In a previous post, the skeptical cardiologist was dealing with a patient about to embark on a 16 day cruise through the Panama Canal who was having frequent episodes of atrial fibrillation.
I was concerned about the medical care on board her cruise ship and had not been able to contact medical personnel on board.
I’m happy to report that I have been in email contact with Dr. C, of Celebrity Cruise Lines who is on board the Celebrity Infinity as it sails down the Pacific coast of Mexico and prepares to dock in Cabo San Lucas today.
Dr. C tells me that they have excellent medical personnel and resources available and should my patient go into afib they will be very comfortable dealing with the situation:
“Well I can not speak for any other cruise line but Celebrity, Royal Caribbean and Azamara (the 3 are part of Royal Caribbean Intl), which I have work on the 3 lines. As requirements for the Physicians and Nurses is to have BLS, ACLS, PALS and ATLS certification every 2 years, but most of us like to perform it at least once a year. Most of the ships have 2 Physicians and 3 Nurses, except the Oasis class ships, where there are 3 Doctors and 5 Nurses.
Regarding equipment, we have the necessary equipment to stabilize cardiac emergencies (obviously not all of them)… we have the mentioned monitors with described capabilities, a portable pressure/volume ventilator (used in the US Army in areas of combat). For IV cardiac medications, we have Adenosine, epinephrine 1:1000 and 1:10000, atropine, amiodarone, procainamide, dopamine, dobutamine, furosemide, metoprolol, diltiazem, verapamil, labetalol, digoxin, calcium gluconate and chloride, furosemide lidocaine 2%, magnesium sulfate, norepinephrine, sodium nitroprusside, nitroglycerine, enoxaparin, clopidogrel (oral), aspirin and tenecteplace as fibrinolytic.”
What Is The Scope Of Cruising Cardiac Emergencies?
After publishing my last post , Dr. Sergio Pinski tweeted me a link to a paper from 2010 entitled “Cardiovascular Emergencies in Cruise Ship Passengers” that he co-wrote.
The Cleveland Clinic Florida apparently provides “contracted cardiology consultations” to cruise ships and they recorded the nature and outcome of their consultation over a two year period.
“One hundred consecutive patients were identified (age 66 +/- 14 years, range 18 to 90, 76% men). The most common symptom was chest pain (50%). The most common diagnosis was acute coronary syndrome (58%; ST elevation in 21% and non-ST elevation in 37%). On-board mortality was 3%. Overall, 73% of patients required hospital triage. Of the 25 patients triaged to our institution, 17 underwent a revascularization procedure. One patient died. Ten percent of patients had cardiac symptoms in the days or weeks before boarding; all required hospital triage. Access to a baseline electrocardiogram would have been clinically useful in 23% of cases.”
As a result of these observations they recommended the following:
“A pre-travel medical evaluation is recommended for passengers with a cardiac history or a high-risk profile. Passengers should be encouraged to bring a copy of their electrocardiogram on board if abnormal.”
Finally, the authors write (and this seems a little self-serving and not supported by data) that:
“Cruise lines should establish mechanisms for prompt consultation and triage.”
Dr. Pinski also tells me he has witnessed two electrical cardioversions performed onboard cruise ships.
I don’t know if Cleveland Clinic is consulting with my patient’s ship but I’d prefer cardioversions be done on land, preferably in a hospital with appropriate anesthesia (see my post on defibrillation).
More Research Needed: Volunteers Saught
If any of you are aware of cardiac emergencies or episodes of atrial fibrillation on cruise ships and how they were handled please let me know. I’ll collect as much first hand information as I can and share it with you.
In my office this morning I spoke with an afib patient who is planning on a several week cruise in the Mediterranean on a Royal Caribbean ship. He has agreed to be my investigative reporter on the status of medical care on that cruise.
I don’t know if you can expect this level of cardiac medical care on every cruise but it makes sense, if you are a heart patient, to find out what is available in terms of medical personnel, cardiac and pulmonary monitoring/pacing/cardioversion equipment and medications should you go into afib or another cardiac emergency on your particular ship.
Finally, ask the cruise company if they contract for cardiology consultation services with any entity and, if so, what that entity is and how the consultation works.
This question popped into my head as I was talking to a patient (we’ll call her Barb) who has paroxysmal atrial fibrillation (PAF) and was about to embark on a 17 day cruise from San Diego through the Panama Canal and on to Fort Lauderdale.
