Plastics

 

"I just want to say one word to you... just one word...Plastics."

 

One of the many great quotes from the 1967 film “The Graduate” finds the main character, Ben, floundering and undecided as to his future. His future father-in-law tries to guide him and suggests a career in plastics. Over the ensuing 57 years, he certainly would have been proven correct from the business standpoint. Plastics are everywhere. The worldwide production of plastic has grown from less than 2 million tons in 1950 to about 400 million tons in 2020. Plastic production is expected to double by 2040 and triple by 2060. While plastics have made our lives better there is a downside. Plastic waste is ubiquitous in the environment.  Plastic bottles, plastic wraps for food and other plastic products are dumped in the ocean and found in the soil. These plastic products break down into smaller particles called microplastics. Microplastics are picked up by fish, especially tuna, oysters, and mussels. The burning of plastics results in the release of microplastics into the air. Humans are exposed to microplastics by ingestion (for example by eating fish) or inhaling air laden with these particles. The Center for Disease Control suggests that microplastics are present in the bodies of nearly all Americans. Microplastics have been found in the colon, liver, spleen and lymph nodes. Now we find out that plastics are present in our arteries. 

 

A study from the March 7 2024 New England Journal of Medicine was eye opening and thought provoking. The researchers examined plaque from patients undergoing surgery for blockage in their carotid (neck) arteries. 304 patients had plaque removed and analyzed. In 58% of patients, microplastics were found in their arteries. Over the next 3 years, the patients who had microplastics in their blood vessels were 4 times more likely to die or have a heart attack or stroke compared to patients without microplastics. The proposed mechanism is that microplastics penetrate the cells in the blood vessel wall, producing chronic inflammation and resulting in worsening plaque production and outcomes. The authors proposed microplastics as a new cardiac risk factor. The study generated lots of discussion in the medical community. The study itself had many flaws (single center, small number of patients). The bottom line is association does not mean causation. Microplastics may be associated with adverse cardiac outcomes but may not be causing the adverse events. Further studies are needed to confirm the findings.

 

Plastics may be another in a growing number of environmental pollutants that have cardiovascular consequences. Known risk factors are air pollution (http://sportscardiology.blogspot.com/2017/08/paris-polluted-arteries-r-not-in-style.html)

and noise pollution 

(http://sportscardiology.blogspot.com/2020/02/the-cardiac-consequence-of-sound.html). Pollution is defined as the presence of a substance in the environment that can cause adverse health effects as well as damage to the ecosystem. Air pollution is the most important environmental cardiac risk factor. Of all of the air pollution related deaths, cardiac disease accounts for 45% of the total, while lung disease is only 8%. In addition, there is soil and water pollution due to farming and industrial activity as well as waste disposal (plastics falls into this category). In addition to plastics, other pollutants include pesticides and heavy metals. Despite different chemical compositions, pollutants lead to cardiovascular disease through common pathways. Pollutants trigger stress reactions leading to systemic inflammation leading to plaque and blockage in arteries, increased blood clotting, and abnormal hormonal secretion. 

 

Controlling pollution is important for overall cardiac health. Decreased air pollution over the past 50 years has contributed to the decline in overall cardiac mortality in that time period. Given the scope and magnitude of the pollution problem, what can a single person do? While most of the heavy work decreasing pollution must be left to governments and industry, there is much the individual can help with. To decrease exposure to air pollution one can stay indoors during high pollutant levels, commute by public transportation or bike or on foot and avoid spending time in high pollution areas, such as near highways. In addition, plastic pollution can be decreased by minimizing single use plastics (products designed for one use and then thrown away). This includes food and beverage containers, bottles, straws, cups, plastic forks and knives and disposable plastic bags. Follow some of these easy measures and your arteries will thank you. 

 

 

 

The Dawn of a New Day

 

When the child of morning, rosy-fingered Dawn, appeared, Odysseus rose and led the way to the place of assembly, which was near the ships.

