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DIABETES
and
CARDIOVASCULAR DISEASE
The continuum…
Dr.O.Adikesava Naidu M.D.,D.M.,FACC
Assosciate Professor,Dept. of Cardiology,
Osmania General Hospital, Hyderabad.
Consultant, YASHODA HOSPITALS, Somajiguda.
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Diabetes…..the CVD equivalent
“From the point of view of cardiovascular disease it is appropriate
to say, Diabetes is a cardiovascular disease.”
- AHA Scientific Statement Diabetes and Cardiovascular disease.
Circulation 1999;100:1134-1146
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Discovery of
Insulin*
The Miracle
“Drug ??”
1921
Charles Herbert Best
Sir Frederick Grant Banting
University of Toronto,CANADA
From latin word
Insula
meaning islet/island
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Leonard Thompson
First Person to Receive Insulin
Purified by John Clamp in 1922,
for his Type1 Diabetes at the age of 14.
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The “unlucky” man – Clark Noble.
Prof.W.J.R Macleod Professor in Physiology
Awardee of Nobel Prize in Medicine.
“Allowing for experiments in his laboratory”
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On his discovery of Insulin….
Insulin is not a cure for diabetes; it is a treatment. It
enables the diabetic to burn sufficient carbohydrates, so
that proteins and fats may be added to the diet in
sufficient quantities to provide energy for the economic
burdens of life.
— Sir Frederick Grant Banting
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s
First Insulin Vial
First Manufacturer of Insulin.
Funded the Scientists
Insulin Syringe used for experiment by Best and Banting
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Tom Hanks Salma Hayek
Wasim Akram
Halle Berry
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Introduction
Diabetes, is one of the most common noncommunicable
diseases.
It is an ongoing epidemic in many developing countries.
Cardiovascular disease is the most common cause of death.
Management of a Cardiovascular disease in Diabetics is of
great challenge for the physicians and cardiologists.
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Contents
1.Definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Contents
1.Definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points with regards to CVD
6.Evaluation of patient with diabetes for CVD
7.Management
8.Prevention
9.Take home message
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Definition
Diabetes Mellitus is a metabolic disorder, characterized by chronic
hyperglycemia associated with disturbances of carbohydrate, fat and
protein metabolism due to absolute or relative deficiency in Insulin
secretion and/or action.
“Metabolic cum vascular disorder”
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Contents
1.Diabetes Mellitus definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Epidemiology
The prevalence of diabetes across the world has tripled during
the last three decades.
Approx. 382 million people ( 0.05 % of world population)
have diabetes(world population 7.125 billions).
Approx half of them are undiagnosed (178 million).
Among adults (>20 yrs of age) 9.6% of population have
diabetes( 10.5% men,8.8%women).
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Diabetes is a huge and growing problem, and the costs to
society are high and escalating
382 million people have
diabetes
By 2035, this number will rise
to 592 million
IDF ,Global burden of
diabetes ,2013
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IGT to be given equal importance
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5-20%
60-70%
20-25%
Most of them are in 40-59 yrs of age
IDF,2013 report
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Almost half of all people with
diabetes live in just three
countries
China
India
USA
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Across the world 548 billion USD --
11% of total health expenditure on adults.
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5.1 million deaths in 2013
Every 6 seconds one person die of diabetes
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More than 79,000 children developed type1 diabetes in
2013.
More than 21 million live births were affected by diabetes
during pregnancy in 2013.
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Statistics in India
More than 62 million Indians have diabetes. (ICMR-INDIAB)
65.4 million as per IDF statistics (2013).
Projected to increase to 100 million by 2030.
Present prevalence rates are 15-20% (2.3% in 1971) in urban areas,
10-12% (1.2% in 1971)in rural areas.
There is overwhelming rise of diabetes in rural areas compared to
urban areas in recent times.
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Disease Burden of Diabetes Mellitus
• 2-4x increase in cardiovascular mortality.
• DM responsible for 25% of cardiac surgeries.
