As I’ve previously mentioned in earlier essays, coronary artery disease caused by the underlying disease of ATHEROSCLEROSIS is by far and away the Number One cause of dying per year in the United States. Death occurs most commonly by Ventricular Fibrillation with over 400,000 people dying suddenly, most of them with underlying coronary artery disease. Another million people will have heart attacks, which may or may not kill them, and they may also end up with Congestive Heart Failure, which can be treated, but can also lead to significant incapacity and death. (I refer you back to my earlier essay on HEART DISEASE which explains the underlying disease process of Atherosclerosis and how it can suddenly create a sudden event causing a Heart Attack (Myocardial Infarction). In fact, most of our efforts as Cardiologists, are based around, not only taking care of these emergency- based problems, but also trying to thwart the progress and ongoing development of Atherosclerosis so that it doesn’t cross over to the clinical expression of coronary artery disease).
So, this topic, is Public Health Enemy Number One!
An actual heart attack is referred to in medical language as a Myocardial Infarction, (or MI), and is divided into 2 subtypes: Acute STEMI (ST Segment Elevation Myocardial Infarction), or NON-STEMI.
This type of heart attack is the big 500-pound gorilla. A STEMI heart attack brings on a "full court press" at the hospital. When a patient arrives in the emergency room of any hospital with chest pain, they are triaged very quickly and evaluated if there is a heart problem. When an EKG is done- usually immediately-, and the EKG shows an ST elevation MI, very quick emergency protocols are triggered. This is all based on a concept called “ Door to Balloon Time”.
This means, that if a person is having an acute heart attack (myocardial infarction, or MI, with the findings of ST elevation in the ER, certain medications are immediately given, the interventional cardiologist is called as is the heart catheterization lab team, and everyone gets to the Cath Lab as quickly as possible!
The time sequence of entry into the hospital to the moment the artery is “ballooned” open is measured and must be initially under 90 minutes, and is now expected to be under 60 minutes. This is a national health policy and something every hospital is assessed on.
We at Hoag, on a quarterly basis, are usually at the 100% level!
The reason why this time interval is so important, is because “Time Saves Heart Muscle”.
In other words, when a total blockage of an artery occurs, there is no flow of blood going down the artery and the area of heart muscle cells that are fed oxygen and nutrients are suddenly deprived. As time goes by, heart cells start to get injured and begin to die off. The longer the time, the more degree of injury and eventual cell death.
If the blockage is high up towards the source of the artery, the greater the area of heart muscle at risk. The farther down the blockage is, the area would become relatively smaller, so the damage to the heart may not be as big an area of injury and cell death.
A non-STEMI MI, is also known as an Acute Coronary Syndrome (ACS). The presentation of the patient may be the same with chest pain and other symptoms, but the EKG does not show the ST segment elevation. It will show other EKG changes, but the bottom line is that this type of presentation does not usually suggest an acute blockage of a specific artery, and is not considered as being the same type of immediate emergency as the acute STEMI MI is.
In this regard, we would usually observe and stabilize the patient first with a variety of heart medications. Certain tests may follow including further EKG’s, lab tests, echocardiogram and nuclear imaging tests, or special CT angiograms, and if necessary, a heart catheterization study to do an angiogram. This may lead to further intervention with angioplasty and stenting, or even bypass surgery... or none of the above, and the patient is taken care of with the use of long-term medications. The reason for this is that the artery in this context is not usually completely blocked, and there may be various degrees of limited flow going through, and there may also be more complex coronary issues involving narrowing of other arteries.
Let me mention the immense skill, training, knowledge, and trouble-shooting capabilities of the Interventional Cardiologist, and the Cath Lab Team.
Firstly, because of the urgency to get to the hospital as fast as possible to “Get That Artery Open”, is a whole different story when an emergency occurs during the day , during regular “business hours” versus evening, night time, holidays and weekends. The stress level is very high. The On-Call Phone is always at your side, even if you’re going to the bathroom, or having a shower, or you’re trying to sleep in the middle of the night. When the call comes, you go, and you go as quickly as you can.
The doctor and the team are walking into a completely unknown situation, each and every time. Some of the issues are: how much time went by before the patient even showed up? What is the clinical stability of the patient? What is the intensity of their pain? What is the extent of the damage and the degree of heart failure? Is the blood pressure stable, or are they in cardiogenic shock? Are they having arrhythmias? Which ones? Are they having cardiac arrest and ventricular fibrillation? Do they need balloon pumps and other heart augmentation devices? (On many occasions we don’t even know who the patient is, or what the story was.)
