All posts by Dr. AnthonyP

Cardiologist, blogger, musician

What Cold Medications Are Safe For My Heart: 2020 Update

Little has changed in the 8 billion dollar world of useless and confusing over the counter (OTC)  cold, flu, and sinus medications since I wrote: “What Cold Medications Are Safe For My Heart” in 2015.

I still advise avoiding combination OTC cold meds and utilizing specific medications for specific symptoms.

The original post covers most of the usual suspects in this mostly useless arena. I updated it in 2016 with comments on a few additional OTC components: Alka-Seltzer, phenylephrine, and doxylamine which I have included below.

Alka-Seltzer Plops Into The OTC Cold Market 

 

I had always viewed Alka-Seltzer as an effervescent tablet which was a treatment for acid reflux, a.k.a. upset stomach, but the brand (now owned by Bayer) has moved aggressively into the bewildering morass of over the counter OTC cold meds. Indeed, when Alka-Seltzer began in 1931 it was a combination of aspirin and sodium bicarbonate (baking soda) marketed for upset stomachs. Popular commercials from the 1960s featured the catchy jingle (still stuck in my head) “Plop, Plop, Fizz, Fizz. Oh What a Relief It Is” often sung by Speedy, an odd anthropomorphic creature with an Alka-Seltzer thorax and cap.

(The jingle was written by Tom Dawes of The Cyrcle (Red Rubber Ball) and not by the father of Juliana Margulies)

Recently, I  received a request from an out-of-town guest who was suffering from a cough and upper respiratory infection (URI) to purchase Alka-Seltzer plus in the form of a tablet that dissolves in hot water .

At his request, Alka-Seltzer Plus Day Multi-Symptom Cold and Flu was purchased at the local Walgreen’s.

The ingredients are typical for many of  the Alka-Seltzer products:

-dextromethorphan (promoted for cough but ineffective with considerable side effects, see my initial post)

-acetaminophen (Tylenol, for pain and fever)

-phenylephrine (decongestant )

Phenylephrine: Ineffective Substitute for Pseudoephedrine

 

I didn’t cover phenylephrine in my previous post. It has taken the place of pseudoephedrine in  on the shelf over the counter URI (OTSOTCURI) medications.

Like pseudoephedrine, phenylephrine is a sympathomimetic drug, meaning it stimulates receptors of the sympathetic nervous system. Unlike pseudoephedrine, phenylephrine is useless as a decongestant when taken in the dosages available over the counter.

A study published in February, 2015 confirmed what previous studies had suggested: phenylephrine in dosages of 10 to 40 mg daily was no more effective than placebo in reducing symptoms of nasal congestion.

An accompanying editorial called on  manufactures to remove this useless drug from their products.

Alas,  all of the Alka-Seltzer preparations that claim to treat congestion utilize phenylephrine as the decongestant.

The transition to useless phenylephrine took place when pseudoephedrine was taken off the shelves and put behind the counter to reduce its usage in making methamphetamine.

Therefore, Alka-Seltzer plus multi-symptom cold and flu contains two useless ingredients plus acetaminophen (Tylenol).

You can buy a large bottle of cheap generic acetaminophen and take exactly the right dose you need for relieving fever or body aches without paying for two useless accompanying drugs that have the potential for giving you unwanted side effects.

Nighttime Sleep Aids In OTC Cold Meds

I covered the most common drug found in OTC cold meds that are promoted for nighttime use, diphenhydramine/benadryl, in my previous post.

Nighttime Alka-Seltzer products contain a similar sedating antihistamine called doxylamine succinate. For example , Alka-Seltzer Severe Cold and Cough Liquid Night (ASCCLN) contains:

-Acetaminophen 650 mg

-Dextromethorphan hydrobromide 30 mg

-Doxylamine succinate 12.5 mg

Doxylamine is the active ingredient in the brand name sleep aid Unisom and the “ZZquil” products from the Nyquil brand that are promoted for inducing sleep. It is available in cheap, generic form at a cost of 7.90$ for 96 25 mg tablets.  According to drugbank.ca:

“It is also the most powerful over-the-counter sedative available in the United States, and more sedating than many prescription hypnotics. In a study, it was found to be superior to even the barbiturate, phenobarbital for use as a sedative.”

Note that the effective dosage recommended in separate sleep aids is 25 mg not the 12.5 mg found in Alka-Seltzer OTC cold meds, Thus, if you want an effective dosage of doxylamine to help you sleep, you must double the recommended dosage of Alka-seltzer  SCCLN  which gives you too much acetaminophen and dextromethorphan.

Doubling these drugs raises the potential for side effects. Common dextromethorphan side effects include nausea/vomiting, dizziness, diarrhea, nervousness. Too much acetaminophen can damage the liver.

In addition, both dextromethorphan and acetaminophen interact with multiple other medications. Dextromethorphan is known to interact with 76 medications.

Acetaminophen can increase the INR (measure of blood thinning) in patients taking warfarin and increase the risk of dangerous bleeding.


My advice for 2020 is unchanged from 2015. As I summarized previously:

“I think you are much better off avoiding these brand name mixtures of different active ingredients.

Instead, you should take what you need for a specific symptom in the appropriate dosage and time interval.

Thus, if you have pain, take  the minimal dose of tylenol that relieves it and repeat when it comes back.

If you have a cough, recognize that the OTC ingredients are no better than placebo and are being abused as recreational drugs. Most coughs go away shortly but if one is particularly troublesome and persistent get a cough suppressing drug from your physician.

If you have a really runny nose with a lot of sneezing it is probably OK to take pseudoephedrine even if you are a heart patient or have high blood pressure. Take it as I described above. Start with 30 mg of the little red pseudoephedrine pills , wait an hour to see how you feel. Take a second if it has not been effective.  Repeat at 4-6 hour intervals as needed. Take your blood pressure at least once after starting it.

Don’t buy the multi-symptom multiple ingredient combinations which are simply a marketing tool to get you to spend more money on something from which you won’t benefit.”

Hypnotically Yours,

-ACP

N.B. Consumer Reports seems to agree with me in a 2017 post on this topic (which doesn’t credit me.)

N.B/ 2 My original post includes a Duane Allman reference.

