Enhanced inotropic state of the failing left ventricle by cardiac contractility modulation electrical signals is not associated with increased myocardial oxygen consumption
被引:74
作者:
Butter, Christian
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机构:
German Heart Inst, Berlin, GermanyGerman Heart Inst, Berlin, Germany
Butter, Christian
[1
]
Wellnhofer, Ernst
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机构:
German Heart Inst, Berlin, GermanyGerman Heart Inst, Berlin, Germany
Wellnhofer, Ernst
[1
]
Schlegl, Michael
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机构:
German Heart Inst, Berlin, GermanyGerman Heart Inst, Berlin, Germany
Schlegl, Michael
[1
]
Winbeck, Georgia
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机构:
German Heart Inst, Berlin, GermanyGerman Heart Inst, Berlin, Germany
Winbeck, Georgia
[1
]
Fleck, Eckart
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German Heart Inst, Berlin, GermanyGerman Heart Inst, Berlin, Germany
Fleck, Eckart
[1
]
Sabbah, Hani N.
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Henry Ford Hlth Syst, Div Cardiovasc Med, Detroit, MI USAGerman Heart Inst, Berlin, Germany
Sabbah, Hani N.
[2
]
机构:
[1] German Heart Inst, Berlin, Germany
[2] Henry Ford Hlth Syst, Div Cardiovasc Med, Detroit, MI USA
Background: Previous studies in patients and in dogs with experimentally induced heart failure (HF) showed that electrical signals applied to the failing myocardium during the absolute refractory period improved left ventricular (LV) function. We examined the effects these same cardiac contractility modulating (CCM) electrical signals on myocardial Oxygen Consumption (MVO2) in both patients and dogs with chronic HF. Methods and Results: Six dogs with microembolizations-induced HF and 9 HF patients underwent CCM leads and generator (OPTIMIZER 11) implantation. After baseline measurements, CCM signals were delivered continuously for 2 hours in dogs and for 30 minutes in patients. MVO2 was measured before and after CCM therapy. In dogs, CCM therapy increased LV ejection fraction at 2 hours (26 +/- I versus 3 1 +/- 2%, P = .001) without increasing MVO2, (257 +/- 41 versus 180 +/- 34 mu mol/min). In patients, CCM therapy increased LV peak +dP/dt by 10.1 +/- 1.5%. As with dogs, the increase in LV function after 30 minutes of CCM therapy was not associated with increased MVO2 (13.6 +/- 9.7 versus 12.5 +/- 7.2 mL O-2/min). Conclusions: The study results Suggest that unlike cAMP-dependent positive inotropic drugs, the increase in LV function during CCM therapy is elicited without increasing MVO2.