Where is the culprit blockage? Which vessel? How complex is it? Does it involve one artery, or is it at a bifurcation of 2 arteries? How long is it? How many other narrowings are present? Can we get the wire passed? Can we get it through the blockage? How do we prevent the wire from perforating of dissecting the artery which can lead to death? How can we stabilize the heart rhythm when recurrent cardiac arrest keeps continuing?
Now I bet you are wondering WHAT IS AN ANGIOGRAM, ANGIOPLASTY, AND STENT? Click on the link provided to watch this video at your convenience (FYI- Skip the Ads)!. It does a good job of demonstrating what we do as cardiologists in the cath lab.
Here’s a Little Joke:
A mechanic is working on the engine of a cardiologist’s nice car. He had to change a valve. It took several hours. He was complaining to the doctor that he only made $75 an hour, and given the car he was driving, the doctor must obviously make more an hour than he did. Whereupon, the cardiologist said, yes I understand, but when I work on an engine, it’s running! (This is obviously an old joke because in this era, I think plumbers and mechanics are now actually earning more per hour than we are! LOL) ☹
WHAT YOU NEED TO UNDERSTAND ABOUT CORONARY ARTERY DISEASE:
Coronary artery disease does not necessarily always unfold with gradual plaque buildup to the point of blood flow compromise and then the artery finally blocks off. This does happen to many people and their presentation is often one of recurrent exertional ANGINA chest discomfort, and/ or the stress tests and echoes and scans will show abnormalities that will lead to an angiogram and then stenting or bypass surgery. These plaques that compromise coronary blood flow are fixed, rigid, and calcified.
However, the majority of people having an acute Myocardial Infarction do not have these very high grade obstructive narrowings causing that specific event.
These people have plaques that are not fixed, rigid, and calcified. They may not be impairing coronary blood flow at all. They may narrow the artery by 20% to 50% which is not sufficient to cause flow impairment. BUT they are VULNERABLE and INFLAMED and SOFT, and may become UNSTABLE.
I compare these plaques to “Creme Brûlée” because they have a “hard cap” filled with cholesterol and inflammatory products and they can unexpectedly and unpredictably FRACTURE or RUPTURE and when this occurs, the artery is acutely blocked and heart attack has begun.
Here are 2 stories where 2 people survived: One who got to the hospital quickly, and had restoration of blood flow through a blocked artery, and his heart function got back to normal, and he was given a new lease on life.
The other, did not get to the hospital quickly because he didn’t even know he was having a heart attack. Unfortunately, he has been left with a permanently damaged heart. However, with good medical care, he is still alive and doing pretty well, and he realizes how lucky he has been.
Both of these patients had “ruptured plaque”.
Patient # 1 is a 66-year-old man. He considers himself to be in very good shape and goes to the gym a lot and does a lot of weight lifting. He also rides his bicycle several times a week from the Newport Pier to the Huntington Beach Pier. However, he was noticing a sharp and aching pain to his left chest muscle area when he would lift himself into his bed. (It is a bed that is fairly high up off the ground, so he has to face the bed backwards, and use his arms to lift himself up). He also noticed the same pain when he moved his arms across his chest. He did not have any chest discomfort when working out, or when riding his bicycle.
I felt that he was having pain from strained pectoral chest muscles, from his weight lifting, and provoking it with his various movements and body positions. He did not have any pain or discomfort that sounded like angina when he was exerting himself.
However, this patient has risk factors including diabetes and high cholesterol numbers. He was not paying attention to his diet, and he was not on the correct doses of medications- when he took them. I referred him to a different endocrinologist, and I changed his cholesterol medications to get his levels into the correct range. I had him do a treadmill, and he exerted well, without discomfort, however, he did have non diagnostic stress test with non-specific abnormalities on the EKG. Therefore, we went on with a more precise study, called a nuclear imaging study.
All of his heart testing was perfectly normal.
Interestingly, right after he finished his study (which was normal showing no perfusion abnormalities that would indicate blockage), he went to have lunch with some friends. While eating he had the sudden onset of a heavy, crushing, quite severe central chest discomfort, associated with sweating. He never had anything like this before. His friends did not ignore this and drove him immediately to the hospital. His EKG showed an Acute STEMI.
He was taken immediately to the Cath Lab and the angiogram showed a total blockage of his major left coronary artery (left anterior descending artery). Though it may sound straight forward, the artery was successfully opened with a very good door to balloon time and it was successfully stented.
He went home 2 days later, and went on to full recovery (His initial left ventricular function was diminished due to the acute injury, but when we repeated his echocardiogram 6 weeks later, it was perfectly normal).
