What are the causes and treatments of Premature Ventricular Contractions (PVCs)?

From the Guidelines

PVCs are generally benign and do not require treatment, but in symptomatic or frequent cases, treatment may be warranted to improve quality of life and reduce morbidity and mortality risk. The management of PVCs should prioritize lifestyle modifications, such as reducing caffeine, alcohol, and stress, while ensuring adequate sleep and exercise. For medication therapy, beta-blockers like metoprolol (25-200 mg daily) or calcium channel blockers such as diltiazem (120-360 mg daily) are commonly used 1.

In cases where PVCs significantly reduce quality of life or cause cardiomyopathy despite medical therapy, catheter ablation may be considered, especially in patients with a high PVC burden (>24%) and a reduced left ventricular ejection fraction (LVEF) 1. The use of antiarrhythmic medications like flecainide (50-200 mg twice daily) or amiodarone (200 mg daily after loading) may be considered in more severe cases, but their use should be cautious due to the potential increased risk of mortality, particularly in patients with structural heart disease or reduced LVEF 1.

PVCs warrant further evaluation if they occur with structural heart disease, are very frequent, cause symptoms like palpitations or lightheadedness, or appear in patterns like bigeminy or trigeminy. The underlying mechanism of PVCs involves abnormal electrical impulses in the ventricles that override the heart's normal pacemaker activity, often due to increased automaticity, triggered activity, or reentry circuits.

Some key points to consider in the management of PVCs include:

• The presence of PVCs on 2 minutes of monitoring of middle-aged patients is associated with increased risk of both ischemic heart disease events and mortality 1
• Frequent PVCs are associated with increased cardiovascular risk and increased mortality, particularly in patients with structural heart disease or reduced LVEF 1
• Catheter ablation can be an effective treatment option for patients with symptomatic PVCs or PVC-induced cardiomyopathy 1
• The use of beta-blockers and calcium channel blockers can help reduce the frequency and severity of PVCs, but may not eliminate them entirely 1

From the FDA Drug Label

Flecainide acetate tablets, USP cause a dose-related and plasma-level related decrease in single and multiple PVCs and can suppress recurrence of ventricular tachycardia In limited studies of patients with a history of ventricular tachycardia, flecainide acetate tablets, USP have been successful 30 to 40% of the time in fully suppressing the inducibility of arrhythmias by programmed electrical stimulation. Based on PVC suppression, it appears that plasma levels of 0. 2 to 1 mcg/mL may be needed to obtain the maximal therapeutic effect. New or exacerbated ventricular arrhythmias which occurred in 7% of 1330 patients with PVCs, non-sustained or sustained VT

Flecainide can decrease PVCs in a dose-related and plasma-level related manner. The maximal therapeutic effect for PVC suppression is achieved at plasma levels of 0.2 to 1 mcg/mL. However, flecainide may also cause new or exacerbated ventricular arrhythmias in some patients, occurring in 7% of patients with PVCs. 2 2

From the Research

Definition and Presentation of PVCs

• Premature ventricular contractions (PVCs) are arrhythmias with a presentation ranging from asymptomatic and benign to symptomatic, frequent, and capable of inducing cardiomyopathy 3.
• PVCs can be representative of underlying coronary artery disease, hypertension, or left ventricular hypertrophy, and their presence is independently linked to an increased risk of stroke and sudden cardiac death 3.
• Increasing age, taller height, higher blood pressure, history of heart disease, less physical activity, and smoking each predict a greater PVC frequency 4.

Diagnosis and Evaluation of PVCs

• The history, physical examination, and 12-lead ECG are critical to the diagnosis and evaluation of a PVC 4.
• An echocardiogram is indicated in the presence of symptoms or particularly frequent PVCs, and cardiac magnetic resonance imaging is helpful when the evaluation suggests the presence of associated structural heart disease 4.
• Ambulatory monitoring is required to assess PVC frequency 4.

Management and Treatment of PVCs

• No treatment is indicated in patients with asymptomatic PVCs in the absence of cardiac disease 5.
• Symptomatic patients without cardiac disease may be managed by identifying and correcting reversible causes 5.
• In patients with cardiac disease, management includes treating the underlying cardiac disease to improve both symptoms and prognosis 5.
• Medical treatment or catheter ablation are considered first-line therapies in most patients with PVCs associated with symptoms or a reduced left ventricular ejection fraction 4.
• β-blockers or nondihydropyridine calcium channel blockers are reasonable drugs in patients with normal ventricular systolic function 4.
• Catheter ablation is the most efficacious approach to eradicate PVCs but may confer increased upfront risks 4, 6.

Therapeutic Efficacy of Antiarrhythmic Drugs

• Antiarrhythmic drugs, such as metoprolol succinate and carvedilol, are frequently inefficient for idiopathic, frequent, monomorphic PVCs 7.
• Therapeutic efficacy decreases further in patients with relatively high (≥16%) PVC burden 7.
• Relatively higher baseline daily intrinsic total heart beats may be used to predict "good" response before beta-blocker therapy 7.