• Mortality in DM: 70% due to Cardiovascular disease.
• 2.5x increase risk of stroke
• Leading cause of blindness (12.5% of cases)
• Leading cause of ESRD (42% of cases)
• 50% of all non-traumatic amputations
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Contents
1.Diabetes Mellitus definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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• Lack of insulin
• Autoimmune
• Usually children
Types of Diabetes
Type 1 diabetes Type 2 diabetes Gestational diabetes
• Insulin resistance
• Lifestyle factors
• Usually adults
• Insulin resistance
• During pregnancy
• Risks to mother and
child
Other specific types
Monogenic – MODY
LADA
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Contents
1.Diabetes Mellitus definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Risk Factors
1.Hyperglycemia
2.Impaired Glucose Tolerance
3.Insulin Resistance
4.Metabolic Syndrome
5.Dyslipidemia
6.Obesity (Diabesity)
7.Hypertension
8.Smoking,Alcoholism
9.Genetic predisposition
10.Environmental factors
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What is the effect of hyperglycemia on
CVD ?
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Retnakaran R, Zinman B. Lancet 2008;371:1790-99.
Hyperglycemia is toxic at several steps in the atherosclerosis process
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NEW ENGLAND JOURNAL OF MEDICINE March 4, 2010
Glycated Hemoglobin, Diabetes, and Cardiovascular Risk in Non-
diabetic AdultsElizabeth Selvin, Michael Steffes, Hong Zhu, Kunihiro Matusushita, et al.
There is a clear epidemiologic association between glycemic control and CVD
Data from 11,092 black and white
subjects in the ARIC trial
(Atherosclerosis Risk in
Communities)
Median follow approximately 14
years.
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ADA position on glycemia
and macrovascular disease in
2010 Standards of Care
Guideline
ADA Standards of Care.
Diabetes Care 2010;33:S11-62
Despite clear epidemiology, controversy continues regarding the role
of glucose lowering to prevent coronary events
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2011 ADA guideline
appropriately discusses
microvascular benefits of A1C <
7% while acknowledging lack of
proven macrovascular benefits at
the A1C values that were studied.
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Three large trials of glycemic control published in 2008 failed to find
CVD benefit
Sklyer JS, et al. Intentive glycemic control and the prevention of cardiovascular events. A position statement of the
ADA/ACC/AHA. Diabetes Care 2009;32:187-92.
So hyperglycemia doesn’t matter to the heart?
Non-fatal MI significantly reduced 24% (p=0.001)
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Failure to find benefit may have related to the A1C levels tested:
6.4% vs. 7.5% 6.3% vs. 7.0% 6.9% vs. 8.5%
Sklyer JS, et al. Intentive glycemic control and the prevention of cardiovascular events. A position
statement of the ADA/ACC/AHA. Diabetes Care 2009;32:187-92.
So hyperglycemia matters to the heart but intense control (A1C < 7%) provides little additional
benefit over moderate control (A1C 7-8%)
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DECODE: IGT Increases Mortality Risk
Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe
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HbA1c Predicts MI in Type 2 Diabetes
UKPDS 35
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Fatal and Non-Fatal Myocardial Infarction
14% decrease per 1% decrement in HbA1c
p<0.0001
0.5
1
5
0 5 6 7 8 9 10 11
Updated mean HbA1c
Hazard
ratio
UKPDS 35. BMJ 2000; 321: 405-12
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Insulin Resistance: Associated
Conditions
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The Metabolic Syndrome
InsulinResistance
Hypertension
Type 2 Diabetes
Disordered
Fibrinolysis
Complex
Dyslipidemia
TG, LDL
HDL
Endothelial
DysfunctionSystemic
Inflammation
Athero-
sclerosis
Visceral
Obesity
Adapted from the ADA. Diabetes Care. 1998;21:310-314;
Pradhan AD et al. JAMA. 2001;286:327-334.
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How all these lead to DIABETES ?
