The Sunshine Vitamin and the Heart

A 65-year-old woman is seeing her cardiologist for follow up of an elevated heart artery calcium score on CT scan.  They discuss various treatment options including starting a statin. She asks, “Should I continue to take my Vitamin D and calcium supplements since there is higher than normal calcium seen in my heart arteries?” How do vitamin D, calcium and their supplements affect the heart?

 

Vitamin D is necessary to maintain bone health and strength.  Vitamin D is also an integral part of normal cell metabolism.  Vitamin D receptors are present in almost every tissue in the body and vitamin D plays a role in regulating cell growth. Vitamin D is obtained by the body through 2 avenues: external sources (food and supplements) and internal sources (produced by the body). Vitamin D can be obtained from the diet (there are a few food sources that naturally contain vitamin D such as oily fish, liver, egg yolks, and vitamin D fortified milk) or by supplements. Vitamin D supplementation is becoming more and more widespread. Between 2011 and 2014, about 37% of the US population took a vitamin D supplement. In the same time period, 61% of adults over age 65 used a vitamin D supplement. Vitamin D can also be produced by the body. The skin turns ultraviolet rays from the sun into vitamin D (thus the name, “The Sunshine Vitamin”). The skin production of vitamin D depends on climate, skin pigmentation, sun exposure and age. Risk factors for low vitamin D levels include older age, colder climates, reduced outdoor activity, and sunscreen use. 

 

Vitamin D levels in the blood can be measured. Vitamin D deficiency is defined as a vitamin D concentration of < 20 ng/ml. Levels of vitamin D between 20 and 29 ng/ml is considered insufficient. The optimal vitamin D level is > 30 ng/ml.  Vitamin D deficiency can cause weak bones and fractures. It is associated with diabetes, autoimmune disorders and rheumatoid arthritis. Vitamin D deficiency can also cause heart problems by increasing inflammation, increasing blood pressure and causing arteries to stiffen. Studies have shown that low levels of vitamin D can increase the risk for heart artery disease, heart attack, stroke and congestive heart failure. Do vitamin D supplements mitigate the risk of low vitamin D levels? The effects of vitamin D on fractures and bone health is uncertain. A recent review showed that vitamin D supplementation does not prevent fractures or improve bone mineral density.  In addition, well-designed trials show that vitamin D supplements do not benefit heart health.  Lastly, vitamin D supplementation does not reduce the risk for cancer, stroke, high blood pressure or dying. Vitamin D supplementation is safe at levels up to 2000 IU/day, however at 4000 IU/day or more toxicity can occur. Vitamin D supplementation does not appear to be harmful to the heart, even at higher levels. 

 

Calcium is the most abundant mineral in the body, with 99% of the body’s calcium stored in the bones and teeth. Adequate calcium intake is essential for bone development and maintenance. Because of their effects on bone health calcium and vitamin D are intricately intertwined. Like vitamin D, calcium can be obtained either in the diet or via supplementation (it is not naturally produced by the body).  Food sources of calcium include leafy green vegetables, low-fat diary products, beans and almonds. The recommended dietary intake of calcium for adults 19 to 50 years old and men 51 to 70 years old is 1000 mg/day. For women 51 to 70 years old and for men and women older than 70 it is 1200 mg/day. Age, vitamin D and other factors influence calcium absorption by the body. People at risk for inadequate calcium intake include those with lactose intolerance and postmenopausal women.  Calcium supplementation is very common with use by 40% of the general US population and more than 65% of postmenopausal women. Calcium supplementation does reduce the risk for bone fractures.  Unfortunately, calcium supplements do appear to increase the risk for cardiovascular events, such as heart attack and stroke, especially at levels over 1400 mg/day. Calcium supplement users also had an increased risk for heart artery calcification compared to those not on supplements.  Of note is the fact that higher intake of calcium in the diet was not associated with increased heart risks. 

 

What are the recommendations for vitamin D and calcium as well as the use of their supplements?  For the general population, obtain vitamin D from food sources and from sunlight. If vitamin D insufficiency persists despite diet and outdoor activity, then supplementation can be used. Calcium recommendations are similar; obtain calcium through the diet and increased physical activity. If calcium deficiency persists or there are increased needs, calcium supplements can be used, keeping in mind that there is a possibility of cardiovascular harm. For both vitamin D and calcium, pill-based supplements may not be better than a healthy life style, including a prudent diet and physical activity.

