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Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency
Tohru Watanabe1, Takeshi Kashimura, Makoto Kodama
1Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences.
Insights
Patients with heart failure have impaired force-frequency relationships (FFR). However, their post-stimulation potentiation (PSP) enhances with heart rate, suggesting refractoriness limits contractile force during tachycardia.
Area of Science:
- Cardiology
- Physiology
Background:
- The force-frequency relationship (FFR), or left ventricular contractile force's response to heart rate, is impaired in systolic dysfunction.
- Post-stimulation potentiation (PSP), the increase in contraction after a pause, is not well understood in this context.
Purpose of the Study:
- To investigate if post-stimulation potentiation (PSP) increases in a rate-dependent manner in patients with idiopathic dilated cardiomyopathy (DCM).
- To compare FFR and PSP between DCM patients and healthy controls.
Main Methods:
- Assessed FFR and PSP using right atrial pacing with a micro-manometer-tipped catheter in 16 DCM patients and 6 controls.
- Measured the increase in left ventricular dP/dtmax (LV dP/dtmax) over baseline (ΔFFR) and after pacing cessation (ΔPSP) at various pacing rates.
Main Results:
- DCM patients had lower baseline LV dP/dtmax and significantly smaller ΔFFR compared to controls.
- DCM patients exhibited a rate-dependent increase in PSP, with greater ΔPSP than controls at higher pacing rates.
- Despite enhanced PSP, failing left ventricles showed limited contractile force during tachycardia.
Conclusions:
- Impaired FFR in DCM is not due to a lack of rate-dependent PSP.
- Refractoriness of contractile force likely underlies the impaired FFR in failing left ventricles.
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.
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