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Predictors for the prolonged R wave peak time among patients with arterial hypertension
Göksel Çinier1, Ahmet Seyda Yılmaz2, Ahmet İlker Tekkesin1
1Department of Cardiology, Dr Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, İstanbul, Turkey.
Insights
Epicardial fat tissue (EFT) and fragmented QRS (fQRS) predict prolonged R wave peak time (RWPT) in hypertension patients. Myocardial fibrosis may significantly impact ventricular activation time more than increased left ventricular mass.
Area of Science:
- Cardiology
- Electrophysiology
- Hypertension Research
Background:
- Hypertension (HT) is a widespread condition linked to severe cardiovascular events.
- Pressure overload in HT triggers significant structural and electrical remodeling of the ventricular myocardium.
- Increased left ventricular mass (LVM) and myocardial fibrosis are associated with prolonged R wave peak time (RWPT), indicating electrical remodeling.
Purpose of the Study:
- To identify predictors of prolonged RWPT in patients with a history of hypertension.
- To investigate the relationship between cardiac structural and electrical changes and RWPT in hypertensive individuals.
Main Methods:
- A cohort of 237 patients with arterial HT was studied.
- Standard 12-lead surface electrocardiography (ECG) and transthoracic echocardiography (TTE) were performed.
- Epicardial fat tissue (EFT), left ventricular mass index (LVMI), and fragmented QRS (fQRS) were assessed to predict prolonged RWPT (upper limit 40 ms).
Main Results:
- The mean RWPT was 41.9±10.8 ms, with 55 patients exhibiting prolonged RWPT.
- Univariate analysis showed EFT, LVMI, and fQRS were associated with prolonged RWPT.
- Multivariate analysis identified EFT (OR 1.211) and fQRS (OR 2.796) as independent predictors of prolonged RWPT.
Conclusions:
- Epicardial fat tissue (EFT) and fragmented QRS (fQRS) are significant predictors of prolonged RWPT in patients with hypertension.
- These findings suggest that myocardial fibrosis, as indicated by EFT and fQRS, may have a greater impact on ventricular activation time than increased LVM in hypertensive patients.
Objective:
Hypertension (HT) is prevalent in the general population and is associated with significant cardiovascular adverse events. Major structural and electrical remodeling occurs in the ventricular myocardium in response to the pressure overload. Increased left ventricular mass (LVM) and myocardial fibrosis contribute to the prolongation of the R wave peak time (RWPT), which may indicate electrical remodeling in patients with HT. We evaluated predictors for prolonged RWPT among patients with a previous diagnosis of HT.
Methods:
Consecutive patients who had a previous diagnosis of arterial HT and presented to the cardiology clinic for routine visit were included in the study. The standard 12-lead surface electrocardiography (ECG) and transthoracic echocardiography (TTE) was performed on all the patients included in the study for evaluating RWPT and the epicardial fat tissue (EFT). The upper limit for the RWPT was accepted as 40 milliseconds (ms).
Results:
Between February 2019 and February 2020, 453 patients were screened; and of these, 237 were included in the study. The mean age was 62.1±11.2 years, and 41.8% of the included patients were men. The mean RWPT of the study population was 41.9±10.8. The RWPT was prolonged in 55 patients, and the remaining 172 patients had normal RWPT. In the univariate analysis, EFT (Odds ratio [OR] 1.222; 95% confidence interval [CI] 1.077-1386; p=0.002), the left ventricular mass index (LVMI) (OR 1.011; 95% CI 1.001-1.021; p=0.026), and fragmented QRS (fQRS) (OR 2.679; 95% CI 1.433-5.004; p=0.002) were associated with a prolonged RWPT. Multivariate analysis revealed that only EFT (OR 1.211; 95% CI 1.061-1.383; p=0.005) and fQRS (OR 2.796; 95% CI 1.459-5.359; p=0.002) predicted prolonged RWPT.
Conclusion:
Among the patients with HT, EFT and fQRS predicted prolonged RWPT. These findings may suggest that compared with increased LVM, myocardial fibrosis had a more significant impact on ventricular activation time.
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