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Most people who get a coronary artery calcium (CAC) scan receive a single number: their total Agatston score. That number is powerful. But it treats calcium in a small branch of a minor artery the same as calcium sitting in the one artery that feeds nearly half the heart. That artery is the left main coronary artery, and when calcium accumulates there, the stakes are meaningfully higher. The research is clear: where your calcium lives matters, not just how much of it you have.
The coronary artery calcium score works by detecting calcium deposits in the walls of the arteries that supply the heart muscle. Calcium in those walls is a marker of atherosclerosis, the slow buildup of plaque that can eventually rupture and cause a heart attack. The standard Agatston method adds up calcium across all coronary arteries and gives you one composite number. Higher numbers mean more disease and higher risk. But this method has a blind spot: it does not weight the location of calcium. A score of 300 from three minor vessels and a score of 300 concentrated in the left main artery are treated identically, even though they carry very different implications.
The left main coronary artery is a short but critically important vessel. It quickly splits into two major branches that together supply the bulk of the heart's left ventricle, which is the chamber responsible for pumping oxygenated blood to the entire body. Because it feeds such a large territory, obstruction or disease in the left main carries an outsized consequence. Calcium there is not just a marker of systemic atherosclerosis; it is a marker of disease in a location where disease is particularly dangerous.
The most comprehensive data comes from the Coronary Artery Calcium Consortium, which followed more than 28,000 asymptomatic adults with non-zero CAC scores. Left main calcium was present in approximately 22% of those patients. Even after fully adjusting for total CAC score and standard cardiovascular risk factors, the presence of left main calcium independently predicted a 20 to 30% higher hazard for both cardiovascular-specific and all-cause mortality. This is not a marginal effect. It means two patients with the same total CAC score have meaningfully different risk profiles depending on whether that calcium involves the left main artery.
The dose-response relationship matters too. For every additional 100 Agatston units of calcium specifically in the left main artery, the hazard for death increases by approximately 6 to 9% beyond what the same calcium in other arteries would predict. The burden within the left main, not just its presence, drives risk in a graded fashion.
At the extreme end, a 2024 study focused on patients with total CAC scores above 1,000, a group already considered very high risk. Among them, severe left main CAC, defined as 300 or more Agatston units in the left main artery, roughly doubled ASCVD mortality, with a hazard ratio of approximately 2.3. When severe left main CAC coexisted with diabetes, the event rates climbed to levels comparable to patients already known to have established cardiovascular disease. In other words, left main calcium combined with diabetes in a very high total CAC context creates a risk profile that resembles someone who has already had a heart attack.
There is also a useful negative finding: in a clinical cohort examined specifically for significant left main narrowing, no patient with 50% or greater left main stenosis had a left main CAC score of zero. This suggests that an absent left main CAC score makes clinically meaningful left main disease unlikely, giving the test real value in both directions.
Despite these findings, the standard Agatston score does not weight the left main differently from any other vessel. Multiple researchers and clinical reviews have argued that future scoring systems should incorporate regional calcium distribution, including left main involvement, to better reflect true cardiovascular risk. Several groups have called for left main CAC to be explicitly noted in clinical reports whenever it is present.