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Development of Type 2 Diabetes
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Natural History of Type 2 Diabetes
Normal Impaired glucose
tolerance
Type 2 diabetes
Time
Insulin
resistance
Insulin
production
Glucose
level
b-cell
dysfunction
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Endothelial dysfunction
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Advanced Glycation Endproducts
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The effect of Diabetes on
Atherosclerosis/CAD
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How is CAD Different in Diabetes ?
> CAD extent
Multi-vessel disease
Distal disease – more difficult to revascularize
Silent ischemia/MI
Younger
Women
Worse outcomes despite revascularization
Increased re-stenosis after PCI even with stents
worse periop & long-term outcomes
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Risk of Cardiovascular Events in DiabeticsFramingham Study
Age-adjusted
Biennial Rate Age-adjusted
Per 1000 Risk Ratio
Cardiovascular Event Men Women Men Women
Coronary Disease 39 21 1.5** 2.2***
Stroke 15 6 2.9*** 2.6***
Peripheral Artery Dis. 18 18 3.4*** 6.4***
Cardiac Failure 23 21 4.4*** 7.8***
All CVD Events 76 65 2.2*** 3.7***
Subjects 35-64 36-year Follow-up **P< .001,***P< .0001
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Framingham Heart Study 30-Year Follow-Up:
CVD Events in Patients With Diabetes (Ages 35-64)
109
20
11
9 63819
3*
30
0
2
4
6
8
10
Age-adjusted annual rate/1,000
Men Women
Total
CVD
CHD Cardiac
failure
Intermittent
claudication
Stroke
Risk
ratio
P<0.001 for all values except *P<0.05.
Wilson PWF, Kannel WB. In: Hyperglycemia, Diabetes and Vascular Disease. Ruderman N
et al, eds. Oxford; 1992.
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Contents
1.Definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Diabetic Cardiomyopathy
First described by Ruber et al. 1972.
Term coined by Ludwack.
Diabetic cardiomyopathy is generally regarded as a unique
pathologic and clinical entity marked by diffuse myocardial
fibrosis and hypertrophy that may result in the emergence of
progressive LV dysfunction and CHF.
Evidence of LV dysfunction in absence of structural heart
disease ( coronary,HTN,valvular,congenital) or other causes of
secondary cardiomyopathy.
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Cont…
Diastolic dysfunction > Systolic dysfunction.
Common in both diabetes and prediabetes.
Presence of microalbuminuria increases the likelihood of diabetic
cardiomyopathy.
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Pathogenesis
Multifaceted,multifactorial
1.impaired calcium homeostasis
2.activation of RAAS
3.Increased oxidative stress.
4.altered substrate metabolism – metabolic cardiomyopathy.
5.mitochondrial dysfunction.
6.increased apoptosis
7.autonomic neuropathy
8.microvascular disease and endothelial dysfunction.
9.disordered copper metabolism
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Sleep apnea
CVD
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Cardiovascular Autonomic Neuropathy
Indicators
Resting tachycardia
Orthostatic hypotension
Peripheral neuropathy
Silent myocardial ischemia or MI
QT prolongation
HR responses to Valsalva,deep breathing,standing up
BP responses to sustained handgrip,standing up.
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Diabetes in pregnancy
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Congenital heart disease in
Newborn of diabetic mothers Risk of congenital anomalies is estimated to be between 2.5-12%
The incidence of malformations is the highest in the group where
mothers were on insulin at the time of conception.
Respiratory problems >CV problems (structural congenital heart
defect and hypertrophic cardiomyopathy) .
Congenital heart disease -5%.
Common are VSD,TGA,Aortic stenosis.
Truncus Arteriosus and DORV are also more prevalent in IDMs.
Paediatr Cardiol. 2000 Apr-Jun; 2(2): 17–23.
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Contents
1.Definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Evaluation of a patient with diabetes for CVD .
