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Realizing what arteries do...

 

If we take the wayback machine to well... wayback, people didn’t know how the heart worked, what arteries do or even that their dysfunction could cause disease. Of course, people have been talking or writing about arteries for millenia. At first, arteries weren’t really seen for what they are. They were felt as the pulse. Chinese physicians pored over the pulse to seek any clue to internal disquiet. Was it fast, slow, regular, irregular, strong or weak? Did it push hard or simply tap and how did it change? Greeks physicians were equally interested but only briefly and moved on to other pursuits. On both fronts, there were some interesting observations. They gave pulses a host of clever names (some of which we still use) and realized that something about the pulse was important. They just were not certain exactly what that important thing might be.

 

The general sense of things (in this discussion, things are the heart and arteries, mostly) went something like this. From food and air, our bodies somehow distilled an essence that fueled life. This mixed in blood which contained life’s most basic and necessary essence. Blood moved, partly of its own accord. It animated the body and provided the fuel for physical activity. In doing so, blood also provided the essential nature of what we are, how we feel and behave. The dispensation of life into the body could be felt in the pulse.  The heart was somewhere in this mix. Exactly what it was doing wasn’t completely clear. Altogether, this scenario is pretty decent guesswork, considering that there was not a wealth of information to guess from.

 

Leonardo looks for life and points at arteries

 

Fast forward to the Renaissance. By this time, most people who were interested in the human body had taken the old understanding of how things worked and found the explanations to be seriously wanting. In part, this was because many of the “experts” expounding upon how things worked liked to sprinkle their writing with personal opinion and some seriously bizarre ideas. The weight of crazy so badly encumbered explanations of the natural world that the scientific method of thought was born. Scientific method meant that if you wanted to put forth an idea, you had to let other people–who might not buy your explanations or even like you–test it and make fun of you when you were wrong.

 

Leonardo da Vinci (just Leonardo apparently) was of this time. In some respects, he probably is the best representative of this time, in that he observed, he described  and he explored ideas by putting them to the test. One of his most important contributions to the new way of thinking was to accurately describe normal and variant human anatomy. His beautiful drawings capture his exploration of the mechanics of how and why different parts of us work as they do.

 

At the time, there was a general understanding that blood moved through the body with arteries as the highways. The heart was in some way integral to the process, but the mechanics were a mystery. In Leonardo’s drawings and writing concerning circulatory anatomy, it is clear that he knew of heart valves, that blood really went in only one direction and that arteries were responsible for the distribution of energy. With energy, he included the body’s heat, the still undefinable essence of life  because it was all too clear that, should blood escape through an open artery, the heat of life would go with it.

 

Famously curious and undoubtedly consulted to explain any mystery, Leonardo’s interest was piqued when he was offered the opportunity to examine an old man who had died peacefully. His purpose was to find where life’s heat escaped at a peaceful end. He examined the anatomy in great detail and reported his observations and musings. From the many observations, one stands out as the beginnings of an idea. Leonardo reported that the supple, straight vessels of youth had been thickened, gnarled, and bent with age, leaving little room remaining for blood.

 

In today’s world, we would interpret this description as evidence of arterial disease. The old man died peacefully, probably having a heart attack as he slept. Thickened and deformed arteries probably signified more than simply age, but also atherosclerosis, the disease of arteries that plagues so many of us. No one really knows what conclusions Leonardo drew from his observations about arteries. He may very well have believed that part of our aging is an attenuation of the channels blood can take to keep us moving and alive. What is most important is that his observations represent the the first inkling that arteries might fail of their own accord and cause disease.

 

Within a relatively short time (in historical terms) arterial failure would be seen more clearly and blamed for an odd type of chest discomfort that eventually became known as heart attack.

