Gilbert is a 58-year old high school science teacher.
When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.
I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero also; it means less intensive efforts less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since the risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.
Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.
Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.
Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.
18 months later, Gil's 2nd heart scan score: 1410--a near doubling. Unsettling to Gil and to us, to say the least.
How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?
I fear that the culprit might be warfarin.
Warfarin, better known by its brand name, Coumadin, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.
It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:
--Accelerate aortic valve calcification
--Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
--Accelerate osteoporosis
--Induce an artificial situation of vitamins K1 and K2 deficiency.
The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are the above list of various pathologic calcifications.
I therefore wonder if warfarin dramatically accelerated the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.
That all said, I am quite certain it was the warfarin.
Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.--serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)
My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweight the risks--including that of possible accelerated calcification of multiple sites.
Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.
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Copyright 2008 House, MD