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.

 

Deconditioning and the Flabby Heart

 

You know the feeling. Every weekend warrior knows the feeling. You spend time building up your exercise capacity by biking, running, swimming, hiking, or going to the gym. Then for some reason (illness, injury, other obligations) you have to stop exercising for weeks or months. When you return to your activity, you are more short of breath, you don’t have the same exercise capacity, and you feel “out of shape”. What happens to the heart during deconditioning (the medical term for “out of shape”)?  Does deconditioning occur with elite athletes or astronauts? Does it happen on weekdays to weekend warriors?

 

The heart is a muscle. With training athletes can build up their arm and leg muscles.  The same process builds up the heart muscle as well. The cardiac effects of long-term exercise include increases in the size of the heart, the thickness of the heart’s muscle and the cardiac mass.  (The heart enlarges to accommodate the increased blood flow during exercise. The walls of the main pumping chamber, the left ventricle, thicken and become more muscular to pump the excess blood.  Cardiac mass is the weight of the heart and represents the long-term effective of blood pressure on the heart). A larger, thick walled heart is called an athlete’s heart. Unfortunately, a thick muscular athlete’s heart resembles a form of cardiac pathology, hypertrophic cardiomyopathy (a congenital abnormality where the heart muscle is very thick and there is a risk for arrhythmia).  Congenital hypertrophic cardiomyopathy is the most common reason for sudden cardiac arrest in the athlete. Athletes are screened to see if they have hypertrophic cardiomyopathy and, if present, vigorous exercise is prohibited. Unfortunately, it is difficult to differentiate between pathologic hypertrophic cardiomyopathy and an athlete’s heart. One way to tell the difference is to have the athlete stop exercising for a period of time, a method called detraining. If the heart muscle reverts to normal thickness during detraining, then it is an athlete’s heart.  Studies on Olympic athletes have shown that after about 12 weeks of detraining left ventricular thickness rapidly decreases (thickness goes down by 15-33%).  In addition, cardiac mass decreases quickly as well, within 4 to 8 weeks. For full regression of left ventricular thickening, detraining should last 6 months.

 

The healthy heart needs exercise, but it also needs gravity. Both of those items are in short supply to astronauts on a long-term space mission. The lack of gravity has the same effect as prolonged bed rest on the heart, worsening the deconditioning that takes place in space.  Studies performed on astronauts who spend months in space show that space flight causes significant cardiac atrophy. After only a few weeks in space, there is a reduction in the heart’s muscle mass. It is estimated that cardiac muscle mass decreases about 1% per week in flight. This deconditioning has obvious consequences for prolonged space missions. A recent study followed astronauts on the International Space Station. The astronauts were in flight for many months and spent 2 hours each day doing endurance and resistance training. Cardiac work load was 12% lower in space than on Earth due to zero gravity and the confines of the station. Despite the lower work load, the astronauts’ heart muscle mass stayed intact. It seems that exercise can preserve the heart’s structure and function offsetting space flight deconditioning. 

 

Most people don’t have to worry about their heart becoming too thick from exercise or losing cardiac muscle mass on a space flight. However, deconditioning occurs in the average person, with changes similar to the detrained athlete or the astronaut in space. Deconditioning is defined as the adaptation of the body to a less strenuous environment and the decreased ability to function with physical exertion. The body resets to a lower level of functioning so that when it is asked to increase physical activity, it is unable to meet the demand. Deconditioning occurs when people stop exercising; the most extreme example is bed rest.  Many studies of patients during bed rest show that skeletal muscle strength is lost rapidly (10-20% in a week, 50% in 3 to 5 weeks). Skeletal muscle mass also decreases 3% within a week of bed rest. In addition, bone density decreases as well. From the cardiovascular standpoint, blood volume goes down and heart rate goes up with bed rest. This means that the body cannot compensate when going from a supine to a standing position; blood pressure drops on standing and patients can pass out. Lastly, bed rest causes cardiac atrophy. With 2 weeks of bed rest, there is a reduction in cardiac muscle mass of 5%, similar to what happens with astronauts in space and the detrained athlete.

 

Can the “weekend warrior”, someone who only exercises one or two days per week, become deconditioned during the work week? Likely this is not the case as loss of cardiac structure and function occurs after weeks to months of inactivity. In fact, a recent study showed that as long as weekend warriors exercised for 150 minutes per week or more, they had similar reductions in their risk for heart attack, stroke, atrial fibrillation and heart failure as people who exercise daily. 

 

You worked hard to build up your exercise capacity. Don’t stop now and let your heart become flabby and deconditioned. Keep active and keep exercising a minimum of 150 minutes per week, even if it is only two days a week.

 

 

 

The Café Coffee Culture and Cardiac Disease

 

Imagine yourself walking down a street in a French town. You spot a picturesque café in the square, perhaps one that had been painted by Van Gogh. People are in the café, relaxed, sipping their coffees. It looks so inviting. You want to join them and order a nice café Americano, but you wonder how good is coffee for the heart? 

 

Before we drip into the medical data, some fun facts about coffee. Coffee grows on a bush and the beans are actually the pit of a berry, which makes coffee a fruit. Coffee has been consumed for about 500 years. In the US, about 85% of adults drink coffee daily, averaging 1.5 standard cups per day. Brazil is the largest exporter of coffee in the world and Finland is the worldwide leader in coffee consumption.Now let’s pour over the physiological effects of coffee. Coffee is not just caffeine; the beans have over 100 active substances which have a variety of metabolic effects. Drinking coffee causes the heart rate and blood pressure to increase. Effective sleep may be suppressed. Caffeine increases catecholamines (adrenaline). Coffee stimulates the electrical system of the heart. For these reasons, many cardiologists recommend decreasing or stopping caffeine use. Is that recommendation justified?