Book VIII, The Odyssey

Homer

 

The phrase “rosy-fingered dawn” is an epithet (a descriptive term) used many times by Homer in both the Iliad and the Odyssey to say, “the break of day”. The term also signifies a fresh start to a new day and a tribute to the trials and tribulations of the day. How does the body handle the “rosy-fingered dawn” and rising from sleep to face a new day? What physiologic changes occur and how do those changes impact heart health?

 

The human body ticks to a 24-hour clock. This clock determines changes in our bodily functions which guide us between a rest stage (sleep) and an active stage. Our internal rhythms are synchronized with the world through interactions with light. These variations are called circadian rhythms (the term circadian is from Latin, circa which means around and dies which means day; around the day). As the rosy-fingered dawn breaks, we sense the presence of light. This results in the secretion of a number of hormones which serve to rouse us, “rev” us up, to get ready for a new day. The hormones include adrenaline and cortisol, which result in an increase in blood pressure and heart rate, increase our wakefulness, increase body temperature and get us ready to be become active. On the other hand, as light fades, the body secretes melatonin and decreases adrenaline and cortisol, getting us ready for the rest phase, sleep. Disruptions to the well-controlled circadian rhythm can lead to various chronic illnesses including heart disease. 

 

Circadian rhythms are controlled by a number of biological clocks. A central clock is located deep in the brain and regulates the clocks located throughout the body. These peripheral clocks are found in nearly all of the tissues of the body, especially in the gastrointestinal system, the nervous system, the liver and the heart. The circadian clocks are molecules within the cell that provide feedback loops timed to a 24-hour cycle. There are clocks in the heart muscle as well as in the wall of blood vessels. The heart muscle clocks orchestrate cellular processes, ensuring that they occur at the right time of the day. Growth and repair of heart tissue takes place during sleep or rest periods. If this circadian pattern is broken, then cardiac pathology ensues. During a normal day, there are fluctuations of up to 20% in various cardiac parameters. For example, blood pressure is lowest during sleep and highest in the early morning hours.  This is due to the release of the hormones responsible for rousing us at the beginning of the day.  Similarly, the greatest risk for a heart attack or stroke is around 6 AM. This is a direct result of the early morning changes with increased blood pressure and heart rate leading to increased stress with the heart’s blood vessels and an increase in clotting factors caused by the release of hormones. In addition, life threatening arrhythmias and sudden cardiac arrest peak around 6 AM.  

 

Maintaining normal circadian periodicity is important for preventing disease and maximizing longevity. Disruption of the normal circadian rhythm is detrimental and leads to a variety of chronic illnesses. Disruption can be genetic, environmental or behavioral. Irregular sleep and eating schedules misalign the clocks. It is important to keep sleep timed with lack of light, i.e. night-time. Irregular sleep schedules throw off the biological clocks so they can’t synchronize properly with the light-dark cycle. Changes such as jet lag and daylight savings time can disturb internal clocks and lead to cognitive impairment and increased risk for heart attack.  Shift workers who sleep during daytime are especially prone to circadian disturbances. Shift work is a risk factor for heart disease, diabetes, obesity and hypertension. It increases cholesterol and triglyceride levels and increase inflammation. Sleep timing is important as well. Evening types, people who have later wake up and bedtimes, are at increased risk compared to morning people. Evening types have a higher incidence of cardiac disease, diabetes and obesity. Therefore, it is important to keep a regular sleep schedule. Meal timing is another factor as food serves to synchronize the biological clocks. Eating late at night also leads to cardiac disease, diabetes, obesity and high cholesterol. Shifting food toward the beginning of the day reduces those risks. This was proven in a recent study. Late eaters, people whose largest meal of the day was after 12:38 PM, had higher risk for obesity than people whose main meal is at lunch time. Having smaller meals throughout the day was better than eating three “square” meals. In addition, intermittent fasting, food intake restricted to early morning to 6 PM with an overnight fast, can reduce weight and protect against metabolic disease. 

 

To every rule, there is an exception. In this case, the exception lies in a Blue Zone. Blue Zones are areas around the world where there is exceptional longevity, with many people in the population reaching 100 years of age. Blue Zones have been identified in Japan, Costa Rica, California and on the Mediterranean island of Ikaria, Greece. The Mediterranean lifestyle seems to counter the circadian rhythms noted above. Dinner is served after 9 PM at night and bedtime occurs late as well. In addition, there is a day time siesta, so sleep patterns are irregular. On the other hand, the main meal is lunch. 