N.B. 3 Alka-Seltzer Plops Into The OTC Cold Market is one of my favorite sub-headings.

This Week’s Most Ridiculous Heart Health Headline: “Running One Marathon Can Make Your Arteries Healthier”

Yes, CNBC went with that silly headline.

ABC went with “Training For Your 1st Marathon May Reverse Aging.”

The usually reliable Allison Aubrey and NPR went with ” Ready For Your First Marathon? Training Can Cut Years Off Your Cardiovascular Age.”

Aaarggh! As the newly-minted wife of the skeptical cardiologist likes to say.

The media threw caution to the wind and went gaga over this study which proves nothing of the sorts of things described above.

They may have been egged on by the authors who were wildly overstating the implications of the study

“What we found in this study is that we’re able to reverse the processes of aging that occur in the [blood] vessels,” says study author Dr. Anish Bhuva, a British Heart Foundation Cardiology Fellow at Barts Heart Centre in the UK..

Allison Aubrey did manage to quote a sensible person in her report to counter the balderdash being thrown around by the study authors:

The heart health benefits documented in the study likely have much less to do with the one-time race event than they do with the fact that the training program got people in the habit of regular, moderately intense exercise, says exercise researcher Dr. Tim Church, an adjunct professor at the Pennington Biomedical Research Center. On average, the participants ran between 6 and 13 miles per week, during their training, so, not super long distances.”The training program was very practical and very doable,” says Church, who was not involved in the study, but who reviewed the training regimen and results for NPR. “It was a slow build up over six months,” Church says.

I know a thing or two about aortic distensibility. In 1992 I described a new noninvasive method for quantification of aortic elastic properties in a paper published in the American Heart Journal entitled “Evaluation of aortic distensibility with transesophageal echocardiography.”

One thing I know for sure is aortic distensibility is highly dependent on systolic blood pressure and any changes that were seen in this study could simply have been related to lower systolic blood pressure.

The authors acknowledge this limitation along with about a million other limitations at the end of their paper. The limitations are legion and I’ve copied them at the end of this post. I’m quite surprised that JACC published it given those limitations and the absence of any important new findings.

Taking up exercise is really good for you but do not be fooled by these ridiculous headlines into thinking running one marathon has any special way to make you younger.

Take up exercise that you can sustain and that won’t leave you injured or frustrated.

Pheidippidesically Yours,

-ACP

Study limitations

This study was conducted in healthy individuals; therefore, our findings may not apply to patients with hypertension who have stiffer arteries that may be less modifiable (40). From these data, however, those with higher SBP at baseline appeared to derive greater benefit. This study was not designed to provide structured training, but rather to observe the effects of real-world preparation for a marathon, which randomized control trials cannot address. Nevertheless, information on the intensity, frequency, and type of exercise training would have been valuable to understand further the beneficial effects on aortic stiffness. The modest change in peak VO2 may be related to exercise training intensity or low adherence, which reflects the real world. Peak VO2 was performed semisupine to allow concurrent echocardiography, and this may also have reduced sensitivity to changes due to running or running efficiency. We assessed only marathon finishers—plausibly, nonfinishers could have had different vascular responsiveness. The causal link of exercise to measured changes is only inferred—marathon training may lead to other lifestyle modifications (dietary, other behavioral factors), or alterations in lipid profiles and glucose metabolism, although these have not been previously associated with changes in aortic stiffness (11). We did not examine the effect of exercise on peripheral arteries or endothelial dysfunction. Although individual participants served as internal controls, there may have been run-in bias for the initial BP measurement. This appears unlikely, as BP changes would not have been age-related nor correlated with the change in separate measures (e.g., aortic stiffness) with training. Estimated aortic ages are approximations and are based on the same dataset at baseline rather than independent observations. The exercise dose-response curve here is not sampled—only training for a first-time marathon with single timepoint assessment. This area warrants further study. We measured distensibility on modulus imaging acquired at 1.5-T rather than steady-state free precession imaging. The free-breathing sequence we used achieved good temporal resolution, but may be susceptible to through-plane motion. However, this and similar sequences correlate well with breath-held cine imaging, and show similar associations with aging (18). If error was introduced into distensibility measurements related to through-plane motion, the resultant noise would minimize the effect size related to exercise training, and therefore would be unlikely to account for our key findings. PP undergoes amplification from central to more peripheral locations, typically being ∼6 mm Hg higher in the descending thoracic than the ascending aorta (20). This PP amplification is not accounted for in our analysis, because it would have involved invasive measures of aortic pressure at each location. A sensitivity analysis suggested that the likely impact of this effect on the observed changes after training would be minimal; however, we cannot completely exclude the possibility that changes in PP amplification contribute to the observed differences. Diaphragmatic descending aortic distensibility data reported here were, however, higher than expected, although there is limited published data for comparison (41). Unlike Voges et al. (41), central rather than brachial PP was used, which would explain greater distensibility, and the use of 1.5-T phase-contrast modulus may accentuate image contrast differences between 3T gradient echo sequences.

 

Younger Next Year: Can We Forestall Aging?

One of my favorite bands is They Might Be Giants (TMBG), a quirky duo of Johns from Brooklyn which produces eclectic, odd and brilliant music for both adults and children.

I’ve performed (with my old band Whistling Cadaver) the TMBG song “Older” on occasion (often a birthday) which  includes the insightfully weird  lines “You’re older than you’ve ever been and now you’re even older” and the wonderful “Time is marching on (at this point one must insert a long pause of variable duration)  and time is still marching on.”

These words of wisdom have heretofore held true but in the last decade, many researchers and authors have declared that we can forestall the inevitable tide of aging. Books, podcasts, and websites abound on the topic and dominate the bestseller and high popularity lists.

Last week a patient gave me a book entitled “Younger Next Year: Live Strong, Fit, and Sexy – Until You’re 80 and Beyond – turn back your biological clock” which suggests that TMBG may have gotten it wrong.

The book first published in 2004 was written by a physician Henry Lodge (a Boston Brahmin and grandson of Henry Cabot Lodge) and his “star patient” Chris Crowley, a retired litigator. It became quite popular and morphed into an entire cottage industry.

