How to Avoid Holiday Heart Syndrome

 

Labor Day marks the traditional end to summer. Families and friends will celebrate the holiday by getting together, barbequing and having a few cocktails. How many of those holiday revelers will end up in the hospital the following week with atrial fibrillation (Afib) and Holiday Heart Syndrome?

 

Afib is a fast, irregular heartbeat from the upper chambers of the heart (the atria). If left untreated it is associated with stroke and heart failure.  Holiday Heart Syndrome occurs in a patient who has recently had alcohol. It typically will occur two to four days after someone has had more alcohol than they usually are accustomed to. It is often seen after binge drinking, such as occurs during a holiday, thus the name.  The Afib episodes usually start during the night. Most of the time the Afib resolves on its own, but Holiday Heart Syndrome is serious. Patients may need cardioversion (having their heart shocked back into a normal rhythm) or may need long-term treatment with heart medications and blood thinners. In addition, 20-30% of patients will have recurrent Afib events within a year of the initial presentation. 

 

How much alcohol is required to induce Holiday Heart Syndrome?  The exact amount is not known, but some recent studies have shed some light on the question. One study concluded that drinking alcohol increased the risk for Afib within a few hours and the more alcohol, the higher the risk.  After only a single drink of alcohol, the risk of Afib increased two times in the next four hours.  After two drinks, the risk increased to three times and there was a linear increase in risk from there (more alcohol, more risk).  The conclusion of this study was that no amount of alcohol is safe for patients with Afib.  Another trial from England showed that four drinks per week or less did not increase the risk for Afib. Higher amounts did increase the risk (resulting in a J shaped curve).  They also showed that the type of alcohol mattered.  Wine (both red and white) was not associated with increased risk for Afib, while beer and cider, in any amount, increased the risk. 

 

But isn’t alcohol supposed to be cardioprotective?  It is true that light drinkers live longer than those who do not drink and those who drink heavier amounts of alcohol (also a J shaped curve). Light drinking (approximately one alcoholic beverage per day) reduces total cholesterol, increases HDL (the “good” cholesterol) and may be associated with a lower risk for heart attack. However, the data for the harmful effects of alcohol is stronger than the data for its beneficial effects. 

 

Alcohol doesn’t only affect the heart. Alcohol use affects brain function. One study showed that any alcohol use decreased brain structure and function compared to those who do not drink. The conclusion of the study was that no amount of alcohol is safe for the brain. Similarly, when it comes to cancer, no amount of alcohol is safe. Alcohol has been linked to several cancers including cancers of the mouth, throat, esophagus, colon, rectum, and breast as well as leukemia and multiple myeloma. The more alcohol consumed, the higher risk for cancer. Even light drinking was associated with esophageal and breast cancer. 

 

To summarize, the effects of alcohol on the heart are conflicting and confusing. Low amounts of alcohol intake can decrease mortality and help with the plumbing (less blockage in the heart arteries), but even those low levels can increase the risk for electrical problems (Afib). In addition, there is no safe amount of alcohol in cancer and for the brain. However, there is no safe level of driving. If you never get in a car, then you can never have a motor vehicle accident.  No one recommends that people stop driving. Some level of risk is present in everything that we do.  The idea is to balance the risk of everyday life versus hiding in a closet.

 

In order to stay safe this Labor Day Holiday and reduce the risk for Holiday Heart Syndrome, here are some recommendations.  If you have a history of AFib, it is likely best to avoid alcohol, or, if you must drink, have only a single drink on rare occasions.  If there is no history of AFib, limit alcohol use to one drink maximum per day and drink only a few days per week. Taking a day off from drinking helps the body to recover. Also, consider consuming wine rather than beer or cider. Stay safe and have a Happy Holiday.

 

Which Sport Wins the Gold Medal for Best Exercise?

The Olympic torch will finally be lit for the 2020 Olympics next week in Tokyo! More than 11,000 athletes will compete in 339 events representing 33 different sports. Before the Opening Ceremony begins, we will explore which sport is the best type of exercise.  Six different Olympic sports, tennis, running, cycling, weightlifting, golf and soccer, will be examined in terms of their exercise benefit but also some rarely considered downsides.  Orthopedic risks will not be covered; that is a topic for another time and for another writer. 

