Impaired fasting glucose and cardiogenic shock

Cardiology Review® Online, January 2005, Volume 22, Issue 1

Impaired fasting glucose and cardiogenic shock

Marianne Zeller, PhD1 • Marie-Claude Brindisi, MD2 • Gilles Dentan, MD3

Yves Laurent, MD4 • Luc Janin-Manificat, MD5 • Isabelle L’Huillier, MD1

Jean-Claude Beer, MD1 • Hamid Makki, MD6 • Jean-Eric Wolf, MD1

Bruno Verges, MD, PhD2 • Yves Cottin, MD, PhD1 • on behalf of the RICO survey working group

From the Service de Cardiologie1 and Service d’Endocrinologie,2 CHU Bocage,

Dijon; Service de Cardiologie, Clinique de Fontaine,3 Fontaine les Dijon; Service de Cardiologie, Centre Hospitalier,4 Semur en Auxois; Service de Cardiologie, Centre Hospitalier,5 Beaune; Service de Cardiologie, Centre Hospitalier, Châtillon sur Seine,6 France

A new definition for impaired fasting glucose has been established by

the American Diabetes Association (ADA). Patients are considered to

have impaired fasting glucose if they have glucose levels from 6.1 mmol/L to 7 mmol/L (110 mg/dL to 126 mg/dL).1 It has been shown that patients with abnormal glucose metabolism are in greater danger of developing macrovascular complications and coronary artery disease (CAD).2 Few

studies have been conducted on the effects of impaired fasting glucose in patients with acute myocardial infarction (MI), however. The importance of assessing risk in patients with abnormal glucose metabolism was highlighted in a recent study, which showed that patients with CAD who underwent percutaneous coronary intervention had a greater risk of mortality if they had abnormal glucose metabolism.3

We compared the in-hospital outcome of MI patients with normal fasting glucose versus patients with impaired fasting glucose from the unselected population of the French regional survey for acute MI, observatoiRe des Infarctus de Côte-d’Or (RICO).

Patients and methods

A total of 999 patients from the French regional study hospitalized for acute MI were included in the study. MI diagnosis was defined based on the criteria of the European Society of Cardiology and the American College of Cardiology.4 We did not include patients in the study if their fasting blood glucose levels had not been taken.

Glycosylated hemoglobin (A1c) levels were taken on the first morning

following admission to the hospital. Fasting blood glucose levels were taken on days 4 and 5. Using the Cockcroft-Gault formula, the baseline serum creatinine clearance rate was estimated, and the peak plasma level of creatine kinase (CK) was assessed.5

Patients were considered to have diabetes mellitus if they had a history of diagnosed diabetes mellitus or a mean fasting blood glucose level of 7.0 mmol/L or greater, based on the ADA’s definition of diabetes mellitus. Also using ADA’s definitions, if patients had a mean fasting glucose of 6.1 mmol/L or more (110 mg/dL) but less than 7.0 mmol/L, they were considered to have impaired fasting glucose; normal fasting glucose was defined as a mean fasting glucose less than 6.1 mmol/L.1


Characteristics and outcome. Of 526 patients (53%) who had abnormal glucose metabolism, 381 (38%) had diabetes mellitus and 145 (15%) had impaired fasting glucose. Patients with diabetes mellitus and impaired fasting glucose had greater peak

CK plasma levels and greater body mass index than those with normal fasting glucose levels (P < .01; table 1). Compared with the normal fasting glucose group, the impaired fasting glucose group had a marked-

ly higher rate of cardiogenic shock

and mortality (P = .049 and P = .011, respectively).

