How the Cardiologist Stole Holiday Treats

The holidays bring visions of sugar plum fairies dancing and tables filled with fruitcake, sugar cookies, gingerbread, red velvet cake, macaroons and chocolate yule log. These delectable holiday treats are as much a staple of the holidays as family gatherings and celebrations. Unfortunately, these sugary delights are not quite part of a heart healthy diet and can wreak havoc with cholesterol levels.  As we head into the peak holiday and treat-eating season, it’s a good time to review what is new in cholesterol management.

Who should be treated with a statin for high cholesterol in 2019? In 2013, the American Heart Association and the American College of Cardiology published a guideline to address this topic.  This guideline was just updated in November 2018, adding more nuance to the original. The guideline focuses primarily on LDL cholesterol (low density lipoprotein, “the bad cholesterol”). In general, there are four categories of patients for whom a statin should be prescribed: 

1) secondary prevention (trying to prevent a second event in patients who have already had a heart attack or stroke), 

2) diabetic patients (a high risk group) whose LDL is greater than 70 mg/dl, 

3) patients with an LDL greater than 190 mg/dl (severe familial high cholesterol).  For these three groups, especially secondary prevention, the medical literature is quite consistent in showing the benefit of statin therapy. The data for statins is less robust in the fourth group, primary prevention (trying to prevent a heart attack or stroke in a patient who has not had an event).  The 2013 guideline used a risk calculator (which can be found at: cvriskcalculator.com) to identify high-risk patients for primary prevention.  This was a controversial issue at the time and many cardiologists felt that the calculator overestimated the risk, thus exposing more people to statin therapy.  The updated guideline attempts to clarify who should be on a statin by adding risk enhancers and using coronary calcium score. If the calculator places the patient at high risk for a cardiac event over the next ten years with a score of 20% or greater, then a statin should be given.  If the patient is at low risk (a score of 5% or less), then no statin is necessary.  If the patient is at intermediate risk (a score between 5% and 20%), then risk enhancers are used.  These risk enhancers are: 

LDL > 160 mg/dl,

high-sensitivity C reactive protein level (a measure of inflammation) > 2.0 mg/L, 

triglycerides > 175 mg/dl, 

apoliprotein B level > 130 mg/dl, 

lipoprotein (a) level > 50 mg/dl, 

peripheral arterial disease, 

chronic kidney disease, 

chronic inflammatory disease (rheumatoid arthritis, psoriasis, or lupus), 

metabolic syndrome (hypertension, diabetes, high triglycerides, obesity- especially a large waist circumference), 

family history of premature heart disease, or 

premature menopause. 

With an intermediate risk score and the presence of one or more risk enhancers, a statin should be prescribed. If the patient and the doctor still are uncertain about starting a statin, then a coronary calcium score can be used. A CT scan of the heart measures the calcium score. Calcium is found in plaque in the heart arteries. The higher the amount of calcium, the more plaque is present in the heart arteries. A coronary calcium score of zero means there is no plaque and a statin can be withheld.  However, if the calcium score is 100 or more, then a statin is indicated. 

What about the other test on the standard lipid panel, triglycerides?  It is well known that patients who have heart disease and good LDL levels on statin but have elevated triglycerides are still at risk for cardiac events. It is thought that reducing triglycerides can provide an additional benefit beyond lowering the LDL. Unfortunately, this hypothesis has never been proven, until recently.  Medications that reduce triglycerides such as niacin or fenofibrate, taken with a statin, did not show a reduction in cardiac events. Omega-3 fatty acids (fish oil) are present in fatty fish and in populations with high fish intake, there is a lower risk for heart disease.  Formulations of omega-3 fatty acids contain either eicosapentaenoic aicd (EPA) alone or a combination of EPA with docosahexaenoic acid (DHA). These medications are prescribed to treat elevated triglycerides but neither the combination nor low dose EPA have been shown to reduce the risk for heart disease. More recently, a high dose, pure form of EPA was tested in patients with heart disease, statin controlled LDL levels and high triglycerides.  For the first time, the pure form EPA was shown to reduce the risk for heart attack, stroke and cardiac death by 25%.  The triglycerides were lower in patients on the medication, but it is thought that other mechanisms, such as an anti-inflammatory effect of the EPA, may also have contributed.  The results of this trial have changed the way cardiologists view and treat triglycerides in their patients with heart artery disease. Is fish oil beneficial for the primary prevention of heart disease? Two recent trials tested patients without heart disease by using a combination of EPA and DHA. Neither showed a reduction in heart attack, stroke or cardiac death. Therefore, low doses of fish oil are not beneficial for primary prevention but prescription high dose EPA is now being used for secondary prevention of heart disease. 