 

Exercise can be divided into two distinct classes: dynamic or isotonic exercise and static or isometric exercise. Most high intensity dynamic exercise is done aerobically. Dynamic exercise increases cardiac output and cardiac endurance.  Static exercise is mostly anaerobic, strengthens and increases muscle mass, increases bone density and helps with balance and coordination.  These two types of exercise are at the opposite end of the spectrum, but most sports involve both static and dynamic components.

 

Tennis is a sport with worldwide appeal, played by professionals as well as recreational athletes. Tennis has a high dynamic component but a low static component: it builds cardiac endurance but doesn’t add a lot of muscle mass.  Do the beneficial cardiac effects of tennis translate into better outcomes? The Copenhagen Heart Study followed 8500 people for 25 years and concluded that playing tennis increased life span by 9.7 years compared to sedentary individuals.  In fact, tennis was the top sport for extending life span, providing more years than running, cycling or weightlifting.  In another study of 80,000 British adults, tennis reduced the chance of death by 47% and cardiovascular disease by 59%.  Tennis certainly provides an exercise benefit, but why is it so effective at extending life compared to other sports? One reason may be that tennis players had the lowest body mass index in the Copenhagen study. In addition, the social aspect of tennis may be a factor. Socializing during and after tennis matches is quite common and it is known that having strong social connections improves quality and quantity of life. In addition, there is the mental aspect of tennis; there is a constant “mental chess game” throughout a match, helping to improve cognition and reduce the risk for dementia. What are the hidden risks for tennis? One study calculated the sun exposure risk for the various Olympic sports in Tokyo.  With higher sun exposure, the risk for melanoma and other skin cancers increases. The study concluded that tennis players had the highest risk for sun exposure due to long daytime matches, the reflective surface of the courts and clothing that is breathable but not protective from the sun’s rays.

 

The track and field events are among the most exciting contests of the Olympics. The men’s 100 meter dash crowns the “World’s Fastest Man” and the marathon is a signature event. Recreational running is one of the most popular sports worldwide with almost 60 million participants. Sprinting is a moderate dynamic, moderate static exercise while long distance running is high dynamic, low static. Running will extend life by 3.2 years (Copenhagen study) and reduce the risk for dying by 43% (British study).  However, running may not be fully protective against the development of heart disease. Several studies have shown that runners have high coronary calcium scores and more plaque in the heart arteries than would be expected.  In addition, studies have found more scar in the heart muscle of long distance runners. The reason for the scar and the heart plaque is not clear, as is the significance of these findings. 

 

Cycling is a high dynamic, high static sport.  Cycling will increase longevity by 3.7 years (Copenhagen study) and reduces the risk for death (British study).  In addition, a long-term study found that Tour de France riders lived longer than the average French male. Cyclists had a lower coronary calcium score and less heart artery plaque than runners, soccer players or tennis players. What are the hidden downsides to cycling? Cyclists had the third highest sun exposure due to long periods of riding outdoors and the body’s position which tends to catch more of the sun’s rays compared to other athletes. Another factor to consider is that cycling is non-weight bearing, so it may put too little pressure on the bones. This was proven in a study showing that cyclists had a lower bone density than runners. 

 

Weightlifting is at the other end of the spectrum compared to the previously mentioned sports. It is the classic low dynamic, high static exercise; it is designed to increase muscle mass and build bone strength.  Does weightlifting reduce the risk for dying? The data is less clear for weightlifting compared to endurance sports. One study of 18,000 US adults showed that weight lifting was not associated with reduced mortality.  Why is this? One study of weightlifters showed that blood pressure rises rapidly and to very high levels during lifting (the average peak systolic blood pressure was over 300 mmHg).  These high pressures thicken the heart muscle. While a large biceps muscle is good for fitness, a thickened heart muscle puts the athlete at risk for arrhythmias and congestive heart failure. 

 

Golf is classified as a low dynamic and low static sport. Despite the low aerobic and muscle building potential, regularly playing golf can raise life expectancy by about 5 years. This proves the point that any activity is better than being sedentary. Another factor may be the socializing aspect of golf. On the downside, golf has the second highest sun exposure risk. In addition, there is the Mark Twain quip about golf being “a good walk spoiled”.

 

Soccer is the most popular sport around the world and a good number of people play soccer for fun on the weekend as well.  Soccer, like tennis and long distance running, is a high dynamic, low static exercise. Soccer will extend life by 4.7 years (Copenhagen study). A study of former Scottish soccer players found a lower risk for dying and heart disease compared to the general population.  However, the same study found a much higher risk for dementia.  All of those headers seemed to have taken their toll. 

