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Cardiac Emergencies In Diabetes Mellitus 415

The possible explanations for hyperglycemia Factors associated with HF in diabetic
worsening the condition of ACS are as patients :
[9]
follows: • Age
• Abolition of ischemic preconditioning and promo- • Ischemic heart disease
tion of myocardial apoptosis.
• Nature of diabetes
• Higher circulatory catecholamine level.
• Duration of diabetes
• Elevation of blood pressures and prolongation of
QT interval. • Poor glycemic control
• Microvascular dysfunction and resultant perfusion • Elevated serum creatinine
defect. • Insulin use
• Endothelial dysfunction. • Peripheral artery disease
• No reflow phenomenon after reperfusion. • Microalbuminuria.

Treatment targets after ACS with DM: Substrate Toxicity and Heart Failure
• Revascularisation If the classical view of myocardial dysfunction in

• Anti-ischemic drugs diabetes emphasized “energy starvation” as a con-
sequence of reduced ability to generate ATP via
• Anti-platelet and Anti- thrombin drugs. glycolysis and glucose oxidation, more recent the-
• Secondary prevention by ories have focused on the countervailing concepts
of substrate toxicity and substrate-mediated intra-
• Modulation of lifestyle including smoking. cellular signaling. This change in perspective arose
• Blood pressure, sugar, lipid control. from the recognition that whereas the overall energy
charge of the diabetic heart is relatively normal un-
• Renin angiotensin blockers
der most conditions, the heart and blood vessels of
• Beta Blockers patients with type 2 diabetes are chronically exposed
to significantly elevated concentrations of glucose,
• Platelet inhibitors.
FFA, and other substrates. As with most other mol-
ecules, intracellular concentrations of glucose and
Heart Failure in Diabetes: FFA are normally maintained within a narrow phys-
Type 2 diabetes mellitus substantially increases the iologic range. Emerging evidence suggests that ex-
lifetime risk of both developing and dying from heart posure to chronic excesses of either substrate may
failure. While this appears to be explained in part by affect such diverse targets as coronary flow reserve,
the well-known association of diabetes with hyper- vascular and myocardial compliance, and myocardi-
tension, dyslipidemia, and coronary atherosclero- al gene transcription. Equally important, the adverse
sis, additional pathophysiologic mechanisms linking effects of excess glucose (“glucotoxicity”) and FFA
type 2 diabetes and heart failure have recently been (“lipotoxicity”) on the myocardium may conceivably
suggested. These include the potentially adverse ef- amplify those of other conditions (e.g., hypertension)
fects of hyperglycemia on endothelial function and commonly associated with type 2 diabetes [9,10] .
redox state, effects of excess circulating glucose
and fatty acids on cardiomyocyte ultra-structure, in- Diabetic Cardiomyopathy :
tracellular signaling and gene expression, and the Independent of the severity of coronary artery dis-
possibility that diabetes may impair recruitment of ease, diabetic patients have an increased risk of de-
the myocardial insulin-responsive glucose transport veloping heart failure. This clinical entity has been
system in response to ischemia. Because many of considered to be a distinct disease process referred
these putative pathophysiologic mechanisms should to as ‘diabetic cardiomyopathy’. Experimental studies
be amenable to normalization of the diabetic met- suggest that extensive metabolic perturbations may
abolic milieu, strategies designed to more carefully underlie both functional and structural alterations of
control circulating levels of glucose and fatty acids the diabetic myocardium. Translational studies are,
might conceivably delay or prevent the development however, limited and only partly explain why diabetic
of heart failure [6-8] .
patients are at increased risk of cardiomyopathy and

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