 

Does coffee cause heart arrhythmias?

Doctors have always felt that coffee may increase the number of premature atrial contractions (PACS) and premature ventricular contractions (PVCs).  Increased PACS may result in atrial fibrillation (Afib) while increased PVCS may cause ventricular arrhythmias. A recent study in healthy volunteers showed that coffee did not increase the number of daily PACs, but may increase PVCs. The accumulated medical literature has shown that coffee drinkers have a lower risk for Afib than those who do not drink coffee. Drinking one cup per day lowers the risk for Afib by 20%. The reason for this may be that long-term coffee drinkers develop a tolerance to the electrical stimulating effects of caffeine. However, there is a lot of individual variation in terms of response to coffee. Approximately 25% of patients report coffee as a trigger for Afib. Clearly those patients should avoid it. Similarly, the literature does not show an increase in ventricular arrhythmias with coffee consumption, despite a possible increase in PVCs. This holds true even for patients with history of significant ventricular arrhythmias. It appears that drinking coffee is safe for most patients in terms of their potential for arrhythmia.

 

Is it the caffeine?

Coffee is the most commonly used stimulant in the world. Coffee activates the central nervous system, boosts alertness and has a variety of psychoactive effects. Are these effects due solely to caffeine? In an interesting study people were given coffee or plain caffeine in water and then underwent MRI scans of the brain. The coffee drinkers had a heightened state of preparedness, were more responsive and had higher executive brain functioning than the plain caffeine group. It appears there is more to coffee than just caffeine. 

 

Does coffee raise blood pressure?

The effect of coffee on blood pressure is still not decided. Drinking a cup of coffee will transiently increase blood pressure for about 30 minutes.  Coffee stimulates catecholamines and stimulates receptors in the blood vessels to constrict, causing an increase in blood pressure. However, this is counterbalanced by an increase in nitric oxide, which dilates blood vessels. Over time, the acute effect of a blood pressure bump with each cup is blunted in regular coffee drinkers. In fact, regular consumption of coffee is associated with lower overall blood pressure readings compared to nondrinkers. It appears that coffee doesn’t cause hypertension.

 

What are the other metabolic effects of coffee?

Coffee has both good and bad effects. Regular coffee drinking lowers body fat and reduces the risk for obesity.  In addition, coffee lowers the risk for type 2 diabetes. On the other hand, coffee may increase cholesterol levels. The effect depends on the type of coffee, the degree of roasting and the type of brewing. Boiled, unfiltered coffee (such as Turkish or Greek coffee, made by boiling water with coffee grounds in a pot) raises cholesterol more than filtered coffee. Other nonfiltered coffees, such as espresso, are significantly associated with raised serum cholesterol levels. Filtered coffee can raise cholesterol but not as significantly as unfiltered coffee. There is no increase in cholesterol with instant coffee. It appears that drinking filtered coffee is the safer than alternatives. 

 

Does coffee reduce the risk for cardiac events?

In the literature, coffee drinkers have consistently had a lower risk for heart problems and death. A study from Europe in 2017 showed that drinking 2 to 4 cups of coffee per day reduced the risk of dying by 15%, reduced the risk of cardiac death by 17% and reduced the risk of dying from cancer by 4%. A more recent study confirms and expands these findings. The study followed 500,000 people for 10 years. In people without known heart disease, drinking 2 to 3 cups of coffee per day lowered the risk for heart artery disease, heart failure, stroke and dying from any cause. People withheart disease also showed improved survival and no increased risk for arrhythmias. The relationship held regardless of instant versus ground coffee, or decaf versus caffeinated coffee. The reason for these favorable benefits may be coffee’s metabolic effects (lower risk for obesity and diabetes), as well as coffee’s anti-inflammatory and anti-oxidant properties. In addition, coffee drinkers consistently do more physical activity than nondrinkers.  It seems that 2 to 3 cups of coffee per day is the sweet spot, a level of consumption where coffee is not only safe, it may be cardioprotective.

 

It can be concluded that coffee is not associated with high blood pressure, significantly elevated blood cholesterol (if the coffee is filtered) or dangerous arrhythmia. It is associated with a lower risk for obesity, type 2 diabetes, heart artery disease, stroke and death.  So find yourself a nice little café. Order one or two cups of (filtered) coffee. Then sit and watch the world go by, guilt free.

 

 

 

Personality Traits And Cardiovascular Disease

 

One of the classic scenarios in psychological evaluations is to show a person a glass that is 50% filled with water.  Is the glass half full or half empty?  How the person answers that question can determine a lot about their psychological state and may show their risk for future heart disease. 

