Is Your Arthritis Medication Hurting your Heart?

Nonsteroidal anti-inflammatory drugs (NSAIDs) are common medications, available over the counter as well as by prescription, used to relieve pain, reduce fever and decrease inflammation caused by arthritis, low back problems and soft tissue injury. There are many NSAIDs on the market including ibuprofen (Motrin, Advil), naproxen (Naprosyn, Aleve), indomethacin (Indocin), diclofenac (Voltaren) and celecoxib (Celebrex).  NSAIDs have been around since the 1960’s and may be the most widely prescribed class of medications in the world. Along with their beneficial effects, NSAIDs have significant side effects including gastrointestinal bleeding, kidney problems and several adverse cardiac effects. What are the cardiac side effects and how important are they?

Can NSAIDs increase the risk for a heart attack? Heart attacks occur when a plaque in a heart artery ruptures, a blood clot is formed over the rupture and blood flow to the heart muscle is stopped. Plaque in a heart artery is comprised of cholesterol and inflammation is felt to play an important role in plaque build up. In fact, in addition to their usual properties, aspirin and statins are felt to lower the risk for a heart attack due to their anti-inflammatory effects.  Do the anti-inflammatory effects of NSAIDs provide the same protection against heart attacks? Unfortunately the answer is no.  Prior to 2004, NSAIDs were felt to be safe for heart patients. In 2004, the NSAID rofecoxib (Vioxx) was removed from the market due to its increased risk for heart attack and stroke, especially with prolonged use and at high doses.  After the withdrawal of Vioxx, a large study testing the heart risks of many NSAIDs was performed and recently concluded. The study found that all NSAIDs (including Naprosyn, which was thought to have acceptable cardiac safety) increased the risk for heart attack. The risk starts in the first week, is greatest in the first month of usage and is increased at high doses.  

Can NSAIDs increase blood pressure and cause swelling? If a patient goes to the doctor with new onset of swelling in the legs or with an increase in blood pressure, one of the first questions asked is whether the patient is taking an NSAID. NSAIDs mechanism of action is to reduce certain factors that result in inflammation. Unfortunately, those same factors have a good effect on kidney function. Reducing these factors leads to a reduction in the blood flow to the kidneys.  If the blood flow to the kidneys decreases, the kidneys feel the body is dehydrated and respond by retaining more sodium (salt) and water.  This leads to increased swelling and an increase in blood pressure. In addition, NSAIDs can block the effect of certain high blood pressure medications (ACE or ARBs), leading to hormonal activation and further retention of salt and water. Due to these effects, all NSAIDs have warnings on their labels stating that they may increase blood pressure or cause swelling.

Can NSAIDs cause congestive heart failure (CHF)? The link between NSAIDs and CHF has been known for more than 20 years. NSAIDs can cause CHF in several ways. NSAIDs can increase the blood pressure, increasing the workload of the heart. If there is a weakened heart for any reason, that extra workload can tip the heart into CHF.  In addition, if more salt and water is retained in a patient with a weak heart, the excess fluid accumulates in the lungs and CHF occurs.  In fact, the use of any NSAID was associated with a 19% increase in admission to the hospital for CHF.

All of this data does not imply that NSAIDs are bad drugs or drugs that should be avoided. On the other hand, NSAIDS are not harmless over the counter medications that can be taken without risk. Patients who are at a high risk for a heart attack, patients with CHF or high blood pressure perhaps should avoid NSAIDs or use them at the lowest possible dose and for a short period of time. Low risk patients should be able to take NSAIDs with appropriate caution.

Medicor Cardiology Donates AED to Flemington-Raritan Baseball Complex

Medicor Cardiology, part of Atlantic Medical Group with offices in Bridgewater and Hillsborough, has donated an Automatic External Defibrillator (AED) to the Flemington-Raritan Baseball Association for use at their baseball complex.

An AED is used to detect an irregular heart rhythm from the lower chambers of the heart, called ventricular fibrillation, the rhythm which causes Sudden Cardiac Arrest.  If this arrhythmia is found, the AED then provides a shock to the heart, a life saving treatment which aborts the arrhythmia.

