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Myocardial energetics in dilated cardiomyopathy
L Thierfelder1, C H Holubarsch, G Hasenfuss
1Universitätsklinik Freiburg, Innere Medizin III, Federal Republic of Germany.
Insights
Drug interventions in idiopathic dilated cardiomyopathy (IDCM) affect myocardial energetics. Vasodilators save energy, while positive inotropes consume it, influencing overall drug effects in IDCM patients.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Idiopathic dilated cardiomyopathy (IDCM) affects myocardial energetics.
- Understanding drug effects on myocardial oxygen consumption (MVO2) is crucial for IDCM management.
Purpose of the Study:
- To assess hemodynamic and energetic effects of different drug interventions on IDCM.
- To determine the impact of vasodilators and inotropes on myocardial energetics.
Main Methods:
- Measured hemodynamic variables and MVO2 in 37 IDCM patients using heart catheterization.
- Analyzed MVO2 from myocardial blood flow and aortocoronary sinus blood oxygen difference.
- Correlated MVO2 with systolic stress time integral (STI).
Main Results:
- Nitroprusside (vasodilator) reduced STI and MVO2 equally, not altering the MVO2/STI ratio.
- Pimobendan (calcium sensitizer/PDE inhibitor) reduced STI and MVO2 similarly, not altering the ratio.
- Enoximone (PDE inhibitor) significantly reduced STI but minimally reduced MVO2, increasing the MVO2/STI ratio.
- Xamoterol (beta-1 agonist) increased MVO2 without changing STI, also increasing the MVO2/STI ratio.
Conclusions:
- Vasodilation demonstrates energy-saving effects in IDCM.
- Positive inotropism is an energy-consuming process in IDCM.
- The net effect of combined inotropic and vasodilating drugs depends on the balance between these properties.
Abstract:
To assess hemodynamic and energetic effects of different drug interventions on idiopathic dilated cardiomyopathy (IDCM), we determined hemodynamic variables of myocardial oxygen consumption (MVO2) in 37 patients with IDCM. Hemodynamics were measured during routine left and right heart catheterization. MVO2 was analyzed from myocardial blood flow (measured by the argon method) and aortocoronary sinus blood oxygen difference. The hemodynamic variable which correlated best with MVO2 was shown to be the systolic stress time integral (STI). Four different representative compounds were tested with respect to their acute effects on myocardial energetics (MVO2/STI) in patients with IDCM who were in compensated heart failure (NYHA class II-III). The drug interventions were performed at rest. Intravenous injection of the vasodilator nitroprusside yielded a 35% reduction in STI and a 30% reduction in MVO2; in other words, the ratio MVO2/STI was not altered. Injection of the calcium sensitizer and phosphodiesterase inhibitor pimobendan also did not alter this ratio, as both STI (36%) and MVO2 (33%) were lowered. The profound reduction in STI (60%) seen with the phosphodiesterase inhibitor enoximone was accompanied by a much smaller decrease in MVO2 (19%); therefore, the ratio of MVO2/STI increased significantly. An increase of this ratio was also seen with the partial beta-1 receptor agonist xamoterol. However, in this case STI did not change, whereas MVO2 increased by 26%. In summary, vasodilation has energy-saving effects, whereas positive inotropism is an energy-consuming process. We conclude that the overall effect on myocardial energetics of a drug which possesses both positive inotropic and vasodilating properties depends on the balance of the two properties.