On a rainy Sunday afternoon while watching the Cardinals pummel the Braves, I had logged onto my AliveCor account to pull up some office patient recordings I had made earlier in the week when I noticed that Barb had made a recording the day before which was interpreted as atrial fibrillation at a rate of 133 beats per minute. I had heretofore been aware that she was having recurrent episodes of PAF and so I called her and found out she was in San Diego.
At her last office visit in early March she was in normal rhythm as usual but reported having spells of palpitations, usually at night. We discussed various monitoring methods and I demonstrated the Alivecor device to her. She purchased one and had been making recordings but had not let me know that some of them were showing atrial fibrillation.
Fortunately, she was on the blood thinner Eliquis and was protected against clots in the heart or stroke but I was worried that she might go into Afib on the cruise, persist in it and develop problems.
What, I wondered, would the cruise ship crew or doctor do in that situation?
Would they be capable of even monitoring my patient’s heart rhythm or would the AliveCor Mobile ECG device she had on her smart phone be the best monitor on the ship?
Are there any medications, like beta-blockers available that could be given to slow the heart rate?
I’m still waiting for the answer to the questions.
What Do We Know About Medical Care on Cruise Ships?
The middle four items are relevant to any cardiac issue:
“-Cruise ships aren’t hospitals
Many ships have a doctor on board who is trained in emergency medicine—but not all of them. According to international maritime law, they aren’t required to; a crew member with medical training is sufficient, says Ross Klein, Ph.D., author of “Paradise Lost at Sea: Rethinking Cruise Vacations.” The medical facilities are generally more like an infirmary or walk-in care clinic than a “floating” hospital. You might find a ventilator and a small X-ray machine and the doctor may be able to perform simple laboratory tests to check for infection or electrolyte or blood sugar levels. But there’s no MRI or CT scanner, intensive care unit, or blood bank (although the crew has usually been blood-typed and may be asked to serve as donors if a passenger needs a transfusion).
– In an emergency, you may be on your own
. You probably could get basic treatment, such as stitches or IV fluids, but for anything serious, there’s a very good chance that you will have to disembark at the next port of call—whether you want to or not. It’s up to the ship’s medical personnel, not you, to decide, You’d be treated at a local hospital, and the ones in more remote areas may not have the same standards of medical care or facilities available in the U.S. And once you recovered, you’d have to arrange another way to get back home.
What if you have a heart attack or develop appendicitis miles from dry land? Don’t assume the Coast Guard will airlift you out. Bad weather can make flying a helicopter dangerous, and the Coast Guard isn’t obligated to take that risk. Even in calm waters, if the ship is 500 miles or more away from shore, it’s unlikely that the Coast Guard will respond, Klein said.
-Get ready for sticker shock
Check with your health insurance company before you set sail to be sure, but most plans don’t cover medical services you get on board, … (In fact, this is usually the case anytime you receive medical treatment from a doctor or hospital outside the U.S.) This means you pay out-of-pocket. The bill can range from a few hundred to several thousand dollars…
Travel health insurance is your best protection. Consumer Reports recommends avoiding commission-driven policies sold by tour operators, cruise-line representatives, and travel agents. Instead check out an online broker, such as insuremytrip.com, that sells coverage from multiple companies and allows you to tailor a plan to your needs. Ask for quotes, but be sure you’re comparing apples to apples. What’s covered under policies can vary. For example, some may not include emergency evacuation.
-Your Ship Does Not Have A CVS
Most ships do have common prescription drugs on board, but you can’t count on it. What’s more, if you needed one, you’d be charged full price—not just your insurance co-pay—for each drug dispensed on the ship.
I developed a plan for my patient and called in a prescription for her to fill prior to getting on the Celebrity Infinity.
Then I tried to get some information on what medical support would be available on her ship.
I called Celebrity Cruise Lines to see if they had a doctor and whether I could communicate with him. I was immediately told yes, however when I asked what the doctor’s qualifications and if I could talk to him this was apparently a novel request. After multiple transfers I spoke to someone in “Special Needs” who gave me an email address. I’m told by email that they have my contact info and the doctor will contact me if needed.
At this time, I’m assuming Barb is on the Celebrity Infinity and cruising down the Pacific Coast of Mexico, enjoying the cool ocean breezes and lounging by the ship’s pool.
Hopefully she won’t have a prolonged episode of afib that needs any urgent medical care.
If she does or if the cruise ship doctor gets back to me, I may get that information I’ve been seeking on how cardiac urgencies and emergencies are handled on cruise ships and I will be sure to share it with all of you.
