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Posts for: October, 2018

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 (,,,, 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.