You are on page 1of 51

:

:

.

30 2015

H CVD
30%

CVD
23.3 . 2030

World Health Organization. Available at www.who.int/mediacentre/factsheets/fs317/en/ [last accessed September 2014]; 2. World Health
Organization. World Health Statistics 2012. Available at www.who.int/gho/publications/world_health_statistics/2012/en/ [last accessed
November 2014].

> 15 Million Heart Attacks Each Year

Source:
World
Heart
Federation

The AEHA 2005 VP Summit

Sudden Cardiac Death or Acute MI as


Initial Presentation of CHD

62%

Men

42%

Women

10

20

30

40

50

60

70

Patients Diagnosed with CHD (%)


Murabito et al


(EF, serum tests,
physician visit)

Stent

140.000.000 > 35

<70%

>70%


Circulation. 2005;111:3481-3488

.
. /
. RBLs
.
.
.
. MMPs

. Ox-LDL
. Apoptotic macrophages
. T-cell

Circulation. 2003;108:1664-1672

J Am Coll Cardiol 2011;57:196179

Circulation. 2003;108:1664-1672

Recurrent events are as likely to originate from a new atherosclerotic


plaque as they are from the initial culprit lesion
PROSPECT study: Prospective study of the natural history of
atherosclerosis over 3 years in patients with ACS who underwent
PCI (n=697)

All events 20.4%


Culprit lesion-related events 12.9%

Non-culprit lesion-related events 11.6%


Indeterminate events 2.7%

PROSPECT, Providing Regional Observations to Study Predictors of Events in the Coronary Tree.
Stone GW et al. N Engl J Med 2011;364:226235.

Eur Heart J 2004;25:1077 82.

(~70%)

(~20%)
- (~50%)
(~30%)


/

ACS is the clinical manifestation of the


rupture or erosion of a vulnerable plaque

Thrombus
formation

Platelet
Fibrous
cap rupture

Lipid
core

Vulnerable plaques have a thin


fibrous cap, a large lipid core
and many inflammatory cells

Several mechanisms are likely


to be responsible for the
transition of high-risk plaques to
obstructive, including:
Subclinical rupture leading to a
fibro-proliferative and
constrictive healing process
Intraplaque haemorrhage
Excessive plaque growth that
exceeds the remodelling
capacity of the arterial wall

Nat Rev Genet 2006;7(3):163173


Cardiovasc Res 2012;96(2):234243


ACUTE PLAQUE
RUPTURE
ACS (UA/NSTEMI/STEMI)


J Am Coll Cardiol 2002;39:14641467

( /
-)

>90%

Circulation. 2003;108:1664-1672

,
( )

( )

Circulation. 2003;108:1664-1672

( ,
, T-cell)

( ,
)

stress

, vasa vasorum,

(MMPs
2, 3, 9, )
(eg, HSP60, C. pneumoniae)

Circulation. 2003;108:1664-1672

VS.

Circulation. 2003;108:1664-1672


(.. LDL, HDL,
())
(.. ,
)
(.. CRP, CD40L, ICAM-1 )
(.. -LDL
-HSP )
(.. ox-LDL and ox-HDL)

A (PAPP-A)
(e.g., Fas/Fas ligand, not specific to plaque)
(ADMA)
(.. NEFA)

200

Grayscale IVUS

Virtual Histology-IVUS (VH-IVUS)

Integrated Backscatter-IVUS (IB-IVUS)

Angioscopy

Near-Infrared Spectroscopy (NIRS)

Optical Coherence Tomography (OCT)

Thermography

Intravascular MRI
JACC Cardiovasc Imaging. 2012 September ; 5(9): 941955

Circ Cardiovasc Imaging. 2011;4:169-178

IVUS E


(
)
.
J Am Coll Cardiol 2000;35:106 11

(TCFA)

Circ J 2008; 72: 1631 1639

OCT

J Am Coll Cardiol 2012;59:105872

OCT

J Am Coll Cardiol 2012;59:105872

OCT

J Am Coll Cardiol 2012;59:105872

CT
Angiography



<30 Hounsfield units

MRI

(
)
,

PET

ULTRASOUND


contrast

J Am Coll Cardiol 2011;57:196179

CT -




J Am Coll Cardiol. 2009; 54:4957.

MRI

J Circulation 2005;112:e3 4

Amsterdam EA, et al. 2014 AHA/ACC NSTE-ACS Guideline

STEMI

European Heart Journal (2012) 33, 25692619

NSTE-ACS

European Heart Journal (2014) 35, 25412619

NSTE-ACS

European Heart Journal (2014) 35, 25412619

TIMACS-trial

NSTEACS
, , 6 ,

(<24h)
(>36h)
N Engl J Med 2009;360(21): 21652175.

Analysis from the ACUITY-trial

NSTE-ACS
24 h PCI

30
1 .

-
TIMI risk score.

J Am Coll Cardiol 2010; 55:141624.

European Heart Journal (2011) 32, 29993054

NSTE-ACS

European Heart Journal (2011) 32, 29993054

NSTE-ACS

European Heart Journal (2011) 32, 29993054

(life style,
rehabilitation)

J Am Coll Cardiol 2015;65(8):846

CANAKINUMAB

METHOTREXATE

microRNAs -

mRNA.
,

.