Obesity is a global epidemic that is associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden cardiac death. As excess adipose tissue accumulates, the heart undergoes various structural and functional changes even without other health issues. This includes an enlarged heart size and thickened muscle walls due to increased workload on the heart to meet higher metabolic demands. Over time, this process can lead to cardiac dysfunction and heart failure if left unaddressed. Physical exams and electrocardiograms may underestimate cardiac abnormalities in obese individuals due to morphological changes from excess fat.

1. Cardiovascular Effects Of
Obesity
Dr. Atul Dixit, Mohak Robotics & Bariatrics, Indore.

2. Obesity: A Global Epidemic!
Dramatic increases in both adults & children
Explosive increase in number of people with Metabolic Syndrome (MetS)
MetS associated with increased risk of both diabetes & cardiovascular disease
(CVD)
41 sites on the genome identified as possible links to development of Obesity in a
favourable environment
A variety of adaptations/alterations in cardiac structure & function occur in the
individual as adipose tissue accumulates in excess amount, even in absence of
co-morbidities

3. On the whole:
Overweight or Obesity predisposes or is associated with numerous cardiac
complications such as:
Coronary heart disease (CHD)
Heart failure
Sudden death (Sudden Cardiac Arrest or SCA)

4. Cardiomyopathy of Obesity (Adipositas Cordis)
Initially, the fatty heart is probably not an infiltrative process but most likely a
metaplasic phenomenon.
Cords of cells can gradually accumulate fat between muscle fibers and/or result in
myocyte degeneration resulting in cardiac dysfunction.
Small irregular aggregates and bands of adipose tissue separate myocardial cells,
a potential result of pressure-induced atrophy from the intervening fat.
Through different mechanisms (increased total blood volume, increased cardiac
output, LVH, LVDD, adipositas cordis) obesity may predispose to heart failure.

5. Assessment of Obese Individuals & Co-morbidities
Physical examination & ECG often underestimate the presence & extent of cardiac
dysfunction in obese patients.
ECG: like physical examination, the ECG is influenced by morphological changes
induced by obesity such as:
displacement of heart & elevated diaphragm, increased cardiac workload with
associated cardiac hypertrophy, increased distance between the heart & the
recording electrodes induced by accumulation of adipose tissue in chest wall,
associated chronic lung disease secondary to sleep apnea/hypoventilation
syndrome.

6. ECG changes that may occur in obese individuals:
Increased heart rate, PR interval, QRS interval, QTc interval, QT dispersion, late
potentials, left atrial abnormalities.
ST-T abnormalities, ST depression, Left axis deviation, Flattening of the T wave
(infero-lateral leads).
False positive criteria for inferior myocardial infarction.
Multiple ECG criteria for LVH are present more regularly in MO

7. Echocardiography:
In the past, obesity-induced cardiac abnormalities were found post-mortem.
Differentiation between subepicardial adipose tissue & pericardial effusion is often
difficult and epicardial adipose tissue is known to be e common cause of
false-positive effusion.

8. Venous Insufficiency, Venous Thrombosis &
Pulmonary Embolus:
Pedal edema is a common finding, partly a consequence of elevated ventricular
filling pressure, despite elevation in cardiac output.
Severe sustained lower extremity venous stasis disease in MO leads to pretibial
ulceration & cellulitis. In absence of right heart failure, surgically-induced weight
loss is effective in correcting venous stasis disease in the majority.
Incidence of VTE increased. Increased risk of PE in women, less clear in men.

9. Hypertension:
Most patients with high BP are overweight; hypertension is more frequent in obese
subjects.
A 10kg higher body weight is associated with a 3.0 mm Hg higher systolendoic &
2.3 mm Hg higher diastolic BP. Leads to an estimated 12% increased risk for CHD
& 24% increased risk for stroke.
Increase in BP is greatest when obesity is of abdominal distribution.
Factors to be considered in linking obesity to Hypertension include: 1). Direct
effects of obesity on hemodynamics: increased blood volume, stroke volume &
cardiac output. 2). Mechanisms linking obesity & an increase in peripheral
vascular resistance: endothelial dysfunction, insulin resistance, sympathetic
nervous system, substances released from adipocytes & sleep apnea.

10. Coronary Artery Disease
Examination of arteries post-mortem from individuals 15-34 years revealed that
the extent of fatty streaks & advanced lesions (fibrous plaques & plaques with
calcification or ulceration) in the RCA & in the abdominal aorta were associated
with obesity and with the size of the abdominal panniculus. PDAY study.
Of note, the maximal density of macrophages/mm2 in the lesions was associated
with visceral obesity.
Follow up data over more than two decades suggests obesity is an independent
predictor of clinical CHD. In the TRACE register, the mortality rate was increased
23% compared with patients who were not abdominally obese.

11. Congestive Heart Failure
Elevated BMI predisposes to congestive heart failure (CHF) by promoting
hypertension, diabetes & CHD.
There is an increase in the risk of CHF of 5% for men & 7% for women for each
increment of 1U of BMI with the existence of a continuous gradient without
evidence of a threshold.

12. Arrythmias
In the Framingham study, the annual sudden cardiac mortality rate in obese men
& women was estimated to be ~40 times higher than the rate of unexplained
cardiac arrest in a matched non-obese population.Specifically, in severely obese
men, a 6 & 12 fold excess mortality rate was reported in the age group 35 to 44
and 25 to 34 years respectively.
Prolonged QTc interval was observed in ~30% of subjects with impaired glucose
tolerance & there is a positive association between BMI & QTc.
Extremely obese patients often have a dilated cardiomyopathy, fatal arrhythmias
may be the most frequent cause of death.

13. Arrhythmias contd....
Obesity & cardiac autonomic nervous system are intrinsically related. High
glucose concentrations may promote increased vasomotor tone & ventricular
instability by reducing nitric oxide availability.
A 10% increase in body weight is associated with a decline in parasympathetic
tone accompanied by a rise in mean heart rate, & conversely heart rate declines
during weight reduction.
It was demonstrated that a 10% weight loss in severely obese patients is
associated with significant improvement in autonomic nervous system cardiac
modulation.

14. Conclusions
A variety of adaptations/alterations in cardiac structure & function occur as
excessive adipose tissue accumulates, even in the absence of systemic
hypertension or underlying organic heart disease.
To meet increased metabolic needs, circulating blood volume, plasma volume &
cardiac output all increase. The increase in blood volume in turn increases venous
return to the right & left ventricles, eventually producing dilatation of these cardiac
cavities, increasing wall tension. This leads to LVH, accompanied by a decrease in
diastolic chamber compliance, eventually resulting in an increase in LV filling
pressure & LV enlargement. As long as LVH adapts to LV chamber enlargement,
systolic function is preserved.