Sudden cardiac arrest occurs in 450,000 people in the United States each year and is usually fatal.  It is most commonly caused by a heart attack, but it can occur if a projectile, such as a baseball, strikes the chest at just the right time in the heart cycle. With sudden cardiac arrest, the arrhythmia prevents the lower chambers of the heart, the ventricles, from pumping blood to the body. If no blood is being pumped to the brain, the victim passes out and collapses. If a patient suffers sudden cardiac arrest, 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 can be life saving.

On October 4 2017, Medicor Cardiology presented the AED to the Flemington-Raritan Baseball Association solidifying Medicor’s long-term commitment to the heart health of the Hunterdon and Somerset County communities.  Prior AED donations by Medicor include Bridgewater Baseball’s Prince Rogers Complex, Somerville Recreation’s Carol Pager Sports Complex and the Hillsborough Baseball League fields in Mountain View Park. The Flemington AED will be kept outside of the snack shack at the baseball complex.

Is Oxygen Really Neccessary?

A 55-year-old man presents to the Emergency Room with crushing chest pain. He is diagnosed with an acute heart attack.  The nurse, following the American Heart Association Advanced Cardiovascular Life Support guidelines and out of habit, puts the patient on oxygen.  A football player comes off the field after a particularly grueling set of plays. He sits on the bench and puts on an oxygen mask. A patient with stable chest pain asks his doctor for oxygen to be used at home. Would oxygen be helpful in any of these scenarios? When is oxygen therapy useful and necessary?

Oxygen was discovered by Joseph Priestly in 1774 and is the second most abundant element in the air (after nitrogen).  Oxygen takes up 21% of the Earth’s atmosphere.  Oxygen is necessary for all of the functions of the body. As we breathe, the oxygen in the air is brought to tiny sacs in the lungs. In these lung sacs, oxygen is absorbed by the blood stream. In the blood stream, oxygen binds to the red blood cells. The oxygen, attached to red blood cells, travels through the lungs to the heart where it is pumped to the rest of the body. Oxygen is then extracted by the muscles and organs of the body to aid in metabolism.

Since oxygen is so essential to the body, how can we be sure we are getting enough? In medicine, the most common way to measure oxygen is with a pulse oximeter, an infrared device that provides the oxygen saturation in the blood. An oxygen saturation between 90% and 100% is normal while a saturation below 90% is considered low. Low oxygen saturation, or hypoxemia, causes shortness of breath, an increased heart rate and it can be very dangerous. To treat hypoxemia, oxygen therapy is delivered in a variety of ways. A nasal cannula has two prongs, which are placed in the nose, and gives extra oxygen. A facemask can provide higher dosages of oxygen, with concentrations up to 100% (ie, the gas in the mask is 100% oxygen versus the 21% oxygen present in the air).  Lastly, in extreme cases of hypoxemia and breathing distress, a tube is placed in the throat and the patient is placed on a respirator to help aid in process of breathing.

Oxygen has been a key treatment in cardiology for more than 100 years. In 1900, it was shown that oxygen could relieve chest pain, a finding that led to the routine use of oxygen in all heart patients. Over the years it has been found that oxygen therapy in patients with hypoxemia is undeniable but in patients with normal oxygen saturation the benefit is not as clear. In patients who are hypoxemic and have an acute heart attack or who are in congestive heart failure (CHF), with fluid filling their lungs, oxygen can be life saving. In cases with hypoxemia, oxygen therapy increases the oxygen saturation in the blood, decreases the resistance to blood flow in the lungs and eases the work of the heart by lowering the heart rate and blood pressure, thus reversing the body’s adaptation to a low saturation.

While the body has mechanisms to counter act low levels of oxygen in the blood, high levels of oxygen saturation is a man-made phenomenon caused by oxygen therapy. The body has no mechanism to handle this situation and in fact oxygen therapy can be damaging. There are two possible reasons for this. First, the red blood cells are nearly saturated with oxygen. Adding extra oxygen doesn’t increase the amount of oxygen delivered to the cells of the body. Secondly, excess oxygen can cause spasm or narrowing of the heart arteries, reducing blood flow to the heart. In CHF patients with normal oxygen saturation, high flow supplemental oxygen caused a decrease in the heart’s pumping capacity and increased the pressure in the lungs, causing worse outcomes. In heart attack patients with normal oxygen saturation, excess oxygen therapy can cause a reduction in flow to the heart arteries. Patients with oxygen therapy had larger heart attacks than those not given extra oxygen.  In a recent study of over 6000 patients with a heart attack and normal oxygen saturation, there was no change in the rate of death or recurrent heart attack with oxygen therapy.

