Flatline: A Heart [Under] Attack

If thou examinist a man for illness in his cardia, and he has pains in his arms, in his breasts and on one side of his cardia…it is death threatening him
– Ebers Papyrus

Just recently I finished covering the heart and cardiovascular system of an introductory anatomy and physiology course. As always, I have recorded a fair amount of notes along the way that I would like to share with you all.

But lets start with a few historical facts. There’s no doubt the prominence of the heart was paved by the practices of the Egyptians. Through a forty seven case medical treatise, known as the Edwin Smith Papyrus, we find that the heart was the only organ left inside of a corpse during mummification as it was believed to contain the essence of a person. This essence often referred in the Book of the Dead as the Ka, was thought to be all that a person was, i.e., spirit, intelligence, passions, humors etc. Modern medical interventions of the heart had their beginning with Werner Forssmann, a German physician known for performing the first cardiac catheterization. Forssmann performed this experimental procedure on himself and then shot an X-ray to prove to the medical community the validity of his work. His courage was awarded the 1956 Nobel Prize in medicine for his contributions to humanity. Three years later in 1959, Norman Shumway and Richard Lower, two physicians at Stanford University interested in the heart perform the first transplant in a dog; this was a huge accomplishment for medical science though the real reward went to Christiaan Barnard a South African doctor at Cape Town University. Barnard had almost no experience in cardiac transplantations, and bypass many ethical dilemmas that would have otherwise kept him from becomig the first to perform one. But he was ambitious and on December 3, 1967 he performed the first heart transplantation on a human. Louis Washkansky became the first recipient of a heart. Washkansky lived a total of 18 days and die of an uncontrolled infection caused by klebsiella and pseudonomas.

Heart anatomy and physiology is one of a kind. The heart is under the control of the autonomic nervous system, which means that we don’t consciously control it. It never stops working. This relatively small organ is the size of a clenched fist, it beats approximately 100,000 times each day pumping about 2,113 gallons of blood daily. The heart and its four chambers direct the blood to its appropriate destination; deoxygenated blood to the lungs, oxygenated blood to the rest of the body via the aorta. The exchange of gasses occurs at the capillary level (next time you go to the doctor pay attention when he/she presses on your skin, they are checking your capillary refill which should be at 2 seconds or less). I don’t want to get into a lot of biochemistry here but oxygen is absolutely necessary in the body as cells utilize it as the ultimate electron acceptor during cellular respiration in the generation of energy. The heart muscle, which is contracting and relaxing at all times needs to have a free flowing supply of fresh oxygenated blood. Problems in the heart occur when this flow of blood is compromised by a blockage in the coronary system. We call this, a heart attack or in medical terms a myocardial infarction (MI).

The coronary arteries that supply oxygenated blood to the heart muscle branch from the ascending aorta, deoxygenated blood then returns from the coronary venous system through the coronary sinus and then into the posterior side of the right atrium to start the cycle again. Returning to our conversation of heart attacks, the CDC states that every 43 seconds someone in the United States experiences a heart attack for a total of 735,000 cases per year.
Here’s a picture showing the most common signs and symptoms of a heart attack:

In an emergency situation, a patient is often times given an aspirin to thin the blood along with nitroglycerine to dilate blood vessels in an effort to allow blood to better flow through the presumed blocked/constricted area (nitroglycerine might not be appropriate for patients experiencing inferior wall acute MIs due to the fact that 60% of these patients develop hypotension and the administration of nitroglycerine further complicates matters). An EKG is performed, if an ST elevation is noted then in many situations catheterization is necessary and the patient is rushed from the ER to the cathlab. Blood tests can further confirm the presence of an acute heart attack through troponin levels (troponin is a protein that is release into the blood when the heart muscle is dying).

Here’s a pointer, coronary artery disease (CAD) is caused by a build up of plaque that constricts the artery, which causes the flow of blood to the heart muscle to be compromised. Plaque is composed of cholesterol and other substances. This collection leads to a condition known as atherosclerosis (hardening of the arteries). Interestingly, this problem only occurs in arteries and not in veins, so it is now believed the process begins with damage to the inner most layer of an artery, the endothelium that sits in the tunica intima. Arteries are like veins but on steroids, this is due to the high turbulence and pressure they must endure. Just Google an image of the right and left ventricles and you will see how thick the left is compared to the right. This is an obvious anatomical necessity as the contraction of the left ventricle (high pressure) sends the blood to the rest of the body while the contraction of the right ventricle (low pressure) sends the blood to the nearby lungs. As the strong contractions of the left ventricle send the blood to the aorta and then to the coronary arteries high pressure blood smashes against the inner walls causing damage. Clotting factors gather to start repair mechanisms. The problem here occurs when high levels of LDL (low density lipoprotein) are found in the blood, but it isn’t just LDL that is detrimental to cardiac health, it’s a particular type of LDL known as Lp(a). This particular type of LDL shares a similar structure with plasminogen and both compete for binding at the site of endothelial damage. It is important to mention that plasminogen is incorporated into blood clots as they form; when active it turns into plasmin and performs the action of cleaving the clot apart. You can start seeing the problem now, when Lp(a) binds instead of plasminogen the clot remains in place and a layer of endothelium grows over it, over time this becomes an issue as the path of blood starts to constrict ultimately becoming blocked. Malcolm Kendrick, general physician and author of The Great Cholesterol Con advices against elevated levels of Lp(a) reporting that more than 30 mg/dL puts an individual at risk of developing acute problems. In fact, some professionals believe that a good indicator of cardiac health can be determined by inflammation levels, which could be initially indicated by a C-reactive protein blood level (nonspecific).

Though procedures such as balloon angioplasty (use of an inflatable balloon to flatten the plaque) and coronary artery bypass graft (graft of one’s own blood vessels, often times the great saphenous vein, to bypass the blocked area) exist, there is no better treatment than preventive. Regular cholesterol screening, exercise, and a balance diet are great protectors against CAD.

I hope you have found this short blog informative as well as interesting. As always if you enjoyed reading make it known by leaving your kudos and subscribing. Until next time!

Mounir C. Cejin