AED Density

 

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

 

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

 

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

 

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

 

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

 

The Hibernating Heart

 

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

 

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

 

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

 

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

 

 

Sudden Cardiac Arrest

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

 

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

 

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

 

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

 

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

 

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

 

 

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

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

 

 

 

Resistance is Futile

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

 

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

 

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

 

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

 

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

 

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

 

 

 

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.