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. 

 

 

 

The Radio Blood Pressure Show

 

Hi everyone and welcome to WWAD in New Jersey, number 807 on your AM dial. I’m your host, Brother Brucie from Asbury Park. Today on the Blood Pressure Show we answer all of your burning questions about hypertension. So email me, text me or hire an airplane to pull a banner over the shore with your question. Lets get started.

 

Meryl S from Summit asks, “How common is high blood pressure? Is high blood pressure a bad actor?”

High blood pressure (hypertension) affects nearly 1 in 2 people worldwide between the ages of 35 and 70 years old.  Hypertension is a leading risk factor for stroke, heart attack, death and disability. Hypertension is often called the silent killer, as there usually aren’t any symptoms until an adverse event occurs. In addition to affecting the individual, hypertension impacts the health care system. It was recently shown that about one third of emergency room visits in heart patients were for high blood pressure. This represents about 2.7 million people. In addition, hospitalization for uncontrolled hypertension has increased in recent years. 

 

Jon B from Perth Amboy queries, “How high is too high? What is the optimal blood pressure?”

Blood pressure is considered normal if less than 120 and less than 80. Elevated blood pressure is defined as a systolic pressure between 120 and 129 with diastolic less than 80. Stage 1 hypertension occurs with blood pressure over 130/80. Stage 2 hypertension is defined as a blood pressure of 140/90 or greater. Hypertension should be diagnosed if blood pressure readings are elevated on three separate occasions, several weeks apart. Once hypertension has been established, what is the target blood pressure? The landmark SPRINT study is the current gold standard answer to the question. The SPRINT trial compared two blood pressure goals, treating to under 140 and treating to under 120. The study showed that patients who were treated to under 120 had a significantly lower risk for cardiac outcomes. However, those treated to under 120 were taking more medications and had a higher risk for side effects from the medications. Therefore treating to a blood pressure under 120 is recommended for heart patients or those at high risk for cardiac disease. Other populations, such as diabetics and the elderly, should be treated to under 140.

 

Francis S. from Hoboken wonders, “Is it best to measure blood pressure in the doctor’s office or should I do it my way?”

The doctor’s office is not the ideal location for blood pressure checks. More accurate readings occur when patients take their blood pressure at home. Home blood pressure reading can be obtained either by the patient checking their own blood pressure or 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 can confirm hypertension in patients who have high readings in the office or white coat hypertension (high readings in the office but normal at home). In addition, ambulatory blood pressure monitoring is a stronger predictor of cardiac disease and mortality than office blood pressure values.   

 

Vincent L. from Ridgefield demands, “What is a winning game plan for blood pressure?”

The amount of time patients spend in a target blood pressure range is emerging as a therapeutic goal. More and more research is focusing on time in therapeutic range. The more time in range, the lower the risk for cardiac events. For example, studies have shown that increased time in the blood pressure range of 110 to 130 lowered the risk for cardiovascular death, heart attack, stroke and heart failure. Therefore, a winning strategy is to try to keep the pressure in range for the longest time. This has implications for office visits as well. If a patient comes in with an elevated blood pressure, it has to be placed in context and compared to home readings as well as prior office measurements. When blood pressure readings are taken also help describe the bigger picture. If blood pressure is 120 while sitting but is 160 after walking, or when under stress, or when in pain, then the higher reading again has to be placed in context and likely discounted.

 

Thomas E from Menlo Park, “If blood pressure readings at home and time in target blood range are keys, would wearable devices help achieve these goals?”

The blood pressure cuff was first introduced in 1896. Today, more than 120 years later, there is no significant difference in blood pressure cuff technology. This may be changing. Home blood pressure monitors and ambulatory devices all use a cuff that must be inflated to provide a reading. This limits the usefulness of these devices. There are now several cuffless wearable blood pressure devices on the market. These monitors hold lots of promise: the ability to record blood pressure comfortably, continuously, during the day and at night and provide good unbiased data on blood pressure variation. Several different technologies have been incorporated including photoplethysmography (the green light on the back of the watch). Unfortunately, the cuffless devices currently available on the market have not been shown to be accurate. For example, one smartwatch had a difference of 17 points compared to the standard cuff. Because of this, no device is recommended for use by any medical society. On the other hand, traditional home blood pressure monitors have been independently validated as accurate and a list of these validated devices is available at ValidateBP.org

One cuffless technology may prove to be both accurate and useful. The mechanism is a thin sticker that is worn on the skin and uses bioelectrical impedance, a method that has been used for years in medicine for other reasons. The sticker can be worn on the skin for a week at a time and in trials was very accurate (within 0.2 points of a standard measurement). While not currently available, it may be the future.

