Improved Myocardial Contractility with Glucose-Insulin-Potassium Infusion During Pacing in Coronary Artery Disease

McDaniel, Huey G.; Rogers, W. J.; Russell, Richard O.; Rackley, Charles E.

doi:10.1097/00132586-198608000-00019

Cited by 3 publications

(5 citation statements)

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“…31 Previous human studies of insulin's effects on the heart have mainly focused on insulin's metabolic effect,33-36 and physiological hyperinsulinemia has not been found to affect cardiac hemodynamics in resting condition. 34,37 On the other hand, GIK infusion has been found to increase coronary sinus blood flow38 and enhance left ventricular function during acute myocardial infarction or prolonged ischemia.2o, 39 The mechanism by which insulin increases glucose uptake in dys-…”

Section: Discussionmentioning

confidence: 99%

Identification of Viable Myocardium in Patients with Chronic Coronary Artery Disease and Myocardial Dysfunction: Comparison of Low-Dose Dobutamine Stress Echocardiography and Echocardiography During Glucose-Insulin-Potassium Infusion

Yetkın

Şenen²,

İleri³

et al. 2002

Angiology

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Low-dose dobutamine stress echocardiography (LDDSE) is one of the methods most used to assess myocardial viability. Glucose-insulin-potassium (GIK) has been shown to increase contraction of the ischemic zone. The aim of this study was to compare LDDSE and echocardiography during GIK infusion for detection of myocardial viability in patients with chronic coronary artery disease (CAD) and myocardial dysfunction. Twenty-one patients who had chronic CAD and myocardial dysfunction were included in the study. Glucose-insulin-potassium protocol consisted of a fixed dose of insulin (100 microU/kg/hour IV) and a variable glucose/potassium infusion rate. GIK echocardiography was made at baseline and after 60 minutes of GIK infusion. During continuous electrocardiographic, blood pressure, and echocardiographic monitoring, an intravenous infusion of dobutamine (3 microg/kg body weight/min) was started with an infusion pump and continued for 5 minutes and then increased to 5 microg/kg/min and 10 microg/kg/min for another 5 minutes. The detected viable myocardium was defined as 1 or 2 scores decreasing in at least 2 adjacent abnormal segments during LDDSE and GIK echocardiography. Viability was detected in 19% (52 segments) of the asynergic segments at baseline with GIK echocardiography and 16% (44 segments) of those segments with LDDSE (p>0.05). Left ventricular wall motion score index at baseline was 2.24+/-0.35 and it decreased significantly during both LDDSE (p=0.004 vs 2.11+/-0.36) and GIK echocardiography (p=0.001 vs 2.09+/-0.32). The agreement between LDDSE and GIK echocardiography for detection of myocardial viability was 95%. This study shows that GIK echocardiography is similar to LDDSE for detection of myocardial viability. With the support of further clinical studies GIK echocardiography can be used to detect myocardial viability in patients with chronic CAD.

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Section: Discussionmentioning

confidence: 99%

Identification of Viable Myocardium in Patients with Chronic Coronary Artery Disease and Myocardial Dysfunction: Comparison of Low-Dose Dobutamine Stress Echocardiography and Echocardiography During Glucose-Insulin-Potassium Infusion

Yetkın

Şenen²,

İleri³

et al. 2002

Angiology

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“…l 0 " In patients with stable angina pectoris and coronary artery disease, administration of GIK, together with cardiac pacing, was beneficial in some studies 12 and detrimental in others. 13M A better understanding of the metabolic action of GDC may explain many of these contradictory results.…”

Section: I P Nuclear Magnetic Resonance Studymentioning

confidence: 99%

“…Intracellular metabolites, primarily glycogen and glutamate, were labeled from exogenously supplied [l- 13 C]glucose during a preischemic aerobic perfusion period. Glycogenolysis of the [ll3 C]glycogen was subsequently monitored by 13 C NMR spectroscopy during ischemia as it was utilized in the glycolytic pathway to form [3][4][5][6][7][8][9][10][11][12][13] C]lactate and other products. The extent and rate of glycolysis were estimated from the labeled lactate formed.…”

Section: I P Nuclear Magnetic Resonance Studymentioning

confidence: 99%

“…Infusion of GIK in patients Received November 6, 1986; accepted January 6, 1988. with acute myocardial infarction has resulted in improved left ventricular function, 6 improved electrical stability, 7 clinical improvement, 8 and reduced mortality. 9 Other studies have found no reduction in mortality.l 0 " In patients with stable angina pectoris and coronary artery disease, administration of GIK, together with cardiac pacing, was beneficial in some studies 12 and detrimental in others.13M A better understanding of the metabolic action of GDC may explain many of these contradictory results. Several mechanisms proposed for the action of GDC are 1) to increase anaerobic and/or aerobic glycolysis, 2) to spare glycogen, 3) to reduce "toxic" levels of free fatty acids and their consequent detrimental effects, 4) to stabilize membranes, and 5) to replete intracellular potassium."…”

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confidence: 99%

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Rates of glycolysis and glycogenolysis during ischemia in glucose-insulin-potassium-treated perfused hearts: A 13C, 31P nuclear magnetic resonance study.