 

Currently choosing a sport is a matter of personal preference but can a more precise exercise regimen be tailored to the individual? The answer is yes. By using your own data from a stress test, a cardiologist can issue a personalized exercise prescription (http://sportscardiology.blogspot.com/2017/08/an-exercise-prescription-to-get-fitt.html).  Even more precision may be on the horizon.  Researchers at Harvard found 102 proteins in the blood that may be able to predict a person’s response to physical exercise. So, based on their blood profile, one person may be prescribed endurance exercise while another might be nudged towards a high static exercise. 

 

Until personal physical exercise proteins become mainstream, here are some considerations for deciding which sport is right for you. First, choose a sport that you like to do. If you like the exercise, you are more likely to do it, especially on those days when you don’t feel like exercising. Second, minimize the risks. For example, if you like to play tennis, split your time between outdoor and indoor matches to lower the sun exposure and lower the risk for skin cancer. If you like to cycle, don’t ride exclusively. Balance it with an activity that will help with weight bearing and bone strength such as weightlifting.  Lastly, participating in any of these sports is better than sitting on the couch and watching the Olympics on television. At a bare minimum, get on your treadmill or stationary bike and then cheer on your favorite athletes.

 

 

Thumbs Up For Aortic Screening

 

 

The thumb is a remarkable appendage.  By allowing us to grasp objects, to use tools, to write, the thumb has helped us evolve above and beyond all other animal species. Can the thumb also be useful in helping us detect an enlarged aorta? 

 

The aorta is the main artery of the body. It arises from the heart, courses through the chest and abdomen and ends by splitting into two arteries to supply blood to the lower extremities. Arteries arise from the aorta to supply blood and oxygen to the heart, brain, stomach, kidneys and all of the muscles of the torso and the upper extremities. The aorta is divided into two main parts, the thoracic (chest) aorta and the abdominal aorta. One of the most serious, and deadly, problems with the aorta is an aortic aneurysm.  An aneurysm is an enlargement of the aorta. As the aortic diameter increases and balloons out, the wall of the aorta weakens.  At some critical size, the wall is so weak that it can burst open. Unfortunately when that happens, the patient most likely will die from bleeding. The keys to managing an aortic aneurysm is to identify an aneurysm, monitor its growth and size and refer the patient to surgery to repair the aorta before it ruptures.  Aneurysms of the thoracic and abdominal aorta have different causes and different ways to monitor them. 

 

The exact cause of abdominal aortic aneurysm (AAA) is not known. It does occur in families and those with a first-degree relative with AAA are at two times the risk. AAA can occur in the setting of atherosclerosis. Risk factors for AAA include male sex, older age, smoking, and hypertension. Aneurysms that are greater than 5.0 cm in diameter are at increased risk for rupture and at that level of dilatation patients are referred to surgery for repair. AAA can be detected by physical examination. A pulsatile mass is felt in the area around the umbilicus. Ultrasound is very good for detection and screening of AAA. It is recommended that men over age 65 who have ever smoked or who have a family history of AAA have a one-time screening (the benefits of screening women hasn’t been determined). Once identified, yearly ultrasounds are used to follow patients with AAA. If there is rapid growth, or the AAA reaches 5.0 cm, then a CT scan is done to further delineate the anatomy and help in planning for surgery.

 