 

The question

A short time ago, my email inbox contained a query from one of those online information sites. The question posed was, “Do stents prevent heart attack?” My initial impulse was to ignore the question altogether. It is too broad and too general for a simple answer. But then again, it is exactly what most people who are worried about coronary artery disease would like to know the answer to. What makes the question so difficult is that the answer is different, depending upon your perspective. This was my attempt at a reasonably complete, but concise answer.

 

The short answer

Yes. Without question, placement of a stent is an important part of the treatment options to prevent a heart attack. However, the complete answer is important.

 

The long answer

A stent is used to reduce narrowing, open an artery and improve blood flow to heart muscle. For everything, there is a season and for the stent, that season is when the heart is in need of rescue.

 

In order to review the idea of rescue as it pertains for stents, two major concepts require definition. They are angina and stability.

 

Angina pectoris:

A narrowed artery to the heart may cause symptoms of chest discomfort during physical activity, with anger or other types of emotional stress. The particular type of chest discomfort (an uncomfortable uneasiness that doesn’t always hurt) is called angina pectoris, or just angina. The symptoms usually mean an artery is narrowed, but don’t tell you what the narrowing is made of.

 

Stability:

When people experience angina, the discomfort may follow different patterns. The pattern of symptoms provides a clue as to what a narrowing that is causing the symptoms might be made of. Symptom patterns are generally condensed for descriptive purposes.

To the point of our discussion, some people have discomfort that they have noticed for at least two or more months. The discomfort is fairly consistent in its return with repetition of specific physical activity; for example walking up a hill or sweeping a room. This is called stable angina. “Stable” symptoms, or stable angina, is usually an indication that the narrowing responsible for the symptoms made of scar tissue. Scar tissue is relatively dormant and unlikely to change rapidly causing a heart attack.

On the other hand, some people experience symptoms that they have never felt before, that come on for no reason, or keep going away only to return slightly worse. These symptoms are said to be unstable. Unstable symptoms suggest that a blood clot is part of the narrowing responsible for symptoms. Blood clots are unpredictable, prone to grow very rapidly and are the cause of most heart attacks.

 

The important point is that the pattern of symptoms, stable or unstable, provides the indication as to whether or not a heart attack is threatened.

 

People who have stable symptoms are not facing imminent harm. Stable symptoms that are encountered only during time of great effort are easily managed. On the other hand, some people with stable symptoms find it difficult to shower and groom in the morning without stopping to rest. A person who is so limited, even after trying medication, may seek a rescue from his or her disease-imposed prison. By restoring blood flow to heart muscle and relieving symptoms, a stent may hold the key to that prison. This is very much a rescue and the proper use of a stent. However, the use of a stent for this purpose does not prevent a heart attack.

 

People who have unstable symptoms face the threat of a heart attack in the very near future. In fact, in some, the unstable symptoms are an indication of a heart attack that is under way. Since the heart is being damaged by a misbehaving artery, it is in need of rescue from harm. This is the type of rescue where a stent can stop or prevent a heart attack. Unstable symptoms fall into three major categories.

 

ST-segment Elevation Myocardial Infarction (STEMI) is a heart attack that is immediately apparent on an EKG. The diagnosis is recognized while damage is underway, triggering emergency treatment. Medicines that dissolve clot (Thrombolytic drugs) can be given very quickly. In hospitals with the capacity to perform emergency angioplasty, a balloon procedure and stent placement is preferred over thrombolytic drugs.

 

Non-ST-segment Elevation Myocardial Infarction (NSTEMI) is a heart attack that was not apparent on an EKG and recognized only after the fact by finding blood-test evidence of heart muscle damage in someone with unstable symptoms. Thrombolytic drugs are not useful, but rescue treatment with other medications, stents or sometimes surgery may be necessary to prevent additional damage and to speed healing.

 

Unstable Angina (USA) refers to unstable symptoms without evidence of a heart attack on the EKG or blood testing. The evidence of an unstable artery in need rescue is the discovery of a severely narrowed coronary artery that explains the unstable symptoms. In someone with unstable angina, placement of a stent, in addition to equally important medical therapy (cholesterol lowering, blood pressure control, diabetes control, aspirin and related drugs) unquestionably prevents heart attack.