 

Joe P from Passaic asks, “My blood pressure is high when I am working on Saturday night.  When should I take my blood pressure meds?”

There is an old debate regarding when to take blood pressure medications- morning or evening. There is logic to taking medications at night. Blood pressure usually drops at night. Patients who do not have the traditional nighttime blood pressure dip are at higher risk for cardiovascular problems. In addition, taking meds at night may lead to fewer side effects. So, taking meds at night makes sense. Does the data support this approach?  Over the years, most studies supported taking medications at night. Recently a large, well-run trial showed no difference; morning or evening there was no difference in cardiovascular events at 5 years. When is the best time to take meds? The answer is to tailor to each patient’s individual needs, balancing efficacy (remembering to take the meds) versus tolerability (the time with the lowest side effects).

 

Lawrence B from Montclair asks, “Is one blood pressure medication sufficient? Or should I go for a four bagger?”

Doctors traditionally have been trained to use a step wise approach when treating hypertension. One medication is started and the dosage is increased if the blood pressure is not controlled. If one medication is maxed out and the number is still not good, a second or third medication is added. Is this the best approach? Recent trials have compared a single blood pressure pill to a “quadpill”, a tablet containing small doses of four different blood pressure medications. The quadpill dropped the blood pressure 7 points lower than the single agent. The appeal of the quadpill is that it offers better blood pressure control while providing ease of use (only one pill to remember) and lower side effects.

 

Robert J. from New Brunswick asks, “I have arthritis. Can I take Tylenol with my blood pressure medications?”

It is well known that nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided for patients with hypertension. NSAIDs include ibuprofen (Motrin, Advil), naproxen (Naprosyn, Aleve), indomethacin (Indocin), diclofenac (Voltaren) and celecoxib (Celebrex). These medications can raise the blood pressure and can interfere with some blood pressure drugs. Tylenol (acetaminophen) is often prescribed instead. However, recent data shows that Tylenol may not be innocuous. Patients who took Tylenol for two weeks saw their blood pressure increase nearly 5 points above patients who took placebo. Therefore, long-term use of Tylenol may not be safe for patients with hypertension. Short-term (few days) use may still be fine.

 

That’s it for our show. Thanks for joining me and hope to see you next week. This is Brother Brucie signing off (fade to music): 

“This is Radio Blood Pressure

 Is there anybody normotensive out there?

 I was staring at a dumb dial

 Just another lost number in a file

 This is Radio Blood Pressure”

 

 

How High Is Too High?

 

Come and listen to a story about a blood test named HDL (High Density Lipoprotein, the “good cholesterol”). It is an epic saga full of lows and highs. It is a story that spans the globe, from Massachusetts to the Italian Alps. What is HDL and how is it associated with heart disease?

 

The story begins in a town outside of Boston, Massachusetts. In 1977, the famous Framingham Heart Study first identified low levels of HDL in the blood as a risk factor for heart artery disease. In patients with HDL levels less than 40 mg/dl, there is an increased risk for blockage in the heart arteries and cardiac death.  On the other hand, in patients with elevated LDL (the “bad cholesterol”) normal or high levels of HDL protect against heart disease. The prevalence of low HDL in North America is about 7% in men and 2% in women. How does HDL protect against plaque build up in arteries?  There are several mechanisms. HDL transports excess cholesterol from arteries back to the liver, where it is metabolized and excreted. This process is called reverse cholesterol transfer. In effect, HDL “cleans” the arterial wall, sweeping away cholesterol and stopping plaque in its track. In addition, HDL is anti-inflammatory (plaque formation is an inflammatory disease) and has anti-oxidant and anti-blood clotting properties. Are there ways to treat low HDL?  Aerobic exercise, weight loss and smoking cessation all increase HDL levels. Diet plays a role as well. Low fat diets lower both LDL and HDL levels but diets high in monounsaturated fats (including olive oil) reduce LDL without adversely affecting HDL.  Statins will increase HDL levels. They raise HDL between 5% and 15% with an average increase of 9%. Many, many other pharmacologic agents have been tried to see if they can raise HDL levels and improve outcomes. Niacin and fenofibrate both raise HDL (by concomitantly lowering triglycerides). However, despite the positive impact on HDL levels, both drugs failed to reduce heart attacks, strokes and cardiac deaths. Several other medications have been tried, but in clinical trials they all failed to improve cardiac events, some agents even raised mortality. There are several reasons for the failure of theses medications. The biology of HDL appears to be much more complex than that of LDL.  There are several different subclasses of HDL; we don’t know which ones are the keys to the success of HDL. In addition, the function of the HDL molecule is more important than the level. Increasing the amount of HDL doesn’t mean it works better at preventing artery blockage. 