There are many different causes for thoracic aortic aneurysm (TAA). Connective tissue diseases are an important etiology. In these conditions, patients are born with loose muscles and joints. They can perform all kinds of contortions (they are “double jointed”).  The aorta has muscle and connective tissue within its walls; this makes it elastic, allowing it to expand when the heart pumps blood through it and to  relax when there isn’t blood flow. These elastic properties help the aortic wall handle the high pressure of blood flow, without rupturing. Unfortunately the same connective tissue laxness in these patients also causes weakness within the aortic wall. This leads to TAA and these patients are prone to rupture at smaller aortic diameters than other TAA patients.  The most well known connective tissue disease is Marfan’s Syndrome. These patients are tall, skinny and lanky (Abe Lincoln was thought to have it). They may have TAA, their aneurysms can grow rapidly and are at risk for bursting at about 4.5 to 5.0 cm.  Athletes with Marfan’s Syndrome are barred from playing sports because extreme physical activity can increase the risk for their aneurysm bursting. Therefore it is very important to identify and follow these patients. Other causes of TAA are bicuspid aortic valve (the aortic valve has two leaflets instead of the normal three leaflets), atherosclerosis, vasculitis (inflammation of the wall of the aorta), infection (for example, syphilis) and trauma.  Detection and screening for TAA is more difficult than with AAA. The echocardiogram (ultrasound of the heart) can image parts of the thoracic aorta. It is not an ideal screening tool as it can’t view the entire thoracic aorta and measurement of aortic size is fraught with error.  However, it is noninvasive and doesn’t require intravenous contrast.  The gold standard for measuring TAA is either CT scan or MRI, both of which require intravenous contrast. Due to the contrast, the cost and the radiation exposure (for CT scan) these tests are not ideal for screening.  A good, low cost, low risk screening test for TAA is sorely needed. Enter the thumb test. The thumb test is simple. Hold up one hand and keep the palm flat. Stretch the thumb as far as possible across the palm. If the thumb crosses beyond the edge of the palm, the test is positive.  A positive thumb test indicates that the joints are loose, due to a connective tissue disease and that a TAA may be present. The majority of aneurysm patients do not have a positive thumb test, but if the test is positive there is a very high likelihood of having a TAA. A negative test does not exclude the possibility of an aneurysm.

 

If you are a male, over 65 years old and have ever smoked or have a family history of AAA or if you have a positive thumb sign, talk to your doctor about screening for an aneurysm. It may save your life.

Humor Explains (And Cures) Everything

Plato and a platypus walk into a bar... This isn’t the start of some highbrow joke, but the title of a book by Harvard trained philosophers Thomas Cathcart and Daniel Klein. In the book the authors plausibly spell out how jokes and humor can explain all of philosophy. Jokes and philosophical concepts are similar in that they both make you think; both flip the world upside down and uncover hidden truths about life. Joking about the three main branches of philosophy, ethics, logic and metaphysics, helps us understand these lofty ideas.  Metaphysics tackles the Big Questions, for example: What is reality? What is the meaning of life? If humor can help us understand metaphysics, humor can therefore explain everything! If humor is this powerful, we need to define it.  The humor writer and philosopher Dave Barry defined humor as, “a measurement of the extent to which we realize that we are trapped in a world almost totally devoid of reason. Laughter is how we express the anxiety we feel at this knowledge“. Speaking of anxiety, Sigmund Freud wrote a book analyzing jokes and their relationship to our dreams, our inhibitions and our unconscious thoughts. So a good joke not only provides a hearty laugh, but can have deep philosophical and psychological meaning as well, allowing us insight into the how the world, or our own mind, works (or at least lets us to blow off steam about the randomness of it all).  Does laughter also have physiologic and therapeutic properties?

 

These are my principles; if you don’t like them, I have others- Grouch Marx

The beneficial effects of laughter have been known for many years. An early reference may be found in the Bible, “A merry heart doeth good like medicine” [Proverbs 17:22]. The modern concept of laughter as medicine was eloquently characterized by Norman Cousins, a noted author, professor, world peace advocate and nuclear disarmament activist in his 1976 New England Journal of Medicine article (and subsequent book by the same name), “Anatomy of an Illness (as Perceived by the Patient)”. He attributes laughter to curing his crippling rheumatologic disease, which doctors previously felt was irreversible. He states that 10 minutes of genuine belly laughter would relieve his arthritis and provide at least two hours of pain free sleep.  Mr Cousins’ writing spawned a series of studies on the effect of laughter leading to some interesting findings. In addition, it lead to the development of laughter clinics, including the Gesundheit community lead by Dr Patch Adams, where laughter is used to help patients with chronic, debilitating diseases find a way forward. 

 

What is the cardiologist’s favorite song? “Statin Alive” by the Bee Gees- Francisco Navarro

What effect does laughter have on the body?  Laughter has been shown produce numerous positive physiologic changes. Laughter relieves stress by decreasing stress hormones and by increasing endorphins (hormones that are usually released while exercising to make one feel good and to keep exercising).  It relaxes blood vessels, reduces blood pressure, decreases the heart rate and aids in muscle relaxation. Laughter improves the immune system and aids in healing after surgery.  A good laugh provides a huge psychological boost as well and helps to fight depression.  Humor is used routinely for stress reduction during cardiac rehabilitation programs. Lastly, if humor is injected into the doctor’s office visit, it will result in better patient satisfaction, greater patient empowerment and a stronger bond with the doctor. Most importantly, laughter and humor has no down side (except perhaps a pulled muscle from laughing so hard!).