 

For more information, stay tuned for “Heart Attack: The science and the story of what it is, why it happens and what to do about it.”

 
 

I know that this is a pretty broad question. Therefore, I would like to start by setting my boundaries. First, I would like to take the question from a big picture perspective because that approach helps to understand most of the recommended preventive efforts and treatments. Second, I want to be clear about the meaning of coronary artery disease. Three arteries ring the top of the heart like a crown, giving them the designation coronary, from corona. Any illness that affects these arteries is reasonably called coronary artery disease. But, let’s not ignore the elephant in the room. One disease will affect ⅓ to ½ of us in our lifetime, loves the arteries of the heart and, most importantly, causes heart attacks. The disease is atherosclerosis, a corrosive scarring of the arteries, and almost any time someone says coronary artery disease, that is what they mean.

Atherosclerosis is a disease in the sense that it causes illness and suffering. However, the source of the problem is, to a great extent, in how we are designed to process and store what we eat and maintain our arteries. As most of us make the morning navigation to work, we mull over thoughts of success that center on peace, serenity and financial security. Mother nature sees things from a different perspective than you and I. From the biological perspective, success is navigating our hostile world long enough to reproduce. That is the target of our design and the goal of the genes that help to make us who and what we are. The genes that have made us such a rousing success developed under much different circumstances than we face today. In a hostile world, with scarcely enough to eat, full of predators, large enough to eat us and too small to be seen, those genes carried primitive people through their twenties and thirties, long enough to be fruitful and multiply.

Generally speaking, people are made to survive frequent hardship, long walks looking for food and long times without it. Weather was to be endured, abundance enjoyed and water kept in convenient reach. These were the challenges to be overcome for success and we are well equipped. We have long legs, can eat almost anything and store energy with great efficiency. However, our most important advantage is not physical.

We have the ability to learn, individually and collectively. We can make tools, build houses and, most importantly, write everything down. This advantage brings plentiful food, treatment for infections and longer lives. Under these conditions, our biological design for self-preservation misfires in many forms of cardiovascular disease such as high blood pressure and coronary artery disease. In essence, our heart and arteries are designed to maintain themselves under a set of difficult conditions and last a lifetime. With all of the success born of cumulative learning, we have moved outside of the conditions that shaped us and changed the duration of a lifetime.

Modern society lets us survive long enough to suffer from atherosclerosis and modern technology lets us see it. At any given time, more than 15 million people in the US have symptomatic atherosclerosis. It affects the heart most famously, but can also cause stroke, loss of limb, damaged kidneys and dysfunctional intestines. Of the 1 million people who will have a heart attack this year, almost all are over 40, an age seen by a lucky few of our primitive ancestors.

Atherosclerosis is very much affected by the body’s energy metabolism. It strolls along happily with obesity and inactivity. Obese and inactive adolescent children may already have arteries that misbehave. Their arteries may not be diseased at that young age, but measurable misbehavior is believed to be one of the first steps toward disease. By the age of thirty, some people may have an abnormal appearance of the arteries on an angiogram. Most heart attacks occur much later in life, meaning that this disease starts early and may be present for a very long time before it starts to cause problems.

Atherosclerosis can remain silent for so long because it is alive. Unlike the debris in a clogged drainpipe, atherosclerosis is in constant negotiation with the walls of arteries, forcing them to adapt to its presence. Baudelaire said that the “finest trick of the devil is to persuade you that he does not exist”. Atherosclerosis has mastered this trick as well. Arteries accommodate disease in their walls by enlarging so that blood flows freely. Each step that may help atherosclerosis along does not exact immediate restitution, but lays claim much later, when the arteries can no longer accommodate. Fortunately for us, atherosclerosis is the rarest of all biological cats. By addressing the root cause of disease, we can put it back in the bag… at least part way.