The most effective method for getting a heart that is in atrial fibrillation back to normal rhythm is a called an electrical cardioversion.
I’ve tried to come up with a good alternative or descriptive term for this procedure for my patients, such as “resetting” or “rebooting” the heart, but the term that seems to best resonate with patients is “shocking” the heart.
How Does Electrical Cardioversion Work?
Typically, we all can connect (excuse the pun) to the feeling of a low current electrical shock which occurs when touching an ungrounded electrical source.
Unless the current reaches a certain level, it only results in transient burns and discomfort.
However, at current levels greater than 50 mA, an AC electrical shock traveling through the chest can, if timed properly, cause the heart to go out of normal rhythm into ventricular fibrillation.
We use a “synchronized” electrical cardioversion (termed direct current or DC cardioversion (DCC)) to convert a fibrillating or fluttering atrium back to the normal rhythm by timing the electrical shock so that it doesn’t cause ventricular fibrillation but resets both ventricles and atria safely back to normal.
This may seem like a barbaric and unnecessarily crude and dramatic way to restore normal rhythm, but if patients are properly prepared for this procedure, it is very safe and very effective, resulting in resumption of the normal rhythm 99% of the time.
There are some medications that we can utilize to convert atrial fibrillation (afib) back to normal (antiarrhythmic drugs), but they are far less effective than the electrical cardioversion, and often can bring out more dangerous heart rhythms.
Typically, I do my cardioversions in conjunction with an anesthesiologist, who administers IV propofol (yes, this was Michael Jackson’s sleep aid, his “milk”) to obtain “deep sedation.” At this level of anesthesia, the patient is breathing on his own but will only respond to painful stimulation. The propofol is short-acting and prevents the patient from feeling the intense pain of the cardioversion (often described as like a mule kicking one in the chest), and from recalling any of the events.
The electrical shock is administered through electrodes, consisting of large sticky pads with electrical conducting gel attached to the right anterior chest and the left posterior back (see this brief information from Zoll about optimal placement).
Since I began using “biphasic” energy, the initial cardioversion is successful >95% of the time in my experience, but the heart may revert back to atrial fibrillation anywhere from a few minutes to a few years after the shock. We can reduce the chances of reverting back by the use of anti-arrhythmic drugs.
Multiple Shocks: What Is The Limit?
The DCC may need to be repeated, and we may repeat it after starting one of those anti-arrhythmic drugs I mentioned, in order to increase the time that the heart stays in the normal rhythm.
A common question when I recommend a repeat cardioversion is:
“Doc, how many times can you have your heart shocked?”
One might think it is one and done with the shock but it is not a cure; it is merely a resetting of the chaotic, confused and futile activity of the atria, so that the synchronized and regular electrical pacing provided by the sinus node in the upper right atrium can again resume its rightful role as conductor of the cardiac electrical orchestra that creates the wondrous symphony of normal cardiac contraction.
The factors that brought on the afib in the first place likely are still present: if we don’t address correctable factors we are less likely to maintain the normal sinus rhythm (NSR). Correctable factors include:
abnormal thyroid function
abnormal potassium or magnesium
inflammation of adjacent lung or pericardium
obesity (see my post on fat sheep and afib)
certain cardiac valve problems
There is no evidence that the cardioversion per se damages the heart in any way. The major risks of the procedure (again, assuming proper preparation, see below) are related to the anesthesia.
I am more inclined to recommend a repeat cardioversion if there is clear-cut evidence that the patient does poorly when the heart is in afib.
Why Shock The Heart?
In medicine, there are two reasons for giving medications and doing surgery/procedures: to make the patient feel better or to reduce the chances of dying/having a major complication.
The major complication of afib is stroke. Proper anticoagulation is required to prevent this in patients with afib whether or not they are in normal rhythm. Clots can form in the left atrial appendage within hours of the development of afib, and the electrical cardioversion can increase the chance of stroke as any clot present is more likely to be expelled when the quivering, ineffective atrium converts back to a normally pumping, vigorous atrium.
Primarily, then, we utilize cardioversion for the purpose of making patients feel better.
Some patients feel terrible the moment they go into afib: symptoms of palpitations, chest pain, or shortness of breath predominate and are especially prominent if the heart rate is high. Controlling the high heart rate with beta-blockers or diltiazem will reduce many of these symptoms, but I have a large number of patients who still feel terrible when they are “out of rhythm,” even if the heart rate is normal. Such patients who persist in afib are good candidates for one or multiple cardioversions, with or without the addition of anti-arrhythmic drugs.
