Obesity Cardiovascular and Respiratory Complications - pediagenosis
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Saturday, May 8, 2021

Obesity Cardiovascular and Respiratory Complications

Obesity Cardiovascular and Respiratory Complications
Clinical background
Obesity is associated with a number of complications and comorbidities. Cardiovascular disease is the major cause of death in obese patients and there is a direct link between the degree of obesity and the degree of hypertension. Other risk factors for coronary heart disease, such as smoking and hyper- lipidaemia, should be addressed. There is also a higher risk of thromboembolism and stroke in the obese population. Other complications include osteoarthritis, back pain, ligament and tendon injury, gallstones and an increased risk of certain cancers, in particular those of the colon, rectum, breast, endometrium and prostate (Fig. 47a). Sleep apnoea syndrome is more common in the obese, particularly men.

Respiratory complications of obesity

Cardiovascular complications of obesity
Obesity not only relates to but also predicts coronary atherosclerosis in both men and women, even with minimal increases in BMI (Fig. 47b). Disordered lipid metabolism occurs partly through decreased levels of the enzyme lipoprotein lipase, an insulin-sensitive enzyme that breaks down fat. This results in elevated serum triglycerides and reduced HDL  cholesterol. Hyperglycaemia results in the glycation of more LDL, which increases the affinity of LDL for the modified LDL receptors on macrophages. This in turn promotes endothelial cell cyto- toxicity, foam cell production and smooth muscle proliferation. Plasminogen activator inhibitor (PAI-1) is raised (Fig. 47b), and this prothrombic state is a further risk factor for coronary artery disease. Elevated circulating levels of C-reactive protein, a systemic marker of inflammation, also occur as increased visceral fat appears to enhance the inflammatory pathway response that involves phospholipase A2, intracellular adhesion molecule and C-reactive protein.

Congestive cardiac failure. Left ventricular hypertrophy is a common feature of obesity. In the absence of hypertension, increases in cardiac output and stroke volume with diastolic dysfunction and have been related to sudden death in obese patients. Changes in the right heart are also seen in obese patients. These changes may occur as a consequence of sleep apnoea and the obesity hypoventilation syndrome, and result in right ventricular hypertrophy and pulmonary hypertension, and eventual failure. Right ventricular dysfunction may also occur as a result of left ventricular dysfunction, with subsequent biventricular failure.

Hypertension is often a consequence of obesity, particularly in patients who have also developed hyperinsulinaemia and hypertriglyceridaemia. These patients will be predisposed to myocardial infarction, stroke and renal failure. Obesity-related hypertension is of complex aetiology. Free fatty acids, leptin and insulin may all be raised in the patient’s blood and may act together to activate the renin–angiotensin system and promote sympathetic activity with consequent vasoconstriction and sodium retention.
It has been found, using animal models of obesity, that obesity causes inflammatory changes in small blood vessel walls with adverse consequences for perfusion of vascular beds.

Respiratory complications of obesity Sleep apnoea describes the cessation of breathing during sleep. This syndrome is characterized by snoring and apnoeic episodes culminating in sudden waking associated with a rise in arterial Pa CO2. Patients may experience many apnoeic episodes in a single night, resulting in severe sleep disturbance and daytime somnolence. Fat deposition in the neck may externally compress the upper airways and infiltration of adipose tissue into muscle may decrease upper airway size, render the pharynx more susceptible to collapse and decrease chest wall compli- ance. Furthermore, abdominal fat may impede diaphragmatic movement, especially in the supine position. In obesity hypoventilation syndrome, there may also be a reduced central respiratory drive.
Detailed sleep studies should be performed as, untreated, sleep apnoea syndrome may lead to the development of pulmonary hypertension and right heart failure. Machines exerting continuous positive airway pressure (CPAP; Fig. 47c) are available which effectively ‘splint’ the upper airways preventing their collapse. These provide relief for sufferers of sleep apnoea,and also for their partners.

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