One Stroke Can Ruin Your Whole Day

If It’s Yours or Your Patient’s

Reproduced from Shutterstock by Subscription

I don’t usually push folks to follow my medical advice. I may strongly encourage, but, in my experience, when I pushed too hard the patient “develops” a side effect or some other reason to do what they wanted and not what I suggested. I do push, sometimes pretty hard, however, when it comes to trying to convince patients with atrial fibrillation (AF) and atrial flutter to take anticoagulants.

A stroke can be so devastating if the clot is not “busted” or otherwise treated early. About 40% of stroke survivors have some long-term disability from the stoke. AF is responsible for 20-25% of strokes, and the strokes from AF are big because the clot originates in the left atrial appendage, which can accumulate a lot of clot. So when patients with AF and an elevated risk refuse anticoagulation, I use the line, “I just want you to know that a stroke can ruin your whole day and your life, if it’s yours.”

Clinicians define a patient’s risk of a stroke using the CHA₂DS₂-VaS₂c score. This score is a point summation of seven risk factors where:

C = Congestive heart failure – 1 Point

H = Hypertension – 1 Point

A = Age: 25-74 – 1 Point, >75 – 2 Points

D = Diabetes history – 1 Point

S = Sex: Male – 0 Points, Female – 1 Point

V = Vascular disease, including myocardial infarction, peripheral vascular disease, or atherosclerotic plaque – 1 Point

S = Stroke (previous) or transient ischemic attack or thromboembolic disease – 2 Points

A CHA₂DS₂-VaS₂c score of 2 or greater in men or 3 or greater in women indicates the need for anticoagulation.

Many patients ask me about their risk if they do not take the anticoagulation. The estimated risk scale I use is from a study of hospitalized patients with AF (1) so may overestimate the risk of ambulatory patients, but this study indicated the risk as:

CHA₂DS₂-VaS₂c score Risk per 100 Patients per Year

0 1.9%

1 2.8%

2 4.0%

3 5.9%

4 8.5%

5 12.5%

6 18.2%

This is difficult to remember, so I tell patients that their risk is 2% per year with AF alone and that goes up 1 to 2% per year with each additional risk factor. It’s not exact, but in the ballpark. Remember, that risk occurs every year, so after 10 years, even a 0 score person has a risk of almost 20%.

Each clinician and patient has to make their own decision as to whom to anticoagulate, but even a risk of almost 3% per year with one risk factor makes me twitchy, and I generally suggest that such patients strongly consider anticoagulation.

One of the reasons I have gotten more aggressive is the new oral anticoagulants. Rat poison, also known as Coumadin or warfarin as the generic, was actually discovered as the cause of a problem and it remains a problem (2). Cattle in the 1920s were observed to develop severe, sometimes fatal bleeding either spontaneously or after minor injuries. It was discovered that silage made from sweet clover produced an inhibitor of prothrombin if the silage became moldy. Investigators at the University of Wisconsin in the 1940s found, that the offending agent was 4-hydroxy coumarin. This led to the discovery of warfarin and to its approval as rat poison in 1952 and as a human anticoagulant in 1954. Warfarin actually stands for the Wisconsin Alumni Research Foundation, Warf, plus -arin from coumarin.(2)

Warfarin remains a problem for two reasons:

1. It’s hard to use because the dose needs to be determined by measuring the international normalized ration (INR) of how long it takes blood to clot, and only about 65% of patients on warfarin are in the approved range when tested at any one time.

2. It can cause cerebral bleeding. Warfarin decreases the activity of clotting factors II, VII, IX, and X. I remember this by remembering that warfarin affects 4 clotting factors and that 2 plus 7 equals 9, but I need one more so that it adds up to 10 – Factors 2,7, 9, 10. Factor VII interacts with tissue thromboplastin to activate the “extrinsic pathway”. This pathway contributes to coagulation in tissues such as the brain, so when factor VII is decreased by warfarin, there is increased risk of brain and other tissue bleeding. Spontaneous intracerebral bleeding in patients on coumadin is devastating, and is increased by warfarin. The new oral anticoagulants do not decrease Factor VII so the risk of intracerebral hemorrhage is much less with the newer agents than with coumadin.

The decreased risk of intracerebral bleeds with the new agents makes anticoagulation at lower risk scores, 1 or even 0, less risky. I don’t worry about bleeding as much with these agents, as long as there is “blood in the bank” because, a transfusion can fix most bleeding if it’s not in the head, spine or other critical organs.

