Increased Plasma Levels of Atrial Natriuretic Peptide (ANP) in Patients with Paroxysmal Supraventricular Tachyarrhythmias

Nilsson G, Pettersson A, Hedner J, Hedner T (Department of Internal Medicine, Central Hospital, Halmstad and Department of Clinical Pharmacology, Sahlgrenska University Hospital, Göteborg, Sweden). Increased plasma levels of atrial natriuretic peptide (ANP) in patients with paroxysmal supraventricular tachyarrhythmias. Acta MedScand 1987; 221:15–21. Atrial natriuretic peptide (ANP) is a cardiac hormone originating from atrial cardiocytes. It seems to be involved in the regulatory control of circulating volume and vascular tone. Plasma immunoreactive atrial natriuretic peptide (IrANP) was investigated in 22 patients with paroxysmal supraventricular tachyarrhythmia (16 with atrial fibrillation, 4 with atrial flutter, one with a Wolf‐Parkinson‐White syndrome (WPW) and one with atrial tachycardia). During the aute attack, IrANP was significantly increased (125.3± 11.4 pmol/1) compared to samples obtained during convalescence (55.9±4.7 pmol/1). Heart rate (HR) was 144±4.3 beats/min during the arrhythmia and 75±2.6 during convalescence. The reduction of IrANP in plasma from the acute attack of tachycardia to follow‐up was significantly related to the reduction of HR ( p <0.05). Irrespective of type of paroxysmal supraventricular tachyarrhythmia, 50% of the patients experienced polyuria during the attack. This symptom was more frequent in younger patients with a shorter duration of tachycardia. Polyuria patients had a higher HR during the attack of supraventricular tachycardia. Even though polyuria was not alwavs found in the patients with the highest IrANP values, the symptom was associated with significantly higher concentrations of Ir ANP in plasma compared to the non‐polyuria group. We conclude that Ir ANP is increased in plasma during acute attacks of paroxysmal supraventricular tachycardia. Furthermore, the polyuria frequently associated with this condition may partly be due to excess release of ANP from cardiac myocytes.