title: Atrial electrical and structural remodeling associated with longstanding pulmonary hypertension and right ventricular hypertrophy in humans.
abstract: BACKGROUND
  Pulmonary hypertension (PH) is common to a range of cardiopulmonary conditions and is associated with atrial arrhythmias. However, little is known of the isolated atrial effects of PH and right atrial dilatation (RA) in humans. To avoid the confounding effects of PH-associated disease states, we performed detailed electrophysiological (EP) and electroanatomic (EA) mapping of the RA in patients with idiopathic PH.
  
  
  RESULTS
  Eight PH patients (mean pulmonary arterial [PA] pressure 39.0 ± 15.8 mmHg) and 16 age-matched controls (mean PA pressure 11.5 ± 4.1 mmHg, P < 0.0001) were studied. Corrected sinus node recovery times (cSNRT), atrial effective refractory periods (ERPs), conduction delay at the crista terminalis (CT), and inducibility of atrial fibrillation (AF) were evaluated. EA mapping (pacing cycle length 600 and 300 milliseconds) was performed to determine RA global and regional voltage, conduction velocities, atrial activation times, fractionated electrograms and double potentials. Patients with PH demonstrated a prolongation in cSNRT without significant change in atrial ERP and an increase in AF inducibility. PH was associated with lower tissue voltage (1.8 ± 0.4 mV in PH vs 2.2 ± 0.4 mV in controls, P = 0.02), increased low voltage areas (13.7 ± 8.2% in PH vs 6.2 ± 3.7% in controls, P < 0.01) and the presence of electrically silent areas. Conduction velocities were slower (global 67.3 ± 5.6 cm/s vs 92.8 ± 4.0 cm/s, P < 0.001) and fractionated electrograms and double potentials were more prevalent (14.7 ± 4.4% vs 6.3 ± 4.1, P < 0.01) in PH compared with controls, respectively.
  
  
  CONCLUSIONS
  Idiopathic PH is associated with RA remodeling characterized by: generalized conduction slowing with marked regional abnormalities; reduced tissue voltage; and regions of electrical silence. These changes provide important insights into the isolated effects of PH fundamental to a range of clinical conditions associated with AF.
authors.affiliation: Department of Cardiology, The Alfred Hospital, Australia.
authors.forename: Caroline
authors.initials: C
authors.lastname: Medi
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Kalman
authors.forename: Liang-Han
authors.initials: LH
authors.lastname: Ling
authors.forename: Andrew W
authors.initials: AW
authors.lastname: Teh
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Lee
authors.forename: Geraldine
authors.initials: G
authors.lastname: Lee
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Spence
authors.forename: David M
authors.initials: DM
authors.lastname: Kaye
authors.forename: Peter M
authors.initials: PM
authors.lastname: Kistler
mesh_terms: D000200:Action Potentials; D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D016280:Atrial Function, Right; D001794:Blood Pressure; D006328:Cardiac Catheterization; D002304:Cardiac Pacing, Artificial; D016022:Case-Control Studies; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D065627:Familial Primary Pulmonary Hypertension; D005260:Female; D006325:Heart Atria / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011651:Pulmonary Artery / Q000503:physiopathology; D012032:Refractory Period, Electrophysiological; D012849:Sinoatrial Node / Q000503:physiopathology; D013997:Time Factors; D014739:Victoria; D056969:Voltage-Sensitive Dye Imaging