Can oxygen be beneficial for the athlete? Can it be considered a performance-enhancing drug?  When supplemental oxygen was given to soccer players and other athletes, there was no demonstrated improvement in performance and no reduction in recovery time. On the athletic field, it is felt that oxygen may provide a placebo effect (an expectation of doing something good) without a real physiologic benefit. 

Oxygen clearly has a role and is life saving for those heart patients who have low oxygen saturation. For heart patients with normal oxygen levels, as well as football players and other athletes, supplemental oxygen likely has no benefit and can be harmful. Based on these findings, none of the patients in the scenarios would be candidates for supplemental oxygen.

Are Statins a Pain?

Statins are wonderful drugs which have almost single handedly reduced the global burden of heart disease.  Statins are a class of medications that lower cholesterol, including the “bad cholesterol” (LDL, low density lipoprotein) and raise the “good cholesterol” (HDL, high density lipoprotein). In addition, statins have other properties, such as anti-inflammatory effects, that also contribute to their ability to lower heart disease. For every 40 points that statins lower LDL, the risk of a heart attack is reduced by 20-25% and the risk of dying from heart disease is lowered by 10%. As with all medications, with the good comes the bad; all medications can have side effects. Statins can raise liver enzymes, increase the risk for diabetes and, most significantly, can cause muscle pains.

Muscle pain is the most common side effect of statins. It is also the most common reason that patients stop taking their statin, despite the benefits. The symptoms include muscle pain, aching, cramping or weakness.  Usually both sides of the body are affected and usually large muscle groups (thigh, buttock, back, shoulder) are involved.  A typical example would be muscle cramping in both thighs. Risk factors for statin associated muscle pains include older age, female sex, and lower body mass index (BMI).  Other medications and substances (such as alcohol) that have toxic effects on muscles also increase the risk.  Symptoms usually occur right after starting a statin or after an increase in statin dose. The most extreme side effect of statins is called rhabdomyolysis, a life-threatening condition where the muscles not only are painful they actually break down, releasing a protein that can damage the body.  Symptoms of rhabdomyolysis include weakness, vomiting, confusion, tea colored urine, kidney failure and death.  Fortunately, it is a rare condition, occurring in less than 1 in 1000 patients taking statins.

The true extent of statin associated muscle pain is very hard to determine, even within clinical trials.  In trials, muscle pain from statins is reported in 10-25% of patients, but any seasoned clinician will tell you that, in practice, the number of patients who have muscle pains on statins seems much higher.  The reason may due to a powerful factor called the nocebo effect.  Many are familiar with the placebo effect, the idea that a patient can be given a fake treatment, a “sugar” pill with no real medication, and still derive a benefit from taking that treatment. It is the power of positive thinking; simply because a patient believes a pill with be helpful can cause it to have true physical benefit.   For example, in a hypertension trial a patient given placebo can actually have a lower blood pressure.  In trials, placebos are given to set a baseline. Researchers can see if an active medication provides benefit above and beyond the placebo.  The opposite effect, the nocebo effect, occurs when a patient is given a fake treatment or a sugar pill but still has harm. Just knowing the potential side effect of a medication is enough to bring on real symptoms. The nocebo effect can be triggered by reading package inserts, watching or reading about a medication in the media or by listening to a doctor describe side effects.  The placebo effect is the expectation of benefit from a medication while the nocebo effect is the expectation of harm from a medication.

Statins are especially prone to the nocebo effect, which was nicely documented in a recent trial.  In the first phase of the trial, patients did not know if they were on statin or placebo. The percentage with muscle pain was the same in both groups.  In the next phase, patients could continue on a statin or placebo, but they knew which they were taking. Once patients knew they were on a statin, muscle pains were much more likely among patients taking a statin versus those who were on placebo.  Patients on placebo were twice as likely to have side effects when they did not know which drug they were on. The researchers concluded that the expectation of harm was causing the increased muscle pain rather than the medications themselves.