 

Don’t trust atoms, they make up everything - Richard Feynman

Is there data to support laughter as medicine?  In a study from Norway spanning 15 years and including 53,000 patients, a good sense of humor lowered overall mortality for women and lowered mortality due to infections in both men and women. In a study of 17,000 people in Japan, those who a good hearty laugh more than once per week lived longer and had less heart disease than those who laughed only once per month or less. Laughter can also help with memory and thinking.  A strong laugh can stimulate the brain and lead to higher cognitive activity. Also, older patients had improved short-term memory and improved recall after watching a humorous video.

 

In summary, humor not only explains everything, but can help cure many ills. So for a long and healthy life, exercise 20-30 minutes a day, eat fresh fruits, vegetables, fish and plant based protein, sleep seven hours a night and socialize with friends and family. And it wouldn’t kill you to have a long, loud, hearty laugh each day too.

  

An Addition to the Cardiac Alphabet: “a” Novel Risk Factor

 

Lipoprotein (a) or Lp(a), pronounced “El Pee Little a”, is a lipid particle that is associated with plaque in the heart arteries, heart attack and cardiac death. What is Lp(a), what is its link to heart disease and how is it treated?

 

Lp(a) was discovered in 1963, but has been largely forgotten since then due to the lack of good treatment options.  Newer medications have shown some efficacy in lowering Lp(a) sparking a resurgence in research.  Plaque or blockage in the heart arteries mostly consists of low density lipoprotein (LDL, the “bad” cholesterol). In fact, plaque is more than 90% LDL cholesterol. Lp(a) however is also needed initiate and propagate plaque formation in the heart arteries. In addition, Lp(a) promotes blood clotting and inflammation, two properties contributing to heart disease. Abnormal elevation in Lp(a) is a common genetic entity. Lp(a) elevation above 50 mg/dl affects one in five people in the US or approximately 60 million Americans. Studies have linked Lp(a) to a higher risk for heart attack, stroke, aortic stenosis (thickening and blockage of  the aortic valve, limiting blood flow from the heart), heart failure, kidney disease and heart deaths.

 

Who should be tested for an abnormal Lp(a) level? Lp(a) may be measured in the blood and levels over 50 mg/dl are abnormal. However, the risk for heart disease increases as Lp(a) levels increase. Therefore, slight elevations may not be as clinically relevant as high levels of Lp(a).  There are a couple of scenarios where measuring Lp(a) may be beneficial. One consideration is in a patient with a strong family history for coronary artery disease (first degree relative with heart disease at age 60 or younger). Another possibility is a patient who has had recurrent heart events (heart attack or repeated cardiac stents) despite adequate treatment with a statin. In these cases knowing that there is an elevated Lp(a) level may change therapy. 

 

How should elevated Lp(a) be treated?  Ideally a medication should be chosen that reduces both LDL and Lp(a). Statins are the treatment of choice for patients with heart disease and high LDL levels. Statins lower LDL and reduce the risk for heart attack and cardiac death. Unfortunately, statins do not reduce Lp(a) levels. In fact, statins can increase Lp(a) by 10% to 20%.  Niacin reduces Lp(a) levels by 15-25%. Unfortunately, niacin has not been shown to reduce the risk for cardiac outcomes and has significant side effects (flushing of the skin after ingestion). For these reasons, niacin has not been used for heart patients for some time. PCSK9 inhibitors are new monoclonal antibodies that have very good data in heart disease. PCSK9 agents reduce LDL nearly 50% on their own and by 60% when used with a statin.  They have been shown to reduce the risk for heart attack and cardiac death. They are injected under the skin every two weeks and, since they are not a statin, do not have muscle pain as a side effect. In addition, PCSK9 agents reduce Lp(a) levels by 25%.  Another new medication is currently undergoing trials. Inclisiran reduces LDL by 50% and Lp(a) by 20%. It is also given by injection and is administered twice yearly. 

 

While the data associating Lp(a) with a higher risk for heart artery plaque, heart attack and cardiac death is well established, it is not known whether lowering Lp(a) will improve cardiac outcomes.  This is important because many treatments in cardiology that initially seemed promising (examples include vitamin E, hormone replacement therapy and folic acid) did not reduce the risk for heart attack or cardiac death when tested in large scale clinical trials and have thus fallen out of favor.  Trials are currently underway testing the Lp(a) hypothesis of heart artery disease and cardiac outcomes and the answer should be available very soon. Until then, we should try to identify patients who have significant elevations in Lp(a) and treat them as best we can. 