So, enjoy the holidays with friends and family. Have a holiday treat or two. If you want some heart healthy choices (including treats), try the recipes at heart.kumu.org. Then in the New Year, tackle those high cholesterol and triglyceride numbers.

The Gray Lady of the Medicine Cabinet

Aspirin is the gray lady of the medicine cabinet.  Aspirin, the medication that has been in use for over one hundred years, is tried, true and reliable. Aspirin has been prescribed for a variety of ailments including fever, aches and pains. Aspirin is the standard of care in the treatment of heart disease and stroke. Judging by its longevity and the extent of its use, it would seem that we know all there is to know about aspirin. That assumption would be wrong.

Aspirin’s anti-inflammatory and blood thinning properties are ideally suited for treating an acute heart attack or stroke. Aspirin is usually the first medication given in the ambulance to a patient who is having a heart attack. In addition, there is data going back decades showing that aspirin can prevent a second heart attack or stroke in patients who have already had an event. This is called secondary prevention and aspirin’s role is not controversial and well established.  What about primary prevention, trying to prevent a heart attack or stroke in a patient who has not had an event? Here aspirin’s role is much murkier and the data not as solid. A few primary prevention trials of aspirin were done many years ago and showed a small cardiovascular benefit for aspirin, even though the risk for bleeding increases with aspirin use. In 2016 the US Preventive Services Task Force recommended a low dose (81 mg) aspirin for adults aged 50 to 59 years old, who are at high risk for cardiovascular disease. What about patients who are 70 years of age or older, a population known to be at higher risk for cardiac events? Should an aspirin a day be prescribed?

Several large, well done primary prevention trials have recently been published and have added clarity. In a trial of 15,000 patients with diabetes (average age of 63), aspirin lowered the rate of cardiovascular events but increased the risk for major bleeding. There was no reduction in the death rate.  The next trial included 12,000 nondiabetic patients with the men over age 55 and the women over the age of 60.  These were patients felt to be at low risk for cardiovascular disease. Again, aspirin did not reduce mortality. There was no cardiovascular benefit for taking aspirin and the risk of bleeding was twice as high. The last trial included 17,000 patients all older than 70 years old and without cardiovascular disease. Once again, aspirin gave no benefit with respect to death, cardiovascular events, dementia or physical disability.  The risk for bleeding on aspirin was higher.  Overall these trials were consistent in showing that aspirin provided minimal benefit and significant bleeding risks. On the scale of benefit versus risk, the risk of aspirin outweighed any benefit in primary prevention.  What changed compared to previous primary prevention trials? The difference seems to be that the prevention of heart disease is much better now than in the past. Smoking is less common and the treatment of high blood pressure, high cholesterol and diabetes is better and more aggressive.

What is the correct dosage of aspirin? Even after all of these years, we still do not know for certain. Guidelines recommend a full dose (325 mg) of aspirin for at least one month after a heart attack, a cardiac stent, bypass surgery or a stroke. Then the recommendation is to lower the dose to 81 mg, with the idea that the lower dose confers the same benefit as the higher dose, but with less risk for bleeding. Now a new study questions the efficacy of 81 mg of aspirin.  It was found that low doses of aspirin, such as the 81 mg dose, were only effective in protecting against cardiovascular effects in patients weighing less than 150 pounds and had no benefit for those weighing more than 150 pounds.  This issue certainly will require further study.

All of these studies were reported in the news accompanied by headlines such as, “Aspirin Flops Big Time in Heart Study. Is it R.I.P for Aspirin?” This caused a lot of confusion among patients as to whether they should be on aspirin. To clarify, if you are having a heart attack or stroke, take an aspirin and call for help. If you have a history of heart attack, cardiac stent, bypass surgery, stroke, significant plaque in the neck (carotid) arteries, aorta or leg arteries, congestive heart failure or atrial fibrillation then the benefits of aspirin outweigh the bleeding risks.  If you do not have any of these conditions, then you should not take aspirin for primary prevention of cardiovascular disease. Instead, you should refrain from smoking, exercise regularly and take a statin and/or blood pressure medication as indicated.  Of course if there are any questions, talk over the risks and benefits of aspirin with your doctor.

Even One Cigarette is Two Too Many

“Doc, I’m down to one cigarette a day”. That’s great, but you have to stop altogether. “I don’t want to gain weight if I quit. What do you think about e-cigarettes?”

