European Heart Journal has published an important review paper that highlights the potential of vitamin K2 supplementation for calcific aortic valve stenosis (CAVS), a common cardiovascular condition in the ageing population for which no medical therapy currently exists
According to researchers, once symptomatic severe CAVS has developed, the prognosis without intervention is dismal.
Currently the only treatment for (symptomatic) severe CAVS is surgical or trans-catheter aortic valve replacement (AVR), to which not all patients are suited.
Although multiple trials have attempted to repurpose commonly used pharmacological interventions to slow CAVS progression, pharmacological interventions have thus far failed to alter the course of CAVS.
The review paper notes that studies have demonstrated that statins, widely used for lipid lowering in atherosclerosis and inflammation, have no effect on CAVS progression or clinical outcomes, and might actually exacerbate the condition.
However, the researchers noted promise with vitamin K2, specifically the long-chain menaquinones (MK7), as they are transported efficiently beyond the liver.
“Vitamin K supplementation is an attractive option to replenish vascular vitamin K stores to ensure optimal calcification inhibition,” the researchers wrote.
“This review is so very significant,“ says Dr Hogne Vik, Chief Medical Officer with NattoPharma ASA, world leaders in Vitamin K2 research and development.
“Recognising that medical therapies are proving ineffective, researchers are shining a light on efficacious supplemental alternatives, which leads them to the clinical research that NattoPharma has spearheaded."
"Specifically, our 3-year cardiovascular study in healthy postmenopausal women taking just 180 µg daily of vitamin K2 as MK-7 (as MenaQ7), which demonstrated a cessation and even regression in arterial stiffness."“The relevance of our 3-year study has resulted in several studies by the medical community for patients with existing coronary artery calcification, aortic valve calcification and peripheral artery calcification,” adds Dr Vik.
The review paper concluded: The pathophysiological mechanisms involved in CAVS initiation and progression are being rapidly elucidated and include inflammation, fibrosis and calcification.
With this advancing knowledge, we have identified novel therapeutic targets such as vitamin K and new imaging techniques that can be used to test the efficacy of novel agents and further inform our pathophysiological understanding.