Ventricular Extrasystoles Without Structural Heart Disease: Epidemiology, Clinical Presentation, Pathophysiology, and Prognosis

Premature ventricular contraction (PVCs) is a com­mon pathology observed across all age groups, albeit with a higher prevalence among older individuals (1). It can manifest in both healthy individuals and those with structural heart disease (2). While PVC without underlying heart disease may be benign, it can lead to arrhythmic cardiomyopathy – structural and functional changes in the heart (3). PVCs are classified into several categories based on their frequency and morphology, with higher classes associa­ted with an increased risk of mortality, especially in pa­tients with structural heart diseases (4). Often, patients with PVCs do not experience any symptoms. However, symptomatic patients may report episodic palpitations, dizziness, and possible symptoms of heart failure such as shortness of breath, chest pain, and palpitations (3). These symptoms help identify patients at higher risk who require thorough specialised evaluation. PVCs without structural heart disease typically originate from the right ventricular outflow tract (5), located bene­ath the pulmonary artery. The main pathophysiological mechanisms are believed to be re-entry, increased ectopic automatism, and triggered activity (6). The prognostic significance of PVC varies and fluctua­tes depending on the patient’s medical history, overall condition, any other cardiac dysfunction, and concurrent diseases. PVC is generally associated with a good pro­gnosis; however, comprehensive clinical studies have revealed that it may entail several potential long-term complications. Detailed clinical studies have indicated a higher risk of developing cardiomyopathy in patients experiencing PVCs (2). The aim of the work is to review the literature on the epi­demiology, clinical presentation, pathophysiology, and prognosis of ventricular extrasystoles in patients without structural heart disease.