Chapter 63
Cardiovascular Disease — 2
The principal basis for heart and blood vessel disease is atherosclerosis. The literal translation of that medical term is hardening of the porridge, from the Greek words athero, meaning gruel or porridge, and skleros, meaning hard. Make oatmeal, then let the unwashed saucepan sit in the sink, and you will understand why this is bad. When the German pathologist Felix Marchand coined the term in 1904, he was referring to the fatty material with an appearance like gruel he observed inside the arteries. The fatty material is now called plaque, which forms when LDL and other lipoproteins, or molecules made of proteins and lipids that carry cholesterol, build up. The plaque accumulates over decades from progressive trapping of these lipoproteins, which is accompanied by inflammation in the wall of the artery. The atherosclerotic process can lead to different outcomes. It can be sudden, from a sudden crack or plaque rupture and blood clot, the proximal cause of a heart attack, or chronic, with the arterial pipe becoming narrowed from accumulation of plaque, limiting (but not usually completely blocking) the normal blood flow into the heart. The cumulative exposure to elevated LDL cholesterol over time and its magnitude drives atherosclerosis and is preventable with early intervention. The same process can occur in any of the arteries of the body, whether it be to the brain (cerebrovascular), the aorta with branches to the intestine and kidney, or peripheral pipes to the extremities.
The process of atherosclerosis is highly influenced by factors that damage the wall of the artery, such as cigarette smoking, uncontrolled high blood pressure, diabetes (and attendant high sugar levels in the blood), or abnormal lipids in the blood, especially LDL cholesterol. Atherosclerosis has been likened to a tumorlike disease driven by the smooth muscle cells in the artery wall. In parallel, the shared lifestyle+ risk factors and underpinning of chronic body-wide inflammation with cancer have been duly noted. There’s also a component of self-directed immunity that has been increasingly documented, adding to the knowledge that people with autoimmune diseases have a considerably higher risk of developing heart disease. Even though coronary disease typically shows up in older adults, it’s a lifelong process with clear-cut evidence of early plaque formation in teenagers and young adults. Some mild coronary artery plaque formation is remarkably common, some would say pervasive, as we age; by age thirty, the majority of people have at least some evidence of early coronary atherosclerotic plaque (fig. 5.2).
The sooner in life all underlying, driving lifestyle+ factors are addressed, the less chance there will be of significant accumulation of plaque or plaque ruptures. What can’t be emphasized enough about the major age-related diseases—heart, brain, and cancer—is that they typically are incubating for about twenty years or more before they declare themselves clinically. What an opportunity that represents to prevent their occurrence.