Over the past several years, the number of people who smoke has dropped to an all time low. About 13% of US adults smoke, but that still represents about 37 million active smokers. The risks of smoking are well known. Heart attack, stroke, lung disease and cancer all increase with more smoking: the greater the number of cigarettes smoked and the longer a person smokes, the higher the risk for problems. Many people believe that cutting from smoking 20 to 25 cigarettes per day to only one or two per day will cut their risk. The idea is that a cigarette a day can’t be harmful. What is the data?  Researchers examined 5.6 million people and found that cutting the number of cigarettes from 20 per day to one per day reduced the risk for cancer, but the risk for heart disease persisted.  Compared to a nonsmoker, smoking 20 cigarettes per day increased the risk for heart disease in men by 100% (doubling the risk) and by 184% in women. Compared to those who never smoked, smoking only one cigarette per day increased the risk for heart disease by 50% in both men and women.  In addition, there is an excess risk for stroke with only one cigarette a day. The conclusion was that even one cigarette per day puts a person at significant risk for a heart attack or stroke. The goal must be zero cigarettes.

One of the barriers to quitting is that smokers don’t want to gain weight when they stop smoking. Given the fact that both smoking and obesity put people at risk for heart disease, which is worse, smoking or weight gain? Weight gain in quitters is the result of an increased appetite and lower energy levels.  The amount of weight gained after quitting is usually less than 10 pounds, but can be as high as 30 pounds. Weight goes up for about 5 years after smoking cessation and then slowly comes down.  In a recent study, it was found that stopping smoking reduced the risk for cardiac deaths regardless of weight gain.  This reduction occurred in those who gained weight and those who didn’t gain weight; the weight gain didn’t offset the benefits of smoking cessation on the death rate. The patients who gained weight also had more diabetes than those who didn’t gain weight. Even with weight gain and diabetes, there were less cardiac deaths. This data shows that smoking is worse than weight gain. 

What is the best way to stop smoking?  The main determinant is the smoker’s desire to quit. If you don’t really want to stop, then quitting will be nearly impossible. Some people can stop cold turkey. Most, however, need help in some form. Smoking cessation aids (such as nicotine patch, Chantix and Wellbutrin) can help people quit.  How safe are they? The cardiovascular safety of these aids has been tested in the general population of smokers and they do not increase the risk for heart attack and stroke.  The safety in patients with heart disease is not yet known. How effective are they? In a recent large trial only 3% of people using these aids were smoke free at six months. An emerging method of quitting is the use of the electronic cigarette (e-cigarette) or “vaping”.  The e-cigarette is a battery-powered device that heats liquid nicotine and flavorings (such as vanilla or cinnamon) into a vapor cloud that is inhaled. The data on e-cigarettes are still evolving, but preliminary studies show that they are less harmful than traditional cigarettes. Less harmful does not mean safe, however the degree of harm has not yet been defined. By altering the amount of nicotine in the device, smokers can titrate the nicotine down and quit slowly. However, a recent study showed that smoking cessation with e-cigarettes was not any better than other smoking cessation aids. The other major concern with e-cigarettes is their use in the adolescent population. Vaping has exploded amongst teens. Many studies have shown that e-cigarette use in young people doubles the odds of smoking traditional cigarettes. The FDA is now cracking down on e-cigarette manufacturers, trying to stop their advertising and sale of these products to teens.

In summary, the number one priority for any smoker is to stop smoking, using any means (going cold turkey or using smoking cessation aids or e-cigarettes) and then work to lose the weight that is gained. 

My Apple Watch says that I am in Afib!

Apple just came out with a new watch. In addition to telling time and reading text messages and email, the new watch has electrocardiogram (EKG) capabilities. When the EKG detects an irregular heart beat (atrial fibrillation, Afib) it alerts the wearer. How well will this new technology perform in the real world?

Using Bayes calculation and assuming (a big assumption) that the Apple watch can detect Afib with a sensitivity of 99% and a specificity of 99%, we need to determine the prevalence of Afib in the population. This is not easy and there is scant data. Using Dr John Mandrola’s recent article in JAMAnetwork (“Screening for Atrial Fibrillation Comes with Many Snags”, August 2018), we can get a starting number. A study screening 75 to 76 year old Swedes found new Afib in 0.5% of the screened population.

If we put these numbers into Bayes formula, a pretest probability of 0.5% yields a post-test probability of 33%. In other words, if the chance a person has Afib is 1 in 200 and the watch detects Afib, the posttest probability of Afib is 1 in 3. This is a substantial increase and may be worth additional testing and perhaps treatment.

But…

We don’t know the true sensitivity and specificity. A sensitivity and specificity of 99% is almost never achieved by a diagnostic test, even the best tests come in at 90% to 95%. Testing the sensitivity and specificity of the Apple watch’s ability to detect Afib can be done and it won’t be a difficult undertaking. For example, Apple watches can be given to patients with pacemakers who go in and out of Afib. The watch can then be compared to the pacemaker interrogation to see if it accurately detects Afib and then the sensitivity and specificity can be calculated.  This study would not require too many patients, can be done in a short time and would not be that costly.

