chest pain…now what

Tuesday, November 22, 2016

Bruce Arians, the Arizona Cardinal coach, had an eventful weekend and ended up batting .500 with a loss to the Vikings and a win for his heart. After returning home, he developed chest discomfort and rightfully so, made his way to the ER where tests were done to sort out the cause of the chest pain. Rightfully so, because the medical world spends lots of time, effort and money to convince people that chest pain is not normal and potentially could be deadly. Getting chest pain checked out is not something that should be delayed.

Once you get to the hospital, the science of diagnosis mixes with the art of medicine and a healthy dose of Las Vegas probability gets thrown into the mix to decide how much or how little needs to be done to make the diagnosis. If a heart diagnosis is suspected the full force of hospital technology may come raining down on the patient. It is just the suspicion of atherosclerotic heart disease (ASHD) also known as coronary artery disease (CAD) that sets events in motion.

The first step in sorting out chest pain is taking a history. It is the story of the pain that is most important: what it feels like, what brought it on, where it radiates, and whether there are other symptoms including shortness of breath, sweating or nausea. The doctor may try to find risk factors for the patient having narrowed arteries: is there a history of high blood pressure, high cholesterol, diabetes or smoking? What about family history? Or does the patient have a previous history of heart attack, stroke or peripheral artery disease.

If, after taking the history and examining the patient, the doctor thinks that the pain is not cardiac, then the story ends there. Of course, there are other killer causes of chest pain that have to be considered, including pulmonary embolus (blood clot in the lung) and aortic dissection (tearing of the main artery as it leaves the heart), but if the story is not consistent with major disaster, clinical skill allows the doctor to diagnose and treat other things that can cause chest pain, from chest wall injuries to pneumonia to reflux esophagitis.

But if there is worry that the cause of the pain comes from the heart, the next step is an EKG to look for signs of a heart attack. The heart is an electrical pump and if narrowed arteries can’t supply enough blood, that part of the heart conducts electricity differently and those changes can be seen on the EKG tracing. A heart attack means that a blood vessel is completely blocked and the next step is opening the artery either with clot busting drugs or a trip to the cath lab where a cardiologist can open the artery with a balloon and place a stent to keep the artery open.

If the EKG is normal, the next step is to look for heart muscle that is under stress; perhaps an artery not completely blocked but narrow enough not to get enough blood to meet the muscle’s needs so that it begins to ache or hurt. Blood test can measure chemicals (troponin) leaked from heart muscle cells that are irritated, but it takes at least 4-6 hour for troponin to accumulate in the blood to be detectable. Most often, people arrive in the ER within that time frame, so one troponin test begets another beyond that 4-6 hour to make certain the test remains normal.

If the EKG and troponin are normal, the worry is not yet done. Perhaps the heart artery is narrowed enough to cause pain but not narrow enough to cause damage. That might mean a patient at risk for a heart attack in the near future. The next step is imaging and stressing the heart. This testing may be done immediately but can also be safely delayed f0r 24-48 hours. And there are numerous ways to look at the heart, from a stress test on a treadmill, to chemical stress tests, to stress echocardiograms (ultrasound of the heart) and CT or MRI of the heart and finally, the gold standard, heart catheterization, the same procedure used in a heart attack but this time used to look for a narrowed artery.

Chest pain is a big deal because one only gets one heart and it has to last a lifetime. Showing up to a doctor’s office or ER complaining of chest pain will most likely get you to the front of the line. Aside from dying, that heart muscle can be electrically very irritable and puts the patient at risk for sudden death from ventricular fibrillation, a fatal heart rhythm. While Cardinal fans bemoan the loss of a football game, Coach Arians came through with a bigger win later that evening and lived to have his team play another Sunday.


This entry was tagged , , , , , ,

hypertrophic cardiomyopathy

Tuesday, March 10, 2015

Anniversaries allow memories to be rekindled and sometimes, introspection regarding what might have been. Perhaps 25 years after the sudden death of Hank Gathers allows another look at the philosophy behind how society decides to spend its resources and how much it’s willing to invest.