 

There are numerous factors involved in greeting many rosy-fingered dawns. Listening to our biologic clocks and following our circadian rhythms can help stave off disease and increase longevity. In order to do this, regular sleep habits and timing sleep patterns to light and dark seem prudent. In addition, shifting caloric intake to earlier in the day, eating smaller meals and doing some overnight fasting will improve the chances of seeing the dawn of a new day. 

 

 

Cold-Hearted

 

CLEOPATRA: Ah, dear, if I be so,
From my cold heart let heaven engender hail,
And poison it in the source

 

The expression cold-hearted means showing no understanding, no feeling towards another. It is unsympathetic, unemotional, uncaring and cruel. If used in a sentence it might look like this: “The cold-hearted landlord evicted the poor family with a sick child”. The first known use of the adjective cold-hearted is in Shakespeare’s play, “Antony and Cleopatra”. Certainly, Cleopatra could be considered cold-hearted due to her various plots to overthrow her brother and rule Egypt. Heart attacks can also be considered cold-hearted. A heart attack does not discriminate; it can affect men or women, young or old, rich or poor. It can strike at any time of the day or night, often without warning. Despite that, heart attacks do have some predictable variation. For example, heart attack risk changes with the season of the year and is associated with extremes of temperature, both hot and cold.  The only known example of Cleopatra’s handwriting is a single Greek work, γίνεσθοι, which she wrote on a papyrus addressed to a tax collector in 33 BC. It translates to, “so be it” or “make it happen”. Heeding the queen’s order, we will now “make it happen” and outline when heart attacks are the most cold-hearted.  

 

A heart attack occurs when a plaque in a heart artery breaks open. When the blood is exposed to foreign material (such as an exposed plaque), it does what it is supposed to do and forms a blood clot within the artery. If the clot totally obstructs the flow of blood, the type of resulting heart attack is called a STEMI (ST elevation myocardial infarction). If there is still some residual blood flow through the blockage and clot, then the heart attack is a nonSTEMI. For both types of heart attack, there is a U-shaped association with temperature. There is an increased risk for heart attack on very cold and on very hot days. Since we are in the throes of winter, we’ll concentrate on the cold weather effects on the heart. An increase in heart attacks and heart attack deaths in the winter was first noticed in the 1930’s. A large database studied heart attacks from the 1980’s and 1990’s and quantified the risk. A seasonal distribution was confirmed; there were 50% more heart attacks in the winter months compared to the summer time. The peak number of cases were in January, followed by February, March, November and December. Another series, also from the 1990’s, concluded that coronary events were 20-40% more likely to happen in the winter and spring versus other times of the year. One other study (1980’s-1990’s) also showed that the month with the highest mortality rate due to a heart attack was January.  Lastly, a study from Minnesota (1979-2002) showed that a temperature below 0 degrees Celsius (32 degrees Fahrenheit) was strongly associated with death due to a heart attack.

 

A lot has changed in the 25 to 30 years since this data was reported. At least two factors have changed significantly. First, heart attack care has vastly improved. Catheterization and coronary stenting during the acute event (especially STEMI) restores blood flow and subsequently fewer patients die from their heart attack. Secondly, there is global warming. Since the 1950’s each decade is hotter than the previous one. Globally, the temperature has risen 0.17 degrees Fahrenheit each decade, with steeper rise since the 1970’s. Has the combination of warmer weather and improvement in cardiac care reduced the risk for having a heart attack in winter? To answer this a group from Germany looked at temperature and heart attacks in two distinct periods, 1987 to 2000 and 2001 to 2014. During those time periods, the average daily maximum temperature rose from 14.5 degrees C (58.1 degrees F) during 1987-2000 to 15.1 degrees C (59.2 degrees F) in 2001-2014. They found no significant decline in cold related heart attacks when comparing the two eras. Heart attack risk remained high with very cold temperature. Another group studied data from five European countries between 1994 and 2010. They also found that cold weather was associated with an increased risk for heart attack, without change over time. With a drop in temperature from 5 degrees C (41 degrees F) to – 5 degrees C (23 degrees F) there is about 20% increased risk for heart attack and cardiac death. Lastly, a study from Taiwan looking at data from 2000 to 2017 showed that below 15 degrees C (59 degrees F), every 1 degree drop in temperature increased the risk for heart attack by 0.9%.

