Mary Boudreau Conover, BSNed
Inloving memory of Henry J. L. Marriott, M.D., F.A.C.C. (1917-2007), mentor, teacher, consultant, brilliant Cardiologist, terrific dancer, loyal friend, and at the end—courageous warrior.
Dr. Marriott once began his lecture with this question: “How many of you have ever had chest pain?” All of us, right? At least that was the case when we first began intense CrossFit workouts. A muscle ache in the vicinity of the ribs or sternum would make you pause with: “What’s that?” “Oh yea--those last two reps”--a superficial muscle pain.
Chest pain is a whole lot different when it comes from a heart muscle deprived of oxygen. Such pain may or may not involve the chest per se and it even has a different name—“angina”. According to reports from those who have experienced it, pain originating in oxygen starved heart muscle (myocardium) can be mild or severe, but it’s a deeper more alarming type of pain than the chest muscle twinges or aches experienced by many of us days after or during exercise.
J. Willis Hurst M.D. once published descriptions of angina given by his patients. These colorful accounts reflect the common perception of the sensations felt behind the sternum (substernal), in the back, abdomen, shoulders, either or both arms, chest, or mouth that are described as tightness, heaviness, squeezing, strangling, aching, burning, a weight, numbness, pressure, a suffocating feeling, nausea or feeling of “heartburn”.
Here are some very expressive quotes from patients with angina:
- “A red hot poker”
- “A shoe box in my chest”
- “A toothache”
- “Hot flame in the upper part of my mouth”
- “An elephant on my chest”
- “Jaw pain”
- “A bad feeling in the upper portion of my back”
- “Sternal whisper” [This one is hard to imagine!]
- “Dryness in my throat produced by effort or emotional stress”
- “Smoke in my chest” [This one too! Would only a smoker use this description?]
- “Someone choking me from behind”
One patient described different degrees of his pain like this:
Severe: “A large fish hook stuck under my jaw and hung up from a scaffold.”
Moderate: A small fishhook caught in my lower jaw”.
Mild: “A needle and thread being pulled through two lower teeth.”
Angina: Pain originating from the heart muscle
Athero-: A buildup of anti-inflammatory and marker cells along with some cholesterol within the walls of an artery
Coronary: Pertaining to the heart
Endothelium: A thin layer of cells lining blood vessels
Myocardial infarction (MI): A condition in which a localized area of myocardium is dying or dead because of insufficient blood supply.
Myocardium: Heart muscle
Sternum: Breast bone
Heart attacks are more accurately known as myocardial infarctions. They are the result of a total occlusion in a coronary artery, depriving the muscle supplied by that artery and its distal branches of its blood supply. The area immediately affected by the blocked artery is dead or dying. The muscle surrounding the dead area is injured--still living but not functioning (unable to contract), and the area surrounding the injured muscle is weak and ischemic (oxygen-deprived).
Cause. Occlusion of a coronary artery is caused by the formation of a plaque in the lining of the artery (the endothelium). This plaque is called “ath-er-o-scler-osis”. “Athero” comes from a Greek word meaning “a lump of hardened porridge”.
Atherosclerosis is caused by a chronic inflammatory response to an injury or irritation of the lining of the coronary arteries (endothelium). Major factors that result in the injury are high blood sugar, cholesterol, cigarette smoking (active and passive), some drugs, and high levels of sugar in the blood (Perry 2008).
Pathophysiology (mechanism of the disease process). As you know, the normal protective response to inflammation anywhere in the body is the accumulation of white blood cells to fight the inflammatory process, so too in the walls of coronary arteries. However, in the heart the well-meaning white blood cells do more harm than good because they migrate across the inflamed cellular lining of the artery along with many types of cellular markers for inflammation. Additionally, inflammatory cells (monocytes) circulating in the blood stick to the blood-facing surface of the plaque like Velcro.
In any other place in the body, such a reaction would be protective. In a coronary artery it becomes a threat, forming a potentially obstructive plaque within and on the endothelium. Thus, most of the plaque is not made up of cholesterol, as we always thought, but rather white blood cells and specific markers for inflammation, as well as cholesterol crystals.
Where do the LDLs and HDLs come in?