How should statin associated muscle pain be treated? The first step is to stop the statin. If muscle pains persist after two months, there is likely another cause for the pain.  Once the symptoms resolve, the patient can be challenged with another statin. Patients often tolerate one statin better than another.  Longer acting statins can also be given once or twice per week, to achieve the benefit with fewer side effects. Patients should also be evaluated for other conditions know to cause muscle pains such as an underactive thyroid or low levels of Vitamin D. These conditions should be corrected. Coenzyme Q10 is purported to counteract muscle pains, but it was not shown to be effective in clinical trials. Lastly, if patients cannot tolerate two or three different statins, other cholesterol lowering medications should be used.

PARIS: Polluted Arteries R not In Style

The Great Smog gripped the city of London for four days in 1952.  Smog was not an unusual occurrence in London, but this one was different. It started after a prolonged cold front caused coal fireplaces to work overtime to heat homes. Next, a high-pressure system caused warm air to lie over the cooler ground air. These events prevented the smoke generated from burning coal from rising and escaping.  The smog crippled London, paralyzing transportation. Londoners could not see their feet as they walked and their faces were black with soot if they ventured outside. The Great Smog was deadly as well with approximately 4000 deaths directly attributed to the smog. About half of the deaths were attributed to respiratory disease, but about 25% were due to heart disease.  Due to the Great Smog, Parliament passed the Clean Air Act of 1956, restricting coal use in cities and switching to gas, oil and electricity for heating. In the US in the 1940’s and 1950’s, Pittsburgh symbolized the evils of air pollution. The smog from the steel mills was so thick that street lights had to be turned on during the day. In 1948, Donora Pennsylvania, a town near Pittsburgh, was hit with thick yellow smog that resulted in 20 sudden deaths, 400 hospitalizations and caused 7000 of the 14000 residents to become ill.  As a result, Congress passed the Clean Air Act of 1963 and the Air Quality Act of 1967, both of which helped limit the unhealthy effect of air pollution on the US population.  Air pollution has been associated with heart disease for many years. How and why does air pollution affect the heart?

The unhealthy effects of air pollution are caused by inhaling fine particles in the air. These fine particles can be produced by natural sources, such as dust and wildfires. They are also caused by industrial activity and burning fuel in homes. In addition, a major contributor is emissions from cars and airplanes.  Inhaling these fine particles from the air can stimulate localized and more widespread reactions in the body. These fine particles provoke inflammation in the lungs and the inflammatory cells and proteins produced are released into the body, causing a systemic inflammatory response. Levels of C Reactive Protein, a measure of inflammation, are elevated in the blood after exposure to air pollution.  Local inflammation can trigger asthma and emphysema in the lungs. Exposure to the particles in air pollution has been shown to increase the risk for heart artery disease and increase blood pressure. Since plaque within the heart arteries is an inflammatory process, anything that increases inflammation can increase the severity of blockage in the coronary arteries. This was shown in a ten-year study of calcium in the heart arteries (a marker for plaque in the arteries).  Patients exposed to high levels of traffic-related air pollution in cities had progressive worsening of the calcium in their arteries.  In other words, constant exposure to air pollution accelerates atherosclerosis in the heart arteries. Lastly, air pollutants can increase the risk of blood clotting within the body. All of these factors, elevated blood pressure, the systemic inflammatory response and the increased the risk for blood clotting are mechanisms whereby air pollution can destabilize plaque and trigger a heart attack.  The association between long term exposure to air pollution and heart attacks has been corroborated in many studies worldwide. In addition, exposure to air pollutants has been shown to increase admissions for congestive heart failure and to increase the risk for atrial fibrillation.  Those at higher risk for air pollution related heart disease include people with pre-existing heart disease, those with diabetes and the elderly.

Given the global burden of disease caused by air pollution and the fact that it is a leading modifiable risk factor for heart disease, how can the effects of air pollution be reduced? On an individual level, those at risk should: 1) travel by walking or public transportation rather than by car; 2) avoid being outside in rush hour traffic; 3) exercise in parks and avoid major traffic roads; 4) limit time outdoors during highly polluted periods and 5) use a ventilation system with filtration for homes in high pollution areas.  On the global level, countries should work together to reduce industrial pollution, stop the rise in the global average temperature, reduce emissions and switch from fossil fuels to greener sources of energy.  Signing on to the Paris climate agreement would be a good first step.