A second group of patients, I think, benefits the most from maintaining sinus rhythm (rhythm control strategy): patients who develop heart failure when they go into AF.
These patients may not even know they are in AF because they don’t feel the typical symptoms initially. After a few days or weeks or months of being in afib silently, however, they develop shortness of breath, weakness and leg swelling – classic signs of heart failure.
When we look at the heart of such a patient by echocardiography, we often find one of two things causing the heart failure: a weakening of the heart muscle (cardiomyopathy) or significant leakage/backflow from the mitral valve (mitral regurgitation). Following cardioversion and maintenance of SR for weeks to months, the heart muscle strengthens back to normal and/or the mitral regurgitation improves dramatically and the heart failure resolves.
Multiple Shocks: Rationale
Yesterday I did an electrical cardioversion on an elderly patient of mine for atrial fibrillation/flutter; this was her fifth DCC in the last year.
She falls into the second category of afib patients; she had developed severe heart failure due to mitral regurgitation after silently going into afib a year earlier. After long-term loading on the anti-arrhythmic drug amiodarone, followed by her fourth cardioversion, she had stayed in NSR for 10 months, her MR resolved, and she felt great. In patients like her, I think it is particularly important to maintain NSR and thus, multiple shocks are definitely warranted.
On the other hand, if you feel fine in afib without any evidence that it is effecting your heart muscle or valves, then it is hard to justify multiple attempts to shock the heart.
Any patient that has recurrent symptomatic afib or afib associated with heart failure, should be considered a candidate for an atrial fibrillation ablation. The risks and benefits of afib ablation are worthy of another blog post, but the patient-centered afib website stopafib.org has a reasonable discussion here. Suffice it to say, it is a much more complicated and risky procedure than a cardioversion, but it attempts to address the underlying cause(s) of afib, and in some cases creates what could be considered a “cure.”
It has for the most part taken the place of the more elaborate, but cumbersome and time-consuming, 12-lead ECG in patients where heart rhythm is my only concern.
I’ve also convinced about a dozen of my patients who have intermitent atrial fibrillation to obtain the device and they are actively using it to monitor at home their heart rhythm. Through the AliveCor website, I can view their recordings and see what their heart rhythm is doing when they have symptoms.
Last week, a patient of mine (I’ll call her Suzy) who has had significant prolonged episodes of atrial fibrillation associated with heart failure (but cannot tell when she is in or out of rhythm) notified me that her device was interpreting her rhythm as atrial fibrillation. She had not had any symptoms, but was making daily recordings for surveillance.
Suzy called our office and we brought her in the next day and confirmed with a 12-lead ECG that she was indeed in atrial fibrillation with a heart rate of 120 beats per minute.
It’s pretty amazing that this little, inexpensive device can now replace expensive and elaborate long term cardiac monitors for many of my patients.
AliveCor Rebrands Itself to Kardia
I’ve noticed that AliveCor has rebranded itself as Kardia. If you go to http://www.alivecor.com now you see the fourth generation device along with promotion of a “Kardia band” which apparently works with an Apple Watch to record your ECG.
The Kardia band is not available for purchase at this time but if and when I can get one, it might motivate me to purchase an Apple watch.
When I purchased my AliveCor device in June, 2015 it cost $74.99 from Amazon.com. The newer version is priced at $99 at both AliveCor and Amazon websites. I’m told by Dr. David Albert of AliveCor that this “fourth generation” version is more accurate, so I have purchased it to see if it reduces the problem of occasional bad recordings.
You can see in this picture from the website that the formerly flat metal electrodes now have bumps. Dr. Albert says these result in more surface area for better contact with skin. We will see.
The Value of Early Detection Of Atrial Fibrillation
Meanwhile, I will be doing an electrical cardioversion (shocking or resetting the heart) on Suzy to get her back to normal sinus rhythm. If we had not detected the asymptomatic onset of her rapid atrial fibrillation using the AliveCor/Kardia device, chances are we wouldn’t have known about it until her heart muscle weakened again and she became short of breath from heart failure.
I have Suzy on blood thinners to lower her risk of stroke associated with her Afib but for my patients who are not on blood thinners, detection of silent or asymptomatic AFib is even more important.
p.s. The skeptician in me feels this post borders on infomercialese.