 

For years the face of heart disease was a man who was highly ambitious, competitive, aggressive, impatient, goal- directed and willing to take risks. The type A personality was originally described in the 1950's by two cardiologists. They went on to show that the type A person had higher levels of cholesterol and a higher risk for heart disease. In addition, they found that the opposite of the type A, a relaxed, easy going, laid-back person, a type B personality, had a lower risk for heart disease. These stereotypes have persisted to this day.  More recent data found no significant link between type A personality and heart disease. However, two components of the type A personality, anger and hostility, are strongly associated with cardiac disease.  Studies have shown that anger and hostility significantly increase the risk for cardiac events in healthy people as well as those with established heart disease.  Anger causes excess catecholamine (adrenaline) release, an increase in heart rate and elevated blood pressure which can lead to angina and a heart attack. An outburst of anger is a well-established trigger for an acute heart attack. Chronic anger and hostility lead to the initiation and progression of blockages in the heart arteries, especially in young men. A new personality type was identified in 2000 and named type D (or “distressed”) personality. The type D personality has two components. The person exhibits negative emotions (anxiety, worry, neurotic) and social inhibition (can’t express emotions, thoughts or behaviors in a social situation). It is often associated with anger, hostility and social isolation as well. The type D personality is associated with cardiac disease including angina, heart attack and an increased risk for cardiac death

 

Neuroticism is another personality trait tied to adverse cardiac disease. Neurotic individuals have emotional instability, difficulty handing stressful situations and “fly off the handle” when under pressure. On the other hand, those with low neuroticism scores are more emotionally stable, calmer, even-tempered and less reactive to stress. Individuals with high neuroticism scores have more anxiety, moodiness, fear, anger, frustration, pessimism, and loneliness than those with lower scores.  They often turn to maladaptive behaviors (substance abuse, alcohol). In addition, people with high neuroticism scores were more likely to develop atrial fibrillation and to be diagnosed at an earlier age then those with lower scores. 

 

On the other hand, certain personality traits are cardioprotective. These include optimism, conscientiousness, openness to new experiences and curiosity.  Optimism is defined as the expectation of good things in the future (while its opposite, pessimism, is expecting something bad to happen down the road).  Individuals with high optimism scores have lower risk for angina, heart attack, stroke, cardiac death and all cause death. Why is this? Optimists and people with psychological well-being have favorable physiologic parameters including lower blood pressure, better cholesterol levels and less sympathetic activation (lower adrenaline levels).  They smoke less, exercise more, eat better and have less tendency for obesity. In addition, optimists are more likely to seek help in difficult social situations. They have larger and stronger social networks for support. They act on medical advice more readily. Lastly, optimists can weather the harmful effects of stress due to their inner and outer support systems. Meanwhile, pessimism has been shown to increase the risk for cardiovascular mortality.

 

So, when confronted with the question about that glass of water, don’t get angry. Don’t become hostile. Don’t get depressed if you can’t come up with an answer. Look for the positives, try to maintain an optimistic viewpoint and say that it is half full. Your heart will thank you.

 

When Anthropology Meets Cardiology

 

When Mount Vesuvius, a volcano near Naples Italy, erupted in 79 AD, it caught the townspeople of nearby Pompeii and Herculaneum by surprise. Many were able to escape, but many died instantly, buried by lava and volcanic ash. Due to the nature of their death, their bodies were well preserved. Recently, scientists were able to study the bodies of these early Mediterranean people and were able to determine what they ate. How does the ancient Mediterranean diet compare to the modern version?  How can the study of ancient peoples give us insight regarding heart healthy diets in today’s world?

 

The Mediterranean basin has been called the cradle of civilization. It stretches from the Nile to Rome and has housed advanced civilizations for thousands of years, including the Egyptian, Assyrian, Babylonian, Persian, Phoenician, Greek and Roman. The Mediterranean diet is linked to the fertile land of the region.  It is more than a diet; it is a way of life and based on traditions linking the land to the preparation, cooking and enjoyment of the food. The key elements of the Mediterranean diet include oil (especially olive oil), whole grains, wine, vegetables, sheep and goat cheese, seafood and very little meat. Whole grains include bread, cereals, couscous, pasta, rice, corn, oats and barley.  The description of the ancient Mediterranean diet comes mainly from written accounts. For example, texts describe the diet of the ancient Greek Olympic athletes starting around 700 BC. The diet was mostly vegetarian, consisting of barley porridge, cheese, fresh vegetables, lentils, beans, seafood, eggs and fresh fruit, mainly figs. Sweets were frowned upon. Initially meat was not a part of the athlete’s diet, but as time went on, meat was incorporated more and more.  Fast forwarding to Pompeii and the modern day, we now have concrete proof of what Roman era Mediterranean people actually ate. Scientists have been able to test the bones of the people frozen in time by the eruption of Mt Vesuvius. Using bioarcheological approaches they determined that the people of Pompeii ate a lot of fish, more than is consumed with the modern Mediterranean diet.  In addition, locally grown fruits and vegetables were eaten. The majority of their food energy came from seafood and cereals, although grain consumption was less than today’s diet. After the fall of Rome, the Mediterranean diet faded during the Middle Ages. It rose again from the ashes and poverty following World War II when meat was scarce and people turned once again to what could be grown locally. The cardiac benefits of the Mediterranean diet were first described in the 1950’s by Ancel Keys, a University of Minnesota researcher who discovered that people in poor towns in southern Italy were healthier than wealthy people in New York City. He conducted the Seven Countries Study and showed that the Mediterranean diet resulted in low levels of cholesterol in the blood as well as low levels of heart artery blockages. 

 

Anthropological data has shown that pre-agricultural hunter-gatherer populations derived a majority of their energy from animal based foods such as meat, fish, birds and eggs. The keto and paleo diets were developed to mimic these eating patterns.  These diets are very low in carbohydrates and high in saturated fat. It is generally believed that hunter-gatherers had low levels of heart disease. Is this true? A recent study performed CT scans on mummies from four regions, including ancient Egypt, Peru, southwest US, the Aleutian Islands and going back 4000 years. Atherosclerosis (calcified plaque in the wall of an artery) was found in 34% of the mummies and was found in all four regions.  In addition, atherosclerosis was present in 60% of the hunter-gatherers.  Atherosclerosis is felt to be a modern disease, but it is clearly present in our ancient ancestors, including hunter-gatherers. 