ECG
2D ECHO
TMT
Stress Echocardiography
CAG
PTCA - BMS/DES
CABG
Carotid stenting
Peripheral angioplasty
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Exercise stress testing
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Contents
1.Definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Management of comorbidities
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Three points critical to understanding the
evidence base of the ADA guidelines for lipid
management:
1. The etiologic role of lipoproteins in atherosclerosis
2. The etiology of dyslipidemia as seen in patients with diabetes
3. The clinical outcomes literature in patients with diabetes
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How unique is the lipid panel in a diabetic patient
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1. Atherosclerosis is a lipoprotein driven processBasic Science for Clinicians
Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis
Update and Therapeutic Implications
Ira Tabas, MD, PhD;
Kevin Jon Williams, MD;
Jan Borén, MD, PhD
Circulation, October 16th, 2007
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Lipoproteins share structural homology
Chylomicrons, VLDL, IDL, LDL, HDL all share a basic biochemistry
Liver
VLDL
T
G
IDL
LDL
Lipase
enzymes
Lipase
enzymes
LDLc
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Type
(%)
Appearance of
serum
Elevated
particles
Associated clinical disorders TC
T
GI (~1%) Creamy top layer Chylomicrons,
VLDL
Lipoprotein lipase deficiency,
apolipoprotein C-II deficiency+ +++
IIa (10%) Clear LDL Familial hypercholesterolemia,
polygenic hypercholesterolemia,
nephrosis, hypothyroidism, familial
combined hyperlipidemia
++ ↔
IIb (40%) Clear LDL, VLDL Familial combined hyperlipidemia ++ +
III (~1%) Turbid IDL Dysbetalipoproteinemia + +
IV (45%) Turbid VLDL Familial hypertriglyceridemia, familial
combined hyperlipidemia, sporadic
hypertriglyceridemia, diabetes
+ ++
V (5%) Creamy top, turbid
bottom
Chylomicrons,
VLDL (remnants)
Diabetes + ++
Fredrickson Classification of Dyslipidemia
We look at thisArtery wall sees these
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LDL
LDL
Endothelium
Vessel LumenMonocyte
Macrophage
MCP-1
Adhesion
Molecules
Steinberg D et al. N Engl J Med 1989;320:915-924.
The primary atherogenic lipoprotein is LDLlipoproteins of > 70 nm have limited transcytosis past the endothelium
Foam Cell
Modified
LDL Taken
up by
Macrophage
Intima
Nascent
chylomicronNascent
VLDL
ΧΧ
Artery wall
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Proatherogenic LDL
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Am Heart J 2008;156:112-119
2. Dyslipidemia vs. Hyperlipdemia: Prevalence in NHANES 2008 data: High TG or low HDLc more
common than high LDLc
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Prevalence of Dyslipidemia is high in Type 2 Diabetes
Jacobs MJ, et al. Diabetes Res Clin Pract. 2005;70:263-269.
Control of Lipids Patients With
Diabetes, %
Patients Without
Diabetes, %
P Value
LDL-C
> 100 mg/dL74.7 75.7 NS
HDL-C
< 40 mg/dL (men)
< 50 mg/dL (women)63.7 40.0 < .001
Triglycerides
> 150 mg/dL61.6 25.5 < .001
N = 498 adults (projected to 13.4 million) aged > or = 18 years with diabetes representative of the
US population and surveyed within the cross-sectional National Health and Nutrition Examination
Survey 1999-2000.
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Hepatic lipase
Fat Cells Liver
Kidney
Insulin
CETP
CE
VLDL HDL
Lipoprotein lipase
or hepatic lipase
Small, dense
LDLLDL
TG
ApoA-ITG
CE
FFA
‘Dyslipidemia’ is a state of relative insulin resistance resulting in a conversion of adipose tissue
to an exocrine state. Excessive production of free fatty acids (FFA) increases hepatic VLDL
production
CE, cholesteryl esters; FFA, free fatty acids; TG, triglycerides.
Ginsberg HN. J Clin Invest. 2000;106:453–458.
