JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
VOL. 64, NO. 7, 2014
ª 2014 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
ISSN 0735-1097/$36.00
PUBLISHED BY ELSEVIER INC.
http://dx.doi.org/10.1016/j.jacc.2014.06.1163
EDITORIAL COMMENT
Putting TCFA in Clinical Perspective* Jagat Narula, MD, PHD, Jason C. Kovacic, MD, PHD
B
ased on the coronary angiography performed
regardless of the extent of luminal stenosis (3,9,10).
many days or even years before a patient
Histopathologically, the disrupted plaque usually
experienced a myocardial infarction (MI),
demonstrates substantial plaque burden and a large
physicians have long believed that in the majority of
necrotic core, covered by intensely inflamed and
cases, culprit lesions were mild to moderate in
attenuated fibrous cap (FC) (11). The bulky plaque
severity at the time they ruptured and caused MI (1–3).
may variably encroach the lumen because of the
The observation that coronary occlusion and MI
positive remodeling (12). The high-risk plaques or
evolved from a mildly-stenotic coronary lesion has
thin-cap fibroatheroma (TCFA) demonstrate the same
left a more indelible impression on cardiology practice
histopathological characteristics as a disrupted pla-
than other concepts proposed in the past several
que, except that the FC is still intact (13). On the
decades (4). However, contrary to these publications,
basis of these histopathological similarities, TCFA is
subsequent post-mortem studies of subjects dying
considered to be the precursor to plaque rupture. A
from cardiac arrest or acute MI indicated that the
detailed analysis of the histomorphological features
percent luminal area stenosis at sites of thrombus
(including FC thickness, percent luminal stenosis,
was $75% in two-thirds of cases (5), and the mean
macrophage area, necrotic core area, and calcified
stenosis of likely culprit lesions causing MI was >90%
plaque area) in 295 coronary atherosclerotic plaques
(6). The angiographic studies also demonstrated that
from patients who experienced sudden death (11)
the culprit lesion severity, although variable, was
revealed that FC thickness was the strongest single
often significant (7,8), and that only about 10% of
predictor of plaque type. All stable plaques or
culprit lesions had a diameter stenosis
VOL. 64, NO. 7, 2014
ª 2014 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
ISSN 0735-1097/$36.00
PUBLISHED BY ELSEVIER INC.
http://dx.doi.org/10.1016/j.jacc.2014.06.1163
EDITORIAL COMMENT
Putting TCFA in Clinical Perspective* Jagat Narula, MD, PHD, Jason C. Kovacic, MD, PHD
B
ased on the coronary angiography performed
regardless of the extent of luminal stenosis (3,9,10).
many days or even years before a patient
Histopathologically, the disrupted plaque usually
experienced a myocardial infarction (MI),
demonstrates substantial plaque burden and a large
physicians have long believed that in the majority of
necrotic core, covered by intensely inflamed and
cases, culprit lesions were mild to moderate in
attenuated fibrous cap (FC) (11). The bulky plaque
severity at the time they ruptured and caused MI (1–3).
may variably encroach the lumen because of the
The observation that coronary occlusion and MI
positive remodeling (12). The high-risk plaques or
evolved from a mildly-stenotic coronary lesion has
thin-cap fibroatheroma (TCFA) demonstrate the same
left a more indelible impression on cardiology practice
histopathological characteristics as a disrupted pla-
than other concepts proposed in the past several
que, except that the FC is still intact (13). On the
decades (4). However, contrary to these publications,
basis of these histopathological similarities, TCFA is
subsequent post-mortem studies of subjects dying
considered to be the precursor to plaque rupture. A
from cardiac arrest or acute MI indicated that the
detailed analysis of the histomorphological features
percent luminal area stenosis at sites of thrombus
(including FC thickness, percent luminal stenosis,
was $75% in two-thirds of cases (5), and the mean
macrophage area, necrotic core area, and calcified
stenosis of likely culprit lesions causing MI was >90%
plaque area) in 295 coronary atherosclerotic plaques
(6). The angiographic studies also demonstrated that
from patients who experienced sudden death (11)
the culprit lesion severity, although variable, was
revealed that FC thickness was the strongest single
often significant (7,8), and that only about 10% of
predictor of plaque type. All stable plaques or
culprit lesions had a diameter stenosis