Predictors of mortality. The in-hospital mortality was primarily relatedto cardiogenic shock (odds ratio [OR], 4.86; 95% confidence interval [CI], 1.53—15.39; P = .007) and ventricular arrhythmias (OR, 3.62; 95% CI, 1.18–

11.11; P = .014) in the impaired fasting glucose group, according to multivariate analysis. Table 2 shows that, among patients without diabetes mellitus, impaired fasting glucose was a predictive factor for mortality in univariate analysis (P = .0324), but it was not an independent predictive factor for in-hospital death, after adjusting for anterior location, left ventricular ejection fraction, age, reperfusion, ventricular arrhythmia, sex, and cardiogenic shock. Impaired fasting glucose also had no predictive value for ventricular arrhythmias when adjusted for other variables. In contrast, impaired fasting glucose had a strong predictive value for cardiogenic shock (P = .0217), even after adjustment for confounding factors (P = .027).


Based on the results of our study, in-hospital mortality is twice as high in patients with impaired fasting glucose compared with those with normal fasting glucose, mainly because of the increased risk of cardiogenic shock.

Among the unselected MI patients, we found a high preponderance of patients (53%) with abnormal glucose metabolism, with 15% of patients having impaired fasting glucose. In the National Health

and Nutrition Examination Survey (NHANES) III study, only 7% of healthy adults had impaired fasting glucose.6 In that study, 8% of patients with impaired fasting glucose had CAD, compared with only 6% of patients in the normal fasting glucose group (relative risk [RR], 1.47). In another study, abnormal fasting glucose metabolism was more prevalent than expected in 1,612 patients with CAD undergoing percutaneous coronary intervention.3 These findings are similar to those in our study, which went one step further by including patients with acute MI.

Previous studies have pointed out the strong predictive value of fast-ing glucose levels in CAD patients for all-cause mortality at long-term follow-up, even after adjustment for potential confounding variables.7 In acute MI patients with admission

or fasting hyperglycemia (glycemia threshold range, 6.1 to 8 mmol/L), Capes and colleagues found a higher risk of in-hospital mortality (RR, 3.9; 95% CI, 2.9—5.4) for hyperglycemia.8 A higher risk of in-hospital death was associated with impaired fasting glucose in patients with acute MI, which highlights the importance of using the new definitions of abnormal glucose levels for patients with acute MI, as well as the need to determine specific therapy during the acute phase of MI.

Because impaired fasting glucose was not a persistent prognostic factor for death after adjusting for covariates, especially for cardiogenic shock, it is believed that the increased risk of death associated with impaired fasting glucose was mainly the result of a high occurrence of cardiogenic shock. In patients with MI who have blood glucose levels

above 10 mmol/L, without adjusting for potential covariates, previous studies have shown a greater risk of severe pump failure.9,10 After adjusting for age, nondiabetic patients with abnormal glucose metabolism have also been found to have a greater risk of congestive heart failure or cardiogenic shock.11

The reasons for the greater risk

of cardiogenic shock in patients with impaired fasting glucose are not well understood, although it is theorized that increased glucose levels are involved because high blood glucose levels have been found to be damaging to cardiomyocytes.12 High blood glucose levels also indicate

a relative insufficiency of insulin, which correlates with greater lipolysis and increased circulating free fatty acids, which may harm cardiac cells.13

Study limitations. We measured fasting glucose levels in patients with acute ischemic stress and disturbed metabolic state, which may interfere with glucose metabolism. We cannot rule out the fact that increased blood glucose levels may be the result of acute metabolic stress following acute MI. A previous study of nondiabetic patients that measured serial glucose concentrations, however, showed that the fasting blood glucose level after acute MI was stable from day 4 and was an independent predictor for abnormal glucose metabolism at the 3-month follow-up (P < .017). These findings indicate that the increased glucose levels are not just caused by the stress related to an acute MI.14 The A1c level, which is an indicator of preexisting glucose metabolism, in our study was also markedly greater in patients with impaired fasting glucose, thus confirming the presence of abnormal glucose metabolism before the acute MI.


Our study showed that in-hospital mortality was significantly increased as a result of a higher risk

of developing cardiogenic shock

in acute MI patients with impaired fasting glucose. This highlights the importance of assessing specific therapy during the acute stage of MI for patients with impaired fasting glucose. n