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Two-thirds of coronary thrombi were organizing prior to sudden death
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Most thrombi within coronary lesions in those with sudden death were later stages of healing and may require a refined treatment strategy, results from a study suggested.
Researchers examined coronary lesions with thrombi from 111 cases of sudden death. Thrombi were either ruptures (n=65) or erosions (n=50). Thrombus healing was classified as either early (less than one day) or as one of three late phases, including the lytic stage (one to three days), infiltrating stage (four to seven days) and healing stage (more than seven days).
The researchers identified late-stage thrombi in 79 of 115 (69%) culprit plaques and reported that women had a greater prevalence of erosions in late-stage thrombi than ruptures (88% vs. 54%; P<.0001). Coronary artery area measurements were greater in ruptures than in erosions (P<.0001), as were plaque area, necrotic core size and plaque burden. The majority of early thrombi were observed in plaque ruptures as compared with erosions (46% vs. 12%; P<.0001). The majority of thrombi in erosions were either infiltrating or healing (P<.001). The internal elastic lamina area (P<.0001) and percent stenosis (P=.02) were both smaller in erosions compared with ruptures. The researchers reported no established relationship between macrophage infiltration and thrombus organization, despite the observation of lower macrophage infiltration in erosions vs. ruptures (P=.03).
“The current data widen this view, where coronary thrombi in fatal erosions are in later stages of maturation as compared with ruptures,” the researchers concluded. “Considering that STEMI patients with healing thrombi of >1 day have poorer prognosis, the present findings that erosions are the main cause of healing thrombi — which occur predominantly in women and younger men — together with the increased risk for distal intramyocardial embolization would further indicate that women and younger men might require different strategies of treatment.”
In an accompanying editorial, Richard I. Levin, MD, dean of the faculty of medicine at McGill University in Montreal, Canada, wrote that the study results confirmed earlier observations regarding the relationship between coronary thrombosis and sudden death and that the researchers further refined the concept by examining the plaque’s specific architectural disruptions while relating them to clinical expression and pathological description.
“The differences impressed the authors enough that they suggest that we think about the possibility that erosions and ruptures be treated differently, another application of the developing principles of personalized medicine in which better pathophysiologic understanding — whether genomic or pathologic — allows the therapeutic targeting of subsets rather than the whole set,” he wrote. “These are very interesting observations and confirmations of reports that used other methods of study.”
Kramer MCA. J Am Coll Cardiol. 2010;55:122-132.