ISCHEMIC HEART
DISEASE
CORONARY CIRCULATION :
The heart supplied with arterial blood by the right and left
coronary arteries which branch from the aorta .The coronary
arteries receive about 5% of the blood pumped from the
heart ,although the heart comprise a small proportion of
body weight (225 g ) ,this highlight the importance of the
heart to body function.
The left coronary artery supply mainly the anterior and
lateral portions of the left ventricle, whereas the right
coronary supply most of the right atrium as well as the
ventricle posterior part of the left ventricle .
Coronary heart disease CHD occur due to imbalance
between myocardial oxygen supply and myocardial oxygen
demand. This imbalance is caused by either an increase in
myocardial oxygen demand (as in anxiety ) or by a decrease
in myocardial oxygen supply(due to thrombosis or coronary
artery spasm ) which cause myocardial ischemia ,and if
prolonged it may cause cardiac muscle death (myocardial
infarction).
IHD may present as an acute coronary syndrome
(acute coronary syndrome includes unstable
angina, non–ST-segment elevation myocardial
infarction or ST-segment elevation myocardial
infarction; chronic stable exertional angina
pectoris, and ischemia without clinical symptoms.
Coronary artery vasospasm (variant or Prinzmetal
angina) produces similar symptoms but is not
caused by atherosclerosis. Other manifestations of
atherosclerosis include heart failure, arrhythmias,
cerebrovascular disease (stroke), and peripheral
vascular disease.
RISK FACTORS FOR IHD :
-Hypercholesterolemia.
-Hypertension.
-Diabetes mellitus.
-Smoking.
-Sedentary lifestyle .
Risk factor identification and modification are
important interventions for individual patients with
known or suspected IHD and as a population-based
policy to reduce the impact of this disease.
ANGINA PECTORIS :-
Angina pectoris is the primary symptom of ischemic
heart disease. It is manifested as Sudden , severe ,
pressing chest pain starting substernal &radiate to left
shoulder and arm or to the jaw.
It last for several minutes(0.5-30min).
Types of angina pectoris :
1-Stable angina ;
It is the most common type and occurs due to atherosclerosis of
large coronary arteries. It is induced by exercise, emotional
stress, heavy meals.
2-Unstable angina ;
means increased frequency, severity and duration of anginal pain
at rest. It is caused by platelet adhesion and aggregation on an
atheromatous plaque with coronary thrombosis
.
3-Variant angina ;
It occurs at rest and is caused by coronary artery spasm .
PATHOPHYSIOLOGY
Angina pectoris typically occurs when myocardial
oxygen demand exceeds myocardial oxygen supply.
The underlying pathologic condition of this mismatch
invariably is the presence of atherosclerosis in one or
more of the coronary arteries.
If the size of the atherosclerotic plaque obscures less
than 50% of the diameter of the vessel, coronary blood
flow can be augmented sufficiently during exertion by
the intramyocardial arterioles(resistance vessels), and
the patient is pain free.
In patients with chronic stable angina, most coronary
artery stenosis are greater than 70%. A linear
decrease in coronary blood flow occurs as the plaque
occupies more of the arterial lumen until high-grade
(>80%) obstruction develops. At this point, the
decrease in blood flow is out of proportion to plaque
size. The impaired blood flow with atherosclerotic
lesions may be adversely affected by vasomotor
dysfunction, leading to inappropriate vasoconstriction
and further reduction in blood supply. Functionally,
coronary blood flow is absent when lesions obstruct
greater than 95% of the vessel lumen.
Collateral blood vessels (i.e., side branches of a
coronary artery that join one of the three principal
arteries or connect two points along the same artery)
may offer protection against myocardial ischemia.
The distribution and extent of collateral vessels are
variable. These usually are very small and have no
function in the normal heart.
If blood flow is obstructed, however, collateral vessels
assume more importance and can restore some
myocardial blood flow. When myocardial oxygen
demand is increased excessively, however, collateral
blood flow usually is insufficient, and angina or other
myocardial ischemia syndromes develop.
Stable versus Unstable Plaque
Clinical Presentation:
A detailed description of chest pain is vital in order for the
clinician to determine whether chest pain represents chronic
stable angina, ACS, or is non cardiac in origin. Chest pain
stemming from myocardial ischemia is often described as a
sensation of pressure or heavy weight located over the
sternum.
Patients may also complain of SOB , nausea, vomiting, or
diaphoresis. Pain may also occur in the neck, jaw, shoulder,
or arm.
The precipitation of pain is typically associated with exertion
and rapidly resolves with rest or the administration of
nitroglycerin.