“Younger Next Year” and the rest of the series, “Younger Next Year for Women: Live Like You’re 50 — Strong, Fit, Sexy — Until You’re 80 and Beyond” (2005), “Younger Next Year Journal” (2006) and “Younger Next Year: The Exercise Program” (2015), have more than two million copies in print and have been translated into 21 languages.

I found the book to be an easy read, written in a folksy, conversational style and alternating between brief sections written by each of the authors which present both the star patient’s perspective and the learned physicians. This makes the book appealing to the large audience that might benefit from its words of wisdom but less appealing to those who seek a more science-backed and advanced look at methods for enhancing longevity.

The blurb from the inner flap serves as a good summary of what is within:

“YOUNGER NEXT YEAR draws on the very latest science of aging to show how men 50 or older can become functionally younger every year for the next five to ten years, and continue to live like fifty-year-olds until well into their eighties. To enjoy life and be stronger, healthier, and more alert. To stave off 70% of the normal decay associated with aging (weakness, sore joints, apathy). and to eliminate over 50% of all illness and potential injuries.”

Ultimately, according to YNY, the secret to successful aging centers on following Dr. Lodge’s simples rules:

  • Exercise six days a week for the rest of your life.
  • Do serious aerobic exercise four days a week for the rest of your life.
  • Do serious strength training, with weights, two days a week for the rest of your life.
  • Spend less than you make.
  • Quit eating crap!
  • Care.
  • Connect and Commit.

For the most part, I agree with these rules. In particular, the immense value of regular aerobic, strength and flexibility exercise in prolonging one’s healthspan cannot be overemphasized.

Exercise is the most powerful medicine we have against aging and the authors spend a lot of time trying to convince readers of this and suggesting ways to facilitate and activate a good exercise program.

It is for this reason that I would recommend the book to any patient or reader who is not currently regularly exercising.

In 2015, “Younger Next Year: The Exercise Program” was published which gives more specific details and recommendations. I haven’t read this but you can read a well-written review of the book from a discerning physical trainer here. I’m on a continuous quest to find the best exercise program for myself and my patients and realized that I already have incorporated many of the 25 resistance exercises (downloadable PDF here) mentioned in the book into my regular routine.

Harry’s Death

When my patient gave me this book he told me that Dr. Lodge had died at a youngish age. Alas, sadly this is true.  He died of prostate cancer at age 58 and his NY Times obituary can be found here.

 

 

As I’ve discussed previously with respect to diet gurus (Atkins and Pritikin) we should not put much stock in the mechanism of death of our lifestyle and diet authors.

It’s never too late to start an exercise program.  A year ago I bought Pops Pearson, my 92-year-old father, a recumbent exercise bicycle. He had become unable to walk on his exercise treadmill due to balance and orthopedic issues with a subsequent decline in his overall physical and mental well-being. After starting regular work-outs on the bicycle he now feels stronger and better than he has in years!

Antisenescentally Yours,

-ACP

N.B. The authors of YNY imply that we all know what qualifies as “crap.” The brief details they provide on what we should and should not eat are not unreasonable, however, they mistakenly promote skim milk and non-fat dairy. Best to follow Dr. P’s diet recommendations.

N.B.2 Since my patient was kind of enough to give me this book and I’ve finished reading it I’m going to pass it on to the first patient of mine to leave a comment indicating they want it.

Bernie Sanders Is Back: Is His Heart Healthy? Why Is His Ejection Fraction Not Reported?

While campaigning in Las Vegas last October, Vermont Senator Bernie Sanders began experiencing tightness in his chest. He was rushed to a hospital where he was diagnosed with a heart attack and had two stents implanted to open blocked arteries.

Despite little details about his cardiac condition, the event cast a cloud over his candidacy.

At the time I asked (and answered) a few questions): Is it appropriate for voters to lose confidence in Sanders at this point? He was already the oldest candidate in the race at age 78 years. Would he survive a 4 year term in the grueling position of head of the free world?

We now have more details to better answer these questions.

On December 30 of 2019, a letter from Brian P. Monahan, MD MACP on a letter head which reads in all caps “THE ATTENDING PHYSICIAN:Congress of the United States” to The Honorable Bernard Sanders was released.

This letter summarized Sanders’ “general health history and current medications” as Sanders had requested

Monahan, an oncologist by training, examined Sanders on 12/19/2019 at which time he found the senator was:

” 6 feet tall and 174 pounds. His blood pressure was 102/56, with a pulse of 62 beats per minute. His total cholesterol was 117 milligrams per deciliter of blood, HDL cholesterol (or “good” cholesterol) was 32 milligrams, and LDL cholesterol (or “bad” cholesterol) was 58 milligrams.”

With the exception of the low HDL these are good numbers and they indicate that Sanders LDL/bad cholesterol was at the appropriate goal post MI of <70 mg/dl. I would be a little concerned about the lowish BP of 102/56 in a 78 year old man but this likely reflects to some extent medications he is receiving to strengthen and protect his heart muscle.

Past Medical History

Next, Monahan summarizes Sanders’ past medical history

Over the years you have been treated for medical conditions including gout, hypercholesterolemia, diverticulitis, hypothyroidism, laryngitis secondary to esophageal reflux, lumbar strain, and complete removal of superficial skin lesions. Your colorectal cancer screening is up to date. Your past surgical history consists of repair of left and right-side inguinal hernias by laparoscopic technique and a right true vocal cord cyst excision. In November 2019, a follow-up ENT evaluation of your vocal cords for hoarseness was stable. You have no history of tobacco use, exercise regularly, and seldom drink alcohol.

Now we know some Bernie’s characteristic voice is due to a vocal cord cyst and that he is following a healthy lifestyle with regular exercise and no cigarette smoking.

What Happened In Vegas: The Myocardial Infarction

Monahan’s description of the heart attack (myocardial infarction or MI) Sanders suffered in Las Vegas gives more information than I had seen previously but is still lacking in details which I felt were important to know: troponin level and ejection fraction

The most significant event in your recent health was your admission to the Desert Springs Hospital in Las Vegas Nevada on October 19 2019. You experienced myocardial infarction due to an acute blockage of a coronary artery. In the initial hours of your evaluation, you were found to have an elevation of cardiac muscle proteins in your blood accompanied by diminished heart muscle strength and chamber wall motion reduction as determined by echocardiogram. You underwent prompt cardiac catheterization with identification of the narrowed segment of the midportion of the left anterior descending coronary artery. The narrowed segment was re-opened followed by the placement of two drug-eluting stents, a procedure that is referred to as primary percutaneous coronary intervention (Per). You received standard treatment with medications to improve your heart function and provide antiplatelet therapy required by your stents. You were released from the hospital three days later and returned home.