 

What should we tell our postmenopausal woman with an elevated coronary calcium score about her supplement use? There should be a frank risk/benefit, shared decision making conversation.  Vitamin D supplements are neutral; they don’t seem to confer any benefit for heart health, but they are not harmful either.  Calcium supplements help with bone health, but may come with added cardiac risks, including the possibility of worsening her coronary calcium.  The supplements can cautiously continue as long as there is an understanding of the risks and benefits and with close monitoring. 

The Eyes Have It

William Shakespeare once said, “The eyes are the window to your soul.” This is poetic and philosophical, but can the eyes be more practical and be a window on the heart as well? A cataract is a common eye disorder that occurs as people get older. Are cataracts associated with heart disease or a higher risk of dying? Could a cataract be a new risk factor for cardiac disease?

 

A cataract is a clouding of the lens in the eye.  The eye uses a natural lens to alter the light coming into the eye to help us see.  With aging, the proteins in the lens start to break down, causing vision to become cloudy, like looking through a foggy or dusty windshield.  Aging is the most the common cause of a cataract. People over 60 years old may start to have clouding, although severe symptoms may not develop for years.  Aside from older age, other risk factors for cataracts include diabetes, smoking, heavy alcohol use, hypertension, working in direct sunlight, certain medications such as corticosteroids and a family history of cataract. Once symptoms become severe, the treatment is surgery. An eye doctor can replace the cloudy lens with a clear artificial lens and restore sight. Cataracts are quite common and a major cause of visual impairment worldwide.  Approximately 90% of Americans over age 65 will develop cataracts and 4 million cataract surgeries are performed each year in the United States.  

 

Are cataracts associated with heart disease or a higher risk of dying? Many studies have been done to try to answer these questions, with conflicting results.  More recent data points to an association between these processes. The Nurses Health Study followed 60,000 women, aged 45 to 63, for 10 years. The study found that cataract extraction significantly increased the risk of dying from heart disease. A recently published study looked at 15,000 Americans over the age of 40 with a follow up of 10 years.  This study found significant associations with cataract surgery and the risk of dying. Patients who have had cataract surgery had a 13% higher risk of dying from any cause and a 36% higher risk of dying from heart disease. Lastly, a study from Israel showed that cardiovascular disease was significantly more prevalent in cataract patients undergoing surgery. 

 

How are cataracts and heart disease connected? There are several possible unifying mechanisms. Cataracts and heart artery disease share some common risk factors, such as older age, hypertension, diabetes and smoking. Oxidative stress causes damage and break down of the proteins in the lens. Of course, stress also causes plaque and blockage in the heart arteries. Another mechanism involves proteins in the lens called crystallins. These proteins are present throughout the body and help regulate the body’s response to inflammation and ischemia (low blood flow). The break down of these proteins in the eye and throughout the body may a more widespread systemic disorder rather than a localized problem involving just the eye. Lastly, both cataract and heart patients are more prone to depression.

 

Does this mean that cataracts are a new risk factor for cardiac disease? Not necessarily. Both cataracts and heart disease are common problems and both occur as we get older. It is possible that the both conditions are a consequence of ageing or some other systemic process and not causally related. The research doesn’t show that cataracts cause heart disease. Even so, it seems prudent for patients with cataracts to keep an eye out for symptoms of heart disease and see their doctor quickly if symptoms develop.

NASH

Candy is dandy, but liquor is quicker

 

How easy for those who do not bulge, to not overindulge

- Ogden Nash

 

Ogden Nash was a famous American poet and humorist.  Unfortunately the NASH to be discussed in this column is not as well known and certainly is not humorous. 

 

NASH (or non-alcoholic steatohepatitis) is a subcategory of non-alcoholic fatty liver disease (NAFLD). NAFLD is the most common chronic liver disease, affecting about 25% of adults worldwide.  It occurs when fat builds up in the liver, without associated liver damage. It can progress to NASH, which is a fatty liver but with inflammation, liver injury and scarring (fibrosis).  NASH is quite serious and can lead to cirrhosis (liver failure) or liver cancer. NASH is the most common reason for liver transplantation. About 20-30% of patients with NASH progress to cirrhosis or cancer.  NASH is seen in about 3-5% of people around the world. NAFLD is the liver manifestation of the metabolic syndrome (a systemic condition characterized by obesity, diabetes, high blood pressure and abnormal lipids, especially high triglycerides and low HDL).  Because of this association, NAFLD is linked to cardiovascular disease and both conditions are considered the end-organ damage of the metabolic syndrome.  NAFLD is diagnosed by liver ultrasound or liver biopsy, both methods show the fatty infiltration of the liver. Liver enzymes in the blood (alanine transaminase, ALT, and aspartate transaminase, AST) are mildly elevated. To make the diagnosis, daily alcohol consumption must be less than 30 grams in men and 20 grams in women per day (for perspective one glass of wine is about 17 grams).