Let me make it clear that I have no connection with the company formerly known as AliveCor and have received nothing from them (not even free test devices or Apple Watch Kardia Bands!) but I’m just really excited about the device and how it can help my patients (oh, please excuse me, this really sounds like marketing) “empower” themselves to take control of their heart rhythm.
In the course of writing this, I’ve discovered an academic paper evaluating 13 ECG smart phone type ECG devices so there are other devices you could try. I haven’t had the time or resources to evaluate them.
The skeptical cardiologist has been evaluating the AliveCor mobile ECG device for use with a smartphone to detect atrial fibrillation. In my initial post on this I found it to be accurate in identifying atrial fibrillation in my patients.
I’ve been using it in my office fairly regularly and encouraging my patients with intermittent AF to acquire the device and use it to monitor their heart rhythm.
When they make recordings they can be uploaded to me via internet for my review.
The other day I was examining a patient who I was seeing for syncope (passing out) and I noticed when listening to his heart that his pulse was very irregular.
I pulled out my iPhone with AliveCor stuck on the case and made the recording you see below.
Although the AliveCor app diagnosed it as “possible AF” it is very clearly normal sinus rhythm with frequent premature ventricular contractions (PVC), a totally different (and more benign) rhythm.
I’ll continue on with this evaluation and I’ll be particularly interested in how AliveCor performs in other patients with PVCs which are a common cause of palpitations in the general population.
If AliveCor cannot differentiate AF from PVCS it may lead a lot of users to become unduly concerned about their heart rhythm.
Until the last year or so when patients asked me what they could do to help their atrial fibrillation (AF) I would tell them to avoid excessive alcohol consumption and take their medications as prescribed.
My response has changed because new data suggest that losing weight and exercising can significantly reduce the recurrent rate of atrial fibrillation. Now, in addition to my standard reasons for staying at ideal body weight and exercising regularly I can toss in the fact that atrial fibrillation will be less frequent and troublesome.
I had noted previously that the majority of my patient’s with AF were obese and sedentary (although there are definitely many AF patients who exercise regularly, eat a great diet and stay at their ideal body weight0 but data was lacking to suggest cause and effect.
In addition, I had noted that when I looked at the left atrium of the vast majority of patients with AF using an imaging tool called trans-esophageal echocardiography they had evidence for fatty infiltration into the area between the atria (atrial septum) and the wall of the left atrium.
I strongly suspected based on these observations that somehow the fat infiltrating into the walls of the left atrium was triggering AF but I had no way of proving it. Isolated observations like these can only generate hypotheses on causality.
Science has many different approaches to solidifying or proving hypotheses and one such approach is to induce a disease in an animal similar to humans and make detailed analyses of the cause and consequences.
Australian researchers writing in JACC in July present their observations on the electrical, physiologic and structural changes that result when sheep get fat.
How Do You Make Sheep Fat?
Apparently you just let them eat as many pellets made of energy-dense soybean oil (2.2%) and molasses–fortified grain as they want.
After 36 weeks the 10 sheep given ad libitum pellets weighed twice as much as the sheep who were restricted and kept lean
After 36 more weeks of obesity the sheep were studied extensively. All sheep underwent “electrophysiological and electroanatomic mapping; hemodynamic and imaging assessment (echocardiography and dual-energy x-ray absorptiometry); and histology and molecular evaluation”.
The investigators found
“Sustained obesity results in global biatrial endocardial remodeling characterized by LA enlargement, conduction abnormalities, fractionated electrograms, increased profibrotic TGF-β1 expression, interstitial atrial fibrosis, and increased propensity for AF. Obesity was associated with reduced posterior LA endocardial voltage and infiltration of contiguous posterior LA muscle by epicardial fat, representing a unique substrate for AF”
The fat sheep developed AF and had multiple abnormalities in the left atrium, the source of AF, that made them more likely to develop atrial fibrillation. In fact, the investigators believe it was fat collecting around the heart and specifically around the posterior left atrium that was triggering all these changes.
The pictures to the left show a heart from one of the fat sheep. The arrow points to the extensive amount of fat collecting posterior to the left atrium.
When the posterior left atrial wall was viewed microscopically, fat cells could be seen infiltrating between the muscle cells in the fat sheep (right, blue arrow) but not in the lean sheep.
In the fat sheep, fat cells (adipocytes) were enlarged and infiltrated between the muscle cells of the left atrium, presumably disrupting the normal electrical activity and contributing to the development of atrial fibrillation.
More Reasons To Stay At Your Ideal Body Weight!
If you were previously unmotivated to avoid obesity perhaps this will motivate you.