The true prevalence of Afib, however, is another story.  This will require a much larger and more extensive study. It would require many thousands of people, monitored for long periods of time (likely years) and would be very costly. In addition, the prevalence noted above is for older patients. The prevalence will be lower in younger unselected patients. If we cut the prevalence in half, to 0.25% or 1 in 400 people, then the posttest probability becomes 20%, still a substantial increase, but less impressive and more likely the watch will have produced a false positive. If the true prevalence is even lower, say by an order of 10 (1 in 2000 people or 0.05%), then the posttest probability is only 5%. It would be much more likely that the result would be a false positive.

The bottom line is that we don't know how accurate the Apple watch will be in detecting Afib. However, even if it's detection rate is nearly perfect, it ability to find Afib is dependent on the prevalence of Afib in the community. If there is a higher prevalence (as would be the case in older patients or heart patients who are hospitalized) then the chance of finding Afib is higher. If the prevalence is low, an irregular heart beat on the watch is more likely a false positive and not Afib. So, if your Apple watch says that you are in Afib, try to keep this in perspective.

Low T

We have all seen the advertisement. An ex-ballplayer, a Hall of Famer, is approached by a couple of pretty women in the gym. They comment on how muscular the player is, that he hasn’t changed a bit since his playing days. They inquire, “How do you do it?” The player then launches into his pitch. His supplement keeps him fit and virile due to its “man-boosting” properties. What are these “man- boosting” properties? Can it help boost the heart muscle as well?

The “man-booster” is the male sex hormone testosterone (T).  T is responsible for normal sperm production, maturation of the male sex organs, growth of the beard and pubic hair and deepening of the voice. In addition, T increases muscle mass and strength and helps with bone density.  Low T is a syndrome where T is not secreted in sufficient amounts. Low T may be caused by radiation, trauma, mumps and medications (such as opioids and steroids like prednisone).  In addition, levels of T decline as men get older. About 25% of men over 65 will have Low T while 54% of hospitalized patients and 50% of diabetics have Low T.  The condition is diagnosed by checking levels of T in the blood. Levels are drawn on two separate mornings before 10 AM (T levels drop after 10 to 11 AM).  Total T and free T are measured, with free T the more accurate test. Symptoms of Low T include hot flashes, decreased libido, depression, fatigue, erectile dysfunction and reduced muscle mass. In addition, there is a relationship between Low T and blockages in the heart arteries as well as heart attacks and cardiac deaths.  Many studies have shown lower levels of T in men with significant blockage in the heart arteries, especially when those blockages occur at younger ages (45 years old or younger). However it is unclear whether Low T causes the blockages or whether the Low T is just a marker of poor overall health. 

There are several different ways to replace T in patients with Low T. A patch containing T can be applied to the skin. This isn’t used much as the patch is very irritating and can cause a rash. A gel with T can be applied to the skin. T may also be injected into the muscles.  Oral T replacement (a pill or tablet) is not recommended as it can cause liver toxicity (injection and skin application bypass the liver and are safer).  Regardless of the formulation used, the goal of T replacement is to restore T levels in the blood to normal and reverse the symptoms of Low T.  T replacement has been shown to improve libido but it is less effective at improving mood and depression. Fatigue and vigor improve with T replacement. In addition, there is a decrease in fat, and an increase muscle mass and strength.  Lastly, T replacement reduces blood sugar and triglycerides with no significant improvement in cholesterol and blood pressure.  There are serious side effects with T replacement.  The prostate increases in size under the stimulation of T, which can lead to difficulty urinating.  T replacement can trigger prostate cancer to grow. Before being placed on T, screening for prostate cancer should be performed either with an examination of the prostate or a blood test (PSA).  T replacement may make sleep apnea worse. Lastly, T replacement may cause blood clots in the legs. 

Since most studies have shown that Low T is associated with heart disease, what is the role for T replacement in the cardiac patient?  Unfortunately, the answer is not clear. Many studies have shown an increased rate of cardiovascular events in those taking T replacement.  However, there are an equal number of studies showing the opposite; that T replacement can decrease the risk for a heart attack. There are no high quality studies looking at T replacement and cardiac outcomes as the primary endpoint. Therefore, at the present time, the issue of cardiovascular safety in T replacement is controversial. One area where T replacement may be beneficial is congestive heart failure.  Although the heart’s pumping ability (ejection fraction) was not improved on T replacement, patients on T replacement could exercise more, have less shortness of breath and did not have an increase in heart attack or death. 

Due to aggressive advertising, marketing and celebrity pitches, there seems to be an epidemic of Low T, but who should be treated? The bottom line is that young men with low levels of T in the blood and with symptoms of Low T should be offered T replacement.  Symptoms should be significant; just having fatigue is not enough to warrant T replacement. While on therapy, these patients need careful surveillance to make sure they don’t develop prostate cancer or any of the other side effects of T replacement. The use of T replacement in older men and those with heart disease is still controversial and those patients should be counseled about the potential cardiac side effects. Those with recent heart attack, heart stent, or stroke likely should avoid T replacement, given the uncertainty of the risk.