 

The relationship between cold weather and heart attack has been seen across the globe, in different eras, with different populations and with different weather conditions. It even holds up locally. Over the past five years, the month with the second highest risk for STEMI at Robert Wood Johnson Somerset has been January. How does cold affect the heart and who is at risk?   Elderly patients (over 65 years old) are more susceptible to cold related heart attacks than younger people. The highest risk are older patients with hypertension (high blood pressure). Cold weather increases blood pressure and causes spasm of the heart arteries. This leads to an increase in the work load of the heart. Cold weather increases the thickness of the blood, increases clotting factors and increases inflammation. All of the factors can cause a vulnerable heart plaque to open and trigger a heart attack. The winter months also increase the risk for respiratory infections (for example, flu) which act as a trigger for a heart attack. Other cold related factors include less physical activity, weight gain and holiday stress adding to the risk for heart attack in the winter. 

 

For the elderly heart patient, the cold weather can be as deadly as an asp. For those with significant heart disease, here are some cold weather recommendations. Skip strenuous activity outdoors when the temperature (or the wind chill) is below 30 degrees F and do your exercising indoors. When outside, try to cover all exposed skin. Make sure the heating system in the house is working and use it! The World Health Organization suggests keeping the indoor temperature above 68 degrees F. Lastly, relax with a cup of tea by the fire and count the days until spring. 

 

 

 

 

Vive La Resistance (Training)!

 

The holidays are over. It’s a new year. The decorations are stored away and the New Year’s resolutions are made. What are the top New Year’s resolutions? According to Forbes magazine, the number one New Year’s resolution for 2024 is to improve fitness and exercise more. That is a worthy goal, but what type of exercise should be targeted in 2024? Another top resolution per Forbes is to lose weight. That is also a good goal, but how long will it take to get the holiday weight off?

 

If you are feeling bloated and have gained weight during this holiday season, you are not alone. A study tracked the change in weight for participants in three countries, the US, Germany and Japan. In these three diverse countries, weight started to go up in November and peaked on New Year’s Day. On average, it took until March to lose the weight gained and get back to the pre-holiday weight. How can holiday weight gain be prevented? One strategy is to have smaller meal portions at the family table and eat fewer desserts. Another is to exercise. It has been shown that people who continue exercise training during the holidays can prevent weight gain.

 

It is established that exercise will help with losing weight. It is established that exercising more is the top New Year’s resolution, but what kind of exercising should be done? Aerobic training has well known benefits. The scientific evidence is vast and consistent in showing that cardio exercise (such as running, cycling, swimming or hiking) has many cardiovascular benefits, in addition to increasing longevity. Therefore, aerobic exercise should be a main component of any exercise regimen. What about resistance training? It has been perceived that aerobic exercise is better than resistance training but in fact each is important. It has been estimated that only 28% of US adults perform any form of resistance exercise. Resistance training lowers the risk of dying from any cause by 15% and lowers the risk for cardiovascular disease and death by 17%. Resistance exercise will lower systolic blood pressure by 4 mmHg and diastolic blood pressure by 2 mmHg. It will lower fasting blood sugar by 2 to 5 mg/dl, increase HDL cholesterol (2 to 12 mg/dl), lower total cholesterol (by 8 mg/dl) and reduce triglycerides (7 to 13 mg/dl). Combining resistance and aerobic training gives even greater benefit in terms of weight reduction, diabetes prevention, cholesterol lowering, cardiovascular disease prevention and mortality reduction. 