Think about fat cells gathering around your heart and pouring their evil humours into the tissues of your left atrium and making it more likely that you will develop AF. With AF comes increase risk of stroke, heart failure and death.
Atrial fibrillation (AF) is a common abnormal rhythm of the heart which causes 1 in 4 strokes. Those afflicted with AF may lack any symptoms or only have a vague sense of irregularity of their heartbeat and thus the first symptom of AF can be stroke.
The gold standard for diagnosing AF has long been the electrocardiogram (ECG or EKG) and typically the ECG involves placing 12 electrodes on the chest/arm/legs and recording the electrical activity of the heart on an expensive device.
I’ve been checking out a device made by Alive Cor which works with your smart phone to record a single channel ECG and is capable of accurately diagnosing if you are in the normal (sinus) rhythm or in AF. You can purchase the third generation (significantly smaller then earlier versions) AliveCor Mobile ECG from Amazon or from AliveCor directly for 74.99$ and it works with an app with both iOS and Android devices.
I used mine with my iPhone 6. At first I carried it separately, fearing the added bulk when stuck on to my iPhone case but after a while I realized that it was never with me when I wanted to use it and that there was a huge risk of losing it and so I used the backing adhesive to attach it to my case.
After pairing the device with the app you put two fingers on each of the metal pads and the smartphone screen displays the recording. After 30 seconds of recording it then interprets the rhythm.
Above is a typical recording I made in my office on a patient who had a history of AF. The quality is good and I can clearly see that he is in normal sinus rhythm. The app correctly made the diagnosis of NSR and calculated his heart rate at 68 beats per minute.
One day I had most of my patients record their ECG’s using AliveCor and compared it to the standard 12-lead ECG we normally record. The device correctly identified the two patients with AF out of this group and correctly identified the normals.
This recording is from a patient with persistent AF which had recurred two weeks earlier. The device correctly identified AF.
Studies have documented that AliveCor Mobile ECG can accurately diagnose AF in a screening setting and the FDA approved the device for AF screening in 2014.
Given the high prevalence of silent AF, the strong association of AF with stroke and the availability of anticoagulants which reduce AF associated stroke by 70%, screening for AF with devices like AliveCor holds the promise of preventing large numbers of stroke.
(For my comments on taking the pulse and stroke prevention see here and on the inadvisability of a routine 12-lead ECG see here)
AliveCor allows physicians utilizing the Mobile APP and ECG to have a “dashboard” into which their patients can transmit their AliveCor ECG recordings.
I will be discussing this remarkable new device with my AF patients who are smartphone enabled. I think it will advance our ability to more efficiently and quickly diagnose AF in them.
My standard approach if a patient with AF calls and says that they feel like they are out of rhythm is to have them come into the office for a full 12-lead ECG. If they are AliveCor enabled, they could make their own recording, and we could review that remotely and make a diagnosis without the office visit.
It’s not a word I hear outside of medical circles but it serves a great function in the clinical arena.
When used in medicine as in the phrase “clinical equipoise” it means that medical experts are uncertain as to whether a treatment for a disease is helpful.
Thus, for digoxin, a drug which has been utilized for patients with heart failure or atrial fibrillation for 240 years, we still don’t know if the benefits outweigh the risks.
Digoxin is the major medicinally active chemical in the foxglove plant which was first described by Leonhart Fuchs (the plant and color fuchsia are named after him), a German botanist and physician in 1542. It was given the latin name digitalis purpurea, reflecting the plant’s purplish color and similarity to a thimble (German finger hut).
A vague understanding that the foxglove had medicinal and toxic properties existed in subsequent centuries, but it took a very observant physician from the West of England, William Withering, to give it a sold footing in the medical pharmacopeia.
Withering collected 10 years of his observations, using various preparations of foxglove to treat various diseases including the mysterious “dropsy” in the (now famous) An Account of the Foxglove and some of its Medical Uses.”
He writes of his rationale for beginning to give patients foxglove:
“In the year 1775, my opinion was asked concerning a family receipt for the cure of the dropsy. I was told that it had long been kept a secret by an old woman in Shropshire who had sometimes made cures after the more regular practitioners had failed. I was informed also, that the effects produced were violent vomiting and purging; for the diuretic effects seemed to have been overlooked. This medicine was composed of twenty or more different herbs; but it was not very difficult for one conversant in these subjects, to perceive, that the active herb could be no other than the Foxglove.”