If you are interested in participating in a study examining Low T and heart disease, please call the Medicor Cardiology research department at 908-243-5009 to see if you qualify.

The Mediterranean Diet Melodrama

The Mediterranean diet has long been the standard for heart healthy eating.  It is a diet that emphasizes olive oil, fresh vegetables, nuts, whole grains over refined grains, fish and plant-based protein over red meat, herbs and spices to flavor food over salt, and fresh fruit for dessert instead of refined sweets. The US News and World Report even named the Mediterranean diet its number one diet for 2018. In addition to diet, the Mediterranean lifestyle incorporates moderate alcohol consumption, exercise and socialization with meals.  There has been a lot of data to support the claim that this diet and lifestyle is good for heart patients. However recent revelations may have knocked the Mediterranean diet off its pedestal.

The most important and influential trial of the Mediterranean diet, the PREDIMED study, was published in 2013.  The trial looked at 7,400 people who were at high risk for heart disease. They were randomized to either the Mediterranean diet or a reduced fat diet.  After five years the trial was stopped early and in dramatic fashion. The Mediterranean diet was declared the winner because it lowered the risk for heart attack, stroke and cardiac death by a substantial 30% compared to the reduced fat diet. Reductions of this magnitude are rarely seen with medications much less with dietary therapy. Since this trial was published, cardiologists have prescribed the Mediterranean diet to their patients. PREDIMED was felt to be an excellent study providing rock solid evidence in a field (nutritional science) that is filled with flawed studies. However in a shocking and rare move in June 2018, the New England Journal of Medicine printed a retraction of the PREDIMED trial, questioning the outcomes. It turns out that about 1,500 patients (about 20%) were not properly assigned to the various diet groups. The researchers recalculated the data, without the 1,500 people, and found that the results were much the same, but the evidence was now much weaker.

Does the PREDIMED retraction nullify the Mediterranean diet? Does this mean that the diet is not beneficial for heart disease? Likely not.  The Mediterranean diet remains the standard for heart healthy eating. Each of the components of the Mediterranean diet has been shown to be beneficial and make common sense for the heart patient. In separate and independent studies, fish, fresh fruit, vegetables, nuts, olive oil and plant based protein have all been shown to lower the risk for heart disease. In addition, the Mediterranean diet is nutritious and sustainable (people can follow it rather easily for years).

Another component of the Mediterranean diet, a glass of wine per day, has also recently come into question. A recent study looking at 600,000 current alcohol drinkers showed that imbibing seven or more glasses of wine per week was associated with an increased risk of death from all causes.  The more alcohol consumed per week, the higher the risk of death.  They estimated an upper safe limit of alcohol was five standard glasses of wine per week for both men and women. Drinking above that limit was associated with shorter life expectancy.

These new data and retractions point out that nutritional studies are notoriously difficult to perform. In general, there are several different problems with these studies. It is hard for people to eat the proper foods consistently without straying (ask anyone who has been on a diet).  There is a huge influence of culture and society on what a person eats and the amount of alcohol consumed.  There is a complex interplay between diet, alcohol and other behaviors (for example exercise and smoking).  In addition, heart disease takes a long time to develop, so diet studies must be carried on for years to see a possible effect.  Lastly, nutritional studies are often funded by industry and thus subject to bias. For example, a study sponsored by the National Institutes of Health looking at alcohol and heart disease was halted in June 2018 when it was discovered that it was partially funded by the alcoholic beverage industry. 

Why is this important? It underscores the fact that even professional researchers, who are trying to conduct a scientifically sound study, have a hard time. Keep this in mind while reading the next sensational newspaper story touting the effects of the latest diet or watching television and hearing about the benefits of alcohol. Please evaluate these types of stories with some healthy skepticism.

Get a Haircut, Lower Blood Pressure

“My blood pressure is all over the place”. This is a common refrain from patients. What is a “good” blood pressure? Where is the best place to measure the blood pressure? How does getting a hair cut affect the blood pressure?

The blood pressure is never a single solitary number. It will fluctuate over the course of the day and is affected by many things, such as activity or drinking a cup of coffee. Think of the blood pressure as a wave on the ocean, it will have highs and it will have lows.  It is best to avoid tsunamis with wild swings between the peak and the trough. Large fluctuations in blood pressure are associated with an increased risk for heart disease. A controlled blood pressure will have gentle swings from high to low and be centered around an ideal number. That ideal number, or target blood pressure reading, has been a source of controversy. In late 2017 the American College of Cardiology published new guidelines declaring that patients with blood pressure greater than 130 systolic now have hypertension, supplanting the previous recommendation of 140. This reclassification means that there are 31 million people who now have hypertension and about 45% of Americans are considered to have hypertension, up from about 32% using the previous level. However, according to the new guideline, not all of the people with blood pressure > 130 should be treated with medication. Blood pressure lowering medications are recommended for patients with systolic pressure > 130 and who already have established heart disease or those whose estimated ten year cardiac risk is greater than 10% (based on the risk calculator cvriskcalculator.com).  Those with lower cardiac risk should continue with life style modification (exercise, weight loss, smoking cessation).  For patients with systolic blood pressure > 140, medication is recommended.

