title: High blood pressure and ventricular arrhythmias.
abstract: Here we review the blood pressure-ventricular arrhythmia relationship. An increase in blood pressure, by any means, may induce ventricular arrhythmias both experimentally and in patients with a history of ventricular ectopic beats. Conversely, a decrease in blood pressure may eliminate ventricular arrhythmias due to other causes. The increased pressure is sensed in the ventricles. Both systolic and diastolic loading may induce important electrophysiological changes. However, an increase in systolic pressure may induce ventricular ectopy even though the left atrial pressure remains low; on the other hand, raising the atrial pressure does not induce ectopic rhythms unless associated with an increase in arterial pressure. This phenomenon (mechanoelectrical association or contraction-excitation feedback) seems to be a direct one not mediated by either ischaemia or adrenergic stimulation. Both refractoriness and intraventricular conduction are affected by mechanical loading, although the direction of change depends on several factors. The mechanism of pressure-related arrhythmias remains obscure. Triggered activity due to early after-depolarizations is one possibility. Ventricular arrhythmias observed in chronic hypertension might be a clinical manifestation of mechano-electrical association, especially when they occur in conjunction with acute blood pressure elevations. Several antihypertensive agents with different mechanisms of action also have an antiarrhythmic effect. Extensive research to establish the antiarrhythmic effectiveness of antihypertensive treatment in cases with ventricular arrhythmias is still warranted.
authors.affiliation: Department of Clinical Therapeutics, Medical School of Athens University, Greece.
authors.forename: D A
authors.initials: DA
authors.lastname: Sideris
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology; D001794:Blood Pressure; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology