JOURNAL READING

“Endothelial function and inflammation in

coronary artery disease”

Fathia Kesuma Dinanti

30101407183
JOURNAL IDENTITY

 Correspondence to: Dr Dimitris Tousoulis, Cardiology Unit,

Hippokration Hospital, Athens University Medical School, Athens,
Greece; drtousoulis@hotmail.com
 Cardiology Unit, Hippokration Hospital, Athens University Medical
School, Athens, Greece
 Accepted 13 August 2005 Published Online First 13 September 2005
BACKGROUND

 Coronary artery disease (CAD) remains the principal cause of

death and disability leading to increased burden in health care
costs in developed countries.
 CAD is characterised by a long asymptomatic phase of
development, which starts as early as the first decade of life and
progresses eventually to the formation of atherosclerotic plaques.
 Inflammatory processes have a key role not only in the initiation
and progression of atherosclerosis but also in the stability of the
established atherosclerotic plaques.
ENDOTHELIUM IN CAD  IMPORTANT ROLE

It secretes numerous mediators such as

Nitric oxide
Prostacyclin
Endothelin
They regulate vascular tone, platelet activity, and coagulation
factors but also influence vascular inflammation and cell
migration.
Risk factors and vascular endothelium

 Non-modifiable risk factors  older age and male sex.

 Modifiable risk factors  hypercholester-olaemi (as one of the most important
contributors to atherosclerotic disease progression) and others such as smoking,
hypertension, and diabetes.
 In addition, epidemiological data have suggested that infection and chronic
inflammation may trigger endothelial dysfunction.
 Inflammatory vascular disease is associated with persistent endothelial
dysfunction. More recently mild non-specific viral infections have been found to
have an apparent detrimental effect on the vascular endothelium.
PROGNOSTIC ROLE OF ENDOTHELIAL
FUNCTION IN CAD

 Endothelial vasodilator function was assessed as a test that can integrate the
impact of multiple environmental and genetic influences on the vasculature and
thus serve as a useful diagnostic prognostic tool but also as a therapeutic target
to improve outcome.
 Studies performed at the time of cardiac catheterization clearly show a direct
association between endothelial dysfunction and event rates
 Adhesion
INFLAMMATORY molecules and
MECHANISMS IN monocytes
ATHEROSCLEROSIS

Inflammation in
atherosclerosis

Cytokines and
B and T inflammatory
lymphocytes markers in
atherosclerosis
 Adhesion
molecules and
monocyte

Macrophages Macrophages also

The recruitment of contribute to the local contribute to lesion
inflammatory cells from the Recruitment of monocytes
inflammatory remodelling and to
circulation and their into the arterial wall is one
responses through plaque rupture by
transendothelial migration. of the earliest events in
production of secreting matrix
atherosclerosis. Intimal
This process is mediated by cytokines, free metalloproteinases
monocytes develop into
cellular adhesion oxygen radicals, and contribute to the
macrophages.
molecules. proteases, and evolution of
complement factors. atherosclerosis.
B and T
lymphocytes
Cytokines and
inflammatory markers
in atherosclerosis
PROGNOSTIC ROLE OF INFLAMMATION IN CAD

 The total white blood cell count is an inexpensive, reliable, easy to interpret
inflammatory marker, which has been associated with adverse prognosis in
patients who have stable coronary heart disease after a myocardial infarction.
 Myeloperoxidase concentrations are increased in persons with angiographically
documented cardiovascular disease.
 Myeloperoxidase has been linked to the development of lipid laden soft plaque,
the activation of protease cascades affecting the stability and thrombogenicity
of plaque, the production of cytotoxic and prothrombogenic oxidised lipids.
 CRP, serum amyloid A protein, interleukin 6, and interleukin 1 receptor antagonist,
are also commonly found in acute coronary syndromes.
At the moment, however, the most
attractive candidate marker of
cardiovascular outcome is CRP.
CONCLUSION

 Current evidence supports the central role of endothelium and

inflammation in all phases of the atherosclerotic process.
 Further studies are needed to evaluate whether a combination of
treatments will provide additional anti-inflammatory effects and
protection from cardiovascular events.
Critical appraisal
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ABSTRAK

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Thank You