Where is the best place to measure the blood pressure? The doctor’s office is not the ideal location for blood pressure checks. Patients are often stressed about getting to the office on time and are often nervous. They are rushed into the exam room, not given time to relax, and a blood pressure cuff is slapped on their arm. None of this reflects a true reading of the pressure.  More and more these days doctors are relying on patients taking their blood pressure at home, where they are relaxed and comfortable. Another reliable method is an ambulatory blood pressure monitor, a blood pressure cuff worn for 24 hours, which gives an average blood pressure reading during the day and at night.  Both methods, home blood pressure readings and an ambulatory blood pressure monitor, can confirm hypertension in patients who have high readings in the office. Both can show if the patient has white coat hypertension (high readings in the office but normal at home) to avoid over diagnosis and over treatment.  Most importantly, ambulatory blood pressure monitoring is a stronger predictor of cardiac disease and mortality than office blood pressure values.  Given this data, the guidelines recommend the following for blood pressure targets: 140/90 in the office, 135/85 for home measurements and 130/80 for ambulatory monitors.  Lastly, the systolic blood pressure is a better predictor of mortality than the diastolic pressure. 

What does having a haircut have to do with blood pressure? Black men have more hypertension, more hypertension resistant to treatment and a higher risk for cardiac death due to blood pressure than white men or black women. Until now, this population has been very difficult to treat.  A trial involving 15 black owned barbershops in Texas was able to reduce blood pressure by 27 points and was very successful at reaching blood pressure goals. How was this done? Blood pressure checks were done with the men in a relaxed environment while getting their haircut. A pharmacist was present in each barbershop and medication was prescribed and increased based on blood pressure readings each time the men came in.  These checks occurred every two to four weeks and the results were as dramatic as had ever been seen.

In general, the blood pressure should be lower than 140 systolic while avoiding wild swings. Ideally the blood pressure should be measured at rest and when comfortable, either at home or in your favorite hair salon.

Getting to the Heart of Vitamins

By any measure, the vitamin supplement industry is booming.  Estimates put vitamin sales around $12 billion annually.  According to a 2013 Gallop poll, more than half of Americans take vitamin supplements.  Vitamin use is even higher in older Americans, with 68% of those over 65 years old regularly taking a vitamin supplement. More women (54%) take vitamins than men (46%). A 2017 study found that 54% of adults older than 60 took at least one vitamin supplement, while 29% took four or more supplements. With more than 90,000 vitamin products available to choose from, is there evidence to recommend vitamin supplementation? Does taking a vitamin lower the risk for heart disease?  Let’s look at the data for some specific vitamins.

First there are the B vitamins, whose story is closely tied to homocysteine. In the late 1960’s and early 1970’s it was observed that patients with high levels of homocysteine in the blood tended to develop blockage in their heart arteries at an early age.  This began the homocysteine theory of atherosclerosis. Homocysteine is an amino acid (one of the building blocks of protein) and is metabolized using folic acid (a B vitamin) and vitamin B12. Patients with high levels of homocsyteine in the blood can have a genetic defect, but two thirds are due to deficiency of folic acid, vitamin B6 and vitamin B12.  Giving folic acid supplementation decreases the level of homocysteine.  It seemed plausible that giving vitamin supplementation with folic acid would reduce homocysteine levels and decrease heart artery blockages.  However well done studies showed that giving folic acid did reduce homocysteine levels but this did not translate into lower risk for heart attack, stroke and cardiac death.  It is now felt that homocysteine rises as a consequence of a vascular event, rather than as a cause of the event and that vitamin B supplementation doesn’t reduce cardiovascular risk. 

Next up are the antioxidant vitamins, C and E.  Foods rich in antioxidants, such as fruits and vegetables, are known to protect against heart disease.  Does supplementation with the antioxidant vitamins, C and E, provide the same heart protection?  To test this theory, the British Heart Protection study gave vitamin C and vitamin E to patients at high risk for cardiac death.  They found that there was no benefit of vitamin C or E in reducing heart attack, heart death or cancer. The Women’s Health Study followed nearly 40,000 healthy women for 10 years to see if supplementation with vitamin E would reduce cardiac events. Vitamin E did not decrease the risk for heart attack, stroke or death.  Lastly, vitamin E was given to patients with known heart artery disease to see if it reduced cardiac events.  Once again there was no difference in heart attack, stroke or death. In fact, congestive heart failure occurred more often in patients taking vitamin E, showing that excess vitamin E may be harmful. Because of this, cardiologists have stopped prescribing vitamin E.