 

There are several mechanisms linking NAFLD and cardiovascular disease.  In NAFLD, a diet high in cholesterol and saturated fat leads to high triglycerides in the blood and fat deposition in the liver. The same high triglycerides and low HDL cholesterol cause plaque build up in the heart arteries and blockage.  In diabetic patients with metabolic syndrome, persistently high sugar levels lead to vascular inflammation and coronary artery disease. Fat is present in the liver, but is also deposited around the heart.  The heart arteries run through this fatty tissue, exposing them to inflammation and subsequent blockage.

 

NAFLD is associated with higher mortality compared to the general population.  With more advanced disease (more fibrosis, cirrhosis, cancer) the higher the death rate.  Patients with NAFLD are also at higher risk for developing heart attack, stroke, angina (heart related chest pain) or cardiac death.  Patients with more advanced disease (especially more severe liver fibrosis) are at higher risk for developing cardiovascular disease. Because of this, all NAFLD patients should be evaluated for their risk for heart disease. 

 

NAFLD is treated with weight loss, exercise, diet and medication. A total body weight loss of about 10% is needed to reverse the liver fibrosis. However, weight loss alone is not sufficient to reduce the cardiac risk for NAFLD patients, other lifestyle modifications are necessary. Exercise is needed and the recommended amount is 150-200 minutes per week of moderate exercise. This includes both aerobic activity (“cardio”) and resistance (weight training).  Following a diet high in calories, saturated fats, and refined carbohydrates can lead to obesity, type two diabetes, NAFLD, metabolic syndrome and cardiovascular disease. In addition, consuming sugar-sweetened beverages that are high in fructose (a type of sugar) produces the metabolic syndrome.  Patients with NAFLD should restrict foods high in fructose, saturated fats and simple carbohydrates. Following a Mediterranean diet was shown to reduce the fat in the liver. In addition, the timing of food consumption is a factor. Intermittent fasting, with no food intake for 10 to 16 hours, helps reduce unhealthy metabolic abnormalities. This strategy involves eating during the day with nothing consumed after 6 PM.  Medications may also be beneficial for reversing NAFLD. In patients with concomitant diabetes, metformin and sodium glucose linked transport inhibitors (SGLT2 agents, such as Jardiance or Farxiga) reduce fat accumulation and decrease inflammation. These agents also reduce the risk for heart attack and congestive heart failure in diabetics. All patients with NAFLD should have their cholesterol lowered with statins. This has been proven to be safe and effective in NAFLD (despite the mild liver enzyme elevation).  Lastly, new agents that block key metabolic, inflammation and fibrosis pathways in NAFLD are being developed.

 

So, the cardiologist’s retort to Ogden Nash is that liquor may be quicker, but candy is not benign. Enjoy the holiday season, but try to limit the candy, fatty foods and sugar-sweetened beverages.  And no matter what your weight, try not to overindulge. Your heart and your liver will thank you. 

 

 

To Aspirin or Not To Aspirin

To aspirin or not to aspirin

That is the question

Whether ‘tis nobler in the mind to suffer

The slings and arrows of cardiovascular disease

Or to take meds against a sea of troubles

And by opposing end them.

 

Unlike Shakespeare, medical recommendations are not timeless. A medication may presently be prescribed for a given condition, but if new information comes out casting doubt on it’s effectiveness, then it may fall out of favor. The use of aspirin in the primary prevention of heart disease is the latest example of this, as reported by a new US government document. 