Clinicians can also calculate the risk of bleeding using a bleeding score. This used to be done using the HAS-BLED score, but that score included variation in the INR when using coumadin as one of the criteria so HAS-BLED has been replaced to some extent by the Direct Oral Anti-Coagulant or DOAC score. This score predicts the risk of “major bleeding” defined as reducing the hemoglobin by 2 g/L, or requiring transfusion of at least 2 units of blood, bleeding related death, or bleeding into a critical organ or area (intracerebral, spinal, ocular, pericardial, retroperitoneal, joint or intramuscular causing compartment syndrome). For each 1 increase in the score the risk increases 48.7%.

I never calculate a DOAC score because it’s complex, but here are the criteria and the points and the risk factors are worth thinking about when considering anticoagulation:

Age - <65 = 0, 65-69 = 2, 70-74 = 3, 75-79 = 4, ≥80 = 5 Points

Creatinine clearance (mL/min) - >60=0, 30-60=1, <30=2 Points Underweight (BMI<18.5 kg/m²) – 1 Point

Stroke or embolism by history – 1 Point

Diabetes – 1 Point

Hypertension – 1 Point

Antiplatelet use – Aspirin – 2, Dual antiplatelets – 3 Points

Nonsteroidal use – 1 Point

Bleeding history - 3 Points

Liver disease - AST or ALT ≥3X or ALP ≥2X upper limit of normal or cirrhosis – 2 Points

Scores of 8 or higher are cause for caution with anticoagulation.

But even with all this scoring, there are times when consensus opinion recommends anticoagulation in patients with AF who have a 0 CHA₂DS₂-VaS₂c score. These patients include those with hypertrophic cardiomyopathy, thyrotoxicosis (according to some experts), severe mitral stenosis, and cardiac amyloidosis. I discussed amyloid heart disease previously (5), but amyloid makes the left atrium so stiff and poorly contractile that some clinics anticoagulated these patients even when the patient is in sinus rhythm. Many congenital heart disease conditions and patients with cyanotic heart disease should also be anticoagulated despite a zero score as well.

Most clinicians know that everyone must be anticoagulated for at least 3 weeks before AF cardioversion, but many do not know to continue the anticoagulation for at least 4 weeks after. Anticoagulation should be continued, in part, because even though there is sinus rhythm on the ECG, the atrium may not restart its contraction for several weeks after the shock. The delay depends on how long the patient was in AF before cardioversion. One of the first studies to show this found that full atrial function returns in 24 hours in patients with AF of less than 2 weeks duration, within 1 week in patients with AF of >2 to 6 weeks duration and within a month in patients with AF lasting >6 weeks before cardioversion.(6) Without atrial contraction patients can develop new clots even after cardioversion and after the appearance of atrial electrical activity. (One of the authors of this article (6) is David Silverman, MD, former director of Hartford Hospital's Echocardiography Lab.)

The delay in the recovery of atrial contraction probably explains why some long-time A fibbers require a month or more to feel better in sinus rhythm. Dr. Silverman also reminded me that this delay in atrial function is another reason to cardiovert patients sooner rather than later.

So, here are the rules:

1. One stroke can ruin a whole day, if it’s yours or your patient’s.

2. You can guesstimate the stroke risk of a patient in AF by starting at 2% per year and adding 1-2% for each CHA₂DS₂-VaS₂c risk factor.

3. The newer oral anti-coagulants cause much less tissue bleeding than warfarin probably because they do not decrease Factor VII so have less effect on the tissue or extrinsic clotting pathway.

4. Adult patients with AF and a zero CHA₂DS₂-VaS₂c score should still be anticoagulated if they have HCM, thyrotoxicosis (?), severe mitral stenosis, or amyloid heart disease and for at least 4 weeks after cardioversion.

5. Some persistent AF patients require a month or more after cardioversion to feel better in sinus rhythm possibly because of the delay in return of full atrial function.

References

1. Gage BR, Waterman AD, Shannon W, Boechler M, Rich MW, Radford, MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA. 2001 Jun 13;285(22):2864-70. PMID: 11401607

2. Pirmohamed M. Warfarin: almost 60 years old and still causing problems. Br J Clin Pharmacol. 2006 Nov;62(5):509–511. PMID: 17061959

3. https://www.google.com/search?q=how+is+major+bleeding+defined+in+DeFY

4. https://www.mdcalc.com/calc/10551/direct-acting-oral-anticoagulants-doac-score

5. https://pauldthompsonmd.substack.com/p/learning-from-experts

6. Manning WJ, Silverman DI, Katz SE, Riley MF, Come PC, Doherty, RM, Munson JT, Douglas BS. Impaired left atrial mechanical function after cardioversion: relation to the duration of atrial fibrillation J Am Coll Cardiol. 1994 Jun;23(7):1535-40. PMID: 8195510

Atrialfibrillation; stroke; anti-coagulation; CHADSscore; cardiology; medicine

David Silverman, MD reviewed this piece for accuracy, but I am solely responsible for the final content.