Hoekenga

Brainard

Hutson

1988

Circulation Research

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The effects of 11.7 mM glucose, insulin, and potassium (GIK) on metabolism during ischemia were investigated in the perfused guinea pig heart using magnetic resonance spectroscopy. Intracellular metabolites, primarily glycogen and glutamate, were labeled with I3 C by addition of [l-13 C]glucose to the perfusate during a normoxk, preischemic period. 13C and 31 P NMR spectroscopy was used to observe the metabolism of "C-labeled metabolites simultaneously with high-energy phosphorus metabolites and pH. The extent of acidosis and the rate and amount of labeled lactate accumulation during ischemia were the same in control (3 mM glucose + insulin) and GIK-treated hearts. In contrast, the rate of labeled glycogen mobilization during ischemia in GIK-treated hearts was one third the rate observed in control hearts. These observations suggest that GIK decreased the rate of glycogenolysis during ischemia without affecting the rate of glycolysis. We propose that glucose contributed as a glycolytic substrate to a greater extent during ischemia in GIK-treated hearts than in hearts perfused with 3 mM glucose and insulin. The glycogen-sparing effect of GIK demonstrated in these studies could delay the onset of ischemic damage in a clinical setting by prolonging the availability of glycolytic substrate necessary for production of high-energy phosphate. (Circulation Research 1988;62:1065-1074 M yocardial ischemia is a common and important clinical problem. Although metabolism of the ischemic myocardium has been an area of active investigation for many years, the metabolic changes resulting from the inadequate oxygen and substrate supply and product removal associated with ischemia are incompletely understood. However, it is clear that one of the important metabolic events leading to cellular damage during ischemia is failure of the rate of energy production to meet the demands for energy utilization.Several therapeutic strategies have been introduced to alter cardiac metabolism during ischemia. A mixture of glucose, insulin, and potassium (GIK) was initially used 25 years ago as a means of eliminating the electrocardiographic abnormalities of myocardial infarction.1 Since that time GIK has been used in numerous studies of coronary artery occlusion in animals and man. Nearly all of the animal studies, using a variety of measures of recovery, have shown reduced infarct size and improved tissue metabolism.2 " 3 Studies in man have been less conclusive. Infusion of GIK in patients Received November 6, 1986; accepted January 6, 1988. with acute myocardial infarction has resulted in improved left ventricular function, 6 improved electrical stability, 7 clinical improvement, 8 and reduced mortality. 9 Other studies have found no reduction in mortality.l 0 " In patients with stable angina pectoris and coronary artery disease, administration of GIK, together with cardiac pacing, was beneficial in some studies 12 and detrimental in others.13M A better understanding of the metabolic action of GDC may explain many of these contradicto...

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“…The search for e ffec tive treatmen t of this low card iac o utput sy ndro me wit hout imposing negative local or systemic effec ts is thus still well moti vated. Glucose-Insulin-Kaliu m (GIK) has long been know n to favorably influence myocardial substrate balance and perfor mance ( 15). -Clinical and experime ntal series have.…”

Section: Su Mmarymentioning

confidence: 99%

Direct Effect of High-dose Insulin on the Depressed Heart after Beta-blockade or Ischemia

Krukenkamp¹,

Sørlie²,

Silverman³

et al. 1986

Thorac cardiovasc Surg

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The direct cardiac effects of high-dose insulin (HDI) were assessed in 13 canine hearts supported by cardiopulmonary bypass. Isovolumic peak developed pressure (PDP, mmHg), coronary blood flow (CBF, ml/beat/100 g LV) and myocardial oxygen consumption (MVO2, ml O2/beat/100 g LV) were determined during incremental left ventricular balloon inflation before and after functional depression by beta-blockade (0.2 mg/kg propranolol) or 2 hours cardioplegic ischemia at 28 degrees C. The 2 regimens gave an overall functional reduction of 46 +/- 3% and 42 +/- 2%, respectively. The hearts were then challenged with an aortic root bolus of 1000 IU insulin. A glucose clamp was maintained at physiological levels. Insulin reversed the negative inotropic effect of propranolol to 80% of control function and normalized heart rate. Despite the significant amelioration of systolic function by HDI, MVO2 indexed for cardiac effort did not change. Neither systolic function nor heart rate was changed in the ischemically depressed hearts. In conclusion, HDI reverses the negative inotropic effect of beta-adrenergic receptor blockade without augmenting oxygen utilization. Apart from effects ascribable to systemic vasodilation and metabolic shifts, no direct cardiac inotropic stimulation can be expected on the post-ischemically depressed, nondiabetic myocardium unless there is a persistent negative effect of beta-blockers.

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Improved Myocardial Contractility with Glucose-Insulin-Potassium Infusion During Pacing in Coronary Artery Disease

Cited by 3 publications

References 0 publications

Identification of Viable Myocardium in Patients with Chronic Coronary Artery Disease and Myocardial Dysfunction: Comparison of Low-Dose Dobutamine Stress Echocardiography and Echocardiography During Glucose-Insulin-Potassium Infusion

Identification of Viable Myocardium in Patients with Chronic Coronary Artery Disease and Myocardial Dysfunction: Comparison of Low-Dose Dobutamine Stress Echocardiography and Echocardiography During Glucose-Insulin-Potassium Infusion

Rates of glycolysis and glycogenolysis during ischemia in glucose-insulin-potassium-treated perfused hearts: A 13C, 31P nuclear magnetic resonance study.

Direct Effect of High-dose Insulin on the Depressed Heart after Beta-blockade or Ischemia

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