The exact elevation of the cardiac muscle protein, aka troponin, level is not reported.

He indicates “diminished heart muscle strength” determined by an echocardiogram and this is the ejection fraction (EF) but the exact percent EF is not given.

In my previous post on Senator Sanders I wrote

The size of Sanders’ heart attack is an important determinant of his prognosis. The more myocardial cells that died the larger the damage. We can detect and quantify heart attacks with a blood test using a cardiac specific protein called troponin.

Some heart attacks are tiny and only detected by very slight increases in the troponin in the blood whereas larger ones result in large increases in the troponin. What kind did Sanders have?

The more damage to the main pumping chamber of the heart, the left ventricle, the weaker the pumping action as measured by the ejection fraction.  The lower the ejection fraction the more likely the development of heart failure. What is Sanders ejection fraction? Does he have any evidence of heart failure?

Heart Failure?: Signs Or Symptoms?

Later in his letter Monahan indicates

You have never had symptoms of congestive heart failure

This is an interesting turn of phrase. The doctor is not stating clearly that Sanders did not have congestive heart failure (CHF)

We diagnose CHF by eliciting certain symptoms such as shortness of breath or fatigue and observing certain signs such as crackles in the lungs, distention of the jugular veins, or swelling in the legs. These findings are combined with lab tests (BNP or pro BNP) and imaging studies (chest x-ray, echocardiography).

Given Monahan’s phrasing I suspect there were signs and/or abnormal labs that suggested CHF  on his presentation with chest pain. The good news is that subsequent testing indicates no CHF.

Bernie’s Medications:

Monahan goes on to describe current medications:

Your current daily medications include atorvastatin, aspirin, clopidogrel, levothyroxine, and lisinopril

The aspirin and clopidogrel are anti-platelet agents which are standard after implantation of drug-eluting stents like the two Sanders received at the time of his MI.  They help keep the stents from stenosing or clogging up.

The atorvastatin is a statin/cholesterol lowering drug which should be given post MI in high dosages (40 to 80 mg daily) to reduce the risk of progression of the atherosclerotic plaque in Bernie’s coronaries which caused his MI. The atorvastatin has lowered his LDL to <70.

Lisinopril is an ACE inhibitor which is likely being utilized in this case to help strengthen and protect his heart muscle after the MI. Typically this would be used in conjunction with a beta-blocker however later in the letter, Dr. Monahan indicates Sanders was taken off a beta-blocker:

Several of the medications you initially required (blood-thinner, beta blocker) were stopped based on your progress. Your heart muscle strength has improved

Why Was The Beta-Blocker Stopped?

I see two possibilities, one portending a good prognosis and the other a bad prognosis.

Beta-blockers have been shown to significantly improve outcomes post MI in patients with depressed EF. The normal EF is >55%. Did Sanders’ EF improve to the point where the doctors felt beta-blockers would no longer be beneficial? This would be a good prognostic sign.

The other possibility is that Sanders’ blood pressure was so low on the beta-blockers that he was weak or dizzy. This would be a bad prognostic sign.

A third possibility seems less likely to me: excessive heart rate slowing on a beta-blocker. Given his resting heart of 62 bpm on no beta-blocker he should have been able to tolerate at least a low dose of beta blocker.

Cardiac Testing Post MI

After Sanders returned to his home in Vermont he saw his personal cardiologist Martin LeWinter and underwent further testing which according to Monahan showed the following

The heart chamber sizes, wall thickness, estimated pressures, and heart valves are normal.

I’m presuming this information comes from an echocardiogram. One of the key pieces of information that would come from this same echocardiogram is the ejection fraction. Why doesn’t he mention the EF?

Several 24-hour recordings of your heart electrical activity indicated no significant heat rhythm abnormality.

So Senator Sanders had at least two Holter monitors. This is not the norm post MI and I have to think he must have had some significant arrhythmias on telemetry while hospitalized to prompt these investigations. What rhythm abnormalities prompted multilple Holter monitor studies?

Sanders also underwent a treadmill stress test in December which is the norm post MI. Findings were  summarized by Monahana

a successful graded exercise treadmill examination monitoring your heart function, muscular exertion, and oxygen consumption that indicated a maximal level of exertion to 92% of your predicted heart rate without any evidence of reduced blood flow to your heart or symptoms limiting your exercise performance. Your overall test performance was rated above average compared to a reference population of the same age. The cardiac exercise physiologist who evaluated your results determined that you are fit to resume vigorous activity without limitation.

A  letter from Dr. Phillip Ades indicates this was a cardiopulmonary exercise test and it appears maximal aerobic capacity was measured directly but this number is not revealed.

However, this type of stress test is not capable of monitoring “heart function” and Monahan’s statement that there was no “evidence of reduced blood flow to your heart” can only mean there were no EKG changes as blood flow to the heart was not directly measured.

Fitness To Continue Campaigning And Serve As President

Senator Sanders’ doctors conclude based on all the evidence they have that he is fit and able.

In addition to the letters referenced above, Mr. Sanders’s personal cardiologist, Martin LeWinter wrote a letter (which I can’t locate) which states that Mr. Sanders had experienced “modest heart muscle damage” but that his heart function was now “stable and well-preserved.”

Once more, the two things I would like to know are not being precisely described.

Heart muscle damage would be precisely assessed by the maximal troponin level during his MI. Modest is defined as “not large” in the Cambridge English dictionary.

Heart function would be precisely assessed by the ejection fraction. Well-preserved is most frequently used to describe older things or people that are in good condition or don’t appear as old as they really are. It’s often used to describe left ventricular function but is vague. Why not just state the ejection fraction?

It would also be nice to know what coronary artery was stented and what was the status of the other coronary arteries that weren’t stented.

