Professional Documents
Culture Documents
Risk Factors and Pathophysiology of Stroke
Risk Factors and Pathophysiology of Stroke
PATHOPHYSIOLOGY OF STROKE
Christos Savopoulos
Assistant Professor of Internal Medicine
1st Propedeutic Medical Department
Aristotle University of Thessaloniki
Department of Hypertension & Vascular Diseases
AHEPA Hospital
Stroke accounts for 10% of all-cause
mortality
Tuberculosis Malaria
Diarrhoea
Perinatal causes
2% Other causes
3% 3%
Chronic obstructive pulmonary 4%
disease 27%
5%
HIV/AIDS 5%
Respiratory infections 7%
Coronary heart
disease
9%
13%
Accidents Stroke Cancer
10% 12%
Since 80s, a significant increase (> 2-fold ) has been noticed in incidence of stoke : 1–
2 /1.000 people in USA, 2–2.5/1.000 in Western και 3–3.5/1.000 in Eastern Europe
Framingham Heart Study; American Heart Association, Heart and Stroke Facts statistical update, Lees KR, et al. BMJ 2000;320:991–994; Hankey GJ, Warlow
CP. Lancet 1999;354:1457–1463
Non- modifiable Risk Factors
14
Frequency of Stroke 12
Men 12,0
11,5
Women
% of population
related to age & 10
8 6,6 6,3
gender 6
4 3,1 3,0
2,1
1,1 0,8 1,2
2
0,4 0,3
0
20-34 35-44 45-54 55-64 65-74 75+
Age
Risk factors are the same in all atherothrombotic events such as Coronary disease, stroke and
peripheral vascular disease, but with different importance in each condition, according to the
specific role, biological features and mechanical stress of the respective vascular areas.
Hypertension is more important in cerebrovascular disease compared to coronary heart disease,
whereas the opposite concerns dyslipidemia.
Coronary Cerebral
BP SBP,DBP SBP,DBP
Cholesterol
HDL
smoking
obesity
Heart rate
Other factors
(viral, infectious
10yr risk for Stroke in Adults 55 yrs old
according to basic Risk Factors
(Framingham Heart Study)
E s tim a te d 1 0 -Y e a r R a te (% )
30 27
25 22.4
19.1
20
14.8
15
10 8.4
5.4 6.3
4 3.5
5 2.6 2
1.1
0
A B C D E F
Men Women
A B C D E F
Systolic BP 95-105 130-148 130-148 130-148 130-148 130-148 mmHg
Diabetes no no yes yes yes yes
Smoking no no yes yes yes yes
Previous AF no no no no yes yes
Previous CVD no no no no no yes
Stroke 1991;22:312-318
Atherosclerosis
From risk factors to endothelial injury & CVD
Oxidative stress
Endothelial dysfunction
Adhesion molecules
CV Clinical events
VCAM: vascular cell adhesion molecule,
ICAM: intercellular adhesion molecule
PAI-1: plasminogen activator inhibitor 1
Gibbons GH. N Engl J Med 1994
Normal Arterial Wall
(intima, Media, Adventitia)
Intima:
Endothelium
Internal elastic laminae
Media:
Smooth muscle cell
Lumen
Collagen proteins
Penetration of lipoproteins
Leucocyte adhesion
Lipid core formation (fatty streak)
in atherosclerosis
Migration of smooth
muscle cells
T cells activation
Accumulation of macrophages
Intravascular thrombus
Lipid layer
Intima
Lumen
Media
Plaque
Threshold
Thrombus
Intima
Lumen
Media
Plaque
Brain injury
Due to:
Results to:
Functional body disorders which are controlled by the damaged
part of the brain
Thromboembolic
ISCHEMIC
Brain
infarct
HEMORRHAGIC
Brain vessel
thrombosis
Intracerebral
hemorrhage
Incidence – Mortality of
ischemic & hemorrhagic Stroke
The majority of strokes are ischemic
Embolic : emboli originate from heart, aortic arch & major cervical vessels
•Other possible mechanisms during the first 48-72 h after ischemic stroke
initiation are:
- cerebral oedema development and space occupational action,
- metabolic disturbances like hyperglycemia, hyponatremia,
- hemorrhagic transformation,
- fever (infection) aggravating ischemic neuron metabolism
Ischemic infarct: Frequently, up to 50%, there is
delay in CT imaging within 48 h
“Normal CT” at admission of an Large infarct in the area of middle brain artery
ischemic stroke with left hemiparesis| causing compressive effect, 48h after admission
Hemorrhagic Stroke
Admission CT of hemorrhagic stroke with Subdense appearance and severe compressive effect of
left hemiparesis and persistent headacne extented oedema around hematoma, 48h after admission
Thank you for your attention!