 

Since atherosclerosis seems to be a fact of human existence, which diets help protect the most against atherosclerotic heart artery disease? In 2021 the American Heart Association outlined its requirements for a heart healthy diet and ranked popular diets on how well they met the criteria. The recommendations included consuming:

Fruits and vegetables

Whole grains (rather than refined grains)

Plant based proteins (such as legumes and nuts)

Fish and seafood

Low-fat or fat-free dairy products

Lean meat or poultry

Plant oils (such as olive oil) 

Minimally processed foods

Minimal added sugar 

Little or no salt

Low amounts of alcohol

The dietary patterns that aligned the most with these criteria included Mediterranean, DASH (Dietary Approaches to Stop Hypertension), pescetarian vegetarian (excludes meat and poultry, includes fish), vegan and low fat. At the bottom of the list were the keto and paleo diets. Is there data, some meat, to back these rankings? One study reviewed all of the literature on seven diets. It found that the Mediterranean diet lowered all deaths, cardiac deaths, stroke and heart attacks. The low fat diet lowered all cause deaths and heart attacks. All of the other diets, including the very low fat Ornish and Pritikin diets, had little or no benefit. Studies on low carbohydrate, high fat “keto-like” diets have not been good. One study had 1220 people and followed them for 12 years. The keto-like diet patients had high levels of LDL cholesterol and were twice as likely to suffer from cardiac events.  Another study of 370,000 people, followed for 23 years, found a higher mortality rate for those on a low carbohydrate diet compared to a low saturated fat diet. 

 

Clearly no randomized controlled trials were done in ancient times to see if any of the diets conferred benefit from heart disease. This was due to a lack of scientific knowledge as well as the fact that our ancestors succumbed at early ages due to infectious disease, famine, the tip of the sword from an enemy or volcanic ash, well before heart disease became manifest.  What is clear from the study of mummies is that high fat diets, keto or paleo, did not protect against atherosclerosis. In addition, our modern studies show that these diets are detrimental to heart health. Heart patients should avoid these types of diets.  On the other hand, the Mediterranean diet is a sustainable, lifelong eating plan that continues to sit atop Agamemnon’s throne as the king of the heart healthy diets. The Mediterranean diet, along with DASH, vegetarian, vegan and low fat diets should continue as staples for the heart patient. 

 

 

Can Congestive Heart Failure Be Cured By Walking With Friends?

Congestive heart failure (CHF) is the inability of the heart to pump blood to meet the requirements of the body. CHF is classified into two groups based on ejection fraction. Ejection fraction (EF) is the percentage of blood ejected by the heart with each heartbeat. Normal EF is greater than 55%. CHF with reduced EF includes patients with EF less than 40% while patients with CHF with preserved EF have EF greater than 50%. CHF is an enormous global problem affecting more than 60 million people worldwide. CHF is the number one reason for hospitalization in the US and associated with frequent hospitalization, high healthcare use and cost. Symptoms of CHF include shortness of breath, trouble breathing with exertion or laying flat in bed, severe exercise intolerance, easy fatigability, and swelling. In 2021, a universal definition of CHF stated that CHF is a clinical syndrome with symptoms caused by a structural heart problem plus either an elevation in the blood of natriuretic peptides or objective evidence of congestion (by physical examination or chest X-ray). Natriuretic peptides are released when the heart is stretched or stressed, as in CHF. There are two natriuretic peptides; BNP and pro-BNP. CHF is present when BNP is greater than 35pg/ml or pro-BNP is greater than 125 pg/ml.

 

CHF with preserved EF affects half of all CHF patients. It affects women more than men and it is increasing in prevalence compared to CHF with reduced EF.  CHF with preserved EF is associated with and may be caused by hypertension, obesity, diabetes, heart artery disease, sleep apnea, kidney dysfunction and advanced age. Treating CHF preserved EF is difficult and frequent hospitalizations often result. A recent guideline recommends SGLT2 inhibitors as first line therapy. These medications, Jardiance and Farxiga, relieve congestion and promote weight loss. In addition, diuretics such as furosemide (Lasix) and spironolactone help in the treatment of fluid overload. The next line of recommended medications include Entresto, valsartan or losartan. Beyond medication, what else can be done? Recent information postulates that CHF preserved EF is an exercise deficiency and a social isolation problem. Addressing those issues could go a long way to treating the disease.

 

CHF preserved EF is a syndrome of exercise deficiency.

An intriguing article hypothesizes a spectrum of shortness of breath with exertion. At one end is the patient with CHF preserved EF. With exercise, such as climbing the stairs, there is insufficient cardiac output to meet the demands of the muscles, pressure goes up in the heart, and breathlessness ensues. The same series of events happens with an elite athlete. The difference is the workload; the CHF patient just walks up the stairs, the athlete has run 26 miles. The athlete has larger cardiac chambers, more heart muscle mass and a compliant heart that can handle high volumes and work loads. The patient with CHF preserved EF has a small, stiff, less compliant heart that cannot handle increased volumes with exertion.  Normal aging results in a smaller heart size, higher filling pressures during exertion and a greater potential for CHF. Being sedentary over the course of a lifetime exacerbates the effects of aging.  For adults who sit many hours each day the cumulative effects of a sedentary lifestyle plus the effects of aging plus other factors (for example, high blood pressure, smoking, diabetes) combine to cause CHF preserved EF. On the other hand, adults who have spent a lifetime exercising regularly can stave off the cardiac stiffness that occurs with age and can avoid CHF. Fortunately, for patients with CHF preserved EF the adverse cardiac effects can be reversed with physical training. For this reason, the American Heart Association recommends structured exercise for patients with CHF preserved EF. Structured exercise, or cardiac rehab, has been shown to reduce hospitalizations and reduce cardiac events. Not all those with CHF preserved EF fall into the category of exercise deficiency; it is reserved for the subset of patients with habitually low levels of physical exertion.