 

Aspirin’s anti-inflammatory and blood thinning properties are well suited for preventing heart disease. Aspirin thins the blood due to its effect on platelets.  Platelets are cells which circulate in the bloodstream. If there is a tear in the wall of a blood vessel (a cut) or if a cholesterol-laden plaque in an artery breaks open, the platelets rush to the site of the injury and initiate the body’s blood-clotting mechanism.  The resulting clot prevents bleeding from a cut or produces a clot within a heart artery, stopping the flow of blood and causing a heart attack.  Aspirin inhibits the platelet’s ability to form a blood clot. This puts the person taking aspirin at risk for bleeding (since the platelets cannot form a blood clot) and the blood is “thinned”.  Aspirin may cause bleeding in the stomach, the colon or the brain. 

 

Aspirin is a mainstay in preventing future cardiovascular events in patients who already have heart disease. This is termed secondary prevention. In a patient who already has had a heart attack, aspirin has been shown to reduce the risk of a second heart attack, stroke or death by 33%. In secondary prevention, the enormous benefit of aspirin in reducing the risk of a second event overwhelms the small increase in the risk for bleeding. Aspirin’s role in secondary prevention is not controversial and well established.

 

Primary prevention attempts to prevent a heart attack or cardiovascular event in a patient who does not already have heart disease. Aspirin’s role in primary prevention is less well established and quite controversial.  The issue in primary prevention is that aspirin lowers the risk for cardiovascular events by a little bit and raises the risk for bleeding a little bit with the bleeding risk outweighing the benefit (for the record, aspirin provides a 0.41% reduction in heart events but a 0.47% increase in bleeding). Whether to start aspirin in primary prevention is based on age, risk for heart disease and the risk for bleeding. In 2016, the US Preventive Services Task Force (USPSTF) recommended a low dose (81 mg) aspirin for adults aged 50 to 69 years old, who have a 10% or greater risk for cardiovascular disease (based on the American College of Cardiology cardiovascular risk calculator: http://tools.acc.org/ascvd-risk-estimator/), are not at increased risk for bleeding, and have a life expectancy of at least 10 years. In 2017, several large primary prevention studies looked at patients over the age of 60. These trials were consistent in showing that aspirin provided minimal benefit but had significant bleeding risks. Therefore, initiating aspirin for those over 70 years old for primary prevention was discouraged. 

 

In October 2021 the USPSTF updated their recommendations based on a review of 13 new trials, encompassing 161,000 patients.  They found that using aspirin for primary prevention:

1)  lowered the risk for heart attack or stroke but not cardiovascular death or all cause deaths

2)  increased the risk for gastrointestinal bleeding by 58% and bleeding into the brain by 31% compared to non-aspirin users.

3)  low dose aspirin (81 mg) didn’t lower the risk for brain bleeding compared to higher doses.

They concluded that aspirin use for primary prevention had a small benefit for people aged 40 to 59 years old with 10% or greater 10-year risk.  There is no benefit for persons 60 years or older. Lastly, the USPSTF saw no benefit for continuing aspirin for primary prevention in patients older than 75 years. 

 

After the release of the recommendations, the news media reporting left many people confused about whether to take aspirin. In an effort to clarify whether to take aspirin, consider the following scenarios. Realize that startingaspirin is different from continuingaspirin. The USPSTF’s recommendations are for initiating aspirin. So, if you are currently taking aspirin for secondary prevention, for any of the conditions listed below, DO NOT STOP ASPIRIN.

Heart attack

Heart stent

Bypass surgery

Stroke or mini stroke (TIA)

Stable angina (blockage in the heart arteries)

 

If you are taking aspirin for any of the following conditions, DO NOT STOP ASPIRIN. 

Plaque in the neck (carotid) arteries, aorta or leg arteries

Congestive heart failure 

Atrial fibrillation

Valve surgery (especially TAVR)

Elevated coronary calcium score

 

If you are taking aspirin for primary prevention, DO NOT STOP ASPIRIN. It would be beneficial to talk with your doctor about the pros and cons of continuing to take aspirin.  If you are considering starting aspirin to prevent a heart attack or stroke, realize that the benefit is only for younger, high-risk patients. For the vast majority of patients, starting aspirin in the absence of any of the conditions noted above is not beneficial.

 

So, farewell aspirin for primary prevention. Parting is such sweet sorrow.

 

 

Don’t Forget About The Flu

 

In September 2021, the United States surpassed 700,000 deaths due to COVID 19. This is certainly an enormous and tragic loss of life, but it is significant for another reason. The US now has more deaths from COVID 19 than it did during the 1918 influenza pandemic (675,000).  While COVID 19 has caused more morbidity and mortality, these sobering numbers remind us not to forget about the flu. How does influenza affect the heart and how much protection does the flu vaccine offer?

