dm and cardio
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Diabetes management in
cardiovascular diseases
Anwar C Varghese
Prof D Rajasekarans unit
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Magnitude of theproblem
Management of diabetesmellitus in ACS
Management of diabetesin CAD patients
Diabetes and cardiac
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Magnitude of the problem Diabetes confers as much CV risk as
a previous MI
Men have 2 times the risk; womenupto 4.
Account for majority of the disease inyounger men and premenopausalwomen.
Worse prognosis after an acutecoronary syndrome
80% of deaths among diabeticpatients are from CHD
Management of Diabetes with Acute Myocardial InfarctionAMI
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Early mortality from acuteMI
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Hyperglycemia as prognosticindicator
Hyperglycemia on admission
for acute MI indicatedincreased mortality.
FPG is a strong predictor ofmortality
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Mortality and CHF after MI
Wahab NN, Cowden EA, Pearce NJ, on behalf of the ICONs Investigators: Is blood glucose anindependent predictor of mortality in acute myocardial infarction in the thrombolytic era? J Am Coll
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FP
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FP an ay morta ty a teracute MI
Suleiman M, Hammerman H, Boulos M, et al: Fasting glucose is an important independent
risk factor for 30-day mortality in patients with acute myocardial infarction: A prospectivestudy. Circulation 111:754-760, 2005
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Reasons for the poorprognosis
Reluctance to apply clinicalmeasures like beta blockers.
Clustering of other risk factors
The lipid rich atherosclerotic plaques more vulnerable to rupture
overexpression of receptor foradvanced glycation end products(RAGE) more metalloproteinaseactivity which destabilize plaques.
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Reasons for the poorprognosis
Increased levels of plasminogenactivator inhibitor type 1 (PAI-1) inplasma and atheromas which rduce
fibrinolysis, increase thrombusformation, and accelerate plaqueformation
Increased endothelin activity andreduced prostacyclin and nitric oxideactivity, lead to abnormal control of
blood flow
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Management of ACS in
diabetes mellitusAspirin resistance
failure to reduce adhesiveness of
platelets related to poor metabolic control
aspirin, 150 mg, 1 week reduced
platelet adhesiveness in 69 % of thenondiabetic patients but in only 29 %of the patients with type 2 diabetes(p = 0.0006)
Braunwalds heart disease
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Beta blockers
Under prescribed due fear ofhypoglycemia, worsening of metabolicstatus
New studies confirm the greater benefitderived by diabetics
Noncardioselective beta blocker carvedilolassociated with better metabolic control.
Beta blockers restore sympathovagalbalance in autonomic neuropathy
Decrease fatty acid utilization within the
myocardium, reducing oxygen demand
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Glycemic control
What is the drug to be used? Insulin
How to give insulin?
Intravenous infusion
How long to give iv insulin?
At least 24 hours What is the target?
Tight glycemic control (4-7 mmol/dl)
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Stop oral hypoglycaemic agents.
Infuse 10% Dextrose iv at 15 mls / hourfor at least 24 hours.
Commence iv insulin infusion at 1u / hour.
Check BG hourly .
Aim for BG of 4 7 mmol/l by adjusting the
insulin infusion rate. Institute all normal post-infarct procedures
and drug interventions using standardcriteria (ACE inhibitor, oral beta blockers,statins, aspirin, etc).
The serum potassium should be monitoredclosely. Potassium supplements can be
given either orally or iv. The serum
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How to treat after the
acute phase?
If prior OHA or Insulin regime
seemed adequate, then continuethe same.
If prior OHA regime was givingpoor control, consider insulin
If prior insulin regime was giving
poor control, consider
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Hypoglycemia and mortality
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Hypoglycemia
Detrimental to the recoveringmyocardium by causing beta
adrenergic stimulation and lackof metabolic substrate.
Hypoglycaemia during admission
may increase re-infarction rates. Predisposes to fatal arrhythmias.
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Glucose-insulin-potassium(GIK) solution
regaining favor as a method toinfluence myocardial metabolismpositively during treatment of MI
polarizing agent maintainingelectrical stability
attenuate the rise in free fattyacids (FFAs) during MI, shiftsmyocardial oxidative metabolismfrom FFAs to glucose oxidation.
Has antiinflammator and
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Treatment of diabetes inCAD
Sulfonylureas Associated with fear of loss of
ischemic preconditioning
Blockage of K+-ATP channels in
myocardium UKPDS findings strongly disprove
this theory
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Thiazolidinediones
not recommended for use in
patients with NYHA Class III orIV CHF
causes fluid retentionUsed in diabeticcardiomyopathy
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Metformin Contraindicated inpatients requiring
pharmacological treatmentof CHF
Cardiac failure increase
lactic acidosis due to
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CABG vs. Coronary stenting
Higher restenosis rates and
worse long-term outcomesafter PTCA
CABG may provide betteroutcomes than standard
PTCA, especially in patients
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Diabetes and cardiac failure
Diabetics 2.5 times more likely todevelop cardiac failure
Increased mortality in cardiac failure
patients; especially in ischemiccardiomyopathy
diabetes and ischemic heart diseaseinteract to accelerate the progression of
myocardial dysfunction1 % increase in average HbA1C was
associated with a 16 percent increase inCHF
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Diabetes-specific factorsrelated to CHF
Advanced glycation end products(AGES) Accumulation of AGE-modifiedextracellular matrix results in loss of
elasticity of the vessel wall and interferewith myocardial function.
Myocardial calcium handling slowsCa removal from the cytoplasm in diastole
increasing diastolic stiffness.
Myocardial metabolism the diabeticheart have exaggerated impairment of
ATP generation during ischemia.
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Diabetes-specific factorsrelated to CHF
Coronary microcirculation
Endothelial dysfunction
(reduced synthesis of thevasodilator nitric oxide),
abnormal angiogenic
responseFailure of ischemicpreconditioning
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Diabetic cardiomyopathy
Diabetic cardiomyopathy affects themyocardium in diabetic patientseventually leading to LVH and
diastolic and systolic dysfunction. The concept is based upon the idea
that diabetes is the factor which
leads to changes at the cellular level,leading to structural abnormalities
DCM may overlap with CAD and
hypertension
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