 

CHF preserved EF is a syndrome of social isolation and loneliness.

Social factors are a well-known contributor to heart disease. A recent study followed more than 400,000 people for more than 12 years to see if social isolation or loneliness were associated with CHF. Social isolation was defined as objectively being alone or having few social connections. Loneliness was defined as a painful feeling resulting from a desire for more social connections. Those with social isolation or loneliness were more likely to be men and to have unhealthy lifestyles (smoking, diabetes, obesity, physical inactivity). The study found that both social isolation and loneliness increased the risk for CHF by 15-20%. 

 

So, if you have CHF, or are at risk for CHF, grab a friend, talk a walk, eat, sleep, repeat.

 

The Taxing Pain Of Statin Intolerance

 

There are certain things in life that are inevitable; death, taxes and, for the physician, patient intolerance of their medication. Statins are wonderful drugs which have revolutionized medicine and almost single handedly reduced the global burden of heart disease.  Statins lower “bad cholesterol” (LDL, low density lipoprotein) and raise the “good cholesterol” (HDL, high density lipoprotein). In addition, statins have anti-inflammatory effects that contribute to their ability to lower heart disease. Unfortunately, statins have side effects including raising liver enzymes and causing muscle pains. Many patients cannot tolerate statins due to muscle symptoms.. What is statin intolerance? What new medications are available for patients with statin intolerance?

 

There are many medications available to treat high cholesterol. However, to be deemed beneficial a medication must meet two requirements. Number one, it must lower LDL substantially. Number two, it must reduce major adverse cardiac outcomes (heart attack, stroke, cardiac death).  Medications such as welchol, niacin, fenofibrate, fish oil (omega 3 fatty acids) lower LDL cholesterol, but do not reduce cardiac risk and are therefore not part of the modern cardiac armamentarium. Statins fulfill the criteria by lowering cholesterol and reducing cardiac events. For every 2 mg/dl reduction in LDL, there is a 1% reduction in cardiac outcomes. For example lowering LDL from 140 mg/dl to 100 mg/dl (a reduction of 40 mg/dl) not only reduces cardiac events by 20%, but also lowers mortality by 10%. The most common reason patients cite for stopping their statin is muscle pain. Muscle symptoms include soreness, aching, weakness or cramping and affect large muscle groups (such as the thigh). Muscle pain causing statin intolerance has been reported between 5% and 50% of patients. A recent large study (including 4 million patients) determined that true statin intolerance occurred in about 9% of patients taking a statin. Statin intolerance has been defined by the FDA as " the inability to tolerate at least two statins at the lowest approved doses due to muscle symptoms". Risk factors for statin intolerance include female sex, obesity, underactive thyroid, diabetes, alcohol use, chronic liver or kidney disease, use of calcium channel blocker, and the use of high doses of statin. Factors not associated include smoking and high blood pressure. Statin induced muscle pain usually occurs early in treatment (the first few weeks up to two months). However, the enormous benefit of statins is such that treatment should not be abandoned if a patient reacts to a single agent. Other statins should be tried and dosing altered to try to keep them on the medication. If a patient is truly statin intolerant after several tries, then there are new, nonstatin alternatives.

 

The first alternative medication for the statin intolerant patient is ezetimbe (Zetia). Ezetimbe alone reduces LDL by 18% and in combination with simvastatin 25%. The combination medication lowers the risk for cardiac events by 8%. Ezetimbe is rarely used by itself, rather it is used to lower the statin dose while still providing cardiac protection. The next class of agents are the PCSK9 inhibitors alirocumab (Praluent) and evolucumab (Repatha) which were approved for use by the FDA in 2015. These medications are given by a self-administered injection under the skin (much like an insulin shot) every two weeks. They lower the LDL by a whopping 58% (Praluent) and 64% (Repatha) and lower cardiac event rates by 15%.  The next agent is inclisiran (Leqvio) which was approved for use by the FDA in December 2021. It too is an injectable medication but this is given every six months. Inclisiran has been tested in patients with familial hypercholesterolemia who still have high levels of LDL despite taking a statin. In these patients, inclisiran lowers LDL by 50% on top of statin treatment. Trials are ongoing evaluating inclisiran’s ability to lower cardiac events.  In addition, it has not been tested in statin intolerant patients. However, it may prove very useful in this population. Side effects include only injection site reactions and no muscle pain. The last medication is bempedoic acid (Nexletol) which the FDA approved in February 2020. Bempedoic acid has been tested in patients with statin intolerance. Alone it lowers LDL by 21% and in combination with ezetimbe LDL is lowered 38%. Importantly, bempedoic acid was recently shown to lower the cardiac event rate by 13%. In addition, it seems to have anti-inflammatory properties (like statins) whereas ezetimbe and PCSK9 inhibitors do not. Side effects include gout and gallstones but no muscle symptoms. All of these characteristics make it a good alternative for statin intolerant patients.