 

Influenza (“the flu”) is a very common, very contagious respiratory illness.  It is caused by an RNA virus. Influenza has three subtypes, A, B and C with A being the most common in humans (influenza can affect animals as well, causing, for example, swine flu or bird flu).  The virus consists of an RNA core surrounded by proteins. The most significant surface proteins are hemagglutinin (H) and neuraminidase (N).  When someone is infected with the flu, these surface proteins are targeted by the immune system.   In addition, these surface proteins help identify the type of influenza virus. For example, in 2009 there was a major pandemic caused by the H1N1 strain of influenza.  There are 17 H and 9 N types, but the most common human pathogens are H1, H2 or H3 and N1 or N2. H3N2 and H1N1 are the most common types of influenza A that infect humans. 

 

Influenza inflicts a huge burden on the healthcare system each year. It is responsible for almost a million hospitalizations and about 30,000 deaths per year in the United States.  Most cases of the flu resolve on their own, but certain populations are at risk for complications from influenza. This includes people over 65 years old, those with weakened immune systems, obese individuals, diabetics, and patients with underlying heart or lung disease. 

 

How does influenza affect the heart? During the acute phase of the illness, influenza stresses the body due to the symptoms and high fever. This causes an elevated heart rate and either a significant increase in blood pressure or severe lowering of the blood pressure. These effects put an increased demand on the heart and can precipitate a heart attack or congestive heart failure (CHF).  The virus may also infect the heart muscle directly and cause myocarditis (infection of the heart). In addition, influenza causes an intense inflammatory response. Inflammation plays a critical role in the progression of blockage in the heart arteries. Influenza infection accelerates the atherosclerotic process resulting in heart attacks. The inflammatory response also depresses heart function, leading to CHF.  Over the years, many studies have shown that influenza infection increases the risk for heart attack, cardiovascular death and overall deaths. The flu vaccine helps to prevent these cardiac complications.

 

The influenza vaccine is designed to produce an immune response to the virus.  Once the immune response occurs (usually within two weeks after vaccination) and someone becomes infected with the flu, the body is able to fight it off.  The key is to include the influenza viruses most likely to cause infection in a given year. The flu viruses are constantly changing and can change from one year to the next or even within a single flu season. Each year an FDA committee meets and picks the strains of influenza that it deems likely to be prevalent that year. Then manufacturers produce the vaccine. Trivalent vaccines include strains of influenza A in the H1N1 and H3N2 families plus a strain of an influenza B virus. Quadrivalent vaccines include the H1N1, H3N2 strains plus two types of influenza B strains. The ideal time for vaccination is before the flu season begins, allowing the body to develop the immune response. Typically this between September and November, but the vaccine may still be effective even in the middle of flu season.  Due to the wide variation in the strains of the influenza virus, the vaccine is only between 40 and 60% effective at preventing the flu (the Pfizer and Moderna COVID vaccines have an efficacy of about 95%). Now Pfizer and Moderna are working on flu vaccines based on the RNA technology used for COVID with trials starting soon. The RNA technology allows for more flexibility and more rapid manufacturing, potentially allowing for better strain matching. 

 

How effective are influenza vaccines at preventing heart complications?  In patients who have been hospitalized with the flu, there is a lower risk of heart attack and CHF in those vaccinated versus those who are unvaccinated. There is an 18% reduction in both heart deaths and overall deaths. In patients hospitalized with an acute heart attack, vaccinated patients had a 28% reduction in death or repeat heart attack over the following year compared to unvaccinated heart attack patients.  In people with CHF, getting the vaccine resulted in a 50% drop in death during the flu season and a 20% risk of death during the rest of the year. This is why every hospitalized patient is asked whether they want the vaccine during their hospital stay. This is why every doctor touts the vaccine for his or her patients.  Yet despite these impressive benefits and the public campaign for vaccination, only about 50% of heart patients over the age of 50 receive the flu vaccine in any given year.   

 

So remain vigilant regarding COVID 19 but don’t forget about the flu. Go out today and get your vaccine, especially if you have underlying heart disease.

