Signs and Symptoms
No matter how old we are, if we could see inside our own coronary arteries (those blood vessels with the important job of supplying oxygen to the heart) we might well be alarmed. Most people believe that heart disease comes with age however this idea is quite incorrect. Autopsies performed on American casualties of the Korean War back in 1953 illustrated that 77% of these young men (their average age was just over 22 years) already had atherosclerosis (plaque build-up) in their coronary arteries. Incredibly one out of twenty of the diseased men already had blood vessels 90% clogged (2,3). Follow-up studies on thousands of soldiers from subsequent wars found the same sobering evidence of heart disease (11). As if that is not bad enough, the beginnings of atherosclerosis has also been observed in children with the appearance of fatty streaks inside their blood vessels. Progression into atherosclerotic plaques is obvious in most young people by their 20s (4,5). In the 1980s the Bogalusa Heart Study observations clearly showed that atherosclerosis, coronary heart disease, and essential hypertension were present in childhood with documented blood vessel lesions appearing in some by the time they were 5 to 8 years old (8). In the early 2000s autopsy studies of 3000 young people between the ages of 15 and 34 who had died in accidents exhibited advanced plaques in the coronary arteries of many of these young people along with high levels of non-HDL cholesterol (6,7).
Just to clarify cholesterol types: LDL (low-density lipoprotein) and other non-HDL lipoproteins deposit in blood vessel wall and create plaques. HDL (high-density lipoprotein) has the ability to remove deposited cholesterol and to carry it away as waste.
Have you ever wondered what exactly is happening when a heart attack occurs? The evolution of this catastrophic event is the gradual build-up of cholesterol and other fat compounds under the delicate inner surface of the coronary arteries. This cholesterol comes directly from the food we eat, from the liver’s metabolism of the saturated fat that we consume and from our own liver’s production of cholesterol. The plaque that results is a waxy substance consisting mostly of cholesterol and other fatty products along with some proteins, cellular waste products, calcium and fibrin (a clotting material in the blood). If this plaque builds up slowly over many years, the blood flow has time to adjust to these new circumstances. The coronary arteries can create tiny new vessels called collaterals, essentially performing their own “bypsss” to route the blood around a blocked area. Though these long-term plaques can cause severe angina (heart pain caused by lack of oxygen for the heart muscle), they are rarely the cause of a heart attack. It is the newer, more unstable plaques that are usually the culprits. These young plaques generally block less than 50% of a blood vessel (12).
Our body’s immune system fights back by sending its best warriors to neutralize this inflammatory situation. White blood cells surround the plaque area and attempt to ingest the oxidized LDL molecules, eventually forming a bubble of fatty pus that becomes part of the plaque. Muscle cells in the artery wall multiply to form a cobweb-like single layer of endothelium to cap the plaque. This cap prevents the blood flowing past the area from mixing with the plaque constituents. However, new plaques can be weak and thin, especially in a situation where a person’s diet supplies lots of inflammation-causing reactive oxygen species and only a poor supply of protective antioxidants. As the blood rushes by the plaque, the cap is steadily worn away until it ruptures, mixing its contents with the blood. Platelets are activated and the blood immediately begins to clot to contain the leak. Sometimes a clot will be successful but unfortunately clots can grow quickly and may extend to block the entire artery. In this case, there is no time to develop collaterals. Blood flow downstream from the rupture is severely reduced or stopped altogether and heart muscle cells begin to die. Soon heart pumping mechanisms fail. The victim may feel a crushing agony in the chest or a burning pain down the arm and up into the jaw. This is a heart attack (1,13). If a person survives a heart attack, the portion of the heart that was affected remains as dead scar tissue. Further events with more scarring weaken the heart and can lead to congestive heart failure or heart rhythm problems that in turn may cause death.
One out of every three people that have a heart attack die. Often the heart attack is the first outward sign of heart disease.
Symptoms of a heart attack (9,10)
Symptoms can be extremely variable. Some people have no symptoms at all or at least none that they can identify as being signs of a heart attack. Heart attacks can start slowly with only mild sensations or they can be sudden and intense. People with diabetes may notice no symptoms at all.
The most common indicatiosn of a heart attack are chest pain or discomfort in the centre or left side of the chest. This pain can last a few minutes or longer and then disappear and it may or may not return. The pain can be mild or severe and is variably described as a pressure/squeezing feeling or a heartburn/indigestion type pain. Upper body discomfort may appear in one or both arms, the back, shoulders, neck, jaw or just above the belly button. Some people report light-headedness or dizziness.
Women are more likely to experience the following symptoms although men may have them too;
Sudden sweating or breaking out in a cold sweat, shortness of breath, nausea and vomiting, unusual tiredness that may last for days and pain in the upper body (jaw, neck, back and shoulders). Women in particular may experience pain in either or both arms.
The more symptoms you have, the more likely it is that you are having a heart attack.
Watch for Part Two of this article to discover good news about the prevention of heart attacks.
1 Campbell, Colin T., and Campbell, Thomas M.II. The China Study: Revised and Expanded Edition: The Most Comprehensive Study of Nutrition Ever Conducted and the Startling Implications for Diet, Weight Loss, and Long-Term Health. Benbella Books. Dec 27 2016
2 Enos, W.F., Holmes, R.H., Beyer, J. Coronary disease among United States soldiers killed in action in Korea preliminary report. Journal of the American Medical Association. 1953; 152(12): 1090 – 1093.
3 Enos Jr, W.F., Beyer, J.C., Holmes, R.H. Pathogenesis of coronary disease in American soldiers killed in Korea. Journal of the American Medical Association 1955; 158(11): 912 – 914.
4 Strong, J.P., McGill, H.C. The pediatric aspects of atherosclerosis. J Atheroscler Res 1969 9(3):251 – 265.
5 McMahan, C.A., Gidding, S.S., Malcom, G.T., Tracy, R.E., Strong, J.P., McGill, H.C. Jr. Pathobiological determinants of atherosclerosis in youth risk scores are associated with early and advanced atherosclerosis. Pediatrics 2006; 118(4):1447 – 1455.
6 McGill, H.C. Jr., Herderick, E.E. Atherosclerosis in youth. Minerva Pediatr 2002 54(5):437-447.
7 McMahan, C.A., Gidding, S.S., Malcom, G.T., Tracy, R.E., Strong, J.P., McGill, H.C. Jr.
Pathobiological determinants of atherosclerosis in youth risk scores are associated with early and advanced atherosclerosis; Pathobiological Determinants of Atherosclerosis in Youth Research Group. Pediatrics. 2006 Oct; 118(4):1447-55.
8 Newman, W.P., Freedman, D.S., Voors, A.W., Gard, P.D., Srinivasan, S.R. et al. Relation of serum lipoprotein levels and systolic blood pressure to early atherosclerosis. The Bogalusa Heart Study. N Engl J Med. 1986 Jan 16; 314(3):138-144.
11 McNamara, J.J., Molot, M.A., Stremple, J.F., et al. Coronary Artery Disease in Combat Casualties in Vietnam. JAMA. 1971; 216(7): 1185-1187.
13 Esselstyn, C.B Jr. Prevent and Reverse Heart Disease. Penquin Group, New York. 2007.