Heart disease is the leading cause of death in the United States (with 596,577 each year), barely edging out cancer which has 576,691. One-third of all deaths is, in fact, due to heart disease.
Several factors are known to play a critical role in relation to heart disease, and it’s now well-known that one of the major things that lead to a heart attack is excess stress. Stress can, of course, come from several sources, but it is usually either physical of emotional.
In this article, we’ll look at exactly how stress triggers a heart attack.
What Causes Heart Attacks?
Heart disease starts with the buildup of plaque on the walls of the arteries of your heart. Plaque consists of cholesterol, other fats, calcium, cellular waste, and various products of inflammation.
Since cholesterol plays a major role, let’s look at it first.
As you probably know, cholesterol comes in two varieties referred to as LDL (the bad kind) and HDL (the good kind). But it’s the LDL cholesterol that we’re mainly concerned with in relation to plaque (HDL also plays an important role in relation to it, as we’ll see later).
Under the microscope LDL, cholesterol particles are seen to be different sized; some are large while others are small, and it’s the small ones that do the most damage. The reason for this is that they are small enough to easily slip through the cells that line the walls of the arteries, and they become oxidized when they enter this region.
As a result, the immune system sees them as foreign invaders and sends what are called macrophages to deal with them (destroy them). The macrophages gobble them up and in the process, become bloated and are referred to foam cells.
These foam cells form a relatively large mass within the artery wall that usually protrudes into its interior. Indeed, in time, a fibrous “cap” develops over the mass of foam cells. This is the plaque mentioned earlier (with the area near the cap being the most dangerous section of it).
In practice, it usually takes years to build up plaque in this way, and surprisingly it rarely develops to the state where it completely blocks off the artery. Indeed, plaque buildup by itself only causes a heart attack in about 15% of cases.
Most attacks occur because inflammatory substances are eventually secreted by the foam cells, and they invade the cap and cause it to rupture. This creates a “channel” through to the surface of the cap, and material from the core (referred to as “tissue factor”) rises through it and emerges out the top—much like the lava in a volcanic eruption.
When the tissue factor encounters the blood passing through the cap it causes a blood clot to form. If this clot is large enough to halt the normal flow of blood in the artery a heart attack occurs.
For those visual learners, here’s a video that explains what happens during a heart attack.
How Does Stress Affect This Process?
To understand how stress might affect this we have to look at how stress, and particularly, a stress response, occurs. First of all, let’s consider the difference between physical and emotional stress.
The major way physical stress is produced in the body is through exercise or other rigorous activity. Exercise causes the heart to beat faster, and it also causes our arteries to pulse at a greater rate.
This means that they move in and out further, and this will obviously have an effect on the cap and the nearby plaque. But exercise also keeps arteries supple and flexible, which is important. So moderate exercise will not usually cause a heart attack; in fact, it’s good for the heart and arteries.
In the case of emotional stress, the heart also beats faster and the arteries flex more. What is important here is the “stress response;” it’s what occurs in your body when you experience something that causes stress.
This response involves two hormones called adrenaline and cortisol along with another hormone called norepinephrine. In a stress response adrenaline is called up first. It causes the heart to pulse faster, which sends extra blood to the muscles and organs.
It also triggers the release of what is called fibrinogen, which increases the rate of blood clotting. Finally, it helps increase the body’s energy by releasing glucose from its stored form called glycogen.
Once this first stage is well underway, a second stage comes into play. It triggers the production of cortisol. One of its first jobs is to replace the energy that the adrenaline rush has depleted.
Cortisol is also used by the immune system; it alerts it to respond to any infection or injury in the body. In response, the immune system sends out white blood cells.
Cortisol also acts as a check on the overall response, shutting it down when it is no longer needed. Norepinephrine works alongside adrenaline to help produce energy. It is also involved in controlling blood pressure and maintaining sugar levels.
How Does All This Affect a Heart Attack?
Our problem now is: how does the action of adrenaline, cortisol, and norepinephrine create a heart attack?
It might seem strange that it could do this, as it’s obviously an important process in the body.
We’ve also seen that inflammation, that is controlled by the immune system, plays a large role in heart disease.
Inflammation creates the foam cells within the plaque. It’s important to note, however, that a single stress response does little damage. It’s when the responses get out of control and come one after the other that the problems begin. When this occurs your immune system can become desensitized to cortisol and since cortisol controls the overall stress response, this can allow inflammation to get out of control.
Adrenaline also triggers the release of fibrinogen, a blood-clotting agent, and if too much adrenaline is created, too much fibrinogen will also be created, which is a serious risk factor for a heart attack.
It’s also important to note that in most cases several small attacks that are barely noticed frequently preceded the main one. A small crack occurs in the cap and a corresponding small blood clot occurs that does not block off the artery and may be barely noticed.
Clots of these types dissolve quickly and the cap heals over, but several of them set the stage for a larger crack and much larger blood clot as the cap weakens. And these smaller attacks are usually triggered by stress.
High blood pressure is also a risk factor. It puts the artery walls under an increased load as the artery pulses. With chronic stress and its associated increase in cortisol along with norepinephrine, problems can also arise.
Excess norepinephrine, for example, can cause small deposits of plaque to break loose and cause problems.
So it’s not a single factor associated with stress that causes heart attacks, it’s actually several things.
How to Lower The Chances of Stress-Induced Heart Attacks
One of the best measures of your heart attack risk is your cholesterol numbers, in particular, the ratios of the numbers. The ratio of your HDL to your triglyceride is one of the most important ones. Triglyceride levels of greater than 120 mg/dL and HDL levels less than 40 mg/dL for men and 50 mg/dL for women indicate small, dense LDL particles.
So, in general, your triglyceride/HDL ratio should be less than 2. Also your ratio of HDL/total cholesterol should be less than 24%.
But there are several steps you can take to lower your stress and improve your cardiovascular health:
- Exercise at least 30 minutes a day, 3-5 times a week.
- Eat a healthy diet with plenty of fresh vegetables and nutrient packed foods.
- Try to get at least 7 hours of restful sleep every night. (Magnesium can help you out there)
- Keep your stress levels low with these stress management techniques.
If you have a high-stress lifestyle, or a history of cardiovascular disease in your family, make an appointment with your doctor to get your cholesterol checked. They’ll be able to tell you how at risk you are, and give you some tips to keep your heart strong and healthy!