CETP
↑ TG
↑ ApoB
↓ HDLc
↔ LDLc
XInsulin
resistance
Liver
IDL
FFA
While LDLc is similar,
particle burden is heavier
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LDL particle count vs. cholesterol contentTo carry the same amount of cholesterol, a larger number of particles are needed
if they are smaller
apoB is a measure of number of atherogenic
lipoproteins (essentially VLDL, IDL, LDL).
Non-HDL is measure of cholesterol carried in
these same particles
LDLc measures cholesterol
carried in LDL and IDL
Small, dense: 25-30 nmLarge, buoyant: 30-35 nm
LDLc=115 mg/dl LDLc=115 mg/dl
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Summary: Patients with diabetes have
elevated TG and lower HDLc but also a
greater number of LDL particles which
confers greater risk at any measured LDLc
value
3. What are the data for LDLc lowering?
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ADA guidelines: Major statin trials or sub-studies in diabetic
patients
Lancet 2004;364:685
Diabetes Care 2006;29:1220
Lancet 2003;361:2005
Diabetes Care 2006;7:1478
Diabetes Care 1997;20:614
*Num. needed to treat (NNT) for moderate-high risk DM to avoid one death or MI:
3-50
ADA Standards of Care; Diabetes Care, January 2011
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Reduction in 10-year CVD events with statin therapy in patients with diabetes:
Event reduction correlates with relative risk – more risk, more benefit
Endpoint: 10-year Fatal CHD/Non-fatal MI and LDL lowering
Relative Risk reduction ARR LDL reduction
4S-DM 85.7 to 43.2% (50%) 42.5% 186 to 119 mg/dL (36%)
ASPEN 20 35.1 to 23.2% (34%) 11.9% 112 to 79 mg/dL (29%)
PS-DM 20 43.8 to 36.3% (17%) 7.5% 123 to 84 mg/dL (31%)
CARE-DM 40.8 to 35.4% (13%) 5.4% 136 to 99 mg/dL (27%)
TNT-DM 26.3 to 21.6% (18%) 4.7% 99 to 77 mg/dL (22%)
HPS-DM 10 17.5 to 11.5% (34%) 6.0% 124 to 86 mg/dL (31%)
CARDS 11.5 to 7.5% (35%) 4% 118 to 71 mg/dL (40%)
ASCOT-DM 11.1 to 10.2% (8%) 0.9% 125 to 82 mg/dL (34%)
ASPEN 10 9.8 to 7.9% (19%) 1.9% 114 to 80 mg/dL (30%)
10: Primary prevention data 20: Secondary prevention
2○
1○
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The differential benefit of LDLc lowering in patients with diabetes has
been evident from the earliest statin trials and is more evidence that
higher risk=greater benefit : 4S study: Major Coronary Events
1 2 3 4 5 6
0
50
60
80
90
100
55%
0
Diabetic – simvastatin
Diabetic – placebo
Nondiabetic – simvastatin
Nondiabetic - placebo
Diabetic - simvastatin
Diabetic - placebop=0.002
Risk reduction
Coronary Death and non-fatal MI
Years since randomization
Pyörälä K, et al. Diabetes Care. 1997;20:614–620
Per
cent
of
pat
ients
wit
hout
maj
or
CV
even
t
70
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Within a given population, lower goals do further reduce CVD
events: Risk Curve ConceptHigher risk patients have more to gain from aggressive therapy
Robinson JG, Stone NJ. Am J Cardiol. 2006;98:1405-1408
0Car
dio
vas
cula
r E
ven
t R
ate
(%)
0 20 40 60 80 100 120 140 160 180 200
LDL (mg/dL)
No CVD - No diabetes
Diabetes - No CVD
CHD - NoMS or IFG
CHD + MS or IFG
CHD + Diabetes
80
70
60
50
40
30
20
10
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What aggressive LDL lowering does: reduces atheroma
volume in arterial wall providing plaque ‘stabilization’
Brown et al. Arter Thromb Vasc Biol 2001;21:1623
Treated: LDLc of 84 mg/dL (47%
reduction)
Untreated: LDLc of 163 mg/dL with
statin+resin
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0
10
20
30
40
50
60
70
80
90
100
4S LIPID CARE HPS WOS AFCAPS
N 4,444 9,014 4,159 20,536 6,595 6,605
∆LDL -36% -25% -28% -29% -26% -27%
TxLDL 119 154 98 90 113 112
secondary high risk primary
%
CHD
events
on
statin
J Am Coll Card 2005;46:1225-8
LDLc lowering and residual risk – more is neededThe majority of CVD events still occur: CVD events occurring in the on-
treatment groups in major statin trials
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Despite the need beyond LDLc lowering, outcomes
data supporting combination therapy still limited
ADA Standards of Care; Diabetes Care, January 2011
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The lipid arm of the ACCORD trial was relatively disappointing for
combination therapy (as was FIELD in 2005)– WHY?
