Almost half of us will die of a heart attack or stroke; in fact, it’s likely many of us have been developing a type of cardiovascular disease already (1). Just being male increases your risk, and if you happen to be a male, sedentary, obese smoker then you’re in real trouble (1). Adding these risk factors up doesn’t triple your chances, it multiplies them seven-fold (1)!
In light of American Heart Month, don’t forget to donate to cardiovascular disease research—spend with a clear conscience for clear arteries—but although the American Heart Association badly needs your funding, your cash is best suited for a pair of tennis shoes (1).
The conclusion on getting a heart attack is that the problem isn’t the heart, and in stroke, the brain isn’t at fault either (1). By far the greatest culprit is the accumulated thickening of thick sludge in scattered patches in your blood vessels that eventually merge to form large plaques (1). These atheromas represent atherosclerosis (1).
There’s no sign to us that plaque development is occurring (1). We feel no pain or any other symptoms (1). But our blood vessels are narrowing, called stenosis, more and more as they become hardened, due to calcification, and obstructed (1). The volume of blood delivered to tissues lessens (1). Eventually you might notice skin wounds heal slowly especially in the legs, and reduced blood flow to the brain is causing memory loss and confusion (1). The narrowing will sap your energy and ischemic heart disease results (1). Elevated blood pressure from hypertension worsens the problem and taxes the heart (1).
As blood swirls around plaque, splashing up against vessel walls, resulting endothelial damage might lead to a thromboembolic event (1). As platelets activate as well as a cascade of coagulation, an internal blood clot, or thrombus, can narrow the lumen further and consolidate the stenosis and ischemia (1). Another possibility is an aneurysm from blood flow pushing out a weakened vessel wall like a balloon (1). Usually thrombosis is the final case of fatal myocardial infarction (1).
Where hyperlipidemia, if you are obese, and hypercholesterolemia play roles are in contributing ingredients of plaque (1). LDL cholesterol makes multiple contributions to plaque development (1). When it is oxidized by free radicals and taken up by smooth muscle and macrophages, it leaves fats (intended to go to muscle and adipose tissue) to create foam cells that create thickening (1). The oxidized LDL then causes stimulation of plaque through growth factor production, promoting connective tissue desposition, and attracting monocytes that adhere to and modify endothelial surface (1). Further the LDL itself damages the endothelium causing inflammation (1).
In diabetes, sugars that circle LDL and bind to it in a process known as glycation then allows LDL to easily bind to endothelia (1). This in effect leads to more aggressive attraction of macrophages and promotion of connective tissue deposition enlarging the atheroma and inactivating nitric oxide, which is necessary for vasodilation (1).
When smoking, carbon monoxide that replaces oxygen in hemoglobin, causing hypoxia may also be atherogenic by promoting smooth muscle proliferation and LDL accumulation (1). Plus, the nicotine has vasoconstrictive effects, narrowing blood vessels further (1).
Reducing risk factors is the solution. In conclusion, by knowing more about how cardiovascular disease develops, we can help to prevent heart attacks and stroke. While lowering cholesterol is not justified by scientific research, reducing calories to avoid obesity is strongly supported, more so when saturated fat is reduced. Stopping the cigarette habit helps, and so does keeping blood pressure in check (1). Getting in shape, even with moderate exercise, by far can quickly yield results including a reduced heart rate of 10 beats a minute saving your heart more than 5 million beats a year that cause wear and tear (1). The goal is to avoid developing atherosclerosis further and leading a longer, healthier life.
Reference List
1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