Low-density lipoproteins (LDL)---are the bad guys in our cholesterol panel---but only if their level is too high. When the LDL blood level is low, LDL can easily pass in and out of the endothelium. However, high levels of LDL no longer have freedom of passage so that they accumulate within the arterial wall, causing more inflammatory reactions. This process is further abetted by low levels of those good guys---high-density lipoproteins (HDL), that would, in sufficient numbers, be up to the task of removing fats and cholesterol from the cells. This is why we shoot for reference ranges of low LDL and high HDL.
Once collected and trapped within the vascular lining, cholesterol crystallizes and expands, tearing and perforating fibrous tissues. Thus, it is thought to have a role in the rupture of the plaque. As you will see, plaque rupture is a critical event in unstable angina.
THREE TYPES OF ANGINA
The three types of angina are stable, unstable, and variant (Prinzmetal’s angina), all of which are caused by severe narrowing or occlusion of a coronary artery that results in loss of oxygen to the section of myocardium supplied by the occluded artery. The difference among these three types of angina lies in the mechanism (pathology) of the occlusion.
Stable angina is precipitated by activity (running, walking, rowing, intense CrossFit workout). Symptoms abate with rest and resume with activity. Usually, such a person is already under a physician’s care. They should not continue working out without providing the owner of the gym with a copy of their physician’s permission.
Pathology. In stable angina, a growth of atherosclerotic deposits protected by a fibrous cap develops within the wall of the blood vessel, but does not completely occlude blood flow. Anginal attacks can be precipitated by temporary constriction of the already narrowed, but stable, blood vessel. The pain experienced has pretty much the same character each time. There is danger that stable angina will become unstable without warning. You should never see this person in your gym until after the volatile occlusion has been dealt with and the person is released to an exercise rehabilitation program.
Unstable angina is an acute coronary syndrome and a critical prophecy of an imminent heart attack. In the U.S. there are at least 1 million hospitalized patients each year admitted with a diagnosis of unstable angina. There are many more who are unknown to physicians and who never reach the ER.
Any one of the symptoms listed below is a serious indicator of unstable angina and an impending heart attack, requiring urgent medical attention.
- Angina that occurs unpredictably at rest (or with minimal exertion), usually lasting >10 min
- Severe and new onset angina (i.e., within the prior 4–6 weeks)
- Angina that occurs with a crescendo pattern, i.e., builds gradually, plateaus, and subsides gradually.
Pathology. Other than the symptoms, it is the pathology that differentiates unstable angina from stable angina. Understanding the events that occur within the blood vessel helps one to understand the reason for the symptoms and to remember them.
For a moment, visualize a case of stable angina with plaque covered by a protective cap within the wall of a coronary artery. Suddenly, the cap ruptures, allowing blood clots to gather on the disturbed surface of the rupture and block blood flow. This catastrophic event is called unstable angina. The sequence of events leading up to total occlusion clearly explains why the unexpected onset of pain may be independent of activity, sudden in appearance, and crescendo in nature, becoming severe as the clot builds and gradually subsiding as the clot shrinks.
An understanding of this mechanism, leaves no doubt that such pain requires immediate medical attention—the occlusion is developing and moving toward total blockage of the blood vessel and a myocardial infarction. It is only a matter of time—seconds, minutes, hours, days, weeks. There is no way of knowing. Total occlusion has been known to happen during transport from the ER to the cardiac catheterization lab.
Emergency response to unstable angina
- Call 911 if the pain is new to the person, severe, crescendo in character, or lasting more than 10 minutes—signs of unstable angina -- a true emergency.
- Call 911 even if you are uncertain about the symptoms.
- Reassure, but be firm in your opinion that the symptoms require emergency medical attention.
- Do not allow the person to continue with the workout nor to drive home.
Prinzmetal’s Angina (Variant Angina)
Prinzmetal’s angina refers to chest pain caused by a decrease in blood flow because of spontaneous spasm of a coronary artery, possibly without significant atherosclerotic plaques. These symptoms happen at rest and often may awaken the person during the night. Obviously, if the mechanism of the angina has been misdiagnosed and there is actually a plaque---that plaque could rupture and result in total occlusion of the vessel. Therefore, a definitive diagnosis is of great importance.
It has been proposed that the positive effects of aerobic training on cardiac structure during rehabilitation are neuro-hormonal and that they improve microcirculation within the heart muscle and functional endothelial integrity. This of course results in an enhancement of the blood supply to the injured myocardium and faster healing.
In preconditioned hearts, i.e. hearts that were exercised regularly prior to the coronary occlusion, there are fewer negative effects, in that the damage (infarct) is smaller, arterial inflammation less, hospital stay shorter and the myocardium returns to and retains a strong structure (a.k.a. remodeling).