Dr. LeWinter concludes

“At this point, I see no reason he cannot continue campaigning without limitation and, should he be elected, I am confident he has the mental and physical stamina to fully undertake the rigors of the presidency,”

I have a lot of confidence in Dr. LeWinter’s (see below) integrity and judgement and therefore would agree with his conclusions. I’d feel even more confident if I had access to all of Senator Sanders’ relevant data.

Skeptically Yours,

-ACP

N.B. I recognized Dr. LeWinter’s name as he has been a prominent figure in the area of pericardial disease and heart failure research.

His CV is very impressive.

Dr. LeWinter is Professor of Medicine and Molecular Physiology and Biophysics and Director of the Heart Failure and Cardiomyopathy Program at the University of Vermont. He received his undergraduate degree from Columbia University, his M.D. from New York University and sub-specialty training in Cardiovascular Disease at University of California, San Diego.  In addition to heart failure, cardiac hypertrophy and myocardial dysfunction Dr. LeWinter has had a longstanding interest in pericardial disease. Dr. LeWinter has received continuous research support from the NIH for over 35 years and is the author of over 190 original research papers, over 60 book chapters and review articles, and the Editor of two books. He is a Fellow of the American Heart Association, the American College of Cardiology, the Cardiovascular Section of the American Physiological Society and the International Academy of Cardiovascular Sciences, and a member of the Association of University Cardiologists. Dr. LeWinter has served on numerous Editorial Boards and research review committees and is an Associate Editor of the journals Circulation and Coronary Artery Disease

An In-depth, Objective Comparison of Mobile ECG Devices: Emay versus Kardia

The skeptical cardiologist has been a huge advocate of personal mobile ECG monitoring to empower patient’s in understanding/monitoring their heart rhythm.

The deserved leaders in this field are the Apple Watch (4 and later) and Alivecor’s Kardia device which comes in single-lead and six-lead flavors.

Both Apple and AliveCor have gotten FDA approval for their mobile ECG device and have a body of published studies supporting their accuracy.

In contrast, there are a number of “copy-cat” mobile ECG devices which have been feeding on the success of Apple Watch and Kardia but do not have the bona fides the two leaders have.

I reviewed the SonoHealth ECG here and found it sorely lacking in comparison to Kardia in terms of accuracy of diagnosis and quality of recordings, the two most important aspects of a personal ECG monitor.

Dan Field, a physician  and reader of my blog, has been evaluating a device similar to the SonoHealth ECG made by Emay.

He has provided a point by point comparison of the two  devices in the chart below

Emay versus Kardia

His summary:

“The Kardia6L was clearly superior in almost every way except for price and even that was within the margin of error. ”

It should be noted that the single lead Kardia mobile ECG is actually cheaper than the Emay and retails for $99.

Let The (Mobile ECG) Buyer Beware

I ended my post reviewing SonoHealth’s ECG with a warning which applies equally to the Emay device:

The SonoHealth EKGraph is capable of making a reasonable quality single lead ECG. Presumably all the other devices utilizing the same hardware will work as well.

However, the utility of these devices for consumers and patients lies in the ability of the software algorithms to provide accurate diagnoses of the cardiac rhythm.

Apple Watch 4 and AliveCor’s Kardia mobile ECG do a very good job of sorting out atrial fibrillation from normal rhythm but the SonoHealth EKGraph does a horrible job and should not be relied on for this purpose.

The companies making and selling the EKGraph and similar devices have not done the due diligence Apple and AliveCor have done in making sure their mobile ECG devices are accurate.  As far as I can tell this is just an attempt to fool naive patients and consumers by a combination of marketing misinformation and manipulation.

I cannot recommend SonoHealth’s EKGraph or any of the other copycat mobile ECG devices. For a few dollars more consumers can have a proven, reliable mobile ECG device with a solid algorithm for rhythm diagnosis. The monthly subscription fee that AliveCor offers as an option allows permanent storage in the cloud along with the capability to connect via KardiaPro with a physician and is well worth the dollars spent.

Skeptically Yours,

-ACP

 

A Septuagenarian Hockey Player With Subclavian Stenosis Hangs Up His Skates

Three years ago I asked “Is There A Difference in Blood Pressure Between Your Right and Left Arms.?”

In that post I stressed the importance of measuring at least once the “interarm BP difference” (IAD) and I promised to give a second post which would “give my recommendations on how to reliably measure IAD and ….tell the story of a 75 year old competitive ice hockey player with a totally blocked subclavian artery to his right arm.”

I saw that remarkable patient, Alan Gerrard, in follow up recently and the visit reminded me of my promise. After 25 years of playing competitive hockey he had finally decided to hang up his skates and retire from the sport he loves.

Here’s what I initially wrote:


The Ancient Hockey Player

The skeptical cardiologist started thinking about IAD because of Alan Gerrard, a most remarkable 77 year old who is still playing competitive ice hockey. Last year an errant hockey puck shattered his shin bone but after 6 months of recovery he is back on the ice, older by 11 years than his nearest competitor.

Alan has noted since his time in the military that the blood pressure in his right arm is significantly lower than that in the left. In fact, he would routinely ask that his BP be taken in the left arm to avoid being diagnosed with hypertension.

The pulse in his right wrist is much weaker than that in his left.

A few years ago, after identifying this IAD, I had him get an MRA of the arteries coming off his aorta and it  blockage of the right subclavian artery which supplies blood to the right arm.

Subclavian stenosis
MRA from Alan. The brachiocephalic artery is the first great artery to come off the ascending aorta. It bifurcates into the right carotid artery and the right subclavian artery. The short red arrow points to the almost complete narrowing at the origin of the right subclavian artery. The subclavian beyond this blockage fills by collaterals.

Since identifying this IAD we exclusively utilize the left arm BP to guide treatment of his hypertension.

At home he keeps a meticulous journal of his right and left arm BPs and brings them in for me to review at office visits.

In the first column he records his left arm BPgerrard IAD BP

on arising. On April 1 it was 120/64. The IAD was 15 meaning his right arm BP was 105.

Interestingly, there is a marked variation in the IAD, as it ranges from  +7 to minus 31 (averaging 10 mmHg)

The average systolic blood pressure in both the right and left arms was identical at 139.

