The precise shape of the QRS can give an indication as to where precisely in the heart muscle the abnormal electrical activity arises. If someone has PVCs that all have the same appearance, they are considered "monofocal", if PVC’s have different appearance, they are considerevole “multifocal”. Treatment
Isolated PVCs with benign characteristics and no underlying heart disease require no treatment, especially if there are limited symptoms.The most effective treatment is the elimination of triggers (particularly stopping the use of substances such as caffeine and certain drugs, like tobacco). If frequent, it’s possible to use:

Medications
Antiarrhythmics: these agents alter the electrophysiologic mechanisms responsible for PVCs. In CAST study of survivors of myocardial infarction encainide and flecainide, it was shown that, though those drugs could suppress PVC, they also increased the risk of death. However, while moricizine increased the death rate when used with diuretics, it reduced the frequency of deaths when it was used alone. Beta blockers: do not directly affect or reduce the occurrence of PVCs, but reduce cardiac contractility which makes PVCs less obvious to a person; possibly reduce catecholamine induced PVCs (in catecholamine-sensitive people) due to adrenaline not reaching sinus node as much. Calcium channel blockers
Electrolytes replacement
Magnesium supplements (e.g. magnesium citrate, orotate, Maalox, etc.) Potassium supplements (e.g. chloride potassium with citrate ion)
Radiofrequency catheter ablation treatment. It is advised for people with ventricular dysfunction and/or tachyarrythmia or very frequent PVC (>20% in 24 h) and normal ventricular function.
One study found that the incidence of sudden cardiac death in young competitive athletes declined in the Veneto region of Italy by 89% since the 1982 introduction of routine cardiac screening for athletes, from an unusually high starting rate. As of 2010, however, studies have shown that the incidence of sudden cardiac death, among all people with HCM, has declined to one percent or less. Screen-positive individuals who are diagnosed with cardiac disease are usually told to avoid competitive athletics.HCM can be detected with an echocardiogram (ECHO) with 80%+ accuracy, which can be preceded by screening with an electrocardiogram (ECG) to test for heart abnormalities. Cardiac magnetic resonance imaging (CMR), considered the gold standard for determining the physical properties of the left ventricular wall, can serve as an alternative screening tool when an echocardiogram provides inconclusive results. For example, the identification of segmental lateral ventricular hypertrophy cannot be accomplished with echocardiography alone. Also, left ventricular hypertrophy may be absent in children under thirteen years of age. This undermines the results of pre-adolescents echocardiograms. Researchers, however, have studied asymptomatic carriers of an HCM-causing mutation through the use of CMR and have been able to identify crypts in the interventricular septal tissue in these people. It has been proposed that the formation of these crypts is an indication of myocyte disarray and altered vessel walls that may later result in the clinical expression of HCM. A possible explanation for this is that the typical gathering of family history only focuses on whether sudden death occurred or not.