Next at bat is vitamin D. Vitamin D has been most extensively studied in bone disease, especially osteoporosis, but there is a strong association between vitamin D deficiency and cardiovascular disease.  Studies of hundreds of thousands of patients, followed for more than 20 years, have shown an association between vitamin D deficiency and hypertension, diabetes, high cholesterol and heart disease. Unfortunately, supplementation with vitamin D is not effective in lowering blood pressure, is not useful as a treatment for diabetes and doesn’t significantly change the cholesterol blood panel. It is possible that vitamin D deficiency is a result of cardiovascular disease, rather than a cause of it. The jury is out on vitamin D treatment in heart disease, as some studies show a small reduction in heart deaths, while others show no benefit. The reason for the discrepancy is that most studies looked at vitamin D’s effect on the bones, the heart events were secondary. In addition, these studies tended to involve older patients and patients who already had established heart disease. Studies specifically looking at vitamin D supplementation and heart disease are ongoing, with results due in the coming years. Despite this, it is well established that patients with chronic kidney disease benefit from vitamin D therapy. In this population vitamin D reduces blood pressure and heart deaths. 

It seems that supplementation with B vitamins, vitamin C and vitamin E have struck out with heart disease while vitamin D is still in play. The US Preventive Services Task Force, a group of independent physicians, agrees. They reviewed all of the data on vitamin supplements and could not recommend them for heart protection.  This appears to be a common phenomenon with supplements in general. Whenever humans try to capture the good ingredients found in food and produce a pill, the pill comes up short in terms of benefit. In the case of vitamins, there may be a couple of reasons for this.  Perhaps it is not the vitamin that is beneficial, but some other substance.  For example, fruits and vegetables are high in fiber, vitamin supplements are not. In addition, the body carefully regulates its use of vitamins. The body uses what it needs and any excess is excreted in the urine.  The typical American diet, for all of its faults, provides plenty of essential vitamins and minerals. Many of our foods are fortified, for example, milk with vitamin D, and flour with B vitamins. Any excess supplementation just isn’t being used.

Appropriate vitamin intake is essential for overall health.  In addition, there are many clinical situations where vitamin supplementation is indicated and useful (such as nutritional deficiencies). However, for heart protection eat fresh and natural foods, especially fruits, vegetables, whole grains, and seafood. Don’t expect vitamin supplements or a daily multivitamin to reduce the risk for heart disease.

Is There Something Fishy About Heart Disease?

In the never-ending quest to prevent heart attacks, many populations with low rates of heart disease have been studied.  What are the unique properties of these people that protect them from heart disease? One factor that seems to protect against heart disease is the regular consumption of fish, especially fish high in omega 3 fatty acids.

Omega 3 fatty acids are polyunsaturated fatty acids that can be found in plants (alpha linolenic acid) and fish (eicosapentaenoic acid or EPA and docosahexaenoic acid or DHA).  The omega 3 fatty acids from fish are felt to be especially cardio protective. The oily (dark meat) fish that contain omega 3 fatty acids include halibut, herring, mackerel, oysters, salmon, sardines, trout, tuna, cod, char and mussels. Fish oil containing omega 3 fatty acids has several properties that may be beneficial for heart heath.  It lowers triglycerides and may lower blood pressure while improving the health of arteries.  Omega 3 fatty acids stabilize heart membranes and reduce the risk of heart arrhythmias. Fish oil may also be a blood thinner and it may have anti-inflammatory effects as well.  Do the benefits of fish oil translate into a lower risk for heart disease?

In studies of populations who consume large amounts of fish rich in omega 3 fatty acids, it was found that there was a very low risk for death from heart artery disease.  For example, one of those populations, the Eskimos in Alaska, eat on average about 20 times the amount of omega 3 fatty acids as compared to people in the continental United States. In studies of patients without previous heart artery disease, those with higher intake of omega 3 fatty acids had a lower risk of dying from a heart attack. The death rate is 15% lower for weekly consumption of fish and 23% lower if fish is eaten two to four times per week. In patients with a prior heart attack, fish consumption was also associated with lower rates of cardiac death.  The effect of fish oil seems to be in the reduction of sudden cardiac (arrhythmia related) deaths rather than nonfatal heart attacks (where there is no real benefit). Fish oil may not stabilize heart artery plaque (which would lower the overall rate of heart attacks). Because of these studies, the American Heart Association recommends that patients who have heart artery disease eat oily fish two times per week.  In addition, the heart healthy Mediterranean Diet advocates for two or more servings of fish per week.