Alan, also shares with me at our office visits a beautiful color-coded graph of his right and left arm BPs which are recorded daily without fail.

altitude left right bp
Graph of systolic blood pressure in left arm (red) and right arm (black). Note that typically left arm SBP> right arm SBP by >10 mm Hg but there is a marked variation in difference and occasionally the right exceeds the left.

At our most recent visit he pointed out that when he was in Colorado at high altitude his blood pressure significantly increased (which, according to a recent European Society of Cardiology report is common.)


Providing Alan’s story was the easy part of my promise. Providing the best method for determining IAD turns out to be much more complicated and likely explains why I never wrote the follow-up post.

It also likely explains why 71% of patients in my poll have never had the IAD checked by a doctor (see below.)

A 2014 study found 8.6% of diabetics had an IAD >10 mm Hg. These patients were 3.5 times more likely to die from cardiovascular disease. An IAD>15 mm Hg conferred a nine-fold increased risk of cardiovascular mortality.

This is how IAD was assessed in this British study:

Carry out two pairs of simultaneous BP measurements:
Swap cuffs over (do not disconnect cuffs from BP machine) and obtain two further pairs of simultaneous readings

They utilized two automatic Omron BP devices. The authors recognized the difficulty of this technique in routine clinical practice:

Confirmation of an interarm difference requires a method of repeated simultaneous measurement, to avoid overestimation of prevalence  This technique, however, may not be practical in routine clinical care. It adds time to the clinical assessment of subjects in primary care, and we have found it to be a barrier to recruitment in our previous study in diabetes. Initially, a sequentially measured pair of readings may be sufficient to rule subjects out of further assessment for an interarm difference, but this requires further evaluation.. Previous small studies that directly compared sequential and simultaneous measurement techniques have concluded that the reproducibility of an interarm difference measured by different techniques is poor (3 although we have found that repeated sequential measures can predict a systolic interarm difference ≥10 mmHg on repeated simultaneous measurement.

Dr. P’s Recommended Method for Measuring The IAD

Here’s what I will be asking my MAs to do to assess IAD:

Simultaneously measure BP with automatic cuff on one arm and manual cuff on the other. Switch arms and repeat measurements.

This should be done at least once on all patients with hypertension or diabetes.

For those wishing to test at home who only have one cuff I would suggest the following protocol:

Rest for 5 minutes in a chair. Check left arm BP. Switch cuff to right arm and measure twice. Switch cuff to left arm and measure. Perform this set of measurements one first thing in the morning and once after dinner. If a significant IAD difference (>10 mmg Hg) is noted on the averaged readings repeat the whole process two more times and if it persists report this to your doctor.

If you note a significant IAD always utilize the arm with the higher BP for measurement.

Dextrosinistrally Yours,

-ACP

N.B. In 2017 I included a poll. Here are the results.

Ablation For Atrial Fibrillation: One Patient’s Experience

The skeptical cardiologist previously shared reader Mark Goldstein’s experience with atrial fibrillation which led him to choose to have an ablation.

Mark has subsequently undergone the ablation procedure and has kindly shared his thoughts and observations on the process. I’ve included a few comments (in green).


The Mystery of Afib and An Ablation

Everyone associated with afib knows how mysterious it seems to be. What triggers it? Why does it stop? Why does it affect marathoners, cross-country skiers, and NBA players more than other groups? Why is everyone’s experience as unique as popcorn granules? Recently Dr. Pearson invited me to talk about my accidental discover of afib, my unsuccessful cardioversions, and my decision to have an ablation.

In the last post, afib was affecting me every day when exercising. Moderate exercise would cause my heart to, as my electrocardiologist would say, “act like a drunken sailor.” It became hard. Exercise is important to me. Medication was not working for me. An ablation was the next step.

Choosing A Doctor

Before you decide on the cardiologist or electrophysiologist (EP)  to perform an ablation, do research. Ablations are not particularly dangerous. No one is opening your chest. The doctor is “redecorating” your heart…OK, killing tiny parts of your heart. People occasionally die. There can be complications like infections. How long has your doctor been doing ablations? How many a year? I asked my EP where he learned the technique. Turned out that he learned it from the French doctor who invented it. Peer recognition is good. My EP leads the Atrial Fibrillation Center at the big regional hospital where I had the work. Find out if they are involved in research since this suggests they keep up on the latest developments. I saw that my EP was doing research via the U.S. government’s Medline Plus clinical trial website (https://medlineplus.gov/clinicaltrials.html). And if you are reading about the latest research on the Internet, you can see if your doctor is keeping up with the latest. I asked my EC about a study that appeared days before our appointment. He read it and talked about it. He passed my tests.

(I’ve been meaning to write about a recent study which looked at the early mortality rate (<30 days after procedure) from catheter ablation for atrial fibrillation which  was 0.46% among more than 60,000 patients treated for A-fib ablation between 2010 and 2015.  These real-world rates are higher than those reported in randomized trials. This doesn’t necessarily make ablation a “dangerous” procedure but patients should know that there is a 1 in 200 chance of dying from it.)

Interestingly, and relevant to Mark’s point about choosing an EP who does a lot of ablations per year, mortality rate was higher in low volume hospital (<21 ablations per year). These data support choosing a high volume operator in a high volume hospital. 

Once you choose a doctor, the remainder is scheduling and insurance paperwork. My experience is that you should assume at least a day in the hospital and a day to recover.

I arrived early the day of the procedure. After my previous cardioversions I was experienced with the registration and prep process. A few hours later I was on a gurney entering “mission control.” The procedure room was full of large TV’s, reminding me of launching a rocket. It can be a bit intimidating, but I thought of it as a sports bar. Instead of watching games people were watching my heart. It wasn’t a long time in the room before I was told I’d be sleeping soon.

They were right because I “woke up” about four hours later in a recovery room. I immediately saw my heart rate was in the 70’s and steady. That was good. I put on my Apple Watch and started the ECG test. Without waiting for the watch to decide, I could see my beats were rhythmic. YEAH! I saw “normal sinus rhythm” on the watch and celebrated. Later I found out that I had almost four hours of a successful ablation. Apparently, that is a lot of work however the afib, aflutter, was gone.