The processes, actions and events leading up to a heart attack are partly determined by our inborn programming and partly by the life that we lead. The almost universal coexistence of plentiful food and heart attack lends credence to the misunderstanding that atherosclerosis is simply a penalty for each moment spent enjoying a cup of coffee and a donut. The truth is a bit more complicated. We each live within a design that dictates how we store energy from food, distribute salt and water, fight infection and function physically. Our design was shaped under different conditions from those that we presently encounter. As a result, many of us may encounter difficulty as we age because the lifestyle that has become normal combines with our design to steer a course that will end in decay of our arteries. For most of us, the inherited parts of our design that predispose to atherosclerosis and heart attack are not genetic errors. They are built-in safeguards for times of need. In a different setting, of environment or of food availability, these tendencies may be advantages for survival. In times of plenty, they are not.

Preventing or treating atherosclerosis requires realignment of modern lifestyle with our design. Alignment with design refers to all of us in a general sense as well as each of us specifically. We do not all share the same inheritance. Therefore, the prescription to align with our design will vary from person to person.

More on coronary artery disease can be found in the educational booklets for CAD and Heart Attack here.

Aspirin prevents heart attacks. I know that you may find this jaw-dropping, but it’s true. On the other hand, you may have seen some recent information that was published in the New England Journal of Medicine that casts doubt on the value of aspirin. Before rushing to a conclusion, let me give you a bit of background. The “new” information about aspirin isn’t really new. However, it is very useful to stimulate discussion about the proper use of this amazing, and sometimes dangerous, drug.

 

What does aspirin actually do?

 

Let’s begin with the fact that aspirin is not really a treatment for the disease that corrodes your arteries. It is a last gasp to keep an artery from closing after the disease has gotten very, very bad. What happens is that the body has to send fat around to all of its parts for use as energy and some other things. The packets that carry the fat around get stuck in the artery walls and constantly irritate, like a stone in your shoe. The body’s response to these irritating little packets corrodes the arteries. Too many packets floating about or arteries where the packets can easily get stuck are the cause of the disease. After the artery has been back and forth trying to rid itself of these fat packets for quite some time, corrosion sets in and eventually a blood clot can form. The blood clot is the final straw to close the artery. Aspirin keeps blood clots from forming properly. That is not a genuine fix. It is not really treating the underlying problem, but when facing the danger of a heart attack, it is better than nothing.

 

“More doctors smoke Camels than any other cigarette”

 

In 1949, this was a real ad and it wasn’t the only one of its kind. No one knew what caused coronary artery disease. However, it was accepted that the final event of coronary artery disease, a heart attack, was due to a blood clot that formed in the arteries that feed the heart. At the time, most people with symptoms of coronary artery disease would suffer a heart attack within five years after symptoms began. Most people died of their disease after about ten years. The heart attacks and the deaths were clearly tied to abnormal blood clotting, but there was nothing that anyone could do about it.

 

Under these circumstances, a California physician named Craven took notice of several small articles about bleeding problems after surgery in people who used aspirin. He reasoned that, if an innocuous drug like aspirin made surgical wounds bleed, it would also prevent blood clots from forming on their own in the coronary arteries. His ideas did not gain much traction. He experimented with his own patients and felt that his efforts were successful. He offered the evidence from his observations. However, it would take another 20 years for aspirin’s effects upon blood clotting to be put to regular use.

 

By the 1970’s, the treatment of coronary artery disease and heart attack remained very limited. Dr. Craven’s ideas had become mainstream and aspirin was tested for the treatment of people with symptoms threatening a heart attack. It was wildly successful and represented a major breakthrough. Aspirin did not help resolve symptoms, but it appeared to keep them from progressing to the point of a full blown heart attack. It also saved lives. However, outside of the people with symptoms of a threatened heart attack, the value of aspirin was not quite certain at first. Survivors of heart attack who continued to use aspirin for long periods of time did not seem to really gain anything. As a result, no one knew if the average person who just wanted to avoid a heart attack should use aspirin.