Hank Gathers was an elite basketball player for Loyola Marymount University and during a game collapsed and died, the victim of hypertrophic cardiomyopathy, ventricular fibrillation and sudden death. The anniversary of his death has reopened the ongoing discussion of how we screen athletes and potentially prevent future tragedies but the decision making is murky at best.

Hypertrophic cardiomyopathy, or HCM, is a genetic disorder, where part of the heart muscle becomes thickened and may affect the ability of the heart to pump block to the rest of the body. It can affect the function of heart valves but perhaps the most frightening problem is the potential to develop life threatening heart rhythms, ventricular fibrillation and ventricular tachycardia, that cause sudden death. HCM is the most common cause of sudden death in young adults. Abnormal muscle fibers potentially conduct the heart’s electricity abnormally and the “short-circuiting” may cause the fatal heart rhythm.

HCM is relatively uncommon, occurring in about 1 in 500 people. The severity of disease depends upon where the muscle thickening occurs within the heart and how abnormally thick that the muscle becomes. Most people are unaware that they have the disease and have normal life expectancy. For those with significant disease, between 10-20% of those with HCM, aggressive exercise can precipitate symptoms including fainting (syncope) shortness of breath, chest pain and the big deal…sudden death.

The question becomes, how we screen people to find HCM, especially in athletes and hopefully prevent sudden death. History and physical examination is not great at finding the disease, but can find those at potential risk, especially if there is a family history of HCM or sudden death, OR if there is a history of fainting, lightheadedness or palpitations with the patient feeling a rapid heartbeat. Examining the heart, listening for abnormal sounds or murmurs, might give a clue that HCM is a potential. An EKG (electrocardiogram) may or may not be abnormal and is not a great screening exam, missing up to 30% of those with HCM. Echocardiogram, an ultrasound of the heart, is very good at finding abnormal heart muscle structures and is the ‘gold’ standard for finding HCM.

The American Heart Association and the American College of Cardiology are at odds with their European counterparts when it comes to screening. The Americans felt that using technology would be unsuccessful. In the 1970s, the Italians mandated full screening as a condition of sports participation for all competitive athletes. This includes full history and physical exam and EKG plus echocardiogram for those to be high risk. The proponents of the Italian model, including the European Cardiology Consortium, the International Olympic Committee and FIFA, the international soccer organization, point to studies where there is a 90 percent reduction in HCM sudden death from about 10 deaths per year to one death per year in the past 25 years.

With that background, consider the US situation. There are 8 million students that participate in high school athletics every year. The expected sudden death rate for HCM in the general population is about 1 in 200,000. This statistics seems to fit the 10-25 deaths per year that are reported. In the freshman class of 2 million, HCM would be expected to affect 4,000 student athletes and without any screening, 10 deaths would be expected per year if no screening procedures were in place. If the Italian model was in place, 9 lives might be saved.

The participation physical examination is often a distraction and inconvenience for students and parents alike. Often, a form gets signed without much more than a cursory provider visit and it is seen as not important. However, there is little infrastructure in place to perform 2 million physical exams and EKGs. Aside from the cost of the visit and the EKG, there may be a lack of medical personnel who are trained to ask the right history questions or to look for the signs of HCM on physical examination. The EKG changes may be subtle. For those whose risk factors would suggest the need for an echocardiogram, there are many parts of the US, where the cardiologist, technologist and machine are not readily available.

Mandating heart evaluations before allowing students to participate in athletics may cause those living in medically underserved areas to be divorced from organized sports. What societal consequence exists for a less active adolescent population? HCM may be progressive and affects those of all ages. Taking the screening requirements past high school, should YMCAs, and health clubs require cardiac screening exams before allowing membership? And for those who work in trades and professions that require manual labor and exertion, should there be screening?

Society has opportunity to choose its priorities. Great time, effort and resources are spent to prevent even one plane crash. Less effort is made to outlaw smoking or aggressively diminish drunk driving rates. The question becomes, how much should society care. Even with the most aggressive screening policies found in Italy, there are still athlete deaths due to HCM.

So how much are 9 lives worth?


This entry was tagged , , , , , ,