Chest pain that occurs at rest, prolonged in
duration, or increased in severity is likely reflective
of unstable disease and warrants immediate
medical attention to prevent complications such as
MI,HF, and death.
Importantly, some patients (women, people with
diabetes) may present with atypical symptoms
such as indigestion or gastric fullness, or may
present with diaphoresis alone without
concomitant chest pain. Lastly, many episodes of
ischemia may not manifest any symptoms and are
termed as “silent ischemia.”
Physical findings in patients with chronic stable
angina are nonspecific and may include SOB,
tachycardia, diaphoresis, and nausea. Other
findings that may be present if the level of
ischemia is severe enough include hypotension,
pulmonary congestion, or the presence of
abnormal heart sound.
Diagnosis:
Given that many symptoms associated with chronic
stable angina are nonspecific, several noninvasive and
invasive testing modalities are available to assist in the
diagnosis of CAD.
In addition to providing diagnostic information, many
of these testing options also are useful in evaluating
the overall prognosis of the patient . Such
information is useful in helping to determine an
overall treatment plan.
1-Electrocardiogram
A 12-lead ECG reading should be obtained in all
patients with symptoms suggestive of angina pectoris.
Although not useful in establishing a definitive
diagnosis of CAD, the ECG will be useful at detecting
important information regarding conduction
abnormalities, left ventricular hypertrophy, ongoing
ischemia, or evidence of a previous myocardial
infarction.
The ECG is normal in about one-half of patients with
angina who are not experiencing an acute attack.
Typical ST–wave changes include depression, T-wave
inversion, and ST-segment elevation. Forms of
ischemia other than exertional angina may have ECG
manifestations that are different; variant angina is
associated with ST-segment elevation, whereas silent
ischemia may produce elevation or depression.
2-Exercise Tolerance Testing
The induction of stress via exercise is a common and
highly useful procedure in the diagnosis of CAD.
Under the controlled circumstances of an exercise
tolerance test, the test would be indicative of CAD if
angina, ECG signs of ischemia, arrhythmias,
abnormal heart rate, or abnormal blood pressure
(BP) response develops.
A normal BP response to exercise is a gradual rise in
systolic BP with the diastolic BP remaining
unchanged. A rise or fall of diastolic BP greater than
10 mm Hg is considered abnormal.
A fall in systemic BP during exercise is especially
ominous because this indicates that the cardiac
output cannot increase sufficiently to overcome the
vasodilation in the skeletal muscle vascular bed.
3-Cardiac Imaging
Radionuclide angiocardiography (performed with technetium-
99m, a radioisotope) is used to measure ejection fraction, regional
ventricular performance, cardiac output, ventricular volumes,
valvular regurgitation, asynchrony or wall motion abnormalities,
and intracardiac shunts. Technetium pyrophosphate scans are
used routinely for detection and quantification of acute
myocardial infarction. Positron emission tomography is useful for
quantifying ischemia with metabolically important substrates such
as oxygen carbon, and nitrogen.
4-Cardiac Catheterization and Coronary Arteriography
Cardiac catheterization and angiography in patients with suspected
coronary artery disease are used diagnostically to document the
presence and severity of disease, as well as for prognostic
purposes. High-risk features during ETT suggesting the need for
coronary angiography include early and significant (≥2 mm)
changes on the ECG during ETT as well as multiple lead
involvement, prolonged recovery from ischemia, low workload
performance, abnormal blood pressure response (reduction in
blood pressure), or ventricular arrhythmias.
Multiple defects with thallium scans as well as lung
uptake during exercise or post exercise ventricular
cavity dilation are also high-risk indications for
catheterization. Interventional catheterization is used
for thrombolytic therapy in patients with acute myo-
cardial infarction and for the management of patients
with significant coronary artery disease to relieve
obstruction through atherectomy, laser treatment, or
stent placement.
5-Catheterization and angiography
May be done after coronary artery bypass grafting
(CABG) to determine if the graft has closed or if
coronary artery disease has progressed. Coronary
artery intravascular ultrasound is useful for directly
imaging anatomy, calcified and fatty plaques, and
thrombosis superimposed on plaque as well as
determining patency following revascularization
procedures. Intravascular ultrasound guidance of
stent implantation may result in more effective
stent expansion compared with angiographic
guidance alone
Coronary
Angiography
Treatment
DESIRED OUTCOME
The short-term goals of therapy for ischemic heart disease
are to reduce or prevent the symptoms of angina that limit
exercise capability and impair quality of life.
Long-term goals of therapy are to prevent CHD events such
as myocardial infarction, arrhythmias, and heart failure and
to extend the patient’s life.