 

The question was put to the test in the Physicians’ Health Study that began in 1982. This was an enormous study of mostly men who presumably followed reasonable health habits (we physicians are really only marginally better than everyone else) and would be compliant with a study protocol (see earlier comment). Aspirin worked. In fact, it worked very well. However, the qualifying statement is to remember when this study was done. The basic forces causing coronary artery disease were not really being treated effectively.

 

So what has happened?

 

In the New England Journal of Medicine for October 18, 2018 (https://www.nejm.org/doi/full/10.1056/NEJMoa1800722, https://www.nejm.org/doi/full/10.1056/NEJMoa1805819, https://www.nejm.org/doi/full/10.1056/NEJMoa1803955, https://www.nejm.org/doi/full/10.1056/NEJMoa1804988), several large-scale studies took aspirin to task and strongly suggested that we rethink its use to prevent heart attack in people who are otherwise reasonably healthy. In older people (>65-70) or people with diabetes, people that often consider themselves at risk of suffering a heart attack, aspirin was a bust. Aspirin may have prevented some problems that we know to be the result of blood clots. However, aspirin caused as many other problems that we know to be the result of bleeding that it harmed as many people as it helped. In short, if you are reasonably healthy and want to do something to lower your risk of death or disability due to heart attack, aspirin is not your best option, or even a good one.

 

How is this possible? How could something so cut and dried look so different now. Well, between then and now, we learned and got better tools to prevent heart attack. In 1990 effective cholesterol-lowering medicines became available. By 1997, cholesterol could be lowered very effectively and the treatment of diabetes became more sophisticated. Ask anyone on the street their cholesterol number and almost ½ will know the answer. Many of them will already be taking steps to address it. In fact, in the studies addressing aspirin’s potential benefit for reasonably healthy people, roughly ⅓ were taking cholesterol lowering medication. Almost ¾ of the diabetics were on such medicine. And not many people were smokers.

 

If the disease that corrodes arteries is prevented by not smoking, cholesterol lowering, diet and effective treatment of diabetes, aspirin may have less to offer than it did in the past.

 

Does this mean aspirin doesn’t really work?

 

The answer to this question is a resounding NO. Aspirin is a tool that, applied properly, performs admirably. The message of these new studies addresses people who do NOT have known disease of the arteries. That means that someone who already had coronary artery disease, a prior heart attack or stroke, or peripheral arterial disease was not asked to participate. Only people who were interested in preventing their first episode of heart disease were studied. There is no question that aspirin and medicines like it remain an important part of the protective medical regimen for anyone with definite arterial disease. On the other hand, if you are among the worried well and want to avoid heart attack, the right answer is diet, exercise, not smoking and a periodic meeting with your doctor to evaluate your cholesterol and blood sugar.


 

Stress Cardiomyopathy, also known as Takotsubo Syndrome, and its related syndromes are most likely a toxic injury to the heart, resulting from a brief but profound, high intensity exposure to adrenalin or noradrenalin. These events have been most closely associated with circumstances, illness and injury that would be expected to activate the body’s self-preservation system. In lesser degrees, fear, anger and anxiety can create symptoms that mimic heart attack, without EKG change, blood evidence of injury or abnormality on any type of testing. In the past, and still unfortunately in some forums, these events have been referred to as panic attacks. This misnomer promotes the misunderstanding that this sometimes crippling disorder is in some way under direct conscious control.

Considered in full, our protective behavior is layered from the very basic pain response to the intricacies of imagination and anticipation. At the very basic level is sudden withdrawal from pain. No thoughts are required to guide this action, though they may follow in the awareness of pain. Far more complicated is the subtle discomfort of fear, driven by nothing more that thought. Fear accompanied by visceral symptoms, like sweating, breathlessness and nausea may be triggered by nothing more than anticipation of an uncomfortable situation.

