Download Ischemic heart disease

Pathophysiology
Lecture 23
Ischemic heart disease is a group of diseases that have a common
feature which is Ischemia (they will result in ischemia).
Ischemia: is decrease in blood supply (Mismatch between supply and
demand).
In most of cases (90%) this ischemia in the heart (ischemic heart
diseases) result from obstructive lesions (atherosclerotic lesion) in the
coronary arteries ---that’s why we call “ischemic heart diseases IHD”
sometimes “Coronary heart disease CHD” or “Coronary artery disease
CAD”.
This does not mean that the only cause of IHD is atherosclerotic lesions
in coronary arteries , there is other causes:
1) Lowered systemic blood pressure will reduce perfusion to the
heart(as in the state of shock)
2) Coronary artery emboli
3) Occlusion in intramyocardial vessels
4) Coronary artery vasospasm
5) Microvascular angina
So ,too many causes can result in ischemia in the heart.
*Factors that can aggravate Ischemia:
1)Factors that will increase demand:
a-increases HR (heart rate) can increase demand ---so number of beats
per minute will increase
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b-hypertrophy(chronic hypertrophy can increase the incidence of
ischemia by increasing demands)
2)Any reduction in blood OR oxygen supply:
a-reduction in blood supplyas in case of shock (lower blood
pressure conditions).
b-reduction in blood oxygen level we are talking about hypoxemia.
here I don’t have a problem in blood supply or flow but I have a
problem in blood content (low level of O2 in blood).
so hypoxemia is low O2 in blood circulation
-hypoxia is a general term and can result from different diseases, such
as severe anemia ,severe lung disease...
hypoxia is low oxygen state in tissue(cells),But in hypoxemia we have
proper blood supply with lower O2 content .
(this means that it’s not necessary when blood supply is normalno
ischemia may happen, because in case of hypoxemia we have proper
blood supply and flow but low level of oxygen).
*Ischemic heart disease ( IHD ) may present as:
1) An acute coronary syndrome ( MI,Unstable angina)
2) Chronic stable exertional angina
3) Ischemia without clinical symptoms
What is the difference between Acute coronary heart syndrome(ACS)
and Chronic stable exertional angina ?
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ACS---here we have disruption, acute plaque change, we have rupturing
and partial or total thrombosis
Chronic stable exersional angina---we have fixed occlusion of 70% or
more in the coronary artery. (there is no acute plaque changes)just
continuous growth of the plaque that will cause some kind of
obstruction and they will experience symptoms upon increase work
(stress)
For the two above; the pathophysiology start with the formation of
atherosclerotic lesions (in both cases)
*the main etiology behind IHD is obstructive (atherosclerotic) lesions in
the coronary arterieswhich coronary artery?? The epicardial
one(which are on the surface of the heart)
The most important lesions are the lesions that affect the left coronary
artery and its two branches:
1)the circumflex branch
2)left anterior descending (LAD)”anterior ventricular artery (another
name)”
Why left branch is the most important? Because this is the artery that
feed the muscle that will pump the blood to the systemic circulation.
*Other manifestations of atherosclerosis include:
a- Heart failure which will be associated with ischemia (chronic
ischemia).
b- Arrhythmia can be precipitated by ischemia
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c- Cerebrovascular disease (stroke)
d- Peripheral vascular disease
Note: ischemic heart disease IHD is the leading cause of death
*Epidemiology(refer to the slides)CHD is responsible for more than
half of CVD death
Common initial presentationin menMI ,
in womenangina
In the recent years , death due to CVD is substantially decreased , why?
1)we accounted for risk factors (prevention) we modified essential risk
factors)
2)advance therapeutic and medical methods.
Angina –> caused by mismatch between supply and demand
Classified bysymptoms severity, disability and specific activity state
Two classification systems
1)the Canadian cardiovascular society (based on activity)(6‫)الجدول بالساليد‬
2)Other classificationTable slide 7(here the clinician will classify his
patient according to questions..this classification also based on the
activity scale)
*What can determine the outcome of angina?
. Since we are talking about condition where 90% of the cases are
due to atherosclerotic lesion formation, anything that might affect the
outcome of atherosclerosis can affect the outcome of angina(in the
most cases)
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Number of vessels involved can affect the prognosis of this condition
Size of the vessels also. We said that tiny vessels are easier to be
obstructed
Metabolic activity of the tissue(location and function).
The more active the tissue is, the higher its demands. because we have
a fixed supply the high metabolic activity of the tissue will increase the
imbalance between demands and supply and this will result in a much
more severe form of the disease.
*factors that will increase the risk of death in patients with angina:
Heart failure
Smoking
Left main equivalent.(left coronary artery and it’s too important
branches: circumflex and LAD)any involvement of these is linked to bad
prognosis, and high risk of death.
Diabetes
Prior myocardial infection(MI)
Those are factors that would increase the risk of death in clinically
managed patients. Those patients have angina, we are managing those
patients, but they have another condition that can increase their risk of
death.
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*Etiology/pathophysiology:
Important measures in understanding the rationale for the selection
and the use of pharmacotherapy for IHD(factors aggravate ischemia)
1. The determinates of myocardial oxygen demand (MVO2)
Because as we said earlier, in 90%of the cases we have a condition
where we have atherosclerotic lesions causing fixed supply and this will
come to the surface once demands have increased. We want to know,
specifically in this situation, what kind of things can increase myocardial
oxygen demands (mvo2) so this is very essential.
As demands increase the chances of ischemia increase because we
don’t have enough supply to tolerate with the situation.
2. Regulation of coronary blood flow
This is very essential when we are talking about a situation where we
have atherosclerosis in myocardial vessel, so we need to know how
auto regulation will occur in this tissue:
Is it capable of meeting the increase of blood flow? Will it vasodilate
enough to meet the demands?
3. The effects of ischemia on the mechanical and metabolic function
of the myocardium
Function of the myocardial cells is another thing that would affect the
outcome of the situation.
*IHD are very late manifestation of atherosclerotic lesions that started
to be formed long time before(decades ago).
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*Determinants of ischemia:
1. The caliber of resistance vessels delivering blood to myocardium
“supply” increased resistance decreased blood flow .
2. MVO2 (myocardial oxygen demands) “demand”.
*Determinant of myocardial O2 demand (MVO2)(the most
important factor)
a) HRwe said that heart rate will affect ischemia lag by two arms:
 It will increase demand by increasing number of contractions per
unit time
 This increase in number of contractions will reduce the time we
spend in diastole during diastole the filling of coronary arteries
occur. So, Short diastoleless time (short time) to fill coronary
arteries low perfusion to the heart.
B) Contractility
C) intra myocardial wall tension during systole.(MOST IMPORTANT)
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