Exercise your hearts! At CrossFit we are exercising our hearts every day, creating a sturdy microcirculation and improving the function of our heart muscle--grossly and at the cellular level. We can think of our WODs as a preconditioning for our hearts for the rest of our lives.
Check your BP. As you age, check your blood pressure occasionally and see that it stays within normal limits, with a systolic BP (the top number) at least below 140 mm.
No smoking! Avoid second hand smoke. I don’t think any of you actually smoke!
LDL down; HDL up. Beat your lipid panel into submission.
Drugs. Don’t even think about trying supplements—those capsules and mysterious powders, with claims to incredible results in terms of muscle size, power and potency, manufactured by guess and by golly under the direction of ignorant operators without background in the science of chemistry or nutrition. Our coronary arteries don’t like to be irritated, nor do our livers that metabolize and our kidneys that filter like to be challenged to excess.
Seriously cut out bad carbs. You’ve had plenty of good info on nutrition, but I would warn you about deep-fried anything. The heat-modified degradation products of fat used for deep-frying are thought to be associated with endothelial irritation, an important initial event in the formation of atherosclerotic plaques (Williams, 2009; Michael 1999).
Take good care of your cells. The walls of our blood vessels are lined with living cells that constantly interact with each other, the fluid that surrounds them, and the blood that flows over them. SO, let’s take care of those cells; feed them well and provide them with a gusty flow of blood--you lucky CrossFitters. Surely not everything spins on genetics.
Ronnie Boose (CFNSC), Catherine Boysen (Bellvue, WA) and Ed Conover (San Jose) reviewed this article from their nonmedical positions and Hein J.J. Wellens M.D. from his expert position. Thank you all.
Dr. Wellens is Professor of Cardiology at the University of Maastricht in the Netherlands and formerly Chairman of the Department of Cardiology at University Hospital, Maastricht. His clinical expertise, influential research, books, innumerable medical journal publications and lectures, and his genuine concern for good outcomes for cardiac patients everywhere have uniquely and indelibly influenced Cardiology throughout the world.
O'Toole TE, Conklin DJ, Bhatnagar A.: Environmental risk factors for heart disease. Rev Environ Health. 2008 Jul-Sep;23(3):167-202.
Abela GS, et al: Effect of cholesterol crystals on plaques and intima in arteries of patients with acute coronary and cerebrovascular syndromes. Am J Cardiol. 2009 Apr 1;103(7):959-68. Epub 2009 Feb 07.
Tatasciore A, et al: Awake blood pressure variability, inflammatory markers and target organ damage in newly diagnosed hypertension. Hypertens Res. 2008 Dec;31(12):2137-46.
Zou N, Hong J, Dai QY: Passive cigarette smoking induces inflammatory injury in human arterial walls. Chin Med J (Engl). 2009 Feb 20;122(4):444-8.
Le Page C, et al: Exercise training improves functional post-ischemic recovery in senescent heart. Exp Gerontol. 2009 Mar;44(3):177-82. Epub 2008 Oct 17.
Taglieri C, et al: Prevention of left ventricular remodeling after myocardial infarction: efficacy of physical training, Monaldi Arch Chest Dis. 2008 Jun;70(2):51-8.
Trzos E, et al: The influence of physical rehabilitation on arterial compliance in patients after myocardial infarction. Cardiol J. 2007;14(4):366-71.
Balen S, et al: Anti-inflammatory effects of exercise training in the early period after myocardial infarction.
Michael J. A, et al: Impaired endothelial function following a meal rich in used cooking fat, J Am Coll Cardiol, 1999; 33:1050-1055
Williams, MJA, et al: Impaired endothelial function following a meal rich in used cooking fat. Dept of Med, U of Otag, Dinedin, NZ. Reprint requests and correspondence: Dr. M. Williams, Department of Medicine, University of Otago, 201 Great King Street, Dunedin, New Zealand firstname.lastname@example.org
Steinberg D, et al: Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med 1989 Oct 26:321(17):1196-7.
Libby P: Atherosclerosis: The new view. Scientific American, November 10, 2008.
Sen K, et al: A study to find out the proportion of prediabetes in patients with acute coronary syndrome in a medical college of Kolkata. J Indian Med Assoc. 2008 Dec;106(12):776-8.