 

At this point, the story of HDL heads overseas to two small towns in Italy.  In 1980, a genetic mutation in HDL was discovered in families in a town outside of Milan. People with this mutation were smokers, did not follow a heart healthy diet, and had low levels of HDL (10 to 30 mg/dl). Yet they had low levels of blockage in the heart arteries and lived well into their 90’s.  Researchers discovered that their genetic mutation (called apolipoprotein A-1 Milano) was protective against heart disease. Subsequent trials tested whether IV infusions of this apolipoprotein could help patients with established heart disease, but again the trials failed. In another town, this one located in the Italian Alps, there is a cohort of people who have longevity and virtually no heart disease. Like their countrymen, their diet is not heart healthy but they have higher levels of HDL than the average Italian. The genetic variant in this healthy town has not yet been identified.

 

The guidelines for lipid management recommend a threshold value for HDL of 40 mg/dl; below that level there is an increased risk for heart disease while levels above provide protection. If an HDL value of 40 mg/dl is good, is 100 mg/dl better? Does the risk for heart disease continue to fall as HDL levels rise? How high is too high?  To answer the question researchers pooled multiple studies of HDL (all told more than a million patients were evaluated).  They found a U shaped relationship between HDL levels and death. Levels below 40 mg/dl were associated with increased risk of death. Surprisingly, levels over 80 mg/dl also were associated with increased deaths. They found the optimal range of HDL to be between 40 and 80 mg/dl.

 

The final chapter to the HDL saga has not yet been written. If you are not genetically gifted and have a low HDL level, do what you can to raise HDL. Stay active, exercise, keep weight down, don’t smoke and take your statin. If you have a very high HDL level, don’t assume that you are protected against heart disease. A healthy lifestyle and a statin may still be necessary if the LDL level is also elevated. Only time and further research will tell whether there is a better approach to HDL and a happy ending to the story. 

 

It Was A Swell Summer

As we say goodbye to the scorching summer of 2022, it is worth noting that heat records have been broken across the globe. Unprecedented heat waves have hit the US, Europe, England and China. According to the National Oceanic and Atmospheric Administration July 2022 was the third hottest July on record, June was the sixth warmest and overall the year 2022 is trending as the third warmest year in history. In the midst of all of this hot humid weather, patients flocked to their doctors with lower leg swelling. What are the causes of leg swelling? Why does it occur with greater frequency in the hot summer months?

 

To understand why the legs swell, we have to review the blood flow to and the drainage from the lower extremities. The arteries bring blood to the legs from heart. The veins drain the blood back to the heart. There are two venous systems in the legs: the deep veins and the superficial veins. How does blood defy gravity and flow back to the heart? As we walk, the contraction of the muscles in the legs causes the blood to be pumped upward and back to the heart. To facilitate the flow, the veins have valves to prevent blood from leaking back.  Another conduit is the lymphatic system. This consists of thin tubes and nodes that drain lymph back to the heart. Lymph is a fluid that includes excess fluid, proteins, cells, fats and nutrients. About 20 liters of blood flow to the legs every day. The veins drain about 17 liters back to the heart. The lymph system drains the extra 3 liters.  Leg swelling occurs if fluid leaks from the veins or the lymph system because of blockage to the flow or excess pressure within the vessels or the vessels become damaged or dilated. 