April 29, 2010 N Engl J Med
Conclusion: “The combination of fenofibrate and simvatatin did not reduce the rate of
fatal cardiovascular events, non-fatal MI or non-fatal stroke, as compared with
simvatatin alone.”
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ACCORD
LIPID: Lipid
parameters
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Statins are safe but nothing is without risk: Review of 35
statin therapy trials
Kashani A et al. Circulation. 2006;114:2788-97.
FDA-approved statin* monotherapy vs placebo (N = 74,102)
*Atorvastatin, fluvastatin, lovastatin, pravastatin,
rosuvastatin, simvastatin
CK = creatine kinase
AE = adverse events
Outcome
Statin
(%)
Placebo
(%) RD P value
Myalgias 15.4 18.7 2.7 0.37
CK elevations 0.9 0.4 0.2 0.64
Rhabdomyolysis 0.2 0.1 0.4 0.13
LFT elevation 1.4 1.1 4.2 <0.01
AE discontinuation 5.6 6.1 -0.5 0.80
Statin better Placebo better
-30 -15 0 15 30
Risk difference per 1000 patients (RD)
(95% CI)
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Hypertension
Diabetes along with Hypertension increases risk of CVD by 5
times.
Assosciation of SBP with macroand microvascular
complications – UKPDS 36
Treatment of HTN has beneficial aspects with respect to
diabetes
SHEP trial – Chlorthalidone
HOPE trial – Ramipril
Aggressive BP control has protective effect on CV mortality –
HOT,UKPDS.
Aggressive BP control > aggressive glucose control -UKPDS.
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AJKD 2004;43(suppl 1):S120
Historic goal SBP of < 130 mmHg in diabetes is an
extrapolation of data regarding benefits in nephropathy
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Haven’t previous trials found a benefit from tighter BP control in diabetes?
…ended up comparing mean of 154/87 to 144/82
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Cochrane review 2009
Four trials looked at major CVD outcomes based on randomized BP control;
Two trials (ABCD) were exclusively in patients with diabetes
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April 29th, 2010 N Engl J
Med
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ACCORD BP: Results
Conclusions: “In patients with type 2 diabetes at high risk for cardiovascular
events, targeting a systolic blood pressure of less than 120 mmHg, as compared
with less than 140 mmHg, did not reduce the rate of fatal and nonfatal major CVD
events.”
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ACCORD BP: Using an average of 3 drugs, the authors
achieved a SBP of 119 mmHg vs. 133 mmHg
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Implications on practice
Summary of the evidence:
Lower BP goals
Lower BP goals:
Do not change overall CV outcomes (all 3 trials).
Do reduce rates of stroke (ABCD (H) and ACCORD, but how clinically sig?).
Do help to reduce the progression of nephropathy in terms of urinary albumin
excretion and progression of microalbuminuria to overt albuminuria (ABCD (H)
and (N)).