 

In addition to cardiovascular prevention, resistance training has another very important benefit. As we age, there is progressive decrease in muscle mass and strength. With age, activities such as standing up, sitting down, climbing stairs and maintaining balance are as important as cardiac fitness.  Most of the loss of muscle mass occurs after age 60. Men will lose, on average, 33% of their muscle mass between the ages of 60 and 97. Women will lose 26%. With the loss of muscle mass and strength, significant health problems may ensue as the risk for falls increases by 60% and risk of bone fracture increases by 84%. Resistance training helps to build and maintain muscle strength. Resistance training improves muscle mass (by increasing leg and total body musculature) and muscle strength (by improving handgrip strength, chest and leg press) as well as overall physical performance (by improving sitting to standing, walking speed). 

 

What does a resistance training prescription look like? Resistance training can include free weights, body weight (for example push-ups, squats), machine weights or resistance bands. Resistance training doesn’t necessarily lead to “bulking up” and can be done without great expense (a gym membership or a major set of weights aren’t needed). Ideally 8 to 10 different exercises involving major muscle groups are done (for example, push-up, squat, abdominal crunch, biceps curl). Each exercise is performed for 8 to 12 repetitions. Weight and intensity can be increased gradually over time. Resistance training should be done two or more times per week for maximal muscle strengthening and cardiovascular benefit. 

 

As we get older, we are limited by our heart and/or our orthopedics. Resistance exercise helps with both. So this year resolve to pump up your fitness, build some muscle, lose weight and improve your cardiovascular profile by incorporating resistance training into your exercise routine. 

 

 

Jolly Old Visceral Fat

 

It is holiday season and no single figure dominates this time of year like Santa Claus. The figure of Santa Claus is likely based on a combination of ancient legends including St Nicholas (a Greek saint known for his gift giving), Father Christmas (England) and Sinterklaas (a Dutch legend). The name “Santa Claus” was first used in the US press in 1773. The caricature of Santa Claus as a jolly, rotund, white bearded, red suit wearing elf was first defined by Thomas Nast (a famous political cartoonist who lived in Morristown New Jersey) in an illustration for Harper’s Weekly in 1863. How rotund is Santa? According to NORAD (the North American Aerospace Defense Command), who tracks Santa’s course across the world on Christmas Eve, Santa is 5 feet 7 inches tall and weighs about 260 pounds. This would put Santa’s Body Mass Index (BMI) at 40.72 kg/m2 which places him squarely in the obese category. How does Santa’s obesity, his round belly and visceral fat affect his risk for heart disease?  Should we be worried about Santa?

 

It is estimated that 42% of the adults in the United States are obese. Being overweight (BMI 25-29 kg/m2) or obese (BMI >30 kg/m2) increases the risk for cardiovascular disease and cardiovascular death. The BMI was invented in the 1830’s by a Belgian astronomer who was trying to categorize different types of people. The mathematical formula for BMI relies on only two variables, height and weight. Since its inception, the BMI (and similar calculations) have been used by insurance companies to calculate the risk of dying. Since 1972, the BMI has been used to define obesity, even though it is not a perfect measure.  Amongst its flaws, it cannot distinguish between fat and muscle. Consider a 6-foot 9-inch 250-pound man. His BMI is 26.8 kg/m2 putting him in the overweight category. However, if this man is a muscular perennial NBA All Star, then no one would consider him overweight. His higher BMI is due to muscle, not fat. Another flaw is that the BMI cannot distinguish between subcutaneous fat (fat deposited under the skin; think “pinch an inch” or those love handles that have popped up over the years) and visceral fat. Visceral fat is fat deposited in and around the organs in the abdomen and chest. Visceral fat poses many more health risks than subcutaneous fat. Visceral fat interferes with blood sugar regulation and lipid storage, leading to diabetes, elevated triglycerides, high blood pressure and subsequent heart disease. Waist circumference may be a better measure of visceral fat than BMI. Obesity is defined by a waist circumference >40 inches in men and > 35 inches in women.  An elevated waist circumference is associated with heart artery disease and increased risk for cardiac death. Body fat percentage is an even better indicator of obesity than body weight or BMI. Body fat percentage greater than 30% in men and 35% in women is considered obese (the acceptable range is 20-29%).

