In late July 1992, on a Friday morning, I was at work when I began to feel some strange sensations: a cold sweat, a feeling of acid indigestion, but with no acid taste when I swallowed, and a slight ache in the right shoulder blade, like I'd overdone the lat pulldowns at the gym the day before – except I hadn't been to the gym all week. That was because I'd been out with gastrointestinal problems, leading to a complete physical, including EKG, that Wednesday. My doctor had just called to tell me that the results had shown me to be in great shape.
So I drove across the road to the main building to see the nurse. She checked my blood pressure, which was slightly higher than normal – I'd had it checked regularly there so they had a record – and gave me some oxygen. She said she didn't think it was anything serious, but if I wished she could have the rescue squad check me out. I imagine that there are people who feel worse than I did every day, but it wasn't normal to me, so I said OK.
The rescue squad arrived, tested me with a portable EKG machine, and said they didn't find anything wrong, but if I wished they could take me to the hospital. Since I wanted to find out what was the problem, I said yes. So they strapped me to a gurney and wheeled me out to the ambulance, which was parked in front of the building with the flashers going, to the curious stares of those on the upper floors. There was no rush, so they obeyed the speed limit, stopped at red lights, and eventually arrived at Arlington Hospital.
The advantage of arriving in an ambulance is that there is no red tape at the front desk, and I was immediately wheeled into the treatment area. They hooked me up to a full-fledged EKG machine and in a moment a doctor rushed over and asked me if I knew I was having a heart attack! I said no, although I knew I was experiencing something unusual. I still don't know why the rescue squad didn't detect it – whether their device didn't have enough leads or they weren't skilled enough in their placement. The symptoms were exactly the same throughout.
At the time, my company's health plan was fairly liberal; since then, if you go to an emergency room and it isn't justified, they won't pay. I wonder how many people, having been reassured by a company nurse and a rescue squad, and realizing the substantial potential cost of an ambulance trip and an emergency room visit, would just decide to forgo it.
What I've learned since: a heart attack (or Acute Myocardial Infarction, AMI) is often caused when a blockage caused by plaque buildup on the walls of an artery nourishing a heart muscle causes enough turbulence that the body's defenses think it's being attacked, so it generates a clot. A clot is pretty tough – it includes a mesh network that isn't easily breached, requiring a potent agent to dissolve it. In fact, such agents can also eat through weakened arterial walls, and can't be used on people who have had recent surgeries.
The doctor asked if I was willing to participate in a trial to compare two clot dissolvers. This was known as the GUSTO trial that seemed to indicate that tPA was marginally better (although substantially more expensive) than the previous choice, Streptokinase.1 I asked if he thought one was better than the other, and he said he had no reason to think so. I also asked if one of the possibilities was a placebo – my sense of humor was still intact. Appalled, he exclaimed "NO, NO, NO!"
I agreed, and I found out later that I had received Streptokinase. It worked fine in my case, dissolving the clot a few hours later – I could tell, when the symptoms disappeared. Since it was now Friday afternoon, and my condition had stabilized, they recommended scheduling an angiogram, or catheterization, for Monday. This involves threading a small tube through the artery in the groin to a point near where it supplies the heart muscles and releasing a dye that is opaque to low-dosage X-rays, which they use to monitor the results.
I asked the cardiologist about the risk of the procedure, and he said it was 1 fatality in 1,000. That sounded like pretty good odds, particularly since those in the population referred to were most likely in worse shape than I was. I was 52 at the time and had been regularly running and visiting the gym for over 20 years.
The angiogram showed that I actually had two blockages, one of 90% and another of 95%. The 90% blockage was in a serious location; at the top of the left anterior descending artery, which supplies blood to muscles of the left side of the heart, including the left ventricle. This powerful muscle pumps oxygenated blood from the left ventricle to the farthest reaches of the body. (The right ventricle pumps returning oxygen-depleted blood to the nearby lungs to be oxygenated.)
Such AMIs are nicknamed "widow makers" – an unnecessarily narrow connotation, because I later learned that a woman of similar age and physical condition had also entered with a similar AMI. I had experienced no symptoms, even while running the previous week, but I later read that even a 70% blockage was said to result in pain during exertion.
It seems that what happened in my case is that as the blockage gradually increased, collateral circulation built up around it 2 during running, and in the end the difference between 90% and 100% wasn't that much. The 95% blockage was at the lower part of the same artery. (See below for how it was determined which blockage had resulted in the clot formation.)
I have a copy of the videotape of the X-ray video, which shows the thin black dye stream suddenly decreasing to the size of a pencil lead as it passes through the narrowing.
The next day, allowing time for the dye to be flushed out of the body, they recommended a balloon angioplasty (also called Percutaneous Transluminal Coronary Angioplasty: PTCA). This is similar to the angiogram but with a balloon on the tube, which is inflated at the sites of the blockages, expanding the interior of the artery to its normal diameter. (Today this is often the way they immediately treat a heart attack on arrival.)
This time the cardiologist said the risk was 1 in 100. As a statistician, 99% odds had always sounded very good, but when it's your life involved, you think about it a little more. I asked how many such procedures he had done, and he said over 300, so I figured he'd had enough practice to be pretty good by now.
Since I was conscious during the procedure I could verify that the symptoms I experienced during the inflations corresponded to the site of the 90% blockage.
I'd read that in about one-third of the cases the artery shrinks again (restenosis), which is one reason stents were later developed. However, my cardiologist said that it depends on the skill of the practitioner, and that his restenosis rate was much lower than the average. Also, stents are foreign bodies and can present their own concerns.
In any case, restenosis hasn't occurred, at least according to annual treadmill stress tests since then. Of course, I never had a stress test before the AMI, so the results can't be guaranteed.
As for how much damage was done, one measure of heart function is the left ventricular ejection fraction, which is the ratio of the blood that is ejected from the left ventricle to the total left ventricular volume. Fifty percent is average; below about 25% gets pretty serious. Mine was 65%.
Another measure can be provided by a Doppler echocardiogram, which shows how much the heart walls are moving, after a treadmill stress test. The test involves walking, perhaps eventually running, on a treadmill whose speed and incline increase every three minutes, until one can no longer continue. The Doppler displays the rapidly-moving heart walls in various intensities of white; damaged areas appear black. After my first stress test, it showed a loss of about 8% of heart muscle.
It's now been over twenty-five years and although damaged muscle theoretically can't regenerate, my recent stress tests indicate the opposite. My cardiologist says my echocardiogram looks normal today.
1 GUSTO stands for Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries – you can see why it was abbreviated. However, later trials with much larger populations actually showed no difference in effectiveness.
In any case, these days the preferred treatment is to immediately implement balloon angioplasty, when the proper facilities are available, which includes having a heart surgeon on duty in case of complications.
2 Unfortunately, vascular endothelial growth factor (VEGF), the molecule that encourages the blood vessel growth of collateral circulation has a darker side. It can cause the growth of abnormal blood vessels under the macula of the eye, which can leak blood and fluid that can scar or detach the macula, leading to loss of central vision, a devastating condition.
Fortunately, medications recently have been developed that bind with the VEGF molecule and can halt and even reverse its progress if the condition is caught in time. Unfortunately, medication is delivered by an injection directly into the eyeball! The eye is deadened, but the surface is quite resilient, and the pressure to pierce it can be quite uncomfortable.