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Q. Can Pathophysiology causes cardiovascular disease?
Cigarette use activates platelets, increases circulating fibrinogen, increases heart rate, and elevates blood pressure. It appears to promote plaque disruption. A strong dose response relationship exists between smoke and CAD. Duration of smoking and the daily amount markedly influence risk of CAD. The adverse effect of smoking is present among men and women (but may be stronger in women) of all ages and ethnic groups with or without CAD. Data suggest that risk for cardiac death is two to four times greater among current smokers than non smokers.
Risk for cardiovascular disease begins to decline soon after smoking cessation, irrespective of age and sex. There is 50 per cent reduction in cardiovascular events within the first 2 to 4 years. It is thought to take as long as 20 years to regain baseline risk.
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Neurological symptoms and signs occur in 30 to 40 per cent of patients with IE, are more frequent when IE is caused by S. aureus, and are associated with increased mortality rates.
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