A sensation perceived as threat is processed in an area of the brain called the amygdala. It is the point of communication between rapid, unconscious response and the thinking brain. As a rapid response to pain or threat is carried out, the amygdala invokes base emotional responses to color conscious thought.

Some of this response is probably hardwired. For example, in all but the most thoroughly conditioned, sudden changes in environment, a blinding flash or the peal of thunder provoke a startle. Fear is triggered. A physical response begins. It may be quickly aborted, but it is very difficult to prevent initiation by a typical trigger. Consider the sensation after a near miss on the freeway, when only a quick twist of the wheel avoided certain collision. The act was not truly deliberate. In its aftermath, the event is consciously replayed, the after effects are recognized as adrenalin’s effect wanes and fear is acknowledged.

Individuals with repeated exposure to unpleasant surroundings may become inured to flashing lights and loud sounds so that startle does not occur. Therefore, the process of the, almost reflex, emotional response can bend to conditioning. It is conditioning or modification of the process of a different sort that can become a health problem. Traumatic events carry memories of associated sights, sounds and smells. Conscious replay of events may attach seemingly innocuous sensory input to a perceived life-threatening or traumatic event so that the short path to emotional response is triggered inappropriately, even unconsciously. In addition, the pathway to emotional response may activate with no outward cause. No prior conditioning, no bad experience, in fact nothing at all is needed for this response mechanism to take on a life of its own. When this occurs, bouts of rapid heart rate, hunger for air, sweating, blood pressure elevation and chest discomfort can develop, seemingly out of thin air.

For many people, the symptoms of the fear/anxiety response become like a seizure disorder. They may be completely unpredictable, occurring at home, in public, alone or with family. They may occur while awake or awake someone from sleep. To the affected, the sensations are indistinguishable from severe illness with the threat of death. The conscious mind is indeed seized by the more dominant emotional center producing events that have escaped control. The discomfort is real. The changes in the body’s physiology may be so profound that, without testing, it can be impossible to distinguish such an event from an ongoing heart attack.

In 1871, Dr. Jacob Da Costa, a physician active in the American Civil War, recorded the symptoms of hundreds of soldiers who were crippled by bouts of breathlessness, palpitations, fatigue, sweats, nervousness, and dizziness. Their illness clearly arose from war experience, yet no measurable abnormality could be found. He described the appearance of the suffering veterans in the throes of these events, and afterwards, as that of someone engaged in severe or exhausting effort. Da Costa’s observations were quickly dismissed and forgotten. Many years later, the symptoms, findings, and experience collected by dedicated, scientific study would reawaken interest in this phenomenon. It then received the name "Da Costa’s syndrome". Unfortunately, the concept still did not find firm footing in the medical lexicon. Names like neurasthenia, nervous exhaustion, shell shock, soldier’s heart, panic and anxiety disorder were bandied about. The disorder Da Costa described is an abnormality in nervous function that can be primary or triggered by external stressors. It is genuine, organic, and treatable. Therefore, patients are best served if we use the name DaCosta’s Syndrome in preference to the pejorative, Panic Attack.

The sensations and outward appearance of the affected individual very closely simulate a heart attack. They may occur in response to specific sights, sounds, smells, or situations. When part of another disorder, such as Post-Traumatic Stress Disorder, the triggers may be very specific. However, when the disorder is primary, there may be no trigger. Episodes occur at random and may wake some people from sleep. Anyone may be affected. I have taken care of firefighters who can face a burning building, yet are still troubled by these episodes with no recognized trigger. Unfortunately, there is no test to be certain of their presence. All other sources of discomfort must be ruled out before settling upon DaCosta’s syndrome as the cause of symptoms. On the other hand, there are effective treatments. Several medicines, particularly those affecting serotonin use in the brain, are useful and not habit-forming. Behavioral therapy may also be effective and eventually allow withdrawal of medicines. All should be coordinated with the help of a physician.





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