Vitamin K & Cardiovascular Diseases (CVD)
In 2000 Roseneck looked at the survival as a function of cardiovascular calcification. Patients with cardiovascular disease were divided in those with low or high vascular calcium. Survival after 4 years in the low calcium group was 80%, in the moderate or severe calcium group less than 20%.
Until a decade ago, calcification of arteries was thought to be a passive, clinically irrelevant process, resulting from a high calcium x phosphate product, inflammation, lipid accumulation or diabetes. However, during recent years it has become increasingly clear that vascular calcification is an active process and an important, independent pathology that is strongly associated with increased risk of cardiovascular morbidity and mortality. Clinically, vascular calcification causes stiffening of the vascular wall, which may result in decreased arterial compliance, development of left ventricular hypertrophy and decreased coronary perfusion leading to an increased risk of fatal complications.
Coronary artery calcification (CAC) is now recognised as a key prognostic marker for cardiovascular disease in a number of major patient groups that show no immediate symptoms of cardiovascular disease¹. These include patients with a Framingham 10yr cardiac risk score of 10-20% as well as diabetics. Calcification is common in the elderly population, and in patients suffering from diseases such as chronic kidney disease (CKD), diabetes, aortic stenosis, and atherosclerosis.
Coronary artery disease (CAD) is a condition in which plaque builds up inside the coronary arteries. These arteries supply your heart muscle with oxygen-rich blood. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. When plaque builds up in the arteries, the condition is called Atherosclerosis.
Research has shown that it is possible to create vascular calcification in rats by giving them the anticoagulation drug warfarin (belonging to the group of coumarins); warfarin appears to act as a vitamin K antagonist, which blocks the vitamin K-dependent proteins such as those involved in coagulation as well as MGP. The animals get calcium deposits in their arteries after just two weeks treatment², pointing to the role of vitamin K in the regulation of vascular calcification.
Such vitamin K effects have also been shown in humans. Vitamin K-antagonists like warfarin cause a doubling of the arterial calcifications in humans, as compared to patients not receiving vitamin K-antagonist . Calcification results in an increase of aortic stiffness and hence contributes to systolic hypertension and left ventricular hypertrophy, coronary insufficiency, ischemia and congestive heart failure . Although calcification of the arterial vessel wall commonly increases with age, the presence of these calcifications increases the risk for cardiovascular events independent of age . This is why it is a necessity to prevent the deposition of calcifications in the arteries, or even to block or lower already present arterial calcifications.
- Budoff et al., J Am Coll Cardiol 2007;49:1860-70. Becker et al., Am Heart J 2008;155:154-60. Sarwar, et al. JACC Cardiovasc Imaging 2009;2:675-88. Blaha JACC Cardiovasc Imaging 2009;2:692-700
- Price ATVB 1998