and after therapy was associated with more severe CTEPH after therapy (higher RAP, mPAP, PVR, NT-pro-BNP and NYHA class) and an increased risk of death. Men tend to be affected more frequently. After subgrouping, it was observed that a higher median mPAP was associated with a higher right atrial pressure (RAP), a higher pulmonary vascular resistance (PVR) and a lower cardiac output (CO) before and after BPA. In addition, under these conditions, more and more severe electrocardiographic pathologies were detected before and after BPA. Some patients with low mPAP also continued to show mild ECG changes after BPA. In some cases, very few to no pathological ECG changes were detected, and the ECG could present as mostly normal in some patients (5% before BPA and 13% after BPA). Conclusion: "R V1, V2 + S I, aVL - S V1" seems to be able to support the diagnosis of CTEPH, indicate therapeutic improvement and estimate haemodynamics. It also seems capable of predicting a (persistent) severe disease with probably increased need for therapy and increased mortality. Mild PH has been observed to have either no or few mild ECG changes. This might complicate the (early) detection of PH.