Were cardiovascular events linked to clone burden or clonal change?
Clone size, lineage context, and timing could separate a baseline association from an evolving risk marker. For mutations detected at myeloid neoplasm diagnosis, were cardiovascular or cerebrovascular events analyzed by variant allele fraction, affected lineage, and evidence of prior clonal expansion? A single diagnostic measurement cannot show whether clone growth preceded an event. Serial measurements and event timing would clarify whether expanding clones differed from stable clones in their association with risk.
