Thermal detection of cellular infiltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis.
BACKGROUND
Atherosclerotic lesions are heterogeneous and prognosis cannot easily be predicted, even with intracoronary ultrasound and angioscopy. Serial angiographic and necropsy studies suggest that the risk of plaque rupture correlates only weakly with the degree of stenosis. Most ruptured plaques are characterised by a large pool of cholesterol or necrotic debris and a thin fibrous cap with a dense infiltration of macrophages. The release of matrix-digesting enzymes by these cells is thought to contribute to plaque rupture. Other thromboses are found on non-ruptured but inflamed plaque surfaces. We postulated that both types of thrombotic events may be predicted by heat released by activated macrophages either on the plaque surface or under a thin cap.


METHODS
To test the hypothesis, we measured the intimal surface temperatures at 20 sites in each of 50 samples of carotid artery taken at endarterectomy from 48 patients. The living samples were probed with a thermistor (24-gauge needle-tip; accuracy 0.1 degree C; time contrast 0.15 s). The tissues were then fixed and stained.


RESULTS
Plaques showed several regions in which the surface temperatures varied reproducibly by 0.2-0.3 degrees C, but 37% of plaques had substantially warmer regions (0.4-2.2 degrees C). Points with substantially different temperatures could not be distinguished from one another by the naked eye; such points could also be very close to one another (< 1 mm apart). Temperature correlated positively with cell density (r = 0.68, p = 0.0001) and inversely with the distance of the cell clusters from the luminal surface (r = -0.38, p = 0.0006). Most cells were macrophages. Infrared thermographic images also revealed heterogeneity in temperature among the plaques.


CONCLUSIONS
Living atherosclerotic plaques show thermal heterogeneity, which raises the possibility that an infrared catheter or other techniques that can localise heat or metabolic activity might be able to identify plaques at high risk of rupture or thrombosis.
Casscells
W
W
Texas Heart Institute, St. Luke's Episcopal Hospital, Houston, USA.
Hathorn
B
B
David
M
M
Krabach
T
T
Vaughn
W K
WK
McAllister
H A
HA
Bearman
G
G
Willerson
J T
JT
D002339:Carotid Arteries / Q000473:pathology*; D016893:Carotid Stenosis / Q000150:complications / Q000473:pathology; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000150:complications / Q000175:diagnosis* / Q000473:pathology; D002542:Intracranial Embolism and Thrombosis / Q000209:etiology; D008264:Macrophages / Q000473:pathology; D012307:Risk Factors; D012422:Rupture, Spontaneous; D013817:Thermography