This press release is wildly overselling this research. It's not anywhere near as simple as calcium deposits causing vascular disease. CAC (coronary artery calcification, where this has been most examined) is essentially an inevitable byproduct of the process of atherosclerosis; calcification anywhere is a halmark of necrotized cells. Since atherosclerosis results from necrotic cells (primarily macrophages) which have invaded the vasculature, the extent of coronary artery calcification is a good marker of the extent of atherosclerosis that has occurred and is thus a good predictor of future coronary events.

However, that does not imply that removing coronary calcium will reduce coronary events. In fact, statin therapy by itself actually increases coronary artery calcification.

It turns out that calcified and fibrotic atherosclerotic plaques are not the plaques that rupture and cause thrombosis and myocardial infarction; in fact, the responsible plaques tend to be large, lipid-rich plaques with a thin cap (called thin cap fibroatheromas). Calcium can actually be protective in helping to form robust caps over plaques. There is a lot of work on characterizing cap-Calcium microstructure. Theoretically, removing calcium somehow using drug agents could have an adverse effect.