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.

 

 

 

Resistance is Futile

The letter omega (Ω) is the last letter in the Greek alphabet. As such, omega is often used to denote the last, or the ultimate end, of a list. Therefore, it is a fitting topic for December, the final month of the year. In addition, omega symbolizes the ohm, the unit of electrical resistance. The ohm is named after the German scientist George Ohm who described the mathematical formula of electrical resistance. There is a further connection between electrical resistance and resistant hypertension, since external energy can potentially be used to bring down the blood pressure. What is resistant hypertension and how is it treated? Can new treatments be the omega of high blood pressure?

 

Elevated blood pressure (hypertension) is the leading risk factor for cardiovascular disease, stroke and death. It affects about 1.4 billion people worldwide. In the US, approximately 10 to 30% of patients with high blood pressure have treatment resistant hypertension (10-12 million people).  Resistant hypertension is defined as blood pressure above goal despite taking the maximally tolerated doses of three different classes of blood pressure medications. In the past, the goal was a blood pressure under 140/90, but a new definition now moves the goal to under 130/80. The three medications should include a diuretic (a “water pill”), an ACE or ARB (for example, lisinopril, ramipril, losartan or olmesartan) and a calcium channel blocker (usually amlodipine). A structured approach to resistant hypertension has been developed by the American Heart Association. The first step is to make sure the blood pressure is truly high (not white coat hypertension; high blood pressure in office, but normal at home). The next step is to ensure the patient is taking his or her medications (and correctly). After that, lifestyle modifications may be necessary if the patient is not following a low sodium diet, not exercising, or drinking excess alcohol. In addition, many medications can raise blood pressure. These should be eliminated or reduced. Medications that can raise blood pressure include non-steroidal anti-inflammatory agents (such as ibuprofen or naproxen), over the counter cold medications, oral contraceptives, corticosteroids (for example prednisone), some cancer chemotherapy agents and many supplements (ephedra, ginseng, saw palmetto). Lastly in the lifestyle category is obstructive sleep apnea. Obstructive sleep apnea occurs when the upper airway collapses, air movement into the lungs ceases causing the oxygen level in the body to fall. This prompts the person to wake up and take deep breaths.  These periods of low oxygen disrupt the sleep cycle and prevent the person from getting enough time in the deep sleep, restorative stages of sleep. Because the body does not get enough rest, the person feels “revved up” all the time. Over time, this causes hypertension. Treating sleep apnea can reduce blood pressure. 

 

The next step in managing resistant hypertension is to evaluate for secondary causes of high blood pressure.  A variety of disease processes can raise blood pressure (including kidney, adrenal, and aortic diseases). Identifying such a process and treating it will bring down the blood pressure. One such entity is renal artery stenosis (a severe blockage in the artery supplying blood to a kidney). The most common cause of renal artery stenosis is atherosclerosis of the kidney artery (the same process that causes blockage in a heart artery). It is characterized by a sudden increase in blood pressure, low potassium levels in the blood and an extra “whooshing” sound (bruit) heard over the abdomen. The diagnosis is made by ultrasound, CT scan or angiogram of the blood flow to the kidneys. In the appropriate patient, opening up the blockage, placing a stent and restoring blood flow to the kidney can reduce blood pressure.

 

If the blood pressure is still elevated after all of these evaluations, the next step is to add further medications. The next medication that is recommended is spironolactone, which blocks the synthesis of aldosterone, a hormone that promotes salt retention and increases blood pressure. Spironolactone has been used for many, many years and is quite effective at lowering blood pressure. However it does have side effects including raising the potassium level in the blood (a potentially dangerous situation). If the potassium goes above a certain level, the medication has to be discontinued. 

 

Even though resistant hypertension affects millions of people, no new blood pressure lowering agent has been approved since 2007. A couple of new strategies for lowering blood pressure are on the horizon and look promising. The data for a new medication, baxdrostat, was just published this past month. Baxdrostat lowers aldosterone levels by a different mechanism from spironolactone. In the trial just reported, baxdrostat lowered blood pressure in resistant hypertensive patients 11 mmHg more than placebo, a statistically significant amount. There was no significant increase in potassium.

 

Are there any other therapies besides medication to treat resistant hypertension? A new procedure called renal denervation has been extensively studied recently. Renal relates to the kidneys and denervation means to deaden the signal the nerves give off. One of the ways in which blood pressure is controlled is via the nerves to the kidney arteries. The nerves send a signal to the kidneys, prompting the kidney to start retaining more salt (sodium) and increase blood pressure. In addition the nerves from the kidneys send signals back to the brain. This causes the brain to send signals to the arteries throughout the body, making them contract and stiffen, also raising blood pressure. These are normal mechanisms the body uses to regulate blood pressure, but in some people the nerves are overactive resulting in continuously high blood pressure and resistant hypertension. Renal denervation is a procedure where a catheter is placed in the kidney arteries. The nerves are then deadened using radiofrequency or ultrasound. Many trials have been conducted comparing renal denervation with a sham procedure (the catheter is placed but no energy is given). In patients with resistant hypertension, renal denervation lowered blood pressure by 7 to 11 mmHg. These reductions were sustained at 6 months and 3 years. In addition, renal denervation increased the time in therapeutic range (< 140 in office blood pressure, < 130 in home readings) as well as decreased major cardiac events. One of the advantages to renal denervation is that it is always “on”; the blood pressure effect is there, night or day and is not dependent on whether medication is taken or whether medication has worn off during the course of the day. Taking multiple medications every day, often with several doses spaced across the day, 365 days of the year is a difficult task. If approved, renal denervation may be a reasonable option for people with resistant hypertension.