 

 

 

The Cardiac Consequences of 9/11

The terrorist attacks on the World Trade Center on September 11 2001 shocked the nation, causing deep and lasting psychological and physiological effects.  Over the ensuing twenty years, numerous health problems have been described in the survivors of the attacks as well as the rescue workers. These effects include respiratory illnesses (chronic cough, asthma, bronchitis, sinus disease), several cancers (especially prostate and thyroid cancer, multiple myeloma, lymphoma, leukemia) and post traumatic stress disorder (PTSD).  The diseases are due to two main factors: dust inhalation and stress (both acute and long term). Do these same factors affect the heart? What are the cardiac consequences of the terrorist attacks?

 

Immediately after the World Trade Center attack there was an increase in heart attacks and arrhythmias, in the New York City area and beyond.  One hospital in Brooklyn reported a 35% increase in the rate of heart attack in the 60 days following the attacks. Another study looked at hospitals in New Jersey within a 50-mile radius of the World Trade Centers. The researchers showed a 49% increase in heart attacks within 60 days of the attack.  In addition, there was an increase in severe arrhythmias (irregular heart rhythms). Patients with an automatic implantable defibrillator (AICD) routinely have their devices interrogated. At the time of interrogation, any arrhythmia that has occurred since the last interrogation can be detected and the amount and severity of arrhythmia determined.  In the New York City vicinity, there was a significant increase in life-threatening arrhythmias seen in the AICD patients. The incidence of ventricular tachycardia and ventricular fibrillation (each of which can lead to cardiac arrest) doubled in the 30 days after the attack. This finding was not confined to New York City. AICD patients in Florida had a similar doubling of ventricular arrhythmias in the same time period. 

 

Did the attacks and the aftermath have any long-term effect on heart health? The World Trade Center Health Registry has followed rescue workers and lower Manhattan residents and office workers since the attacks. In 2010, they reported an increase in hospitalization for heart disease and stroke in the enrollees. PTSD (found in 22% of the women and 15% of the men) increased the risk for heart disease. Another study followed nearly 10,000 firefighters who responded on 9/11 and helped in the recovery afterwards. Over 16 years, there was an increase in heart attack, heart stents, heart surgery and heart deaths in this cohort of firefighters. The risk increased in those who responded earlier (44% higher risk for firefighters responding on 9/11 versus those who arrived later) and those who had longer exposure to the World Trace Center dust. 

 

There appear to be two mechanisms which increased the risk for heart disease after the terrorist attacks, exposure to dust and stress. It is well known that people exposed to air borne particulate matter are at risk for heart disease. For example, populations living in cities that have heavy air pollution are at higher risk for heart disease than those who live in cleaner air. The particulate matter from the World Trade Center dust was similar to air pollution. With more than million tons of dust, the exposure was extreme. The highest concentration was during and immediately after the collapse of the towers. This explains why firefighters with early exposure had more subsequent heart disease than others. Acute stress reactions, such as occur with natural disasters, are known triggers for heart attacks. An increase in heart attacks was reported after several earthquakes and the tsunami in Japan in 2011. The World Trade Center attacks certainly provoked acute stress reactions in many people.  Acute stress will activate the sympathetic nervous system, revving up the body. This in turn can lead to a heart attack, analogous to the out of shape man running for a bus in the cold. Since the body is not used to such a severe reaction, plaque in a heart artery can rupture, blood clotting is initiated and a heart attack occurs.  Chronic exposure to stress (for example, PTSD or living in chronic fear of a terrorist attack) keeps the sympathetic nervous activated, causing an elevated blood pressure and heart rate, increases inflammation, and promotes plaque formation in the heart arteries. In addition, the hormonal changes lessen the body’s ability to defend itself from a heart attack.

 

The World Trade Center attack was a horrible and tragic event on multiple levels. However, some good rises from the ashes. There are a couple of lessons for keeping the heart healthy that we can learn from aftermath of the attack.  The first lesson is to try to avoid areas with dust or particulate matter in the air (for example in the workplace or in polluted cities).  The second lesson is the importance of managing stress.  There are two ways to handle stress. The first is to avoid stress, which is difficult in our modern world. The second way is to manage stress by changing the reaction to it; to change the perception of stress. There are a variety of methods to cope with stress. These include meditation, yoga, deep breathing, laughter and pet ownership. In addition, exercise is an excellent way to relieve stress. Try taking a good brisk walk. Preferably outdoors. Preferably in clean air. 

 

 

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.