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FARMACOLOGICO
DE LA ANGINA DE
PECHO
Dr. Persio López Contreras
PUCMM
Marzo 2011
✴ DOBLE PRODUCTO....
Figure. Normal arterial segment (A) compared with a vulnerable plaque (B) in longitudinal and cross-sectional views.
Sunday, March 20, 2011 (ACS), whereas in the remaining studies, experimental pa- proteinases and vascular endothelial growth factor. Study
1666 Circulation October 7, 2003
Figure 2. Different types of vulnerable plaque as underlying cause of acute coronary events (ACS) and sudden cardiac death (SCD). A,
Rupture-prone plaque with large lipid core and thin fibrous cap infiltrated by macrophages. B, Ruptured plaque with subocclusive
thrombus and early organization. C, Erosion-prone plaque with proteoglycan matrix in a smooth muscle cell-rich plaque. D, Eroded
plaque with subocclusive thrombus. E, Intraplaque hemorrhage secondary to leaking vasa vasorum. F, Calcific nodule protruding into
the vessel lumen. G, Chronically stenotic plaque with severe calcification, old thrombus, and eccentric lumen.
The Challenge of Terminology: Culprit and macrophage-dense inflammation on or beneath its surface
Plaque Versus Vulnerable Plaque (Figure 3).
Over the past several years, “vulnerable plaque” has been
Culprit Plaque, a Retrospective Terminology
used sometimes to denote this concept and at other times to
Interventional cardiologists and cardiovascular pathologists ret-
denote the specific histopathologic appearance of the above-
rospectively describe the plaque responsible for coronary occlu-
described plaque. This dual usage is confusing, particularly as
sion and death as a culprit plaque, regardless of its histopatho-
Sunday, March 20, logic
2011 features. For prospective evaluation, clinicians need a
plaques can have other histologic features (see Figure 2) that
1286 Arterioscler Thromb Vasc Biol July 2010
Figure 3. Illus
sizes the imp
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secreted by a
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with the main
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Importantly, t
CD40 ligand
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tion of matrix-degrading enzymes produced by vascular smooth muscle cells and inflammatory macrophages. Activat
within the fibrous cap can secrete tissue proteases that support the breakdown of collagen and elastin to peptides an
The loss of structural molecules provided by the extracellular matrix can thin and weaken the fibrous cap, rendering it
ceptible to rupture and acute coronary syndromes. Additional factors involved in the activation of macrophages includ
factor-" (TNF-"), macrophage colony-stimulating factor (M-CSF), and macrophage chemoattractant protein-1 (MCP-1
Sunday, March 20, 2011
Hansson G. N Engl J Med 2005;352:1685-1695
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FENILALQUILAMINAS:
•Verapamil BENZOTIAZEPINAS:
•Galopamil ! Diltiazem
•Tiapamil ! Clentiazem
•Anipamil
•Riapamil
Dihidropiridina Relación
Lercanidipina 730
Lacidipina 193
Amlodipina 95
Felodipina 6
Nitrendipina 3
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