 

Despite a plethora of good alternatives, the principal is to have patients take a statin. Fortunately, there are other medications if they cannot continue on statins. In terms of life’s inevitabilities, physicians can’t reduce the tax burden. However, there are now viable options for patients with statin intolerance that also reduce the risk for cardiac death. Two out of three ain’t bad.

 

 

AED Density

 

Sudden cardiac arrest is an abnormal heart rhythm most often caused by ventricular fibrillation (an irregular heart rhythm from the lower chambers of the heart).  When the heart’s ventricles are fibrillating, they cannot pump blood to the brain and vital organs. If not treated promptly, this leads to death.  Sudden cardiac arrest is common and affects 350,00 people in the US each year. Surviving sudden cardiac arrest requires prompt cardiopulmonary resuscitation (CPR) and defibrillation with an Automatic External Defibrillator (AED).  Timing is everything; if an AED shock is provided within one to two minutes of going into sudden cardiac arrest about 50% of victims will live. However after 10 minutes, less than 10% will survive. We have all seen this in real time recently. Due to the quick response and the coordinated efforts of a team who practiced for just this type of situation, Damar Hamlin is alive today.  However, most sudden cardiac arrests do not happen in a controlled environment such as a cardiac care unit. The big question then is how to get responders and AEDs to sudden cardiac arrest victims as fast as possible.

 

If a patient has cardiac arrest in the hospital, doctors and nurses with advanced cardiac training can often successfully resuscitate the patient. If someone suffers sudden cardiac arrest outside of the hospital, it is a different story. In studies it has been shown that 8% of cardiac arrests occur in a public setting and witnessed by bystanders, but the vast majority of out of hospital cardiac arrests occur in the home (75%).  The overall survival rate for out of hospital cardiac arrest is only between 2% and 14%. One of the biggest barriers to successfully resuscitating a patient out of the hospital is getting trained responders to the victim. Once a cardiac arrest has been called to 911 or emergency services, a dispatch is placed to first responders; police, fire and ambulance corps. However, if it takes emergency responders more than ten minutes to locate and get to the victim, the outcome is usually not good. If bystanders near a victim are able to start CPR and, even better, use an AED, the chance of survival increases dramatically. Resuscitation by bystanders is associated with survival rates between 53% and 66%. For comparison, survival rates for emergency medical personnel is between 28% and 43%.  Most studies show a 2 fold better chance of living if the patient is treated immediately by a bystander. There are a number of volunteer responder programs around the world, including Denmark, Netherlands, United Kingdom, Australia, US and Canada. The idea is to alert volunteer trained responders about a cardiac arrest and direct them to the victim so that prompt CPR can be initiated.  The programs work in the following way. Once a cardiac arrest has been called in to a central dispatching agency, registered volunteers in the vicinity of the arrest are contacted via text message. Some responders are directed to the nearest available AED, while others are sent straight to the patient to start CPR. The system keeps notifying volunteers until a critical mass have responded and are on their way. How many responders are needed to optimally manage a sudden cardiac arrest?  When 3 or morevolunteersresponded before emergency medical services, there was a greater chance for bystander defibrillation with an AED.

 

The other huge barrier to successful resuscitation is getting an AED to the victim as soon as possible.  AEDs have become ubiquitous. About 500,000 to 1 million were sold in the US last year and there are about 3.2 million AEDs in public settings. Yet, there is still a shortage. AEDs in public places (for example gyms, casinos, airports, arenas, shopping malls) should be prominently mounted with easy to see signs. In addition, emergency services and security personnel should know the exact locations of AEDs. What is the optimal density of AEDs?  In a large public space how close together should AEDs be placed? In 1999 AEDs were installed in O’Hare airport in Chicago. AEDs were placed a “brisk 60-to-90 second walk apart”. The survival rate for cardiac arrest at the airport is 56%. The American Heart Association recommends an AED within a 3-to-5 minute round trip walk from anywhere in a public place. This translates to each AED covering about 100 yards in each direction. 

 

In case of sudden cardiac arrest in the home, getting an AED to the person is very problematic. As described above, formal programs will send out texts to responders and direct them to the location of a known AED.  What is the optimal density of AEDs in residential areas? One study from the Netherlands found that approximately 2 AEDs per square kilometer (5 AEDs per square mile) in residential areas was optimal coverage. However, in Holland there is a national registry for all public and private AEDs, including location. When emergency services are called, responders are directed to the nearest AED. Another study from Copenhagen concluded that the optimal coverage was 16 AEDs per square kilometer (41 AEDs per square mile) in residential areas. Keeping in mind that the Netherlands and Denmark are each about 16,000 square miles, that is not an insurmountable number of AEDs to provide residential coverage. The United States is 3,531,905 square miles.Novel ideas that are being piloted include delivering an AED via a drone to the victim and having ultraportable AEDs carried by volunteer responders.

 

You may ask, “How does this information help me? I can’t afford to outfit the US with millions of AEDs.” This is a valid question, but there are still lessons for the general public.  The first is to get trained in CPR. The local hospitals have CPR classes for the community. You never know when you might need these skills. Next, even if you lack formal training, this should not deter you from attempting to save a life. AEDs are easy to use and they help guide the responder through the process of deploying them. Next, if you see a resuscitation in progress, go and help. Remember, the more hands, the greater the chance to save a life. Lastly, advocate in your community for greater AED density.