 

Leg swelling can be categorized as acute (recent) or chronic. One leg can be affected (unilateral) or both legs (bilateral).  There are many causes of leg swelling including deep venous thrombosis (a blood clot in the leg, DVT), chronic venous insufficiency, lymphedema, heart failure, kidney failure, liver failure, infection (cellulitis), cancer, thyroid disease, medications, and pregnancy. Medications include calcium channel blockers (especially amlodipine), prednisone, and non-steroidal anti-inflammatory drugs (such as ibuprofen and naproxen).  Leg swelling may be asymptomatic or cause pain, aching, heaviness or fatigue of the leg, skin changes or ulceration of the skin. 

 

DVT may cause leg swelling in the acute phase as a blood clot could block the flow in the deep venous system. Many patients have swelling years after an acute DVT, likely because the blood clot has caused damage to the venous valves. Treatment of DVT is blood thinners such as warfarin, Eliquis, or Xarelto.

 

Chronic venous insufficiency is a very common clinical problem. In this condition, the venous valves become incompetent, blood refluxes back into an already congested venous chamber, this increases the pressure in the chamber and fluid leaks from the veins into the surrounding tissue.  Risk factors include older age (peak incidence in women is 40-49 years and men 70-79 years), smoking, pregnancy, hypertension and varicose veins.  Prolonged standing or sitting with the legs in a dependent position also can cause swelling. In this case, the veins are completely filled, the valves float open and fluid leaks out. In addition, warm conditions (such as the hot humid summer weather) tend to aggravate symptoms as the warmth can dilate the veins, causing further venous valvular incompetence.  Conversely, cold conditions relieve symptoms.  The best test to diagnose the cause of leg swelling is a venous ultrasound. The ultrasound can demonstrate a DVT and can show if there is venous reflux/insufficiency.  Chronic venous insufficiency is treated by avoiding prolonged sitting or standing, leg elevation, exercise (walking or calf muscle exercises to help increase the flow) and compression stockings. If swelling persists despite these measures, venous ablation can be performed. Ablation shrinks the refluxing vein, allowing the valves to do their job and decrease or eliminate leaking. Varicose veins are enlarged twisted veins near the surface of the skin. They are usually branches off the superficial or deep vein system. They are quite common (25% of adults have them). Treatment is the same as chronic venous insufficiency but varicose veins can also be surgically stripped or injected with a sclerosing agent to shrivel the vein up. These treatments are more cosmetic than medically necessary. Spider veins are similar to varicose veins, but occur in even smaller surface veins. 

 

Lymphedema may be primary or secondary to another condition. Primary lymphedema occurs with congenital absence or damage to the lymph system. Secondary lymphedema occurs with blockage of the lymph system due to cancer, prior pelvic surgery, radiation, or trauma. Lymphedema can be differentiated from chronic venous insufficiency by physical exam. In lymphedema there is no pitting of the edema, swelling affects the back of the foot, the toes are involved and there is skin thickening. Lymphedema is usually painless.  Treatment includes compression stockings and pneumatic pump compression. 

 

So don’t get pumped up over lower leg swelling. See your doctor and get a diagnosis. Then follow the treatment plan to avoid any long-term complications. Keep in mind that cooler weather and relief is coming.

  

What is Optimal Heart Health?

 

What is optimal heart health? Is it normal heart arteries on cardiac catheterization? Is it the ability to run a marathon? Is it playing a round of golf and walking the course? Is it being able to do moderate exercise without shortness of breath? There are many different and unique perspectives on this question. The American Heart Association’s (AHA) perspective defines optimal heart health using eight variables dubbed “Life’s Essential Eight”.

 

The AHA initially defined seven variables for optimal heart health in 2010. After 12 years and lots of subsequent research, the AHA updated these seven parameters and added a new one this summer. Here is an update to the original seven with a deep dive into the eighth.

Diet- this was updated to encourage everyone to follow one of the known heart healthy diets; DASH (Dietary Approach to Stop Hypertension) or a Mediterranean Diet.

Physical Activity- no change was made. The optimal level of activity is still 150 minutes per week of moderate physical activity or 75 minutes per week of vigorous exercise.

Nicotine exposure- updated to discourage the use of e-cigarettes (vaping) and to reduce exposure to second hand smoke.

