Ischemic heart Disease (IHD)

Ischemia refers to the lack of oxygen due to inadequate perfusion of the

myocardium, which cause an imbalance between oxygen supply and
demand.
Most common cause is obstructive atherosclerotic disease of epicardial
coronary arteries
Has two large groups:
1. Stable Angina secondary to Chronic Coronary Artery Disease
2. Acute Coronary Syndrome (ACS)
a. Acute Myocardial Infarction with ST-elevation
b. Non-ST elevation MI
c. Unstable Angina

Epidemiology

Most common, serious, chronic, life-threatening illness in US.

High fat and energy-rich diet, smoking, and sedentary lifestyle are associated
with the emergence of IHD.
Obesity, insulin resistance and type 2 diabetes mellitus are increasing and
are powerful risk factors for IHD.
Urbanization in the developing world causes the increase of IHD prevalence in
these regions

Pathophysiology

Arteries involved:
o Large epicardial coronary arteries capable of constriction and
relaxation, serving as conduits, thus referred to as the conductance
vessels.
*Prinzmetal angina abnormal constriction of the conductance vessel
that can cause severe ischemia
o Intramyocardial arteriole exhibit changes in the tone thus called
resistance vessel.
*Microvascular angina abnormal constriction or failure of normal
dilation of coronary resistance vessels leading to ischemia.
If luminal reduction is severe, myocardial perfusion in basal state is reduced.
Ischemia can also occur if myocardial oxygen demands are markedly
increased, or when coronary blood flow is limited (e.g. LVH with AS)
Reduction in the oxygen-carrying capacity of the blood (e.g. severe anemia)
or carboxyhemoglobin (rarely cause ischemia) but can lower the threshold for
ischemia with moderate coronary obstruction

Normal Coronary Circulation

 The normal coronary circulation is dominated and controlled by the hearts
requirements for oxygen. This need is met by the ability of the coronary
vascular bed to vary its resistance (and therefore blood flow).
The changing oxygen needs of the heart with exercise and emotional stress
affect coronary vascular resistance and in this manner regulate the supply of
oxygen and substrate to the myocardium (metabolic regulation).
The coronary resistance vessels also adapt to physiologic alterations in blood
pressure in order to maintain coronary blood flow at levels appropriate to
myocardial needs (autoregulation)
Effects of Ischemia

Myocardial tissue oxygen tension falls and may cause transient disturbances
of the mechanical, biochemical, and electrical functions of the myocardium.
Associated with almost instantaneous failure of normal muscle contraction
and relaxation. The relatively poor perfusion of the subendocardium causes
more intense ischemia of this portion of the wall.
Ischemia of large portions of the ventricle causes transient left ventricular
failure
If the papillary muscles are involved, mitral regurgitation can complicate this
event.
When ischemia is transient, it may be associated with angina pectoris;
when it is prolonged, it can lead to myocardial necrosis and scarring with
or without the clinical picture of acute myocardial infarction
Abnormalities in cell metabolism, function and structure underlie these
mechanical disturbances during ischemia.
o The normal myocardium metabolizes fatty acids and glucose to carbon
dioxide and water. With severe oxygen deprivation, fatty acids cannot
be oxidized, and glucose is broken down to lactate; intracellular pH is
reduced, as are the myocardial stores of high-energy phosphates, i.e.,
ATP and creatine phosphate.
o Impaired cell membrane function leads to the leakage of potassium
and the uptake of sodium by myocytes.
ECG: Transient ST-segment depression often reflects subendocardial
ischemia, while ST-segment elevation is thought to be caused by more
severe transmural ischemia. Another important consequence of
myocardial ischemia is electrical instability, which may lead to ventricular
tachycardia or ventricular fibrillation