 

The heart is considered a visceral organ and thus prone to fat accumulation. Normally fat is present in two areas in the heart. Epicardial fat is present between the heart muscle and the pericardium (the sac that encompasses the heart). Epicardial fat provides a layer of fat on the heart muscle and around the heart arteries.  It has beneficial effects both anatomically and functionally. It acts as a buffer and provides mechanical protection for the heart arteries. Epicardial fat also secretes a variety of active substances and since it is in close proximity to the heart arteries these substances help in the regulation of the internal environment of the arteries. These fat depots also store fatty acids and act as an energy supplier for the heart. During times of high demand, the fatty acids are released into the heart muscle. Unfortunately, excess epicardial fat increases inflammation which in turn promotes and worsens blockage in the heart arteries and increases the risk for atrial fibrillation.  Pericardial fat is the second type of fat seen in the heart and is located between the two layers of the pericardium (the pericardium surrounds the heart and the visceral layer is adjacent to the heart muscle while the parietal pericardium faces outside the heart). Like epicardial fat, pericardial fat provides mechanical protection for the heart and helps keep the heart contracting smoothly and friction free (you could say the heart is a well-greased machine!). Also, like epicardial fat, an excess of pericardial fat is detrimental. Excess pericardial fat is associated with congestive heart failure. Both types of fat can be detected and quantified by cardiac CT or MRI scan. CT scan for coronary calcium also provides the opportunity to look for excess epicardial and/or pericardial fat.

 

After Santa has given out all of his gifts on Christmas Eve (and eaten a billion cookies in the process), how should we treat Santa’s obesity and visceral fat? Obesity management involves 5 interventions: behavioral changes, nutrition, physical activity, medications and surgery. Lifestyle modifications can produce 5% to 10% weight loss. Newer medications have been quite effective in reducing weight. Semaglutide (Ozempic) can reduce weight by 10-15% while tirzepatide (Mounjaro) can result in 15-20% weight loss. On average, surgical procedures reduce weight by 20-30%, but even greater reductions can occur. Do these weight loss strategies reduce cardiac outcomes and cardiac fat? Surgery reduces the risk for dying from any cause by 37%, heart failure by 54% and heart attack by 37%. Semaglutide has recently been shown to improve cardiac outcomes by 20%, especially in the those with established cardiac disease or diabetes. Lastly weight loss by lifestyle modification or surgery reduces epicardial fat thickness by 9% to 32%.

 

So, this year instead of leaving Santa milk and cookies on Christmas Eve, perhaps a plate of vegetables and a prescription for Ozempic would be better for his health.

 

 

The Trouble With Triglycerides

In the classic Star Trek episode, “The Trouble with Tribbles”, the crew find themselves on an alien planet. A trader gives a tribble to one of the officers, who brings it on board the Enterprise. The tribbles are purring balls of fluff that ease human anxieties. They are instantly loved by the crew. Unfortunately, the tribbles reproduce rapidly, taking over all of the space on the ship and eating all of the food on board. Because the tribbles are killing their hosts, they have to be removed.

 

Triglycerides transport the fat that we eat to the cells in the body to use for energy. Unlike tribbles, triglycerides are not cute and fuzzy, although high levels of triglycerides make the blood look milky and cloudy. Also, like tribbles, as triglycerides accumulate (the blood level goes up) it can kill its host (the risk for heart disease goes up). Elevated levels of triglycerides are either primary (genetic, running in families) or secondary to other medical conditions or lifestyle choices. Secondary causes include type 2 diabetes, thyroid disease, or fatty liver disease. Lifestyle factors include obesity, being sedentary, smoking, alcohol use, or a diet high in saturated fats or processed sugars. Hypertriglyceridemia is defined as blood levels above 150 mg/dl. World-wide more than 25% of people have high triglycerides. High triglyceride levels have been strongly and significantly associated with elevated cardiovascular risk, independent of LDL (“bad cholesterol”) levels. People can have normal or low LDL values, but if their triglycerides are high, they are still at risk for a heart attack. In addition, a very high level of triglycerides is a risk factor for pancreatitis (a potentially life-threatening inflammation of the pancreas). The trouble with triglycerides is how to treat them or whether to treat them at all.