Trial Goal (mmHg) Achieved (mmHg)
ABCD (H) DBP 75 vs 80-89 132/78 vs 138/86
ABCD (N) DBP 10 < baseline vs 80-89 128/75 vs 137/81
ACCORD SBP <120 vs <140 119/64 vs 133/70
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Exercise prescribing
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Management of diabetes
Oral hypoglycemic agents –
Metformin,Sulfonylureas,Glitazones,Incretin based
therapies.
Insulin
Insulin analogues
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complications
Poor wound healing
Aneurysms
Instent restenosis
Aspirin intolerance
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Precautions
Adequate control of blood sugars
S creatinine
Adequate hydration
Compliance with drugs – on day of procedure also
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Perioperative management
CAD + Cardiovascular autonomic dysfunction + anaesthesia + surgical
stress + postoperative pain ---------- PERIOPERATIVE RISK
Modified Goldman risk index .
Five independent preoperative clinical predictors of postoperative
myocardial ischemia – HTN,LVH on ECG,diabetes mellitus on
Rx,documented CAD,digoxin use.
Risk of postoperative myocardial ischemia - 22% without any
predictors,31% - one,46% with two ,77% with four predictors.
Revised cardiac index
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Contents
1.Definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Prevention
Primordial
Primary
Secondary
Rehabilitation
Primordial – lifestyle changes,healthy diet,exercise.
Primary - Aspirin ? ,metformin (Met Synd),Statins
Secondary – Aspirin,ACEI/ARBS,CCBs,Statins
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ASA: The benefit of anti-platelet therapy is greater in higher risk patients and quite
low in low risk patientsCarlo Patrono, Barry Coller, Garret A. FitzGerald, Jack Hirsh, and Gerald Roth
CHEST 2004;126: 234S-264S.
2 Events prevented per
1000 treated in healthy
population
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Risk vs. benefit in primary vs. secondary prevention with ASAWhile the benefit of aspirin increases as risk increases, bleeding stays constant
So the benefits of antiplatelet therapy in low-risk patients is offset by major
bleeding episodes:
NEJM 2005;353:2373-83
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Nine trial meta-analysis in
ADA/AHA/ACCF statement:
CHD: RR 0.91 (0.79-1.05)
Stroke: RR 0.85 (0.66-1.11)
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What about bleeding in patients with diabetes?
Generic estimate ~ 1/1000 per year for non-stroke bleeding and ~
1/10,000 for hemorrhagic stroke
In patient-level ATT meta-analysis, patients with diabetes examined
separately: 25 GI bleeds with ASA (0.23%) and 22 bleeds with placebo
(0.21%)
Hemorrhagic stroke: 6 events on ASA, 9 on placebo
The Bottom Line
At a 10% 10-year risk of MI and Stroke, aspirin would prevent 1 MI and 1 stroke
and maybe cause 1 major GI bleed. At a 20% 10-year risk, 2 MIs and 2 strokes
would be prevented with no change in bleed risk
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ADA Standards of Care, Diabetes Care; January, 2011
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We have known for decades that platelets are more “responsive” in
patients with diabetes. Reasons are still not fully understood nor
the impact on use of anti-platelet agents
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Contents
1.Definition
2.Epidemiology
3.Types of diabetes
4.Etiopathogenesis
5.Special points
6.Evaluation of patient with diabetes
7.Management
8.Prevention
9.Take home message
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Take home message
Diabetes is an ongoing epidemic.
Diabetes increases risk for virtually all CVD complications and most
notably atherosclerotic vascular disease and HF.
Gap between the accumulated evidence and its application clinically in
patients with diabetes to be addressed.
Unraveling the diabetes –CVD conundrum and reversing the current
trend of expanding diabetes and assoaciated complications require
renewed commitments on the parts of patients,doctors,health care
institutions with primary focus on prevention.
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WORLD DIABETES DAY November 14,every year
An International Diabetes Federation initiative
for creating Global awareness on Diabetes.
In memory of Frederick Banting’s birthday .
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Theme for 2014 -2016
Healthy Living &
Diabetes
Lets Unite for Diabetes
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Thank You