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Coronary thrombi in patients who die suddenly are more likely to display signs of healing if they are caused by a plaque erosion rather than a rupture, researchers found.

Among 111 victims of sudden coronary death examined at autopsy, 69% had plaques with more than day-old thrombi, according to a study by Renu Virmani, MD, president and medical director of the CVPath Institute in Gaithersburg, Md., and colleagues.

Nearly nine out of every 10 erosions had late-stage thrombi -- those displaying some degree of healing -- compared with 54% of ruptures (P<0.0001), they reported online in the Journal of the American College of Cardiology.

Previous studies have shown that late-stage thrombi are associated with worse survival in patients with ST-elevation myocardial infarction, the researchers said.

Thus, they said, "the present finding 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."

This might include more aggressive antiplatelet therapy, Virmani said.

To explore the relationship between the degree of maturation of thrombi and the underlying cause -- either erosion or rupture of the plaque -- Virmani and her colleagues studied 115 plaques from 111 victims of sudden death autopsied at the Maryland Medical Examiner's Office.

Two thirds of the deaths were witnessed and 51 patients had typical signs of unstable angina or MI, including chest pain and malaise. Another eight had atypical signs such as indigestion, paresthesia, and back pain. Fifteen did not have any symptoms.

Of the plaques, 65 had ruptured and 50 had eroded.

Victims who had plaque erosions were younger on average (43 versus 52, P<0.0001) and were more likely to be female (26% versus 11%, P=0.03) than those who had ruptures.

Virmani and her colleagues classified the thrombi obtained from the victims according to the degree of healing displayed:

• Early thrombi, or those less than one day old, were composed of alternating layers of platelets mixed with fibrin and intact neutrophils.
• Lytic thrombi, which were one to three days old, were acute thrombi with degraded acute inflammatory cells without evidence of celluar organization.
• Infiltrating thrombi, which were four to seven days old, showed basal in-growth of smooth muscle cells and/or endothelial cells without accumulated proteoglycan matrix.
• Healing thrombi, which were greater than seven days old, were composed of layers of smooth muscle cells with proteoglycan deposition admixed and endothelial infiltration.

Thrombi in one of the latter three stages were identified in 69% of the plaques, but they were significantly more common in cases of plaque erosion.

Nearly half of the thrombi associated with erosions (46%) were healing, compared with just 9% in ruptures (P<0.001).

Internal elastic lamina area, percent stenosis, plaque area, necrotic core size, and plaque burden were all significantly smaller in plaque erosions (P≤0.02 for all).

Plaque location had no significant effect on the maturation of thrombi.

For lesions with both critical and noncritical stenosis -- greater than or less than 75% cross-sectional luminal narrowing, respectively -- erosions remained more likely to be associated with late-stage thrombi.

The authors acknowledged that the study was limited by the inherent bias in studying patients who come to autopsy and reliance on family members to provide the patient's medical history.