 

The first step in treating elevated triglycerides is lifestyle modification. This starts with reducing excess weight, alcohol intake and dietary carbohydrates. Additional measures include exercise, smoking cessation and diabetes control. Together, these interventions can lower triglycerides by 60%. Medications for high triglycerides include statins, fibrates and omega-3 fatty acids. Certain statins (for example, atorvastatin) lower triglycerides as well as LDL cholesterol and should always be the initial agent chosen. Atorvastatin (Lipitor) reduces triglycerides by about 25%. Fibrates (such as fenofibrate) have the highest potency in reducing triglycerides. However, despite lowering triglycerides by 30-50%, fenofibrates have not been shown to reduce the risk of cardiac events. There are three omega-3 fatty acid formulations in clinical use. These are: eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and icosapent ethyl (IPE, a highly purified form of EPA).  EPA is found in plants and fish. Medications with high dose EPA reduce triglycerides by 14-33%. One study showed that EPA reduced cardiac events by 19%. Another study looked at IPE in patients with heart disease or diabetes on a statin. High dose IPE reduced cardiac events by 25%. However, triglycerides were only modestly reduced in the study and it was felt that other factors improved the outcomes (possibly anti-inflammation or anti-oxidant effects of IPE). On the other hand, a large review of multiple trials did not show a reduction in cardiac events with omega-3 fatty acid therapy. In addition, a study of EPA and DHA did not show a reduction in outcomes. The reason for this discrepancy is currently being hotly debated in the cardiology community. 

  

It is well established that higher triglyceride levels are associated with higher cardiac events. However, while there is strong evidence for lowering LDL (the current principle is lower is better) to reduce cardiac risk, the data regarding triglyceride treatment is less conclusive. So, what should we do about high triglycerides? Should we ignore them and not treat them since there is no therapy that unequivocally reduces outcomes? Should we treat them with our current agents and hope that future research proves these therapeutics useful? Should we beam up to the Enterprise and find a new planet? Right now, there is no definite answer, but a few recommendations can be made. The first and strongest recommendation is to start atorvastatin (Lipitor) in patients with established heart artery disease or high risk for heart artery disease (for example diabetics) and elevated LDL and triglyceride levels. A second recommendation can be made for the high-risk patient (as defined above) who has triglyceride levels above 150 mg/dl and whose LDL is at goal with a statin. This type of patient should be started on high dose IPE. Lastly, patients with triglyceride levels over 300 mg/dl should start fenofibrate to reduce the risk for pancreatitis. What about the lack of data? Never fear, the science officers are combing the galaxy, doing the research, trying to find an answer to the triglyceride question. Stay tuned.

 

My Watch Says I Am in Atrial Fibrillation. What Should I do?

 

Recently there has been an explosion in consumer wearable smart devices. It is estimated that 1.1 billion devices were in use worldwide in 2022. These devices can detect and monitor a variety of health-related parameters including heart rate and arrhythmias (abnormal heart rhythms). Devices include smartwatches worn on the wrist, fitness bands with chest strap, and a stand-alone handheld single lead electrocardiogram (EKG) monitor. Smart devices can monitor heart rate and determine if there is an arrhythmia using two methods. The first method is photoplethysmography (PPG). The second way is to obtain an actual EKG strip, either a single lead or multiple leads, using electrotrodes as would be done with an EKG in a doctor’s office. PPG works by sending light pulses to the skin. The intensity and pulsatility of light reflected from the blood vessels can determine heart rate and algorithms can provide an estimate of whether there is an arrhythmia. Smartwatches such as Apple Watch (series 4 or later) and Samsung Galaxy Watch 3 utilize both PPG and EKG. PPG is used for routine monitoring, but the user can be prompted to obtain a single lead EKG by holding the crown of the watch for 30 seconds. The KardiaMobile device is connected to a phone but is a stand-alone monitor. It has two pads and the user places a finger on each pad to record a single lead EKG. Smartwatches using PPG can accurately detect heart rate, but accuracy drops off with activity.  One study showed a 30% reduction in accuracy during exercise. For a more accurate determination of heart rate with exercise, a chest strap using PPG can be used.  Patients often see their doctor for advice about arrhythmias that are detected on their smart devices. How accurate are the readings? What should one do if the device says there is atrial fibrillation (Afib)?