Body Mass Index(BMI) – BMI is body weight divided by height and is a measure of overweight or obesity (A BMI calculator may be found here: https://www.calculator.net/bmi-calculator.html). There was no change to the ideal BMI: between 18 and 25 kg/m2. 

Lipids- the updated metric for blood lipids is non-HDL cholesterol (total cholesterol minus HDL). The ideal non-HDL cholesterol for optimal heart health is < 130 mg/dl.

Blood sugar- optimal levels for non-diabetic patients are a fasting blood sugar < 100 mg/dl or Hemoglobin A1C < 5.7%.

Blood pressure- the optimal blood pressure is less than 120/80 mmHg; 130/80 and above is considered hypertension.

 

The new variable is sleep duration. According the AHA, the ideal duration of sleep for optimal heart health is between seven and nine hours per night.  The importance of sleep on overall health has been well documented and known for years.  Poor sleep can lead to irritability, anxiety, reduced cognitive performance (including loss of concentration and poor decision making), Alzheimer’s disease and increased risk for obesity, diabetes, heart attack, stroke, hypertension, atrial fibrillation and cancer. Several recent studies outline the risks of not getting a good night’s sleep. A study from the US (6,820 people, mean age 53) looked at various measures of sleep health. Those with poor sleep health had a 54% increased risk for cardiovascular disease. In another study of young healthy people, sleeping only four hours per night added extra weight and specifically added “belly fat”, which has an increased risk for heart disease. The association between sleep and metabolic disease was shown again in a study in women. Sleeping less than 7 hours per night altered glucose (blood sugar) metabolism, leading to diabetes and hypertension. Since sleep is so important, let’s tackle some pressing questions about sleep such as the optimal sleep duration, the best time to go to bed, melatonin and sleep trackers.

 

What is the optimal amount of sleep? There seems to be a “right” amount of sleep, at least as far as cognitive function is concerned as demonstrated in two recent studies. One study of elderly patients showed dramatic decline in brain function for those who slept less than 4.5 hours or more than 6.5 hours per night. In patients who slept less than 6 hours per night, there was a greater burden of amyloid in the nervous system, a marker for Alzheimer’s disease.  Another study from the United Kingdom (500,00 patients, 38-73 years) showed that seven hours of sleep per night was optimal for cognitive performance. Therefore, seven hours of sleep seems to be the sweet spot for optimal health for middle aged and elderly people (children and adolescents need more sleep). Now that we know the optimal amount of sleep, is there an optimal time for bed?  An interesting study (88,000 patients, average age 61) answers the question. Researchers found that going to sleep before 10 PM or after midnight increased the risk for heart disease. Those who went to sleep between 11 and 11:59 PM had a 12% higher risk for heart disease and those who hit the sack before 10 PM or after 12 AM had a 24% higher risk. The people who went to bed between 10 PM and 10:59 PM had the lowest risk for heart disease in the study; thus defining the optimal time for bed. In this study, timing of sleep was actually more important then duration of sleep. 

 

If there is difficulty falling asleep and getting the recommended amount of sleep, does melatonin help? Melatonin is a hormone produced by the brain. As darkness falls, the brain senses that it is nighttime and releases melatonin. The elevated levels of melatonin help us fall asleep and stay asleep. As dawn breaks, melatonin levels go down and we wake up. Can over the counter melatonin help people who have trouble falling asleep (insomnia)?  Melatonin has been available for quite some time and is felt to be safe, but no formal studies have been done. Over the counter melatonin is not benign. It has effects on body temperature, blood sugar and blood vessel tone. In addition, since it is not regulated by the FDA, melatonin doses vary widely. The American Academy of Sleep Medicine is currently reviewing the safety and efficacy data of melatonin. Until the review is complete, they recommend that it not be used for insomnia.

 

Are there devices that can help track sleep? There are a variety of sleep tracking devices that fall into two broad categories: devices put under a mattress or pillow and wearable devices. The devices may help to tell you when you went to sleep and your total sleep time. However, no device can diagnose sleep apnea (stopping breathing). In addition, when compared to a formal sleep study (the gold standard for sleep), no device can accurately measure sleep quality.  In addition, no sleep tracker or sleep app is endorsed for use by national sleep academies or sleep specialists.

