Cardiovascular Journal of Africa: Vol 32 No 5 (SEPTEMBER/OCTOBER 2021)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 5, September/October 2021 248 AFRICA Association of premature ventricular complex burden with elevated left ventricular filling pressure Ahmed Salah Salem, Mohamed Ahmed Elkotby, Gamela Mohamed Nasr, Ahmed Tageldien Abdellah Abstract Background: Premature ventricular contraction (PVC) is considered one of the most common arrhythmias in clini- cal practice. The aetiology of PVC is still unclear, however increased sympathetic activity, electrolyte misbalance and cardiomyopathies are considered the main causes of PVCs. In this study we were trying to find out whether there was any association between PVC burden and elevated left ventricular (LV) filling pressure. Methods: A total of 100 patients (age: 58.6 ± 7.5 years, 52 males) with frequent PVCs observed on 24-hour Holter monitoring (> 1%) and normal LV ejection fraction (LVEF) (> 50% on echocardiography) were enrolled. Clinical charac- teristics and echocardiographic parameters, including E/E ′ to assess LV filling pressure of the patients, were compared with those of an age- and gender-matched control group ( n = 100, age: 57.4 ± 7.5 years, 50 males). Results: Mean E ′ was significantly higher in the controls (7.9 ± 3.1 cm/s) than the cases (6.4 ± 1.9 cm/s) ( p = 0.010) while mean E/E ′ was significantly higher in the cases (12.5 ± 5.3) than the controls (10.9 ± 5.7) ( p = 0.044), reflecting significantly different LV diastolic function. However LVEF by M-mode and biplane imaging showed no significant differ- ence between the groups. Conclusion: Patients with frequent PVCs were associated with high LV filling pressure, which was significantly different from LV filling pressure in the control group. Keywords: premature ventricular contraction, left ventricle, fill- ing pressure Submitted 12/2/21, accepted 9/5/21 Published online 24/6/21 Cardiovasc J Afr 2021; 32 : 248–253 www.cvja.co.za DOI: 10.5830/CVJA-2021-021 Premature ventricular contractions (PVCs) are early depolarisations of the myocardium originating in the ventricle. Ventricular ectopic activity occurs in a wide variety of clinical settings with a spectrum of clinical implications. They are often seen in association with structural heart disease and represent increased risk of sudden death, even in the absence of identifiable heart disease. They may cause troubling and sometimes incapacitating symptoms such as palpitations, chest pain, pre-syncope, syncope and heart failure. 1 PVCs are among the most common cardiac arrhythmias encountered in clinical practice. There has been a recent accumulation of evidence implicating PVCs as a cause of reversible cardiomyopathy. 2 Even though the burden of PVCs seems to be an important determinant of left ventricular (LV) systolic dysfunction, some patients with a high PVC burden do not develop cardiomyopathy. This suggests that in addition to the PVC burden, other characteristics of PVCs might also be contributory. 3 PVC-induced cardiomyopathy has been a subject of great interest and the evidence for this entity is rapidly emerging. In some cases, a high PVC burden may not impair LV function, whereas PVC-induced cardiomyopathy can be observed in patients with lower PVC frequencies. The relationship between LV dysfunction and PVCs is a phenomenon to consider. 4 Why do PVCs occur? The reasons are not always clear. Certain triggers, heart diseases or changes in the body can make cells in the ventricles electrically unstable. Heart disease or scarring may also cause electrical impulses to be misrouted. In our study we were trying to determine whether PVC and PVC burden is correlated with one of the most relevant indicators of LV dysfunction, which is LV filling pressure. Methods This study was a cross-sectional, observational study that was carried out at the Cardiology Department, Suez Canal University Hospital, Egypt. We identified 100 eligible subjects with frequent PVCs (> 1% in 24-hour Holter) and normal LV systolic function [left ventricular ejection fraction (LVEF) > 50%]. Patients with valvular heart disease, congenital heart disease, hypertrophic cardiomyopathy or those with cardiac channelopathies, such as long-QT syndrome, short-QT syndrome and Brugada syndrome, were excluded. The study population was matched regarding all risk factors, such as diabetes, hypertension, dyslipidaemia and coronary artery disease, with a control group with PVC burden < 1%. All patients were subjected to: • a resting 12-lead electrocardiogram (ECG). PVC is caused by an ectopic cardiac pacemaker located in the ventricle. PVCs are characterised by premature and bizarrely shaped QRS complexes that are unusually long (typically > 120 ms) and appear wide on the ECG. These complexes are not preceded by a P wave, and the T wave is usually large and orientated in a direction opposite the major deflection of the QRS. • 24-hour Holter ECG (Schiller MT-Holter recorder). The following information was obtained from the recordings: PVC burden: the ratio between the number of PVCs and the total number of QRS complexes on 24-hour ambulatory ECG Department of Cardiology, Suez Canal University, Ismailia, Egypt Ahmed Salah Salem, MD, alsalem912@hotmail.com Mohamed Ahmed Elkotby, MD Gamela Mohamed Nasr, MD Ahmed Tageldien Abdellah, MD