 

Before diving into wearable devices and Afib, a few words about Afib itself. Afib is a very common arrhythmia. In this condition, the upper chambers of the heart (the atria) fibrillate, beat chaotically, not in a regular coordinated manner. When the atria fibrillate, blood doesn’t flow into the lower heart chambers (the ventricles) efficiently and blood can stagnate in the atria. If blood is not flowing it can form clots. These clots break off and can cause a stroke. To treat this and prevent a second stroke in someone who already has had a stroke, blood thinners are prescribed. How important is the Afib/stroke connection? In a patient with a stroke, or a “mini-stroke” (TIA), a cause for the stroke cannot be found in 30%. This is called cryptogenic stroke, a stroke of unknown origin. It turns out that Afib is a major cause of cryptogenic stroke. If a patient is hospitalized with a stroke and a cause cannot be found, they often are prescribed a monitor to wear for one month to see if they have Afib. If Afib is found, they are prescribed a blood thinner. The use of blood thinners in Afib is quite effective, but comes at a cost. These medications can cause bleeding. In a patient with Afib, who should be placed on a blood thinner? The answer is not easy and there is lots we know, and still lots we don’t know. Some Afib patients are straightforward and should be on blood thinners. These include patients who are known to be in Afib for 48 hours of more. Also, patients with Afib and a history of stroke or mini-stroke should be on one of these agents. Patients with Afib who haven’t had a stroke but who are at high risk for a stroke (older patients, women, diabetics, heart failure patients, hypertensives, and patients with vascular disease) should be on a blood thinner. If a patient is not in one of these categories, how much Afib is needed before committing them to a blood thinner: an hour of Afib? several hours of Afib? a day of Afib? Unfortunately, we don’t yet know that answer, but a recent study did shed some light. The study looked at pacemaker patients without prior history of Afib. A pacemaker can be interrogated and can tell precisely how long a patient has an arrhythmia such as Afib. The study looked at pacemaker patients who had short duration episodes of Afib; the average time in Afib was about three hours. Patients who were given a blood thinner did not have fewer strokes than patients who were not on a blood thinner. In fact giving the blood thinner caused harm, more patients had bleeding. So, putting patients on a blood thinner for short duration episodes of Afib does not prevent strokes and may be causing harm.  We still do not know the burden of Afib necessary to start treating to prevent a stroke. 

 

How accurate are smartwatches and KardiaMobile devices in detecting Afib? More and more studies are being performed to check the validity of these devices. One study found that Apple Watch and Samsung Galaxy Watch were 80% accurate in picking out Afib, while KardiaMobile was 74% accurate. One issue with the devices was the high number of inconclusive tracings: Apple 18%, Galaxy 17%, KardiaMobile 26%. Another study of KardiaMobile also showed 74% accuracy and 16% of tracings could not be classified. The bottom line is that these devices are readily available, not very expensive (KardiaMobile is less than $100), reasonably accurate and the technology will only continue to improve.     

 

So, what should you do if your smartwatch tells you that you are in Afib? First, realize that these devices should only be used as a screening tool. See your doctor, bring your phone or tracings for your doctor to review. Afib should be confirmed with medical grade devices such as a Holter monitor (worn for one to three days) or an event monitor (worn for two to four weeks) or an implantable recorder (used for months to years). Next discuss with your doctor whether you should be on a blood thinner, remembering that short duration episodes of Afib likely don’t need to be treated. However, if you have had a stroke, or mini-stroke (TIA) especially if cryptogenic, then starting a blood thinner may be appropriate. Even if the detection of Afib by your smart device doesn’t lead to a blood thinner, it can make a difference in your treatment plan. Medications may be changed to try to avoid Afib. In addition, triggers for Afib can be discussed and corrected (treating high blood pressure or sleep apnea, decreasing or eliminating alcohol, starting an exercise program or weight loss). Listen to your body and watch your watch.