After the procedure I felt pressure around my heart. Not surprising considering the “redecorating” that was done. It was more of an annoyance than painful. That lasted for a few days. The area around my groin was also sore from the insertion of the ablation instruments. Certainly not unbearable but not fun. A couple of hours after the procedure I asked if I could go for a walk. The staff accompanied me for a walk and saw that I was fine. I asked if I continue walking. After a mile of moderate walking around the hospital (thanks to the Apple Watch’s measurements), my groin felt much better. When my watch showed I walked three miles, I went to bed. The following morning before breakfast, I walked another three miles. After ablation, start walking as soon as you can. It helped me physically and probably more important mentally showing that I was OK.

My groin area was purple for about a week so the worst part of the ablation was I couldn’t wear a Speedo (nor did I want to wear one). It was ugly and a minor nuisance but didn’t affect my activities. Oddly the second day after the procedure I woke up feeling the aftermath of cramps in both of my calves. This was bothersome walking stairs especially. I hadn’t heard of cramps associated with an ablation so it may just have been coincidence. The next day I could walk fine.

Post-Ablation Early Recurrence

My heart was fine after the ablation. I checked it regularly with my Apple Watch and Kardia Mobile EKG. Life was good until 1:55AM a couple of weeks after the ablation. I was sleeping. Without explanation my heart rate jumped from 53 beats per minute to 110 in five minutes. When I woke hours later, I knew my heart was racing. The Kardia Mobile showed I had a “uncategorized” problem. It stayed around 110 beats no matter what I was doing. A few hours later my EP saw my EKG chart and said I needed another cardioversion. He reminded me that he told me the first time we discussed ablation that during the first three or four months I might have more rhythm problems as the heart returns to normal. He was right.

A few days later I had my third cardioversion. My heart immediately went from 110 back to 60/70 beats per minute after the procedure. Yeah! I was beating normally again.

One Month After Ablation

Today is a month after the last cardioversion. My Apple Watch, Kardia Mobile, and body tell me I am fine. The other metric I check regularly is my heart rate while sleeping since it should reflect my heart rate without activity. I’m averaging 54 beats per minute at night which is fine. I can now exercise moderately or intensely. I am celebrating by writing this article.

I continue to take a blood thinner because of my CHADS₂ score. Hopefully my afib adventure is over…but I will not be surprised if it returns.


So far, so good.

Hopefully, Mark will remain free of afib for many years if not a lifetime but given that he is empowered with both a Kardia 6L device and an Apple Watch for monitoring his rhythm I feel confident he will know when and if it returns.

Skeptically Yours,

-ACP

N.B. Here are the charges for the ablation procedure.

Hospital – 86,350

EC/EP – 7,365

Anesthesia – 4,550

Blood test – 120

Misc charge – 22

Mark ended up paying $200 out of pocket.

Mark Goldstein works in the field of cybersecurity in the Washington, DC area and can be contacted at https://www.linkedin.com

Heartening News For The New Year! United Health Care Paid For This Patient’s Coronary Calcium Scan

Unless you live in Texas you will have to pay out of pocket for a coronary artery calcium (CAC) scan. Insurers and Medicare won’t pay a dime for this simple test which  progressive preventive cardiologists and primary care docs rely on to better determine who is at risk for heart attacks and sudden death.

But as we approach 2020 perhaps this failure to cover our best tool to detect subclinical atherosclerosis can be reversed. To my surprise, earlier this week, a patient of mine revealed to me that United Health Care had reimbursed him for the CAC he had done earlier this year.

It wasn’t easy or straightforward but his process may work for others so I asked him to email me the letter he sent that resulted in coverage which I have copied below.

As discussed in your office today, I was able to get my insurance company (United Healthcare) to reimburse me from the Cardiac Calcium Scoring costs of $125 after filing an appeal through my former employer. Below, as requested, is the simple write up I provided to them.

I visited a cardiologist (Dr. Anthony Pearson) in May 2019 regarding heart palpitations I had with increasing frequency. He performed a variety of diagnostic tests (blood work, Holter monitor, echo stress test), which were all covered by UHC. Because these tests did not show any issues, he suggested I have a Cardiac Calcium Scoring Test, which I completed on May 24, 2019. The test showed that I had serious coronary artery disease (score of over 800), which caused the cardiologist to prescribe a daily baby aspirin and a statin medicine (also covered by UHC). While I was told that the Cardiac Calcium Scoring Test cost is not covered by insurance, this is the one and only test that indicated I was at a severe risk for a coronary artery event (significant or total blockage) and, per the cardiologist, may have saved my life or perhaps avoided an unexpected significant cost (e.g. bypass surgery) by catching the issue early.

To recap, St. Luke’s Hospital did not submit a claim for the $125 cost of the Cardiac Calcium Scoring Test because they said no insurance company pays for this test. This test was ordered by my cardiologist, Dr. Anthony Pearson, and was performed at St. Luke’s Hospital in St. Louis. I am requesting reimbursement for the cost of this test for the reasons stated above

The United Health Care EOB contained this claims summary:

Screen Shot 2019-12-31 at 9.34.20 AM

It would appear the mighty wall that insurers and CMS have put up against paying for CAC scans is crumbling and can be breached.

I highly recommend all patients who have gotten an appropriately ordered CAC go through this process with their insurers to attempt to obtain reimbursement.

Happy Antiatherosclerotic New Year,

-ACP

Merry Christmas SkepCard Followers!

It was  an incredibly warm  and sunny Christmas Day here in St. Louis.

So warm, in fact, that I experienced the sun’s  rays on thoracic portions of my skin while semi-exercising in Forest Park.

Remarkable! I hope all my readers and patients had a similarly delightful day. There were residual patches of snow so I’m counting this as a white and a warm Christmas.

Do normal people exercise on Christmas or this is insanity?

Serenity Now,

-ACP

Premature Atrial Contractions: Are They Benign Or Malignant?

In the last few weeks the skeptical cardiologist has had a run on patients with premature atrial contractions (PACs).

I’ve discussed in detail premature ventricular contractions (PVCs) here and here. They are the most common cause of an individual feeling that their heart is skipping a beat or fluttering briefly, something we term palpitations.

