Advances in management of premature ventricular contractions

Abstract

Premature ventricular complexes (PVCs) are a common occurrence in clinical practice. The clinical presentation may range from asymptomatic to left ventricular (LV) dysfunction with congestive heart failure. The decision to suppress PVCs is largely based on the presence of symptoms, interference with other therapy (e.g., cardiac resynchronization therapy), or suspicion of PVC-mediated cardiomyopathy. Catheter ablation has emerged as a safe and effective option for the treatment of frequent PVCs. Careful attention to PVC characteristics on surface electrocardiogram has proven useful for the initial localization of the ectopic focus, which may then serve as a guide to procedural planning. The point of interest is often identified with activation mapping, and the ablation site can be further defined with pace mapping techniques. Clinical experience with PVC ablation has been successful in ≥80 % of cases, and the literature reports multiple cases of marked improvement in LV function after eradicating the culprit ectopic focus in patients with PVC-mediated cardiomyopathy.

Ablating Premature Ventricular Complexes: Justification, Techniques, and Outcomes

“…11 Mechanistically, it has been proposed that RVOT PVCs are caused by delayed afterdepolarizations or triggered automaticity, provoked by catecholamines, exercise, and menstrual cycles, and inhibited by adenosine. 4,[12][13][14] However, anisotropic extensions of cardiomyocytes above the fibrous valvular annuli have also been hypothesized to allow conduction slowing and unidirectional block, which can lead to reentrant PVCs. 4,[15][16][17] Delayed afterdepolarizations also cause pathologic PVCs, frequently in a bigeminal pattern, in channelopathies such as Andersen-Tawil syndrome or catecholaminergic polymorphic ventricular tachycardia (VT), and in digoxin toxicity.…”

“…Thus, the QRS morphology on ECG can predict the PVC's site of houstonmethodist.org/debakey-journal origin or exit to the larger myocardial mass (Table 1). 13 The site of origin or earliest activation is the target of ablation for focal PVCs; for reentrant PVCs, the critical arrhythmogenic tissue can often be targeted in proximity to the exit site. Outflow tract PVCs typically have an inferior frontal plane axis with tall positive R waves in inferior leads (II, III, aVF) and QS complexes in aVR and aVL.…”

Dual-chamber ICD-CRT implantation in a patient with persistent left superior vena cava: testing skills

“…Furthermost of the individuals do not present the symptoms, and the presence of the persistent left superior vena cava is by the way found during or after insertion of a central venous catheter (CVC) or pacemaker electrodes. The correct report of a PLSVC and lack of a right superior vena cava has significant clinical repercussions in definite circumstances, such as oncological therapy, totally implantable vessels catheters, hemodynamic checking in intenive care unit (ICU) or the correct location of pacemakers [1][2][3][4][5][6][7][8][9][10]. The further clinical relevance of the described anomaly could be due to common tachyarrhythmia and conduction disturbances [11][12][13][14][15].…”

“…Nevertheless, it is the most common thoracic venous anomaly [6][7][8][9][10]. Typically, the left superior vena cava fades post embryological developement.…”

Ventricular fibrillation after inadvertent intravascular injection of ropivacaine

“…The pathogenesis of PVC-mediated cardiomyopathy is uncertain, and hypotheses include ventricular dyssynchrony, hemodynamic impairment, increased oxygen demand, autonomic dysregulation, alterations in intracellular calcium handling, and altered heart rate (HR) dynamics [8,9]. Though PVCs are fairly infrequent and asymptomatic in most cases; some patients may experience more frequent PVCs and symptoms such as palpitations, chest pain, and dyspnea.…”