 

So for optimal heart and brain health, go to sleep between 10 PM and 10:59 PM and try to get, on average, seven hours of sleep. Skip the melatonin and the sleep tracker. How many people get enough sleep and score highly on Life’s Essential Eight? It turns out that only one in five US adults (20% of people) have optimal heart health according to the AHA checklist. That certainly is not good; let’s start to improve those numbers. 

It's Summer Time!

Summer has arrived. It is time for all of those fun summer activities: golf, tennis, hiking, swimming, kayaking and sitting on the beach. Unfortunately, summer poses some unique risks for the heart patient. How does the heat affect the heart?  Is vacationing good for cardiac health? If so, what type of vacation is beneficial? These questions and more will be answered!

The extremes of temperature, either very hot or very cold, are known to cause additional stress to the heart patient. It is well known that heat waves cause a surge in deaths and hospitalizations for heart disease. Elderly patients are more prone to dehydration which can lead to low blood pressure and increased blood clotting. In addition, very hot temperatures increase the work load of the heart. These effects can lead to a subsequent heart attack or passing out or congestive heart failure. A recent study showed that for each additional extreme heat day (defined as heat index over 90 degrees) there is a 0.13% increase in deaths from heart disease. This translates to an additional 600 to 700 deaths per year in the US due to the heat. With three times as many heat waves per year now compared to the 1960’s, heat related illness must be taken seriously. 

In the absence of a heat wave can a warm summer night be just as risky?  Recent research showed that a rise of just 1.8 degrees Fahrenheit in the usual summer-time temperature caused a 3-5% increase in heart related deaths in men aged 60 to 64, but not in men over 65 or in women. It seems that nighttime temperature had a more potent effect than daytime warmth on death and heart disease. The reason for this is not clear. Socio-economic factors are an issue; those without air conditioning would be more vulnerable to warm temperatures. An intriguing theory involves sleep deprivation. Hot summer nights, especially without air conditioning, could lead to more tossing and turning, interrupting sleep patterns with subsequent increase in blood pressure, heart rate and risk for cardiac events. 

One way to escape the heat is to go on vacation. Can taking a vacation reduce the risk for cardiac events? The Framingham Heart Study showed that men who didn’t take a vacation for many years were 30% more likely to have a heart attack than men who took a yearly vacation. The same study concluded that women who took vacations once every 6 years were 8 times as likely to have heart disease as those who took more frequent time off. The MRFIT trial followed 12,000 men for nine years. It showed that men who took annual vacations were 21% less likely to die and 32% less likely to die from heart disease. Vacationing may have a direct protective effect on heart health for the following reasons. First, vacationing reduces stress and releases one from job demands. Next vacationing may have restorative effects by promoting social contact with family and friends (“reconnecting”). Lastly, certain types of vacations increase physical activity.

So vacations are good for cardiac health. What type of vacation is beneficial; an active vacation or relaxing on the beach? One study from Austria helps answer the question. It showed that an active vacation involving walking, biking or golfing reduced blood pressure and heart rate and helped improve cardiac function. Therefore, an active vacation may improve cardiac health more than lying in the sun. It seems that physical activity during leisure time (including vacations) is beneficial. How does physical activity during leisure time compare to physical activity at work?  The Copenhagen General Population Study followed 104,000 people over 10 years and had an interesting answer to the question. The study found that physical activity during leisure time reduced the risk for cardiac events by 15% and the risk for death by 40% but physical activity at work increasedthe risk for cardiac events and death. They called this the “physical activity paradox”. Why is this? They theorized that leisure time activity was more dynamic, more likely to improve cardiorespiratory fitness and allows sufficient recovery time. Physical activity at work, on the other hand, is more static, monotonous, often occurring with awkward positioning and did not allow for meaningful recovery time. 

So as we head into summer, make those vacation plans. Then dust off the golf clubs or hiking boots. Lastly, crank up the air conditioning at night and get a good night’s sleep.

