The SA Journal Diabetes & Vascular Disease Vol 8 No 2 (June 2011) - page 19

SA JOURNAL OF DIABETES & VASCULAR DISEASE
REVIEW
VOLUME 8 NUMBER 2 • JUNE 2011
65
assessment.
14
The cardiovascular risk is considered to be driven by
the existence of multiple metabolic comorbidities rather than the
hyperglycaemia alone.
15
This study confirms that identification of
a cluster of metabolic abnormalities should be considered more
carefully for CVD prevention. Although isolated IFG or IGT was not
associated with a more adverse CVD risk profile, applying the new
American Diabetes Association (ADA) criteria,
16
the mortality risk
rises by more than two-fold after conversion from IFG to manifest
diabetes.
17
Thus, the additional information about the biomedical
markers as outlined in this study might be a powerful tool to
classify the cardiovascular risk of patients with IFG. In particular,
overweight or obese patients with IFG/IGT strictly need intensive
lifestyle intervention and medical care by annual OGTT according
to the recommendations of Australian societies.
18
Treatment
regimens for patients with IGT/IFG should therefore be optimised,
e. g. resembling a regular antidiabetic therapy, in order to prevent
manifest diabetes or even prolong the time to develop diabetes and
the related complications.
Finally, it needs to be considered that even among the
normoglycaemic patients, there is an increased risk of
atherosclerosis related to the abnormal phenotype associated with
insulin resistance and/or the metabolic syndrome. In this study,
normoglycaemic insulin resistance, as assessed by the homeostatic
model assessment – insulin resistance (HOMA-IR) score or elevated
fasting morning intact proinsulin concentrations,
19
was present in
one-sixth of the entire patient cohort. They present with normal
metabolic conditions. We have been able to demonstrate that this
particular patient cohort with normoglycaemic vascular insulin
resistance (also referred to as ‘cardiodiabetes’ or ‘angiodiabetes’)
may be considered for insulin sensitisation, using, e.g., lifestyle
intervention and/or drug therapy such as glitazones.
20–22
The patients visiting cardiology specialists with previously
unknown glucose homeostasis abnormalities had a higher
prevalence of macrovascular disease and an impaired laboratory
risk marker profile. Accordingly, the risk of new myocardial
infarction was highest in patients with diabetes.
23
The hazard ratio
did not increase considerably if known heart failure is added in this
calculation. Recently, Wallander
et al
.
24
reported that dysglycaemia
after acutemyocardial infarction reflects a stable glucose abnormality
rather than a stress epiphenomenon. They consider disturbances in
glucose regulation a common feature of patients with acute MI but
without previously known diabetes. The underlying abnormalities
leading to abnormal glucose homeostasis may represent a major
modifiable component of subsequent cardiovascular risk in patients
with acute MI.
25
This study confirms the importance of early
diagnosis and appropriate treatment of diabetes patients suffering
from macrovascular disease. A pattern of cardiovascular surrogate
risk markers as assessed in our study may help the cardiologist to
critically distinguish high-risk individuals who need careful glucose
metabolism-tailored treatment.
In conclusion, 85% of the patients visiting cardiology centres
in Germany suffer from known or unknown diabetes, IGT, or
normoglycaemic vascular insulin resistance (cardiodiabetes). This
finding underlines the importance of joint treatment efforts from
both disciplines when treating this patient group at high risk for
cardiovascular mortality.
Acknowledgements
We are obligated to the following German cardiology care units
for patient enrolment and trial conduct: Dr Bauersachs, Würzburg;
Dr Strasser and Dr Stumpf, Dresden; Dr Kofler, Potsdam; Dr Deeg,
Bad Kissingen; Dr Algenstaedt, Hamburg; Dr Bauriedel, Bonn; Dr
Bierich, Herrenberg; Dr Schwarzbach, Kaiserslautern; Dr Edogan
and Dr Faske, Gießen; Dr Linß, Henningsdorf; Dr Kühl, Aachen;
Dr Gottsleben, Gehrden; Dr Pistorius, Hamburg; Dr Sorges,
Holzminden; Dr Beyer, Erlangen; Dr Müller, Flensburg; Dr Kreuzer,
Limburg; Dr Christoph, Halle; Dr Höher, Bayreuth; Dr Fünfstück,
Weimar; Dr Schneider, Lübeck.
We are grateful to Mirjam Löbig and the entire IKFE lab team
for excellent laboratory work and to Manja Flannery and Bert
Jenke for study assistance and data management. We gratefully
acknowledge the helpful advice and fruitful discussion with the
anonymous reviewers.
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