Q: Crazy Conspiracy Theory or Useful Supplement?

Over the past several months, the news has been reporting about a shadowy figure named “Q”, who has promulgated many baseless and false theories over a wide range of subjects, mostly about politicians and elections. Similarly, the body has a shadowy “Q”, coenzyme Q, which is ubiquitous and is involved in multiple metabolic pathways. Since the election is over, we will tackle questions about the body’s Q.

 

Coenzyme Q10 (CoQ10) is a naturally occurring substance produced by the body. It plays an essential role in generating energy for the cell. CoQ10 is found in abundance in tissues with high-energy requirements, such as the heart or skeletal muscle. CoQ10 is made in all tissues of the body and the pathway that produces it also produces cholesterol. In general, the body produces as much CoQ10 as it needs, but with aging, the levels of CoQ10 can diminish. Also, importantly, statin use can decrease CoQ10 levels.  CoQ10 is also available as a nutritional supplement with a global market estimated at $600 million. The supplement has been studied extensively and is safe with mild adverse reactions such as dizziness, insomnia, nausea and diarrhea. CoQ10 supplementation may play a role in statin associated muscle pain and in congestive heart failure.

 

Statin associated muscle problems can occur in 10 to 20% of patients who take statins to lower cholesterol. It is one of the major reasons why patients stop taking statins.  Symptoms range from minor muscle aches, to severe muscle pain, cramps and weakness, to muscle breakdown and toxicity (called rhabdomyolysis, a serious condition that can lead to hospitalization, kidney failure and even death).  Unfortunately, there is no objective test to determine statin associated muscle pain. A lab test, creatine kinase or CPK, can be elevated if there is muscle damage, but the test isn’t always reliable. The diagnosis is made by clinical symptoms and stopping the statin (if symptoms improve, they may have been due to the statin). No one knows the cause of statin associated muscle pain, but it has been hypothesized that depletion of CoQ10 may play a role. As such, many trials have been conducted to see if supplementation with CoQ10 would be beneficial. Unfortunately, the trials have been inconclusive and contradictory; some trials show that CoQ10 is beneficial while others do not.  One trial reported more muscle pain in patients who took a statin plus CoQ10 compared to statin plus placebo; a finding known as the nocebo effect. Even though benefit is questionable, there is no harm in taking CoQ10 supplements. Therefore, there may be a role. For patients with statin associated muscle pain the following may be an approach:

1)  Stop the statin for 1 or 2 months

2)  If symptoms improve, restart the same statin at a lower dose or try a different statin 

(if symptoms don’t improve, the muscle pains may be due to something else)

3)  If symptoms return at a low dose or on a different statin, a trial of CoQ10 may be used at a dose of 200 to 400 mg per day

 

Congestive heart failure (CHF) occurs when the heart weakens and cannot pump blood effectively. Fluid builds up in the lungs (causing shortness of breath) or throughout the body (causing swelling in the legs and abdomen).  CHF is the number one cause for hospitalization in the US. CoQ10 is involved with the production of energy in cells, especially heart cells. If CoQ10 is depleted, the heart cells will have reduced energy leading to the weakening of the pumping function of the heart. It has been shown that there are reduced levels of CoQ10 in the blood and in the heart tissue of CHF patients. It has been theorized that supplementation of CoQ10 might improve CHF.  Studies have shown that CoQ10 supplementation does improve symptoms, reduces hospitalizations and decreases cardiac death in chronic CHF patients.  It may also improve the ejection fraction (a measure of the heart’s pumping function). It must be noted that these studies are preliminary and that CoQ10 should only be used in the context of a clinical trial, and not for routine use as yet.

 

CoQ10 is emerging from the shadows and being extensively studied in heart disease.  Depletion of CoQ10 may play a role in statin associated muscle pain and in congestive heart failure.  While awaiting definitive data from future research, nutritional supplementation with CoQ10 may be beneficial in these conditions. It must be noted that CoQ10 is not approved for any medical condition by the Food and Drug Administration (FDA).  In addition, routine us of CoQ10 is not needed in cardiac patients as the body manufactures the amount of CoQ10 that it requires.

