title: Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency Relationship.
abstract: The left ventricular contractile force (LV dP/dtmax) of patients with left ventricular systolic dysfunction does not increase effectively with an increase in heart rate. In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval subsequent to tachycardia causes a stronger contraction (poststimulation potentiation, PSP) in a rate-dependent manner.In 16 patients with idiopathic dilated cardiomyopathy (DCM) (48 ± 2 years old, LVEF 30 ± 10%) and 6 control patients (58 ± 4 years old, LVEF 70 ± 7%), FFR was assessed by right atrial pacing using a micro-manometer-tipped catheter. At each pacing rate, the increase of LV dP/dtmax over basal LV dP/dt (ΔFFR) and the increase of LV dP/dtmax of the first beat after pacing cessation over LV dP/dtmax during pacing (ΔPSP) were evaluated.Patients with DCM had smaller LV dP/dtmax at baseline (872 ± 251 versus 1370 ± 123 mmHg/second, P = 0.0002) and developed smaller ΔFFR (eg, at 120/minute, 77 ± 143 versus 331 ± 131 mmHg/second, P = 0.0011). In contrast, they showed a rate-dependent increase of LV dP/dtmax of PSP and had greater ΔPSP (eg, at 120/minute, 294 ± 173 versus -152 ± 131 mmHg/second, P < 0.0001).Failing left ventricles develop little contractile force during tachycardia despite their rate-dependent enhancement in post-stimulation potentiation, suggesting that refractoriness of contractile force underlies impaired FFR.
authors.affiliation: Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences.
authors.forename: Tohru
authors.initials: T
authors.lastname: Watanabe
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kashimura
authors.forename: Makoto
authors.initials: M
authors.lastname: Kodama
authors.forename: Komei
authors.initials: K
authors.lastname: Tanaka
authors.forename: Shinya
authors.initials: S
authors.lastname: Fujiki
authors.forename: Yuka
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Obata
authors.forename: Haruo
authors.initials: H
authors.lastname: Hanawa
authors.forename: Tohru
authors.initials: T
authors.lastname: Minamino
mesh_terms: D002118:Calcium / Q000378:metabolism; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects / Q000379:methods; D002311:Cardiomyopathy, Dilated / Q000150:complications* / Q000503:physiopathology; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods; D005260:Female; D054143:Heart Failure, Systolic / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D012032:Refractory Period, Electrophysiological; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy
chemical_list: D002118:Calcium