Premature Ventricular Contractions
Premature ventricular contractions (PVCs) are early beats from the ventricles causing a "skipped beat" sensation — common and usually benign, but requiring specialist assessment when frequent, symptomatic, or associated with structural heart disease or reduced ejection fraction.
Your heart maintains the beat of life
Premature ventricular contractions are ectopic beats originating from the ventricular myocardium before the next expected sinus impulse arrives, producing a characteristic early beat followed by a compensatory pause. They are among the most common cardiac rhythm disturbances — present in the majority of adults on prolonged monitoring — and are frequently identified incidentally on ECG or Holter recording. Most PVCs in structurally normal hearts are benign. However, high PVC burden, specific morphological features, and the presence of structural heart disease influence prognosis and determine the need for investigation and treatment.
Symptoms
PVCs are frequently asymptomatic and discovered incidentally. When symptomatic, they produce palpitations — typically described as a skipped beat, a thump or flip in the chest, or a brief pause followed by a forceful beat — caused by the enhanced stroke volume of the post-extrasystolic beat. Symptoms are often most noticeable at rest or when lying down, as competing sinus beats are slower and the PVC is more perceptible. Frequent PVCs may cause lightheadedness, chest discomfort, or exertional breathlessness — particularly when PVC burden is high or when they occur in a bigeminal or trigeminal pattern.
PVC Patterns & Morphology
PVCs are described by their pattern and origin. Bigeminy refers to every other beat being a PVC; trigeminy to every third beat. Couplets are two consecutive PVCs; non-sustained ventricular tachycardia (NSVT) is three or more consecutive PVCs lasting under 30 seconds. The morphological origin of PVCs is clinically important: right ventricular outflow tract (RVOT) PVCs — the most common form, producing a left bundle branch block morphology with inferior axis on ECG — are typically benign in structurally normal hearts and highly amenable to catheter ablation. PVCs with other morphologies, particularly those arising from the left ventricle or papillary muscles, require more careful evaluation to exclude underlying structural disease.
When Are PVCs a Concern?
PVCs in structurally normal hearts with low burden are generally benign and do not require treatment beyond reassurance. The following features warrant specialist assessment and further investigation: PVC burden exceeding 10–15% of total beats on 24-hour Holter monitoring; PVCs that increase with exercise (as opposed to suppression, which is reassuring); NSVT on monitoring; associated reduced ejection fraction or structural heart disease; symptoms significantly impairing quality of life; and a family history of sudden cardiac death or cardiomyopathy. PVC-induced cardiomyopathy — a reversible decline in left ventricular function caused by chronic high PVC burden — develops in a subset of patients, most commonly when PVCs exceed 10,000–20,000 per day; ejection fraction typically recovers with effective PVC suppression through ablation or medication.
Causes & Risk Factors
In structurally normal hearts, PVCs are frequently triggered by sympathetic stimulation — caffeine, alcohol, nicotine, stress, sleep deprivation, and stimulant medications. Electrolyte disturbances — particularly hypokalaemia and hypomagnesaemia — are reversible and important to correct. Structural causes include coronary artery disease, prior myocardial infarction, cardiomyopathy, and mitral valve prolapse. Hyperthyroidism and obstructive sleep apnoea are systemic conditions that increase ectopic activity and should be excluded in new or worsening PVCs.
Diagnosis
A resting 12-lead ECG captures PVCs present at the time of recording and characterises their morphology and axis — providing initial information on likely site of origin. Twenty-four hour Holter monitoring quantifies PVC burden, identifies patterns (bigeminy, couplets, NSVT), and assesses for exercise-related changes. Echocardiography is essential to evaluate left ventricular function, wall motion, and structural heart disease — mandatory in all patients with significant PVC burden. Exercise stress testing assesses whether PVCs are suppressed or increase with exertion, providing important prognostic information. Cardiac MRI is indicated when structural cardiomyopathy is suspected on echocardiography, providing detailed tissue characterisation including scar and fibrosis assessment.
Treatment
Observation and reassurance is appropriate for asymptomatic, low-burden PVCs in structurally normal hearts. Identification and correction of reversible triggers — caffeine reduction, alcohol limitation, electrolyte repletion, treatment of thyroid disease or sleep apnoea — reduces PVC frequency in many patients. Beta-blockers are the first-line pharmacological option for symptomatic PVCs, reducing adrenergic stimulation with a favourable safety profile. Calcium channel blockers (verapamil, diltiazem) are an alternative for patients who cannot tolerate beta-blockers. Catheter ablation is recommended for symptomatic PVCs refractory to medical therapy, for PVC-induced cardiomyopathy, and for high-burden RVOT PVCs in patients seeking definitive treatment. Ablation achieves high success rates for RVOT morphology PVCs and offers the advantage of cure over chronic medication. In patients with PVC-induced cardiomyopathy, ejection fraction recovery following successful ablation is well-documented and frequently substantial.
Experiencing frequent skipped beats, diagnosed with high PVC burden, or concerned about heart function? Dr. Peter Chang consults at Paragon Medical Centre, Orchard Road. Book a specialist assessment today.