Though he initially blamed us for missing something, he demonstrated no insight into the fact that he never took his medications in a committed way and the control of his diabetes and cholesterol was, in fact, quite inadequate. He also had a hard time understanding the concept of plaque rupture! But many people have trouble understanding this.
Patient # 1 has not had a recurrence. He is still exercising, and is now on correct medical management involving good diabetes treatment, cholesterol numbers are very good with LDL driven well below 70, and he is on appropriate combination of anti-platelet medications (blood thinners).
Patient # 2 is a 70-year-old man. He was sent over to my office by his family doctor because he was short of breath, weak, tired, loss of appetite and energy, and he was in atrial fibrillation but was not at all aware of his heart beat. His heart rate was moving along appropriately, not too fast. His EKG was very abnormal, showing an anterior wall Myocardial Infarction, though he wasn’t aware that he had ever had a heart attack!
However, on questioning, he recollected that 8 days before, he was walking through the airport and he had upper mid abdominal and upper left abdominal pain that was quite severe. He actually went to a local Emergency Room and was found to have kidney stones. Because it was felt that the pain he was having was due to the kidney stones, no heart work up was done.
I explained to him that the EKG in our office showed he had had a heart attack, and that he was in CONGESTIVE HEART FAILURE, which was completely astonishing to him. He came back the next day for an echocardiogram which confirmed the story: profound weakening of the left ventricle! We measure the performance of the left ventricle which is called the EJECTION FRACTION (EF). A normal EF is from 50% to 75%.
His EF was only 16%! This means he was really in bad shape with very, very weak heart performance, and also with significant leakage of the Mitral Valve.
So he now had a completed event with full and terrible damage done to his heart. He was now in severe Congestive Heart Failure, by which he could die, and he was also at significantly increased risk of dying of SUDDEN DEATH by Ventricular Fibrillation.
He was immediately admitted to the hospital and started on all the appropriate medications for correction of heart failure, protection of life-threatening arrhythmias, as well as treatment for his atrial fibrillation, and appropriate lowering of his cholesterol.
He also had a heart catheterization (angiogram), and interestingly, we found that he had a single blockage of the left anterior descending artery (LAD) which had spontaneously reopened with what was now a 50% to 60% narrowing, so he did not need a stent.
What apparently happened, was that he had a plaque rupture blocking the artery causing the heart attack, likely when he was going through the airport, and by good luck, at some point the artery re-opened! However, not before very serious damage was done to his left ventricular function.
He went home on all of his new medications and he was given a LIFE-VEST that he had to wear all the time because of the increased risk of having a sudden cardiac arrest.
LIFE VEST AND ICD
The Life-Vest is an external defibrillator that you wear for several weeks before we are allowed to put in an Implantable Cardioverter Defibrillator (ICD). In some people we will see an improvement in heart function over a 6-week period, so they do not require a permanent ICD, whereas other people continue to have problems with weak hearts and heart failure and they require an ICD for hopeful prevention of sudden death, and in some cases further therapy for correction of heart failure. The ICD detects life-threatening arrhythmia and will shock the patient hopefully back to normal rhythm if the arrhythmia reaches predetermined thresholds that indicate a life-threatening situation.
(The topic of Sudden Death and the development of the Implantable Cardioverter Defibrillator (ICD) is an entirely separate essay as is the topic of Congestive Heart Failure)
He continued to have problems with breathing, exhaustion, weakness and his heart function over this period did not improve, so he, in fact, received a very special device which is a Bi-Ventricular ICD. This ICD not only treats and terminates life threatening arrhythmias such as Ventricular Tachycardia, and Ventricular Fibrillation, but also paces the heart in both left and right ventricles, and may improve heart contractility and improve the clinical problem of congestive heart failure.
Two years later, he is alive and doing pretty well. He is able to walk now without shortness of breath, and in fact, says he feels pretty well. His heart function has improved but not up to normal range. He still has some weakness of his heart, but his life quality is quite good and he is extremely grateful.
Each patient who has a heart attack is unique and each one is an individual human story. I have given you a picture of the enormity of what we face with CORONARY ARTERY DISEASE and MYOCARDIAL INFARCTION. Heart Attack can be a devastating HEALTH ATTACK and can completely change your life or take your life.
Please refer back to my earlier essays on Heart Disease, Lifestyle, Hypertension, and Statins. These essays will explore many of the topics touched upon in this essay, and will give you further insight into the importance of what we do for disease prevention, as well as provide encouragement for good health.