This ectopy of the ventricles when associated with a structurally normal heart most commonly occurs from the right ventricular outflow tract (RVOT) under the pulmonic valve. The mechanism behind this is thought to be enhanced automaticity versus triggered activity. Molecular basis
There are a number of different molecular explanations for PVCs. calcium excess:  One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the muscle cells of the hearts ventricles leading to increased flow of calcium ions into the cell. This may happen for the following reasons:Activation of the sympathetic nervous system, due to anxiety and/or physiological stress, for example hypovolemia caused by dehydration or bleeding. This activation can cause a release of catecholamines such as epinephrine (adrenaline) which can bind to beta-1 adrenergic receptor (β1 receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called Gs protein. This type of protein stimulates the production of cAMP, ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol. This has the effect of (1) increasing the strength of contraction (inotropy) and (2) depolarizing the myocyte more rapidly (chronotropy). The ventricular myocytes are therefore more irritable than usual, and may depolarize spontaneously before the SA node depolarizes. Other sympathomimetic molecules such as amphetamines and cocaine will also cause this effect.
Hypertension or diabetes, both risk factors for stroke, did not change significantly risk of stroke for people with PVCs. It is possible that PVCs identified those at risk of stroke with blood pressure and impaired glucose tolerance on a continuum of risk below conventional diagnostic thresholds for hypertension and diabetes. Those in ARIC study with any PVC had risk of heart failure increased by 63% and were > twice as likely to die from coronary heart disease (CHD). Risk was also higher for people with or without baseline CHD.In the Niigata study of 63,386 people with a 10-year follow-up period, subjects with PVC during a 10-second recording had triple the risk of atrial fibrillation of those without PVCs, independently of these risk factors: age; male sex; high simple body mass index (a possible signifier of obesity); hypertension (systolic and diastolic blood pressure within certain abnormal limits); and diabetes.Reducing very frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.Recent studies have shown that those subjects with extremely frequent PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy regresses. Epidemiology
Single PVCs are common in healthy persons. When 24-hour ambulatory monitoring is used, up to 80 percent of apparently healthy people have occasional PVCs. Rates vary by age with extremely rare for those under the age of 11 and extremely common in those older than 75 years.