Dropsy was that era’s term for edema: “The dropsy is a preternatural swelling of the whole body, or some part of it, occasioned by a collection of watery humour. It is distinguished by different names, according to the part affected, as the anasarca, or a collection of water under the skin; the ascites, or a collection of water in the belly; the hydrops pectoris, or dropsy of the breast; the hydrocephalus, or dropsy of the brain, &c. [Buchan1785].”
Foxglove was in clinical equipoise in 1775. When Withering started giving it to his patients with dropsy he did not know if it would help or harm them.
After trying various preparations of the foxglove in varying dosages in hundreds of patients he concluded that it was of a great benefit as long as it was carefully titrated to avoid the toxicities of overly slow pulse and vomiting.
With modern medicines that are proven to be safe and effective we demand evidence from randomized controlled trials in which the active drug is compared to a placebo. There are too many factors which affect the course of a disease to accept the kind of observational evidence that Withering collected.
Digitalis is currently utilized in heart failure and atrial fibrillation. Withering’s patients likely had one or both of these conditions.
A recent observational study found that digitalis usage in patients with newly diagnosed atrial fibrillation was associated with a 26% higher risk of dying.
The only large randomized trial of digoxin, the DIG (Digitalis Investigation Group) trial, showed no effect on mortality, but digoxin did reduce hospitalization among patients with heart failure and a reduced ejection fraction (HFrEF)
The DIG study was performed in the early 1990s, before current optimal treatment regiments for heart failure with reduced ejection fraction were developed and may no longer relevant. More recent observational studies suggest digoxin raises mortality in heart failure.
Thus, the foxglove or digitalis, although used for 240 years in hundreds of thousands of patients for both heart failure and atrial fibrillation remains in clinical equipoise.
Doctors must be very circumspect in prescribing this medicine. Personally, I do not use digoxin in heart failure patients.
I use digoxin in chronic atrial fibrillation only as a last resort when other agents do not allow adequate slowing of the heart rate and I carefully monitor levels and kidney function if a patient is on it.
I have, however, decided to start growing foxglove in my garden. I will try to warn the ducks, rabbits and squirrels not to partake of its beautiful flowers as they might prove deadly.
I also plan to visit the grave of Withering on my upcoming trip to Europe, for upon his tombstone it is said, there is an engraving of the foxglove!
The best way we have of estimating a patient’s risk of stroke if they have atrial fibrillation (AF) is by the CHA2DS2-VASc scale.
This scale take the factors we know that increase the risk of stroke and assigns 1 or 2 points. The acronym comes from the first letter of the factors that are known to increase risk as listed to the left.
Most of the factors get 1 point, but prior stroke (S) and age>75 (A) get 2 points.
We then add up your points and use another chart (or app) to calculate the risk of stroke per year.
Your risk of stroke is very low if you have zero risk factor; it gets progressively higher as you reach the maximum number of 9.
Treatment with an oral anticoagulant (OAC), either warfarin, or one of the four newer anticoagulant agents (NOACS), is recommended when the risk gets above 1-2% per year.
The higher the risk, the more the benefit of these blood thinners in preventing stroke.
In lower risk patients, the bleeding risk of OAC of 1% per year may outweigh the benefits conferred by stroke reduction.
Both European and American guidelines recommend using the CHA2DS2-VASc score for initial risk stratification. The European guideline recommends OAC therapy for males with a CHA2DS2-VASc score ≥1 and for female patients with a score ≥2., whereas the American guideline recommends use of OAC if the CHA2DS2-VASc score is ≥2 for men and women.
I’ve been using the CHA2DS2-VASc scale for several years in my AF patients. I try to review the patient’s risk of stroke and their risk of bleeding during every office visit, and decide whether they should be on or off an OAC.
Initially, it was helpful typing all those capital letters and number twos (although I never took the time to make the twos a subscript) because it helped remind me of the factors.
However, I now view this acronym as a big pain in the neck and I am sick of typing it into my electronic medical records. It is also, really hard to say. Do you say “chad -two-D-S-two-vasc?” That is six syllables! I could have told my patient that warfarin is rat poison during that time.
And, what is with the Sc? Sex category? Why not just an S?
An Easier Term For The Stroke Risk Estimator: The Lip Score
I would like to formally request that this be termed the Lip stroke risk score in honor of Dr. Gregory Y. H. Lip who developed it at the University of Birmingham (UK).
because (per his bio):
“The CHA2DS2-VASc and HAS-BLED scores for assessing stroke and bleeding risk, respectively were first proposed and independently validated following his research, and are now incorporated into major international management guidelines.”