Stable Angina

Males constitute >70% of all patients with angina pectoris and an even
greater fraction of those >50 years.
 o man >50 years or a
o woman >60 years
History
complains of chest discomfort ( heaviness, pressure, squeezing,
smothering, or choking)
o Pressing on the sternum, sometimes with a clenched fist, to
indicate a squeezing, central, substernal discomfort (Levines
sign)
o Crescendo-decrescendo in nature, typically lasts 2 to 5 min,
and can radiate to the left shoulder and to both arms.
episodes of angina are typically caused by exertion (e.g., exercise,
hurrying, or sexual activity) or emotion (e.g., stress, anger, fright, or
frustration) and are relieved by rest
*NOCTURNAL ANGINA- at night while the patient is recumbent
(angina decubitus), may be awakened at night distressed by typical chest
discomfort and dyspnea. May be due:
1. to episodic tachycardia
2. the expansion of the intrathoracic blood volume that occurs with
recumbency ( causes an increase in cardiac size and myocardial oxygen
demand that lead to ischemia and transient left ventricular failure)
Anginal equivalents are symptoms of myocardial ischemia other than
angina ( dyspnea, fatigue, and faintness and are more common in the
elderly and in diabetic patients)
uncover a family history of:
o premature IHD( <45 years in first-degree male relatives and <55
in female relatives)
o the presence of diabetes mellitus
o Hyperlipidemia
o Hypertension
o cigarette smoking
o other risk factors for coronary atherosclerosis
Physical Examination: This is often normal in patients with stable angina, but it
may reveal evidence of atherosclerotic disease at other sites

Unstable Angina and Non ST-elevation MI

defined as angina pectoris or equivalent ischemic discomfort with at least
one of three features
(1) it occurs at rest (or with minimal exertion) usually lasting
>10 min
(2) it is severe and of new onset (i.e., within the prior 4 to 6
weeks), and/or
(3) it occurs with a crescendo pattern (i.e., distinctly more
severe, prolonged, or frequent thanpreviously)
 The diagnosis of NSTEMI is established if a patient with the clinical
features of UA develops evidence of myocardial necrosis, as reflected in
elevated cardiac biomarkers.
Pathophysiology
caused by a reduction in oxygen supply and/or by an increase in
myocardial oxygen demand (e.g., by tachycardia or severe anemia)
superimposed on a coronary obstruction.
Four pathophysiologic processes
(1) Plaque rupture or erosion with superimposed nonocclusive
thrombus- the most common cause
(2) Dynamic obstruction [e.g., coronary spasm, as in Prinzmetals
variant angina
(3) Progressive mechanical obstruction (e.g., rapidly advancing
coronary atherosclerosis)
(4) Secondary UA related to increased myocardial oxygen demand
and/or decreased supply (e.g., anemia).
History and Physical Examination
The clinical hallmark of UA/NSTEMI is chest pain
o typically located in the substernal region or sometimes in the
epigastrium, that frequently radiates to the neck, left shoulder,
and left arm
Anginal equivalents such as dyspnea and epigastric discomfort may
also occur.
The examination resembles that in patients with stable angina and may
be unremarkable.
If the patient has a large area of myocardial ischemia or a large
NSTEMI: diaphoresis, pale cool skin, sinus tachycardia, a third and/or
fourth heart sound, basilar rales, and sometimes hypotension, resembling
the findings of large STEMI.

Prinzmetals Variant Angina

This syndrome is due to focal spasm of an epicardial coronary artery,

leading to severe myocardial ischemia.
Many Prinzmetal patients have spasm adjacent to atheromatous plaques.
The exact cause of the spasm is not well defined
May be related to hypercontractility of vascular smooth muscle due to
vasoconstrictor mitogens, leukotrienes, or serotonin.

Serum Cardiac Biomarkers

Creatine phosphokinase (CK) rises within 4 to 8 h and generally returns to normal by 48 to 72 h. An
important drawback of total CK measurement is its lack of specificity for STEMI, as CK may be elevated
with skeletal muscle trauma.
Other potential sources of total CK elevation are (1) skeletal muscular diseases, including muscular\
dystrophy, myopathies, and polymyositis; (2) electrical cardioversion; (3) hypothyroidism; (4) stroke;
(5) surgery; and (6) skeletal muscle damage secondary to trauma, convulsions, and prolonged
immobilization.
The MB isoenzyme of CK has the advantage over total CK that it is not present in significant
concentrations in extracardiac tissue and therefore is considerably more specific. However, cardiac
surgery, myocarditis, and electrical cardioversion often result in elevated serum levels of the MB
isoenzyme.

Myoglobin is released into the blood within only a few hours of the onset of STEMI. Although myoglobin
is one of the first serum cardiac markers that rises above the normal range after STEMI, it lacks cardiac
specificity, and it is rapidly excreted in the urine, so that blood levels return to the normal range within
24 h of the onset of infarction.