 

The Calcified Aortic Valve

 

The aortic valve is a three-leaflet valve situated between the left ventricle (the main pumping chamber of the heart) and the aorta (the main artery leading from the heart). When the left ventricle contracts to send blood to the body, the aortic valve opens to allow the blood to flow out. After the blood is ejected, the valve closes to prevent blood from leaking back in to the heart. The aortic valve opens and closes, under a tremendous amount of pressure, with each heartbeat, for our entire lives. Because of this, the aortic valve is subject to “wear and tear” over time. As the valve wears down, the leaflets become thickened and calcium is deposited to repair microtears in the valve.  As the valve becomes more thickened and calcified, it doesn’t open fully, restricting the blood flow from the heart. This pathologic condition is called calcific aortic stenosis. When there is significant restriction of the blood flow, it is called severe aortic stenosis. Severe aortic stenosis may cause chest pain, passing out, congestive heart failure or sudden cardiac death. Unfortunately, once severe symptomatic aortic stenosis occurs, there is no medication to treat it. The only way to restore blood flow is to replace the valve. This is done by surgically removing and replacing the aortic valve or, more recently, the valve can be replaced without surgery by inserting a new valve through the artery in the groin (TAVR). Currently there are no medications that can prevent calcific aortic stenosis or slow its progression once it occurs. Or is there?

 

Calcific aortic stenosis is very common occurring in 2% of people over the age of 65 and 4% over 85 years old. It is associated with older age and shares other risk factors for atherosclerosis (blockage in the heart arteries). It has been known for some time that plasma lipids (cholesterol) are involved in the process of thickening and calcification of the aortic valve. It seems reasonable to presume that if elevated cholesterol is a risk factor that lowering cholesterol with a statin would halt the process. Many studies with statins have been performed. Unfortunately, statins do not halt the progression of severe calcific aortic stenosis. What if a statin is started before the disease is far advanced? Again, statins did not slow the progression in patients with mild aortic stenosis.  So, lowering cholesterol doesn’t work. Are there other targets? One possibility is PCSK9. PCKS9 is a protein involved in the production of LDL cholesterol. In patients with heart artery disease PCSK9 inhibitors (such as Praluent or Repatha) dramatically lower LDL cholesterol and reduce the risk for heart attack and cardiac death.  Recently it has been shown that patients with calcific aortic stenosis have higher levels of PCSK9. It is felt that PCSK9 plays a role in mediating aortic stenosis through inflammation and the stress responses of the cell. Do PCSK9 inhibitors slow the progression of calcific aortic stenosis? We don’t know, but future trials may give an answer. Another possible target is lipoprotein a. Lipoprotein a is an LDL like particle that is also associated with elevated risk for heart artery disease. Elevated levels of lipoprotein a have been shown to correlate with progression of calcific aortic stenosis as well. Patients with the highest level of lipoprotein a were twice as likely to need aortic valve replacement as patients with low levels of the protein. Statins do not lower levels of lipoprotein a, but PCSK9 inhibitors do. Whether this translates to a beneficial effect for calcific aortic stenosis is not known, but it seems a trial with these agents is badly needed. 

 

Another potential target is cardiac amyloid. What is amyloidosis? The pathogenesis of amyloid involves a protein called TTR which is produced by the liver and aids in transporting thyroid hormone. In some people (older patients, patients with genetic predisposition), TTR clumps together to form amyloid fibrils. These amyloid fibrils are deposited in many tissues in the body, but especially the brain, the nerves and the heart.  Amyloid deposition in the heart can cause a variety of problems including congestive heart failure as well as calcific aortic stenosis. In patients older than 75 years old with aortic stenosis, 14% have cardiac amyloid.  Cardiac amyloid is treated with a medication called Tafamidis, which stabilizes TTR and prevents the formation of amyloid fibrils. Tafamidis slows the progression of cardiac amyloid in patients with congestive heart failure, but it is not known whether it does the same for calcific aortic stenosis. This too may be a promising area and ripe for future research. 

 

Another potential target is calcium. Since calcium is deposited in the aortic valve do calcium supplements increase the risk? A study of 2600 patients with mild to moderate aortic stenosis found the following. Aortic valve replacement was ultimately needed in 50% of patients taking calcium supplements versus only 11% in patients not taking supplements. It was concluded that long-term calcium supplementation should be avoided in calcific aortic stenosis. 

 

If you have calcific aortic stenosis, don’t despair. A newer and better treatment (TAVR) has already dramatically changed the life for many a patient with this disease.  Although we currently cannot stop calcific aortic stenosis or alter its progression, newer targets and newer treatments may be on the horizon offering similar dramatic medical options to improve the lives of patients. In the meantime, hold those calcium supplements.