By Andrew Golin,
The largest artery in the body, the aorta, carries oxygenated blood to all parts of the body via the circulatory system. The coronary arteries branch off from the aorta and supply oxygenated blood to heart tissue. It is thus critically important that the coronary arteries remain healthy in order for the heart to function properly.
Since anatomists first began examining the heart, it was determined that a connection existed between calcium deposits and disease. When x-rays were first used in clinical practice, calcium masses, because of its density, were noticed on hearts of diseased patients. In order for calcification to occur, four important elements (calcium, phosphorous, oxygen, and hydrogen) combine to form a significant mineral in the body, hydroxyapatite. Hydroxyapatite is the predominant inorganic compound found in bone, and is also the predominant crystalline structure in artery calcium deposits1.
The biochemical sequence of arterial calcification is complex, though many researchers agree that the first significant step appears to be the transformation of vascular smooth muscle cells (the cellular components of blood vessel walls that provide structural integrity and regulates blood vessel diameter) towards cells expressing osteoblast-like characteristics2. Osteoblasts are responsible for bone formation and transformed vascular smooth muscle cells execute what osteoblasts do: secrete matrix proteins2. The matrix of bone mainly contains the organic structural protein collagen, and the inorganic salt hydroxyapatite, which surround widely separated cells. These components in addition to others combine to form bone tissue. Proteins, which are the molecules in the cell that function as the cell’s machinery, such as osteocalcin, are involved in the transport of calcium out of vessel walls1. Several theories have been put forward to explain the mechanism behind the mineralization of calcium. These theories include high calcium and phosphate concentrations, presence of self-programmed death bodies where dead debris leads to vascular calcification, loss of molecules that inhibit calcification, and circulating nucleational complexes where calcium can bind and mineralize6. The progression of coronary artery calcification has not been fully elucidated and requires more investigation.
The amount of coronary artery calcification correlates with the magnitude of atherosclerosis, a disease where plaque containing fats, cholesterol in addition to calcium, build up inside the arteries1. Examination of arteries have shown that plaques containing evidence of mineralization are larger versus plaques without calcified minerals1. Increased coronary calcification, and therefore increased atherosclerosis, reduces arterial elastance5. Elastance is the tendency of a hollow organ to return to its original shape after stretching or compression, such as when blood passes through and stretches the artery. Possible effects from coronary artery disease, where the arteries become hardened due to plaque buildup, are angina, heart attack, heart failure and arrhythmias.
Well-known risk factors for vascular calcification include diabetes, hypertension, and dyslipidemia2. People with diabetes generally have increased vascular calcification when compared against non-diabetics2. Experimental results have suggested that increased calcification in people with diabetes is partly due to hyperglycemic blood typically associated with diabetes2. High blood glucose levels found in patients with diabetes plays a role in transforming vascular smooth muscle cells to osteoblast-like cells, which are involved in secreting bone matrix leading to downstream hydroxyapatite production and therefore calcification2. Furthermore, dyslipidemia (high cholesterol levels), is an additional well known risk factor2. Dyslipidemia can be manifested by elevated low-density lipoprotein cholesterol and triglyceride concentrations, and decreased beneficial high-density lipoprotein cholesterol concentration2,3.
Calcium scores are calculated by quantitatively determining the amount of calcium in arterial walls via non-invasive cardiac CT scans. Computed tomography scans, or CT scans, utilize x-rays to take cross-sectional images of the heart and its vessels. These images are combined to create a 3D image of the heart. Quantifying calcium amount uses the Agatston calculation, where each area of calcified plaque is multiplied by the corresponding plaque density, determined from the CT scanner1. The score of every calcified area is summed to produce the total calcium score1. These scores can then be monitored over time to help predict future adverse events in asymptomatic and symptomatic individuals4.
A healthy heart and decreased lipid concentration reduces coronary plaque development and therefore decreased calcification5. Exercise and diet should be the first approach towards lowering one’s lipid concentration, and lastly, if needed, statin therapy.
- Wexler L, Brundage B, Crouse J et al. Coronary Artery Calcification: Pathophysiology, Epidemiology, Imaging Methods, and Clinical Implications: A Statement for Health Professionals From the American Heart Association. Circulation. 1996;94(5):1175-1192. doi:10.1161/01.cir.94.5.1175.
- Chen N, Moe S. Vascular Calcification: Pathophysiology and Risk Factors. Current Hypertension Reports. 2012;14(3):228-237. doi:10.1007/s11906-012-0265-8.
- Ahmed S, Clasen M, Donnelly J. Management of Dyslipidemia in Adults. American Family Physician. 1998;(May 1, 1998).
- Budoff MJ, Gul KM. Expert review on coronary calcium.Vascular Health and Risk Management. 2008;4(2):315-324.
- Demer L, Tintut Y. Vascular Calcification: Pathobiology of a Multifaceted Disease. Circulation. 2008;117(22):2938-2948. doi:10.1161/circulationaha.107.743161.
- Giachelli C. Vascular Calcification Mechanisms. Journal of the American Society of Nephrology. 2004;15(12):2959-2964. doi:10.1097/01.asn.0000145894.57533.c4.