Why are we still Hardening our Hearts?: Part 2

Posted by Heart Niagara on

The underlying disease causing heart attack and stroke is called arteriosclerosis.

Greek physicians in the 4th century BC called it atherosclerosis or ‘hardened porridge’. That is what it looked like when a dead person’s heart was autopsied. The process can cause narrowing and clogging of all the arteries in the human body, (which if laid end-to-end would stretch over 60,000 kilometres —and if weighed ‘en masse’ would be 4 ½ kilos —-not an inconsiderable organ.) All these arterial tubes are lined by a one cell thick layer of tissue called the endothelium which is the site of very complex physiological activities designed to protect the wall of the artery. Inside that are three layers of tissue: the intima, the media and the adventitia which give the tube the elasticity to accommodate the differing pressures and rates of the heart as it pumps the blood around the human body. Thus supplying all the cells and tissues with oxygen and nutrients. Stated simplistically: the oxygen is sent to the heart from the lungs after a breath and then pumped through all this huge arterial tree: from the heart to the aorta to the arteries to the arterioles to the capillaries which feed all the tissue cells. The fuel is absorbed by the intestines following a meal and sent to the heart after filtration by the liver to be pumped though the system. Blockage of this flow of oxygen and fuel causes fatigue, shortness of breath and pain in the area being deprived of oxygen.

The one-cell endothelium, lining the artery, could be compared to the surface of the skin which is vulnerable to scrapes, rashes, abrasions, cuts and lacerations from contact with branches, stones, sharp objects, allergens etc. except that the objects which damage the endothelium are particles, molecules and other substances circulating in the bloodstream. Some of the things that lacerate the endothelium have been around since the origins of Homo Sapiens, (6000 generations of humans ago), such as products from viral and bacterial infections in the bloodstream and some environmental pollutants that are inhaled from the lungs.

But in the last 70 years a new group of substances have arrived to knock holes in the Endothelium wall: the by- products of cigarette smoking, particles from atherogenic food products, (fast food high in adulterated saturated fats), high levels of Low Density Lipoprotein, (LDL) or ‘bad’ cholesterol, and increased inflammation in the artery from being overweight or diabetic.

These endothelial invaders also attack the enzymes, chemicals and particles designed to protect the endothelium against damage to the interior layers: the intima and media. And if there are fatty-sticky substances in the bloodstream they will lodge in that laceration and create a collection of debris, similar to a sandbar in a riverside. In the terminology of arterial disease the sandbar is called an arteriosclerotic streak. As more adverse substances pour down the arterial river and into the hole in the endothelium, and on into the intima and media, this will progress to an arteriosclerotic plaque. Eventually the plaques will coalesce and start to block the arterial flow leading to stenosis and a reduction in flow and eventually chest pain.

The part of the arterial tree that is most vulnerable to this endothelial and intima damage are the four coronary arteries on the surface of the heart. The Left and Right Coronary artery and their two main branches: the Left Anterior Descending and the Circumflex. They only measure twelve inches in length. The original Grey’s Anatomy described the Left as the size of a crow’s quill and the Right a little longer. Not a very large battlefield but for most humans in the last 70 years it has been an ongoing warzone against Coronary Artery Disease (CAD). Keeping a smooth lining like ‘teflon’ in those 12 inches of arterial tubing is the most important commitment to living a long life that any child can make. 

Regrettably, by the age of 25 many young men will have arterial tubes stickier than ‘velcro’. And by the age of 35 many young women will have the same.

Indeed recent data shows that women are developing adult symptoms earlier than before and as they tend to have arteries of a smaller diameter, and a different anatomy from men, their symptoms are often harder to recognize.

Some of these atheroma plaques in the coronary arteries are relatively stable: they have a hard outer shell with a fibrin cap which is calcified and these plaques do not rupture; they lead to chest pain as the blood flow to the heart muscle is restricted but do not cause a ‘heart attack’. But others contain a soft liquid core full of the fatty- sticky substances that started the problem. If the cap ruptures this liquid core is discharged into the main bloodstream of the artery and causes a clot a.k.a. Coronary Thrombosis. The blockage deprives the area of heart muscle supplied by that artery of oxygen and becomes necrotic i.e. tissue death a.k.a. Myocardial Infarction, (infarction is from Greek to ‘plug up’). If the individual has survived the attack Emergency Room MDs will use a chemical “drano” to dissolve the clot prior to having the blocked artery replaced by a stent or an arterial graft.

Unlike the atherosclerosis noticed by the Ancient Greeks Coronary Thrombosis, (and thus Myocardial Infarction), has not been around for a long time. The name Coronary Thrombosis was only coined in 1912 and prior to that death from ‘Heart Attack’ was relatively rare. More common was angina: labelled Angina Pectoris by an English Physician called William Heberden in 1768. Angina caused chest pain but not a Heart Attack and the pain was relieved in the old days by arterial dilators such as brandy. In angina the plaques are more like the hard calcified atheromas that do not have the liquid core and thus do not rupture; they just block the flow causing chest pain and/or shortness of breath.

To stop hardening our hearts, we must take care of our arteries. We must start before the damage is too serve and irreversible. This means addressing CAD in adolescences. In order to reach the whole population, we need to go where we can provide all adolescents the same benefits and opportunities. Schools are the only place where we can see the whole adolescent population. 

Join me tomorrow as I uncover the 9 principle causes of CAD.


About the Author


Dr. Stafford W. Dobbin was a graduate of Queens University Belfast and founded Heart Niagara in 1977. He established the first Department of Emergency Services in Niagara at the Greater Niagara General Hospital in 1976.  Through Heart Niagara he initiated the teaching of citizen cardio-pulmonary resuscitation and advanced cardiac life support for critical care personnel prior to the establishment of the Regional Paramedic program. 

His initial design of Heart Niagara included a cardiac rehabilitation program for survivors of cardiac events staffed by qualified physicians and nurses for which he was the medical director until 2002. He started the Heart Niagara’s Healthy Heart Schools’ Program in 1985 and served as medical director. His EMS system for coverage of mass participation events was first used at the US Olympic Marathon trials in 1980 and he served on the first executive of the International Marathon Directors Association. 

August 25 2020 Dr. Stafford Worrell Dobbin, much loved and cherished husband to Susan moved on into the loving arms of God, much loved son-in-law to Eileen Kennedy. His dear parents Stafford and Jean passed on before him. Churchyard service at Hillsborough Parish Church to place his ashes with those of his parents in Hillsborough, Northern Ireland at a future time. In memory of Stafford if so desired consider The Niagara Schools Healthy Heart Programme of Heart Niagara which he so believed in.

Disclaimer: The views and opinions expressed in blog entries are those of the author(s) and do not necessarily reflect the official policy or position of Heart Niagara.


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