If the Lip score should somehow be unacceptable, then let’s go with the Birmingham score (recognizing, of course, that this is Birmingham, England and not Birmingham, Alabama). After all, this is what the app I use terms itself and I can type Birmingham a lot faster than CHA2DS2-VASc (even without the subscripts).
The Lip Score will be a great advance in the world of stroke risk estimation for AF patients. It will make all of us doctors creating EMR notes much more efficient, shaving precious minutes off the work day. It will be easier to communicate to patients, medical students and other medical personnel.
Finally, it gives, credit where credit is due, to Dr. Lip, who, according to his bio: “In January 2014, was ranked by Expertscape as the world’s leading expert in the understanding and treatment of AF,”
(I have no knowledge of Expertscape but you can be sure I will be investigating them soon)
Giving Lip service to stroke and atrial fibrillation,
I saw two delightful eighty-something ladies recently whose cases highlight some important points about atrial fibrillation, stroke and long term heart monitors.
Ms. M was playing bridge and found that she had 7 spades solid (solid, Mrs M informed me, means you have 7 of the suit with all of the honors (ace, king, queen, jack). Instead of bidding 2 spades which she meant to do, she bid 2 diamonds, and her partner responded by bidding 5 diamonds. This miscommunication resulted in a disastrous hand for the pair.
Ms. K told me she had had an episode of “mass confusion” two weeks earlier during which for 15 seconds her “thinking process was not working properly.”
These cases illustrate the subtlety and brevity with which transient ischemic attacks (TIAs) or mini strokes can manifest. In contrast to the normal forgetfulness that is associated with aging, these women recognized a sudden, transient and disturbing major alteration in their baseline mental processing.
TIAs are basically strokes that resolve quickly, generally within 24 hours, and leave no residual symptoms. They are often a warning that larger, more permanent strokes will follow.
In both of these cases, when I first saw the patients, they were in normal or sinus rhythm but subsequent monitoring revealed atrial fibrillation (AF).
A quarter of the 500,000 strokes occurring annually in America are unexplained (the medical literature tends to use the exotic and Halloween-appropriate term, cryptogenic for unexplained strokes). This means that imaging of the brain and arteries to the brain finds no abnormalities that would cause a stroke and that the patient has no history of AF. Since there is such a strong association between atrial fibrillation, clot formation in the heart, and stroke, (see my post on AF here) doctors assume that an otherwise unexplained stroke in a patient with AF is due to a clot leaving the heart and landing in an artery to the brain. These patients benefit from medications which reduce the risk of clot formation (either warfarin or one of the newer anticoagulants everyone has been hearing about either from negative TV ads from lawyers or positive direct-to-patient drug company ads).
New evidence suggests that if we monitor the heart rhythm for 30 days of patients who have had unexplained strokes a significant percentage will manifest atrial fibrillation.
A Canadian study of 572 men over the age of 55 who had had a cryptogenic stroke or TIA found that atrial fibrillation lasting 30 seconds or longer was detected in 45 of 280 patients (16.1%) in those who underwent 30 day monitoring, as compared with 9 of 277 (3.2%) in those who were only monitored for 24 hours.
Another study evaluated 441 patients following cryptogenic stroke with half randomized to receiving an insertable cardiac monitor (we call these implantable loop recorders (ILR) in the US). The ILR is a small device that can be inserted under the skin in the left chest region and allows continuous monitoring of the heart rhythm. After 6 months, atrial fibrillation had been detected in 8.9% of patients in the ILR group, versus 1.4% of patients in the control group. At 12 months it was 12.4% versus 2%.
Neither of my two ladies felt palpitations (a sense of the heart beating irregularly) that would have suggested a problem with the heart. About half of my patients with AF will feel their heart fluttering or “flip-flopping” or racing when the heart goes out of rhythm but the rest of my patients feel nothing. Thus, AF can be silent and I have many patients whose first symptom was a TIA or stroke.
These two ladies and two studies have taught (or reinforced for) me the following:
TIAs can be very subtle. Patients need to be aware of transient episodes of significant confusion or speech difficulties and report them to their doctors. We doctors need to pay close attention when patients report such episodes.
The patient who has had a cryptogenic stroke or TIA should undergo long term cardiac rhythm monitoring looking for AF. My take on the literature at this point is that we don’t need to do the more expensive and invasive ILR. I think a 30 day monitoring device that is capable of automatically identifying AF is sufficient.