obesity and heart disease

1. OBESITY AND HEART DISEASE
Dr. Prateek Singh
JR1 Internal Medicine

2. Definition
 Obesity is a state of excess adipose tissue
mass
 Medically meaningful distinction between
lean and obese is arbitrary. So obesity is
defined by assessing its linkage to morbidity
and mortality.

3. Causes of over weight & obesity
 Genetics does play a role in obesity
-however in most cases both genes and behaviour
are necessary for a person to be over weight
 body weight is a result of combination of influences
-genetic ,metabolic, behavioural, environmental,
culture and socioeconomic influences
 Therefore behavioural and environmental factors
provide greatest “opportunity” for action and
intervention.

4. Methods to measure adiposity
 Body mass index
 Anthropometry (skin fold thickness )
 C.T.
 M.R.I
 Electrical impedance

5. Assessment of obesity
 Waist circumference
- above 40 inch in men and 35 inch in women is
indicative of health risk
 BMI
- calculated as weight in kilos divided by height
in meters squared.
-Most large scale epidemiologic study suggest
that all cause, metabolic; cancer; cardiovascular,
morbidity begin to rise (at slow rate) when BMI
>= 25

7. Classical risk factors of CAD
 Diabetes
 Smoking
 Hypertension
 Dyslipidemia
 Obesity & lack of exercise

8. Obesity and overweight
increases the risk of
 Hypertension
 Stroke
 T2 DM
 Metabolic syndrome
 CV mortality
 Cancer- endometrial, breast, prostate, colon
 Gallbladder disease
 Osteoarthritis
 Respiratory disease and sleep apnoea

9. CVD risk factors prevalence in Nepal
Prevalence of cardiovascular disease risk factors: A community-based
cross-sectional study in a peri-urban community of Kathmandu, Nepal
Raja Ram Dhunganaa,b,*, PuspaThapac, Surya Devkota, Palash Chandra Banike,
Yadav Gurunga, Shirin Jahan Mumue, Arun Shayami, Liaquat Alie 9 march 2018

10. SitapailaVillage Development Committee (VDC) from February
2014 to February 2015 sample size 345

11. Relationship Between BMI and the
Relative Risk of Comorbid Conditions
0
 21 22 23 24
7
6
5
4
3
2
1
Type 2 diabetes
Hypertension
Cholelithiasis
CHD
RelativeRisk
25 26 27 28 29 30
BMI
Willett WC et al. N Engl J Med 1999;341:427-434.

12. Obesity and Cardiovascular Disease
0
RelativeRisk
Relative Risk of Nonfatal MI and Fatal
CHD (Combined) Based on BMI (Women)
4
3
2
1
< 21 21 – 22.9 25 – 28.9  2923 – 24.9
BMI
(kg/m2)
Willett WC, et al. JAMA. 1995)

13.  How does obesity cause cardiovascular
disease?

14. Patterns of Body Fat
Distribution
Intrabdominal or
Visceral type
(android or
“apple shaped”)
Lower body or
external type
(gynoid or
“pear shaped”)

15. Normal Visceral obesity
Courtesy of Wilfred Y. Fujimoto,
MD.
Visceral Fat
Distribution
Normal vs Obesity

16. BODY FAT DISTRBUTION
 Men are apt to develop visceral type
obesity while women develop the
peripheral type
 Androgens appear to influence this
distribution
 PCO with androgenemia predisposes to
visceral type adiposity
 Corticosteroids and growth hormone
also tend to develop visceral obesity

17. How does obesity causes
cardiovascular disease
 abdominal obesity(deep visceral fat)
Lipolysis insensitive to insulin
Muscle and pancreas
Insulin resistance
Metabolic syndrome,
T2DM
Liver
gluconeogenesis
Increased triglisrides,LDL
Decreased HDL
Blood vessels
Hypertension,
Hypercoagulable state
Endothelial dysfunction
free fatty acids
Cardio vascular disease

18. leptin- energy balance regulation
adiponectin-adipose derived protein
levels decreased in obesity
-enhances insulin sensitivity and lipid
oxidation
-has vascular protective effect
resistin and RBP-4-increased in obesity
-increase insulin resistance

19. Obesity and Insulin Resistance
Hyperinsulinemia
+
Hyperglycemia
Activation of the
sympathetic nervous
system
Increase of arterial tone
Na+ reabsorption
Hypertension
Overstimulation
of pancreatic
-cell function
Reduction of
insulin secretion
Type 2 Diabetes

20. The Insulin Resistance Syndrome
 A syndrome in which the physiologic
response is inadequate for the amount
of insulin secreted

21. Insulin
Resistance
Hypertension
Type 2 Diabetes
Disordered
Fibrinolysis
Complex
Dyslipidemia
 TG, sdLDL,
 HDL
Endothelial
Dysfunction Systemic
Inflammation
Athero -
sclerosis
Visceral
Obesity
Adapted from ADA. Diabetes Care.
1998;21:310-314. Pradhan et al. JAMA.
2001;286:327-334.
The Metabolic Syndrome Associated With
Insulin Resistance

22. Clinical Manifestations
Central obesity
Glucose intolerance
Atherosclerosis
Hypertension
Polycystic ovary syndrome
Biochemical Abnormalities
Carbohydrate:
Insulin resistance
Hyperinsulinemia
Lipid:
High TG
Low HDL-C
Small, dense LDL
Fibrinolysis:
Increased PAI-1
Rf-thrombosis
&atherosclerosis
The Insulin Resistance Syndrome

23. Insulin Resistance and Heart
Disease
 Diabetes
 Hypertension
 Low HDL
 High triglycerides
 Increased number of small, dense LDL
particles
 Endothelial dysfunction
 LVH (left ventricular hypertrophy)
 Increased C-reactive protein

