Key result
The causal relationship between chronic metabolic shifts, such as increased fatty acid oxidation in diabetes or post-ischemia, and contractile dysfunction in the heart remains unclear.
Discusses the role of metabolic shifts in the pathogenesis of contractile dysfunction in the hypertrophic heart, noting that causal relationships remain elusive.
W hen it comes to fuel for energy production, it is commonly accepted that the heart is an omnivore, capable of oxidizing a wide range of carbon substrates, and that this metabolic plasticity is necessary to maintain a high and variable workload in the midst of an ever-changing hormonal and nutritional state. 1 It is also widely appreciated that shifts in substrate utilization in the heart occur in response to chronic metabolic and hemodynamic stresses.[2][3][4][5] What is less clear, however, is whether such chronic metabolic shifts should be considered a cause or consequence in the pathogenesis of contractile dysfunction.In the case of diabetes mellitus, the heart exhibits an increased dependence on fatty acids for oxidative energy production, and this increase in lipid metabolism has been proposed to significantly contribute to the etiology of impaired cardiac function.6 Similarly, increased rates of fatty acid oxidation immediately after an ischemic event have been implicated in exacerbation of reperfusion injury.7 However, in both of these pathophysiological settings, compelling data to support a direct causal relationship between contractile abnormalities and metabolic dysregulation remain elusive.
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Chatham et al. (2012) conducted a review in Hypertrophic heart. The causal relationship between chronic metabolic shifts, such as increased fatty acid oxidation in diabetes or post-ischemia, and contractile dysfunction in the heart remains unclear.
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