If consuming fish is good for the heart, is the same true for fish oil supplements containing omega 3 fatty acids?  Fish oil supplements also lower triglycerides and LDL cholesterol but it is more controversial whether they reduce the risk for heart disease.  In general, these supplements are safe although they can increase the risk for bleeding. Early studies showed a benefit for fish oil supplements but more recent data don’t show the same benefit.  A recent study of 77,000 patients given supplements with omega 3 fatty acids for 4 years showed no reduction in heart attacks, stroke, cancer or death. There may be several reasons for the difference. More recent studies include higher consumption of fish; people have gotten the message and have increased their fish intake on their own.  Adding fish oil supplements to a diet that includes fatty fish wouldn’t reduce risk further. In addition, more recent studies include patients receiving maximal therapy for heart disease.  Adding fish oil supplements won’t reduce risk further. The American Heart Association reviewed all of the available data on fish oil supplements and recommended the following. For patients without heart disease there is not enough data to recommend fish oil supplements. For patients with heart artery disease, already on optimal medical treatment, the role of supplements is not settled. Given the fact that fish oil supplements are relatively safe, their addition may be reasonable.

The best way to prevent heart artery disease is to exercise regularly and follow a prudent diet, including a good amount of fish. Fish oil (omega 3) supplements can be used for patients with established heart artery disease, but only after other medications, especially statins, are maximized and with the realization that the benefit of the supplement may only be minor.

Broken Heart Syndrome

Can a heart truly be broken? Unfortunately many people have suffered the emotional aspects of a broken heart, but can the heart be physically broken as well? Consider the following scenario. A sixty-seven year old woman presents to the emergency room (ER) with chest pain.  She lives alone and earlier in the day she learned that her faithful companion, her dog, passed away.  In the ER, she is found to have a very abnormal electrocardiogram (EKG) and her blood enzymes are suspicious for a heart attack.  She is admitted to the hospital and undergoes a heart catherization the next day. Her cath reveals normal heart arteries, without evidence for blockage, but her heart is severely damaged. What is happening?

She is suffering from a condition known by various colorful names including broken heart syndrome, apical ballooning syndrome, and stress-induced cardiomyopathy (cardiomyopathy is a weakened or damaged heart muscle).  This condition was first described in Japan in 1991. The Japanese coined the condition Takotsubo cardiomyopathy because the heart muscle resembles a Japanese octopus trap with a narrow neck and a wide base.  Stress-induced cardiomyopathy occurs primarily in women (90%), the majority of whom are post-menopausal. It is often associated with a chronic psychiatric disorder such as anxiety or depression.  It is commonly triggered by an emotional event. Stressors include learning of the death of a loved one, public speaking, a surprise birthday party, a lightning strike, or an earthquake. Physical triggers, such as pain or anxiety over a medical procedure can provoke an event as well.  In women, an emotional trigger is more likely, while a physical stressor is more common in men. The vast majority of patients present with chest pain and EKG changes; their presentation often looks like an acute heart attack. In addition, there are high levels of cardiac enzymes in the blood. These enzymes are typically released when the heart is damaged, as occurs with a heart attack. Heart catherization often shows no blockage in the heart arteries but the heart muscle is severely damaged and not contracting. The most common area of damage is the apex or the tip of the heart. Due to this damage, the heart’s pumping capacity, the ejection fraction, is significantly reduced.  Patients are treated with beta-blockers to reduce the effect of adrenaline (catecholamine) on the heart and ACE inhibitors to prevent congestive heart failure from the low ejection fraction. While death and stroke can occur with stress-induced cardiomyopathy, the vast majority recover.  Fortunately, the heart function also usually recovers and returns to normal after several days to several weeks. The prognosis is usually good, although about 10% of patients have a recurrent event, despite treatment.

The exact cause of stress-induced cardiomyopathy is not known. There are many possible explanations but the prevailing theory is that a trigger provokes a “fight or flight response” resulting in a rush of stress hormones (adrenaline, catecholamines) and an exaggerated stimulation of the nervous system. It is well known that adrenaline and nervous system stimulation can cause severe damage to the heart.  The brain is the common factor. Adrenaline is released on command from a part of the brain (the pituitary gland) and the nervous system is activated in the brain. Stress-induced cardiomyopathy is felt to be part of a number of syndromes with a brain-heart connection. For example, patients with an acute stroke or a bleed in the brain often have EKG changes similar to those seen with stress-induced cardiomyopathy. Activation of the “fight or flight” response can also cause irritability of the heart leading to arrhythmias and potentially sudden cardiac death. In fact, the brain-heart axis may contribute to deaths associated with primarily neurologic conditions such as stroke, seizure disorders and head trauma.

For this upcoming Valentine’s Day, let’s keep both the heart and the brain healthy and hope that there are no broken hearts out there.