24. Risk factor of metabolic syndrome:
ATPIII definitions
Metabolic syndrome is 3 or more

25. Cardiovascular Mortality
Associated With Metabolic
Syndrome (MS)
2.2
12
2
0
10
8
6
4
12
14
No MS MS
IncidenceofCVMortality
Diabetes Care 2001;24:683
p <
0.001

26. Goals for Managing the
Metabolic Syndrome
An opportunity to prevent predictable
complications:
» Type 2 diabetes
» Cardiovascular events

27. Management of Metabolic
Syndrome
 Weight loss, proper diet and exercise are
the obvious recommendations.
 drug therapy
- Insulin sensitizers – hyperglycaemia
- Statins- correction of raised LDL
- niacin – for decreased HDL
-fibrate & omega3 fatty acids-for elevated
triglyceride

28. Obesity Hypertension ?

29. Obesity hypertension
Epidemiological studies have shown a
correlation between body weight and blood
pressure
-70 % of hypertension in men and
-60 % of hypertension in women are
associated with extra adiposity

30. Increased Prevalence of Hypertension*
as a Correlate of BMI
BMI < 25 kg/m2
BMI 25 – 26 kg/m2
BMI 27 – 29 kg/m2
BMI  30 kg/m2
18.2
22.5
25.2
38.4
16.5
21.9
24
32.2
20
30
40
Hypertension(%)
0
Men Women
BMI Levels
*Defined as mean SBP ≥ 140 mmHg or DBP ≥ 90 mmHg, or
currently taking antihypertensive medication.
( NIH. Obes Res. 1998)
10

31. Obesity and Hypertension
 Insulin Resistance
+
 Hyperinsulinemia
 Activation of the sympathetic nervous system

Vasoconstriction  Cardiac output
 Na+
reabsorption
Blood
Pressure
(Landsberg L. J Hypertens. 2001)

32. Mechanisms by Which Obesity May Cause
Hypertension and Renal Injury by Activation
of the Renin-Angiotensin System and
Sympathetic Nervous System, Metabolic
Abnormalities and Compression of the Kidney
Obesity
Renal medullary compression
 Renin-angiotensin system activity
 Sympathetic nervous system activity
 Tubular NaCI reabsorption
Renal vasodilation Volume expansion Lipids Glucose
intolerance
Glomerular
hypertension
Arterial
hypertension  Glucose
+
Glomerulosclerosis
ngeli S, et al. Hypertension. 2000)

33. Mechanism of Hypertension Associated
With Insulin Resistance
Reduced sodium excretion
Stimulation of sympathetic nervous system
Increased Na and Ca content of VSMCs enhancing tone
Proliferation of VSMCs
Upregulation of AT1 receptor

34. Obesity and Cardiovascular Risk
Eccentric Hypertrophy
Sodium Retention
Volume Expansion Heart Rate 
Endothelial
Dysfunction
Diabetes Mellitus
Dyslipidemia
Hypertension
Cardiac Output 
Visceral Obesity
Atherosclerosis
Arterial Resistance 
Concentric Hypertrophy
Congestive Heart Failure (CHF),
Coronary Artery Disease (CAD), Sudden Death
(Adapted with permission from Zhang R, Reisin E. Am J Hypertens. 2000)

35. Issues in Choice of Antihypertensive
Therapy for the Obese Hypertensive
 Reduction in pre- and afterload
 No neuroendocrine activation
 Favorable metabolic effects
 No weight gain
 Reduction in renal hyperfiltration and
microalbuminuria
 24-hour efficacy
 Good tolerability
 Reduction in mortality
(Sharma AM, et al. J Hyptertens. 2001)

36. Considerations in Selecting Pharmacological
Agents For Treating Obesity-related Hypertension

37. Pharmacologic Treatment of
Obesity Hypertension
 ACEI/ARB
 Low-dose diuretic
 CCB
 Beta blocker
++++
+++
++
+
Treatment threshold: 135/85 mmHg!

38. Health Benefits of Modest Weight Loss*
 Possible  risk of death
  CHD risk
 MI rate
 stroke rate
– improves serum lipids
 Improves prognosis in type 2 diabetic
patients
 glucose, insulin
 Can significantly reduce sleep apnea
  osteoarthritis symptoms
 Reduces relapse rate of asthma
*Modest weight loss = minimum of 5 lbs.
(Camargo CA, et al. Arch Intern Med. 1999) (Goldstein DJ. Int J Obes. 1992) (Suratt PM,
Findley LJ. N Engl J Med. 1999) (Gelber AC. Am J Med. 1999)

39. Actions and Adverse Effects of
Weight Loss Agents
Drug Action
Sibutramine
Serotonin-releasing agent
Major Adverse Effects
Possible increase in heart
rate and blood pressure
Serotonin-releasing agent
Inhibits pancreatic lipase,
decreases fat absorption
Orlistat
Serotonin and norepinephrine
reuptake inhibitor
Valvular heart disease
Valvular heart disease
Soft stools and anal
leakage
Decrease in absorption of
fat-soluble vitamins
Dexfenfluramine
Fenfluramine

40. Management of Obesity: Treatment Options
Modality Recommendation
Reduced-calorie diet
 Reduce energy intake by 500 to 1,000 kcal/day to
achieve a weight loss of 1 to 2 lbs/week over a 6-
month period
 Start with 30 to 45 minutes moderate activity 3 to
5 days/week, and work up to at least 30 minutes
moderate-intensity physical activity on most or
all days/week
 Use multiple behavioral strategies (eg, self-
monitoring of eating habits and physical
activity)
 Consider for patients with class 3 obesity, or
class 2 obesity with comorbid conditions, for
whom other treatments have failed
Increased activity
Behavior modification
Surgery

41.  Thank you