GENERAL MEDICINE LECTURE(2)

Ischemic Heart Disease

Ischemic heart disease (IHD) is a condition in which there is an

inadequate supply of blood and oxygen to a part of the heart muscle
(myocardium); it typically occurs when the myocardial Oxygen supply is
less than myocardial(heart muscle) demand.

The most common cause of myocardial ischemia is atherosclerotic

disease of a coronary artery(or arteries) so the region of heart muscle
supplied by this artery(or arteries)doesn’t get enough blood /oxygen.

EPIDEMIOLOGY

IHD causes more deaths and disability and have a greater

economic costs than any other illness in the world ,it affects male

and females and high and low social class people.

pathophysiology

the main problem in IHD is that the heart which is the pumping machine
which provide blood (oxygenation) to all organ and tissues doesn’t get his
share!!
The heart contract and relax continuously (systole and diastole),the blood
and O2 reaches the heart when it relaxes (in diastole) more than when it
contract (systole),the arteries responsible for delivering it are called
coronary arteries.

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WHAT ARE THE FACTORS THAT PREDICT HOW MUCH THE
HEART NEEDS BLOOD /OXYGEN??(DEMANDS)
how much blood (O2)the heart need is determined by factors ; heart rate
(more contraction means more work and remember the diastole
(relaxation phase )became shorter, muscle wall tension (stress)(more
work) and how big is the muscle.
WHAT WE NEED TO PROVIDE ENOUGH BLOOD TO THE
HEART?(SUPPLY)
In order to provide the proper supply of blood to the heart we need a
normal pulmonary function , a normal capacity of hemoglobin to carry
oxygen(sever anemia can cause IHD) and a normal coronary
arteries(atherosclerosis decrease caliber of one or more coronary arteries,
thereby causing IHD(the most common cause),spasm of coronary artery
can do the same(much less common occur in prinzmetal angina).

Atherosclerosis:
Major risk factors(high plasma low density lipoprotein(that why we give
antilipid) Cigarette smoking, hypertension and diabetes mellitus
disturb( CHANGE) the normal function of endothelium causing
abnormal interaction between platelets and leukocyte,monocyte mainly,
resulting in subintimal collection of fat ,smooth muscle cells,fibroblast
and inter cellular matrix(ATHERSCLEROTIC PLAQUE).
This plaque can rupture or erode leading to platelet aggregation and
activation of coagulation and eventually thrombus obstructing the
coronary artery (ISCHEMIA)

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ISCHEMIA:
So we have ischemia, what next?
Ischemia is not a uniform fashion, a part from heart doesn’t get
oxygenation , there is a loss in the mechanical a biochemical and
electrical function of that part(this part will not work prperly) what
happened next is determined by how long this last ?if it is temporary and
the heart muscle didn’t die it is called ANGINA PECTORIS (this further
divided into STABLE and UNSTABLE according to the risk of changing
into MI

if part of the muscle became necrotic and die this is a MYOCARDIAL

INFARCTION(MI).(and this again further divided into ST elevation
MI(STEMI) and NON STelevation MI(NSTEMI) (according to the ECG
changes and involvement of full thickness or part of the muscle wall
involved).

Stable angina pectoris

We learned that angina means TEMPORARY ischemia and the cardiac
muscle isn’t permanently damaged.in these patients (typically male in his
50s or a female in her 60s) exertion, whether physical or emotional
produce symptoms.(most common cause is atherosclerosis yet spasm or
aortic stenosis and HOCM may cause it).
Chest pain, discomfort or heaviness in chest radiated to neck or jaw ,
interscapular area ,epigastrium and left(or both) shoulder/s ,last less than
15 min are the typical presentation in response to exertion (yet it can
occurs when lying ,decubitus angina or during sleep ,nocturnal angina).

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Investigation:
ECG (RESTING) may show ST segment deviation(mainly depression)
and T inversion
EXERCISE ECG: whether physical (treadmill test) or pharmacological ,
down sloping depression is more indicative of ischemia
Myocardial perfusion scan
Stress echocardiography
Cardiac enzymes is negative in case of angina(no cardiac muscle death)
Coronary arteriography

Therapy

Intensive lifestyle modification is appropriate for all patients (smoking

cessation, regular physical activity, “heart healthy” diet). Treatment is
indicated to achieve the following goals: BP <140/90 mm Hg, and
hemoglobin A1c <7%.(good suger and blood pressure control)

(the idea is to decrease demands by decreasing heart rate, contractility

and muscle wall tension or to increase supply by preventing further
platelet aggregations or lipid accumulation or by vasodilation).

The three major classes of antianginal medications for stable angina are
β-blockers, nitrates, and calcium channel blockers.
there are a new classes like potassium channel activator (nicorandil)
,vasodilator, and I(f) channel antagonists(ivabradin)(causing
bradycardia).
Most patients with stable angina will require combination therapy.

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Cardioselective β-blockers are first-line therapy in patients with
chronic stable angina. Dosage should be adjusted to achieve a resting HR
of approximately 60/min. Absolute contraindications to β-blockers
include severe bradycardia , advanced AV block, decompensated HF, and
severe reactive airways disease.
Nitrates are as effective as β-blockers and calcium channel blockers in
reducing angina( chest pain). Prevent nitrate tachyphylaxis by
establishing a nitrate-free period of 8 to 12 hours per day (typically
overnight), during which nitrates are not used. For patients using nitrates,
sildenafil, vardenafil, and tadalafil are contraindicated.

For patients with absolute contraindications to β-blockers, calcium

channel blockers should be initiated as first-line therapy. In the setting of
continued angina despite optimal doses of β-blockers and nitrates,
calcium channel blockers can be added.
Bradycardia and heart block can occur in patients with significant
conduction system disease.
Ranolazine should be considered in patients who remain symptomatic
despite optimal doses of β-blockers, calcium channel blockers, and
nitrates.

Cardioprotective drugs reduce the progression of atherosclerosis and

subsequent cardiovascular events.
• Aspirin( antiplatelets) reduces the risk of stroke, MI, and vascular death
in patients with CAD.
(clopidogrel can replace aspirin if gastrointestinal side effect can't be
tolerated)

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• ACE inhibitors reduce risk of cardiovascular and all-cause mortality
for most patients.
• High-intensity statins( antilipid) reduce cardiovascular events,
including MI and death.

INVASIVE THERAPY
PERCUTANEOUS CORONARY INTERVENTION(PCI)
(under radiological monitoring, we pass a guide wire through the
obstruction and a balloon is inflated to dilate the stenosis)it is mainly
used in single or two vessel disease.
Coronary artery bypass surgery
Anastomosis of one or both internal mammary arteries or radial artery
with coronary artery distal to the obstructive lesion is carried out, for
additional obstruction that can't be bypassed by an artery, a section of
vein (usually saphenous) used as a connection between aorta and
coronary artery.

Revascularization therapy with PCI or CABG may be considered in

patients with persistent symptoms despite maximal medical therapy.

The end

Dr. Haidar Alamri