 

The Hibernating Heart

 

It’s February and if you are a bear, it’s the middle of hibernation season. During hibernation, the bear does not merely fall asleep; there are a complex series of changes that occur throughout its body and the heart is no exception. First, the heart rate slows dramatically. When active, a bear’s heart rate is around 70 to 80 beats per minute. During hibernation, the heart rate slows to 14 beats per minute. There are also a series of changes within the heart. The left ventricle stiffens, preventing stretching due to the low heart rate. In addition, there is a change in the biochemistry of the heart muscle itself. A protein called myosin controls heart muscle contractions. During hibernation, there is a switch from the usual myosin to a different variety which produces a weaker contraction. What can we learn from the study of animals to help us understand the human heart better?  What happens when our heart beat is very low? Can human hearts hibernate?

 

The normal human heart beat ranges from 60 to 100 beats per minute. Very slow heart rates, 20 to 40 beats per minute, do occur and can be present in normal hearts as well as various disease states. The heart beat normally slows while sleeping. Athletes often have very slow rates as a result of training. In fact, athletes usually have a heart rate in the 40’s and are symptomatic. It is not considered abnormal until an athlete’s rate is below 30 beats per minute. The most common abnormality causing a slow heart beat is sick sinus syndrome. This occurs in older individuals and is a result of the electric system of the heart “wearing down” over the years. A heart attack can slow the heart rate, especially if it affects the blood flow to the electric system. Low heart rates are also seen in an under active thyroid (hypothyroidism), sleep apnea, and Lyme disease. There are many medications that can slow the heart beat. These include beta blockers (for example, metoprolol), calcium channel blockers (ex, diltiazem), digoxin, rhythm agents (ex, amiodarone, sotalol), eye drops (especially ones containing timolol, a beta blocker) and Alzheimer medications (donepezil and memantine). Patients with very slow heart rates may have no symptoms or they may feel lightheaded, dizzy, sweaty or pass out. If left untreated, a slow heart rate will lead to congestive heart failure or death. The diagnosis of a slow heart rate is made by capturing the event on an EKG strip. A variety of methods can be used. A Holter monitor is an EKG that is attached to patient and worn all day and night for one to three days. An event monitor is a patch that is applied to the chest. A constant signal is sent to monitoring center and if a significant rhythm change occurs, the doctor is notified. The patch is worn for two to four weeks. These monitors are good if the patient has frequent events. Sometimes, events occur weeks or months apart. In that case, an implantable loop recorder is placed. This is a small metal device that is placed under the skin and can monitor a patient for months or years at a time. In the case of an event, the EKG can be downloaded on a computer. For patient centric devices, there is the Apple watch and Kardia mobile. Kardia mobile provides a single lead EKG when the patient places two fingers on the device and an EKG is stored on a cell phone. It is commercially available on Amazon and can be bought without a prescription. The treatment for a slow heart is to correct the underlying cause or stop the offending medication. If that does not improve the heart rate or symptoms, then a pacemaker is placed. 

 

The human heart can hibernate, but for a different reason compared to the hibernating bear’s heart. In humans, the whole heart doesn’t hibernate, like the bear, but only a portion of the heart muscle. If there is a region of the heart muscle that is supplied by a blocked artery for many months or years, the region will hibernate. Normally if there is lack of blood flow to the heart muscle, there is a heart attack and the affected muscle dies (it stops working, contracting). In an area of hibernation, there is enough blood flow to keep the muscle alive, but it doesn’t contract normally. In effect, the area of heart muscle adapts by downregulating- reducing or ceasing contraction and changing metabolism to try to keep the area alive. Similar to the bear’s hibernating heart, there is a change in the biochemistry. Biopsies of hibernating heart muscle in humans has shown a reduction in and disorganization of the contracting proteins, including myosin. If the blocked artery supplying the area is opened (with a stent or bypass surgery) and blood flow restored, the affected hibernating heart muscle returns to normal function. 

 

In the animal kingdom, the adaptations made by the heart are beneficial, helping the animal to survive cold winters and to ultimately thrive. In humans, the hibernating heart can keep us alive, but in the long run the changes are detrimental.  Hibernating areas of heart muscle weaken the overall contraction of the heart resulting in congestive heart failure and ultimately death. Similarly, a slow heart rate seems to confer a survival advantage in the animal kingdom while not a factor in man.  Animals with fast heart rates such as the shrew with a heart rate of 220 beats per minute tend to have short lifespans, a few years at most. On the other hand, the Galapagos giant tortoise, whose average heart rate is six, can live for more than 100 years. If the human heart were to slow down to that level blood would pool in the four chambers, the heart would start to enlarge, the muscle would weaken leading to congestive heart failure and death. Aside from interesting physiology, the study of animal adaptations may lead to advances in human heart disease.  The research has already borne fruit by producing new medications that target myosin. Omecamtiv activates myosin, improving the heart’s contractility and helping with heart failure due to a weakened heart muscle. Mavacamten inhibits myosin, decreasing the force of contraction in patients with a thickened heart muscle who need less vigorous heart pumping. Let sleeping bears lie, we can learn a lot from them.

 

 

Sudden Cardiac Arrest

On January 2 2023 in front of thousands of people at the stadium and millions on a national television broadcast, a Buffalo Bills player made a routine football play, stood up and then collapsed with sudden cardiac arrest. What is sudden cardiac arrest? What causes it? How is it treated? Can it be prevented?