Premature beats, which can be either PVCS or PACs, in addition to causing palpitations, are the most common cause of an irregular pulse detected by a blood pressure device or a health care worker,

What Causes Premature Atrial Contractions?

 

Like PVCs, PACs occur when electrically active tissue in the heart decides to fire off (or depolarize) before it has received the signal from the normal pacemaker of the heart, the sinus node. In the case of PACs, the rogue tissue is in one of the atria, the upper chambers of the heart.

In the ECG recording below, the PAC (labeled APC) occurs earlier than expected (prematurely). The normal (sinus) beats occur at regular intervals and are all preceded by p waves of normal configuration which are the normal electrical signature of atrial contraction. The larger spike that follows the p wave (the QRS complex) represents ventricular depolarization and is unchanged from the normal sinus beats because activation of the ventricle is normal with PACs.

These early beats, in and of themselves, are felt to be benign.

Premature Atrial Contractions Are Very Common

 

They are extremely common when we monitor ECG rhythm for an extended period, even in young, totally normal individuals. More common, in fact, than PVCs.

For example, in a select group of male aviators

Rare, occasional, frequent and very frequent isolated atrial ectopy occurred in 72.9%, 2.6%, 2.3% and 0.3%, respectively. The same categories of isolated ventricular ectopy occurred in 40.9%, 7.9%, 3.3% and 0.0%.

Frequency of isolated ectopy was classified as a percentage of the total beats on the Holter monitor: rare (< or =0.1%), occasional (>0.1 to 1.0%), frequent (>1.0 to 10%) and very frequent (>10%).

Thus, the majority of the time we will see some PACs in normal subjects who we monitor for 24 hours by ECG.

It was also common to see two PACs in a row (an atrial couplet or pair). Atrial couplets occurred in 14.5% of these aviators.

The highlighted box from the 3 lead Holter monitor recording below shows an atrial couplet.

atrial tach holter
The QRS complex of the premature atrial complex (PAC) is usually preceded by a visible P wave that has a slightly different shape or different PR interval from the P wave seen with sinus beats. The PR interval of the PAC may be either longer or shorter than the PR interval of the normal beats. In some cases the P wave may be subtly hidden in the T wave of the preceding beat.

When 3 or more  premature atrial beats occur in a row, we start calling this nonsustained supraventricular tachycardia.

Nonsustained supraventricular and ventricular tachycardia (duration 3 to 10 beats) occurred in 4.3% (13/303) and 0.7% (2/303), respectively of those normal male aviators.

PACs Are More Common As We Age

 

One study found that in normal individuals over age 50 years , 99% had at least 1 PAC during 24 -hour Holter monitoring. The PAC prevalence strongly increased with age from about one per hour in those aged 50 to 55 years to 2.6 per hour among those aged ≥70 years.

Another study analyzed 24 hour holter recordings at 5 year intervals and found the frequency of PACs (and PVCs) increased significantly in all age groups over that time span.

Screen Shot 2019-11-10 at 6.35.20 AM
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724889/

APCs And Atrial Fibrillation

 

Not uncommonly, when a patient has PACs, especially if they are frequent, computer ECG interpretations mistakenly diagnose atrial fibrillation. This happens regularly even with a full, medical-grade 12-lead ECG. Fortunately, such ECGS are still over-read by cardiologists who usually make the correct diagnosis.

The computerized algorithms that single lead mobile ECG devices like Apple Watch 4 and AliveCor’s Kardia similarly are frequently confused by premature beats, especially APCs. I wrote about this in detail in my post on PVCS and PACs here.

Sometimes the devices will diagnose “possible atrial fibrillation” in a patient with frequent PACs in sinus rhythm and sometimes “unclassified.”

In addition, patients with very frequent APCs show a higher tendency to develop atrial fibrillation and a higher risk of cardiovascular complications.

The Various Names Of The Extra Beats

 

Whereas a consensus has been achieved (for the most part) on the term for early beats from the ventricles (premature ventricular contractions or PVCs ) the term for PACS varies from one cardiologist to another and one paper to another.

If I enter in

“atrial premature”

into my EMR problem list search, multiple naming options appear (all with the same ICD code of I49.1)

In addition, you  may also encounter the terms atrial ectopy, premature atrial beats or various combinations of “supraventricular” with either contraction, beats or ectopy.

The two most popular acronyms are APCs or PACs and I am guilty of using these interchangeably and seemingly randomly.

Premature Atrial Contractions: Markers For Atrial Cardiomyopathy?

 

Through most of my cardiology life I had considered PACs to be totally benign. And certainly, in and of themselves they cause no problems other than occasional palpitations. However, studies in the last decade have shown consistent associations between frequent PACs and stroke, death and atrial fibrillation.

Some researchers have suggested the concept of “atrial cardiomyopathy” to explain this association. A diseased atrium could be the reason for PACs and atrial fibrillation as well as stroke and death as opposed to atrial fibrillation being the primary cause of increased cardiovascular events.

Clearly, PACS, stroke and CV disease share common risk factors such as age and obstructive sleep apnea making cause and effect difficult to sort out. Could PACs and atrial fibrillation represent different phenotypes of atrial cardiomyopathy?

These data on frequent PACs raise a whole host of questions which remain unanswered.

Is there a frequency of PACS ( say >100 per 24 hours) which is useful in predicting adverse outcomes?

Are there clinically measurable predictors of which  patients with frequent PACs are most likely to have to poor outcomes?

Does treatment of PACs (say with anticoagulation therapy or suppression) in the absence reduce risk of CV events?

The Bottom Line On PACs

 

  1. Premature atrial contractions are very common in normal individuals and increase with aging.
  2. They can cause palpitations and an irregular pulse but are benign in and of themselves.
  3.  Frequent PACs (more than 1% of total heart beats) are a marker of increased risk of atrial fibrillation, stroke, and death.
  4. The concept of a diseased atrium (atrial cardiomyopathy)  causing both atrial dysrhythmias and raising the risk of stroke and death helps to explain these associations.
  5. More research is needed to answer the important clinical questions related to the independent significance of frequent PACs and what treatments might be warranted.

Semipalpitatingly Yours,

-ACP