 

 

 

Can You Teach An Old Drug New Tricks?

 

It's a warm summer evening in ancient Athens. Archimedes is sitting in the agora and notices redness, swelling and pain in his big toe after drinking a kylix of wine. He goes to the market and is given an herb by a local farmer. After taking the herb, his big toe starts to feel better. He runs through the streets crying "Eureka!".

 

Colchicine is an anti-inflammatory medication which is used to treat acute episodes of gout. It is derived from the plant Colchicum autumnaleor autumn crocus. It was in fact used in ancient Greece, but as a laxative. The ancient Egyptians used it to treat rheumatism.  Colchicum plant extracts were used to treat gout starting about 550 AD. Benjamin Franklin, who suffered from gout, is credited with bringing Colchicum plants to the United States when he returned from Paris after completing his duties as French ambassador. Colchicine was first extracted in 1821 by French chemists and soon thereafter became a popular remedy for gout. It was approved for use in the US by the FDA in 1961. The anti-inflammatory effect of colchicine is very different from nonsteroidal anti-inflammatory (NSAID) medications and aspirin.  For more than 50 years colchicine was used exclusively to treat gout. Over the past ten years it’s anti-inflammatory properties were found to be useful in heart disease. Even more recently, it has been used in COVID-19. So colchicine, an old drug, finds itself at the intersection of inflammation, heart disease and COVID-19. Here are some clinical scenarios where colchicine has found new uses.

 

Pericarditis is inflammation of the sac lining the heart (the pericardium).  The most common cause of pericarditis is a virus, and symptoms are usually preceded by an upper respiratory infection, the flu or, recently, COVID-19.  Chest pain is the main presenting symptom, often associated with changes on the EKG or fluid around the heart on echocardiogram. Acute episodes of pericarditis are treated with anti-inflammatory agents such as aspirin, NSAIDs, colchicine or steroids.  Colchicine has been used since 1987 to treat acute pericarditis and recently it has been shown that colchicine combined with either an NSAID or aspirin was better for treatment than aspirin or NSAID alone.  With the combination, symptoms usually resolve within 72 hours, but treatment should continue for three months to prevent repeat episodes. About 15 to 30% of patients will have recurrent episodes of pericarditis. As with acute bouts, colchicine plus either aspirin or an NSAID successfully treats recurrent pericarditis. 

 

Coronary artery disease (CAD) or plaque in a heart artery can lead to a heart attack or chronic angina (chest pain). Low-grade inflammation within the walls of the heart arteries leads to plaque build up and blockage. Inflammation can also cause acute rupture of a plaque causing a heart attack. Previous research showed that a strong intravenous anti-inflammatory agent (a monoclonal antibody) improved outcomes for CAD patients but was expensive and had significant side effects. Would cheap, easily available colchicine be beneficial? Colchicine has been shown to reduce inflammation within the walls of arteries, so theoretically it should be helpful. Several studies examined the use of colchicine in chronic stable CAD patients and patients who had a recent heart attack. These studies show that colchicine consistently reduces the risk for cardiovascular outcomes (especially repeat heart stents).  Therefore, it seems that colchicine can be added to the cardiac medication armamentarium.

 

COVID-19 is another inflammatory disease. In severe COVID-19, the immune system’s inflammatory response overtakes the body affecting the lungs, heart, and blood vessels especially hard.  High dose, intravenous steroids are used to combat the inflammatory consequences of the disease.  Given colchicine’s anti-inflammatory properties, can it be used to prevent serious complications in outpatients with mild COVID-19? Several trials are underway to answer the question, one of which was recently reported. The trial enrolled 4000 patients with a diagnosis of COVID-19 within the previous 24 hours. In addition, one high-risk characteristic was needed (older age, obesity, diabetes, hypertension or underlying heart or lung disease).  Colchicine reduced hospitalizations, the need for a respirator and deaths. However, the trial was not peer-reviewed and with the sting of hydroxychloroquine fresh in mind, the data are being interpreted with caution. It is felt that colchicine may be beneficial, but that there is still insufficient evidence to use the medication.  Fortunately, other trials are ongoing and may be able to provide yet another use for colchicine.

 

Currently, a massive amount of research is being conducted focusing on inflammation, it’s effects on the body and novel agents to treat it. Meanwhile, the tried and true drug colchicine, with known efficacy, few side effects, wide availability and low cost, may be an answer to treat inflammatory diseases both old and new.