 

Sudden cardiac arrest is an abnormal heart rhythm most often caused by ventricular fibrillation (an irregular heart rhythm from the lower chambers of the heart).  When the heart’s ventricles are fibrillating, they cannot pump blood to the brain and vital organs. If not treated promptly, this leads to death.  Sudden cardiac arrest affects 150,000 to 250,00 people in the US each year. Less than 20% of sudden cardiac arrest victims have their rhythm restored to normal and only 10% survive to ultimately leave the hospital. 

 

The cause of sudden cardiac arrest depends on the age of the victim and the type of underlying heart disease.  In patients over the age of 35, the overwhelming cause of sudden cardiac arrest is a heart attack. A heart attack occurs when the blood flow to the heart muscle is stopped completely. Usually there is a pre-existing plaque or blockage in a heart artery, the plaque breaks open, a blood clot forms and the blood flow is halted. It is important to realize that a heart attack and sudden cardiac arrest are not the same thing. A heart attack is one of the causes of sudden cardiac arrest and primarily a plumbing problem (the artery and the blood flow) while sudden cardiac arrest is an electrical problem (an abnormal rhythm). In those under age 35 and less likely in older victims cardiomyopathy (a primary heart muscle problem) can cause sudden cardiac arrest. This includes dilated cardiomyopathy (a weak, flabby heart), hypertrophic cardiomyopathy (an abnormally thickened heart muscle) and arrhythmogenic right ventricular dysplasia (fatty infiltration of the wall of the right ventricle). Primary rhythm problems such as Wolf-Parkinson-White syndrome (a bypass which circumvents the usual electrical pathway), Long QT syndrome and Brugada syndrome must also be considered. In young patients, especially young athletes, an anomalous origin of a heart artery can be seen in 12 to 19% of victims. The artery follows an abnormal course between the main artery (the aorta) and the lung artery (pulmonary artery). With exercise, the pressure in these arteries goes up, compressing the heart artery and interrupting blood flow to the heart. Another cause that has come to the forefront in recent years is myocarditis (inflammation of the heart muscle). Myocarditis can be due to infection (from various viruses including COVID), cancer chemotherapy agents (check point inhibitors) or idiopathic. All of these causes are due to an underlying heart issue but sudden cardiac arrest may occur in a normal heart as well. Commotio cordis occurs after a blunt impact to the chest (with a projectile such as a baseball). The energy of the impact is transmitted to the heart, disrupting the normal heart rhythm. The vulnerable period for a projectile striking the heart is only about 10 to 15 milliseconds long and represents one percent of the total heart cycle.  It is a rare but not uncommon occurrence. 

 

The successful treatment of sudden cardiac arrest demands prompt recognition, cardiopulmonary resuscitation (CPR) and defibrillation. Recognizing sudden cardiac arrest may not be easy. The patient cannot explain what is wrong and they are often first evaluated by nonmedical personnel. In addition, it may look like another process is occurring, such as a seizure.  If sudden cardiac arrest is suspected, the initiation of prompt CPR has been shown to save lives. The American Heart Association now recommends hands only chest compression (no mouth-to-mouth) and pressing hard and fast.  Sudden cardiac arrest need not be 100% confirmed to start CPR; if suspected start chest compressions. If the victim doesn’t have cardiac arrest they will ask not to have their chest pumped.  Definitive treatment of sudden cardiac arrest is defibrillation, an electric shock to the heart that restores the heart to normal rhythm. The shock is usually provided by an Automatic External Defibrillator (AED), a small portable device that is brought to the victim’s side. The sooner the patient is shocked, the greater the chance of surviving. Fifty percent of victims of sudden cardiac arrest survive if shocked within two to three minutes, but only ten percent will live if the shock is more than ten minutes from the time of collapse.  Timing is everything and having an AED as close as possible to potential victims is life saving.  As such, there is a push to have AEDs placed in areas where there are large public gatherings (such as airports, schools, stadiums, sports complexes). AEDs have been successfully deployed by police, firemen, sports trainers, and bystanders. There is even a study exploring delivering AEDs by drones.

 

Sudden cardiac arrest is often the first sign that a person has heart disease, but there are steps that can be taken to prevent it. For those over 35 years old, following a heart healthy lifestyle is the first step (staying active, watching a good diet, not smoking, keeping weight under control, treating high blood pressure and/or high cholesterol).  For those at higher risk (for example a family history of heart disease at a young age), speak to your doctor about additional testing. Lastly, don’t ignore symptoms such as chest pain, shortness of breath, nausea/vomiting or passing out. Studies have shown that 50% to 75% of sudden cardiac arrest patients had warning symptoms. Many of the symptoms are nondescript; when should you be concerned? If symptoms are new or unusually severe, then seek care immediately. For those under age 35 and who have high-risk characteristics, cardiac testing (EKG, echo, cardiac MRI) as well as genetic testing may be indicated. For people under age 35 not at high risk, screening for sudden cardiac arrest is controversial. Many professional athletes (especially football, basketball and soccer players) are screened before a contract is signed.  In addition, Division 1 college athletes are screened. 

 

The NFL routinely screens players for their risk of sudden cardiac arrest. In addition, NFL sideline training staff routinely practices responses to sudden cardiac arrest. Due to the prompt response, CPR, the use of an AED, and expert team work by the training staff and medical personnel the player was resuscitated on the field and was able to survive a near death experience.

 

 

The Cardiology Department at RWJ Somerset is conducting its annual screening of high school athletes on Saturday February 4 2023. The screening is free and open to athletes from 14 to 18 years of age.

For more information please check the website (rwjbh.org/cardiacathleticscreening) or call  908-685-1414 to reserve a time slot.