Contrary to prevailing opinion among many cardiologists, there is an emerging notion that coronary calcification is an active process, a true part of the disease.
For years, calcium in arteries was regarded as a consequence of age, a marker for "senescence." Some even said that calcium in arteries meant that plaque was "hard," and thereby not prone to cause heart attack, since it's the "softer" elements of plaque that are prone to participate in "rupture" that characterizes the majority of heart attacks.
Those arguments are being dashed by new observations into phenomena behind vitamin K2 and its role in causing calcium deposition and coronary plaque.
Normal deposition of calcium occurs only in bone and in teeth. Abnormal deposition of calcium in the body occurs in three places: the inner lining of the arteries of the body (the intima) that causes atherosclerotic plaque; the muscle layer of arteries ("medial calcification"); and heart valves. K2 appears to be the form of vitamin K responsible for controlling these phenomena (not K1, the form that plays a crucial role in blood clotting).
Matrix Gla-protein (MGP) is an enzyme recently discovered in arteries and atherosclerotic plaque that is under the control of vitamin K2. MGP is found in unusually high concentration at the edge of calcium in atherosclerotic plaque, suggesting an active role in depositing calcium in plaque. In addition, people with coronary disease with reduced blood levels of vitamin K2 show more advanced atherosclerotic plaque.
Likewise, people who take Coumadin® (warfarin), a prescription drug that induces vitamin K (both K1 and K2) deficiency, suffer more osteoporosis (a lack of calcium in bones) along with more abnormal calcium deposition in other areas, such as heart valves-twice as much as non-Coumadin® takers. There is some evidence that coronary calcification and atherosclerotic plaque may be increased over a long period, also.
The Rotterdam Heart Study is the first large clinical trial in humans that suggested a genuinely powerful association of vitamin K2 dietary intake and heart disease. 4,800 Dutch participants were tracked for 7 years. Participants who included the greatest quantity of vitamin K2 in their diet experienced 57% fewer heart attacks than people who ingested the least. The same relationship did not hold for vitamin K1.
Higher intakes of vitamin K2 also corresponded to less calcium deposited on the aorta (an indirect measure of atherosclerosis), while participants who ingested less K2 were more likely to show moderate or severe calcification. The lowest risk of both heart attack and aortic calcification was seen in participants who included more than 32.7 mcg of vitamin K2 per day in their diet (mostly from cheese).
So some investigators are now proposing that calcium should not be regarded as a passive participant in coronary plaque, but an active player. Perhaps it's also something that can be prevented or even reduced.
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