Abstract
ObjectiveAlthough glucose-insulin-potassium (GIK) therapy ought to be beneficial for ischemic heart disease in general, variable outcomes in many clinical trials of GIK in acute coronary syndrome (ACS) had a controversial impact. This study was designed to examine whether “insulin resistance” is involved in ACS and to clarify other potential intrinsic compensatory mechanisms for GIK tolerance through highly statistical procedure.Methods and resultsWe compared the degree of insulin resistance during ACS attack and remission phase after treatment in individual patients (n = 104). During ACS, homeostasis model assessment of insulin resistance (HOMA-IR) values were significantly increased (P<0.001), while serum potassium levels were transiently decreased (degree of which was indicated by ΔK) (P<0.001). This finding provides a renewed paradox, as ΔK, a surrogate marker of intrinsic GIK cascade activation, probably reflects the validated glucose metabolism during ischemic attack. Indeed, multiple regression analysis revealed that plasma glucose level during ACS was positively correlated with ΔK (P = 0.026), whereas HOMA-IR had no impact on ΔK. This positive correlation between ΔK and glucose was confirmed by covariance structure analysis with a strong impact (β: 0.398, P = 0.015). Intriguingly, a higher incidence of myocardial infarction relative to unstable angina pectoris, as well as a longer hospitalization period were observed in patients with larger ΔK, indicating that ΔK also reflects disease severity of ACS.ConclusionsInsulin resistance most likely increases during ACS; however, ΔK was positively correlated with plasma glucose level, which overwhelmed insulin resistance condition. The present study with covariance structure analysis suggests that there are potential endogenous glucose-coupled potassium lowering mechanisms, other than insulin, regulating glucose metabolism during ACS.
Highlights
Substantial experimental evidence with animal models supports the potential benefit of glucose-insulin-potassium (GIK) administration in patients with ischemic heart disease (IHD) in general by promoting glucose metabolism
Insulin resistance most likely increases during acute coronary syndrome (ACS); ΔK was positively correlated with plasma glucose level, which overwhelmed insulin resistance condition
We recently reported a transient decrease in serum potassium (K) level during ischemic attack of ACS compared to remission phase after treatment in individual patients [13]
Summary
Substantial experimental evidence with animal models supports the potential benefit of glucose-insulin-potassium (GIK) administration in patients with ischemic heart disease (IHD) in general by promoting glucose metabolism. The activation of insulin signaling per se has a cardioprotective effect mainly via anti-inflammatory, anti-apoptotic, and provasodilatory properties, as well as by accelerating uptake and utilization of glucose in the heart, which becomes an important preferential substrate for ischemic myocardium [1,2,3,4]. Many clinical trials with variable results have a controversial impact on GIK given to patients with acute coronary syndrome (ACS) [5,6,7,8,9,10,11]. The presence of insulin resistance during ACS attack is believed to be a critical reason for this paradox, few studies have directly evaluated the insulin resistance in the acute phase of ischemic attack [12]
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