title: Improved ECG detection of presence and severity of right ventricular pressure load validated with cardiac magnetic resonance imaging.
abstract: The study aimed to assess whether the 12-lead ECG-derived ventricular gradient, a vectorial representation of ventricular action potential duration heterogeneity directed toward the area of shortest action potential duration, can improve ECG diagnosis of chronic right ventricular (RV) pressure load. ECGs from 72 pulmonary arterial hypertension patients recorded <30 days before onset of therapy were compared with ECGs from matched healthy control subjects (n = 144). Conventional ECG criteria for increased RV pressure load were compared with the ventricular gradient. In 38 patients a cardiac magnetic resonance (CMR) study had been performed within 24 h of the ECG. By multivariable analysis, combined use of conventional ECG parameters (rsr' or rsR' in V1, R/S > 1 with R > 0.5 mV in V1, and QRS axis >90 degrees ) had a sensitivity of 89% and a specificity of 93% for presence of chronic RV pressure load. However, the ventricular gradient not only had a higher diagnostic accuracy for chronic RV pressure load by receiver operating characteristic analysis [areas under the curve (AUC) = 0.993, SE 0.004 vs. AUC = 0.945, SE 0.021, P < 0.05], but also discriminated between mild-to-moderate and severe RV pressure load. CMR identified an inverse relation between the ventricular gradient and RV mass, and a trend toward a similar relation with RV volume. In conclusion, chronically increased RV pressure load is electrocardiographically reflected by an altered ventricular gradient associated with RV remodeling-related changes in ventricular action potential duration heterogeneity. The use of the ventricular gradient allows ECG detection of even mildly increased RV pressure load.
authors.affiliation: Cardiology Department, Leiden University Medical Center, Leiden, The Netherlands.
authors.forename: Ivo R
authors.initials: IR
authors.lastname: Henkens
authors.forename: Koen T B
authors.initials: KT
authors.lastname: Mouchaers
authors.forename: Anton
authors.initials: A
authors.lastname: Vonk-Noordegraaf
authors.forename: Anco
authors.initials: A
authors.lastname: Boonstra
authors.forename: Cees A
authors.initials: CA
authors.lastname: Swenne
authors.forename: Arie C
authors.initials: AC
authors.lastname: Maan
authors.forename: Sum-Che
authors.initials: SC
authors.lastname: Man
authors.forename: Jos W R
authors.initials: JW
authors.lastname: Twisk
authors.forename: Ernst E
authors.initials: EE
authors.lastname: van der Wall
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Schalij
authors.forename: Hubert W
authors.initials: HW
authors.lastname: Vliegen
mesh_terms: D000200:Action Potentials; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D004562:Electrocardiography; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011651:Pulmonary Artery / Q000503:physiopathology*; D012372:ROC Curve; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013997:Time Factors; D014672:Vectorcardiography; D018497:Ventricular Dysfunction, Right / Q000150:complications / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology; D017725:Ventricular Pressure; D020257:Ventricular Remodeling