Because there is little evidence that revascularization
procedures such as angioplasty and coronary artery bypass
surgery extend life, the primary focus should be on altering
the underlying and ongoing process of atherosclerosis
through risk factor modification while providing symptomatic
relief through the use of nitrates, β-blockers, calcium channel
blockers for anginal symptoms.
-Risk Factor Modification
Primary prevention of ischemic heart disease through
the identification and modification of risk factors prior
to the initial morbid event would be the optimal
management approach and should result in a
significant impact on the prevalence of IHD. However,
early recognition of some risk factors may not be
possible in all cases, and in others, the patient may not
be willing to undertake intervention until overt
evidence of coronary disease is apparent.
The presence of risk factors in individual patients plays
a major role in determining the occurrence and severity
of IHD. Risk factors are additive in nature and can
be classified as alterable or unalterable .
Unalterable risk factors include gender; age; family
history or genetic composition; environmental
influences such as climate, air pollution, trace metal
composition of drinking water.
Risk factors that can be altered include smoking,
hypertension, hyperlipidemia , obesity, sedentary
lifestyle , hyperuricemia , psychosocial factors such as
stress .
Hypertension is the most common and a powerful
contributor to atherosclerotic coronary vascular disease.
Morbidity and mortality increase progressively with the
degree of blood pressure elevation of either systolic or
diastolic pressure and pulse pressure, and no discernible
critical value exists . Recent guideline changes from the
AHA recommend goal blood pressure of <130/80 mm
Hg for patients with stable angina, unstable angina, non–
ST-segment myocardial infarction, ST segment
myocardial infarction , and <120/80 mm Hg in patients
with left ventricular dysfunction.
Hypercholesterolemia is a significant cardiovascular risk
factor, and risk is directly related to the degree of cholesterol
elevation. All patients should undertake therapeutic lifestyle
changes. The objective for patients with IHD is to maintain
or reduce to a normal body weight. This may be
accomplished through dietary modification, exercise,
pharmacologic therapy, or surgical therapy. Reductions in
LDL-cholesterol have been shown to reduce total and CAD
mortality and stroke as well as the need for interventions
such as PCI and CABG.
- Revascularization
Revascularization of the myocardium, either via
CABG or PCI, is a mainstay in the treatment of
patients with CAD. The goals of revascularization
do not differ from the overall goals in treating
patients with chronic stable angina, namely, to
relieve symptoms, improve quality of life, and
prevent complications of CAD such as MI and
death. Historically, a great deal of focus was
devoted to comparing CABG, PCI, and medical
management and their relative efficacy in relieving
symptoms and improving prognosis.
In a broad population of patients with CAD,
revascularization with either CABG or PCI was
found superior to medical management therapy alone
at relieving symptoms at 1 year, although there was
no difference in overall mortality between the
treatment strategies. However, CABG therapy
tended to be superior at providing long-term relief of
symptoms, as well as providing a lower need for
repeat revascularization therapy compared to PCI.
1-Percutaneous coronary intervention;
Percutaneous coronary intervention, also known as
angioplasty, involves the percutaneous insertion of a
balloon catheter into the femoral artery in a similar
fashion to angiography. The catheter is advanced up
the aorta and into the coronary arteries at the
coronary sinus. PCI, which was introduced in 1977,
initially involved the inflation of a catheter-borne
balloon that mechanically dilated a coronary artery
obstruction through arterial intimal disruption,
plaque fissuring, and stretching of the arterial wall.
Balloon inflations were repeated until the plaque
was compressed and coronary blood flow resumed.
Since then, alternative devices have been developed,
including rotational blades designed to remove
atheromatous material, lasers to ablate plaques, and
intracoronary stents that are designed to maintain the
patency of the vessel after it is reopened. Stents can
be of the bare-metal (BMS) variety, or contain a drug
impregnated on the surface of the stent to prevent
restenosis (drug-eluting stent, DES).
PCI is indicated in patients with single-vessel or
multivessel disease and who are either symptomatic
or asymptomatic
Because of mechanical disruption of atherosclerotic
plaques and exposure of plaque contents to the
bloodstream during PCI, potent antiplatelet and
antithrombotic strategies are needed to prevent acute
thrombotic events such as MI and death. In patients
not taking aspirin on a daily basis, 300 to 325 mg of
aspirin should be given at least 2 hours before the
procedure. Patients currently on daily aspirin therapy
should receive 75 to 325 mg of aspirin
before PCI is performed.A600-mg loading dose of
clopidogrel on or before the time of the procedure is
currently recommended, producing an antiplatelet
action within 2 hours
With the development of the GPIIb/IIIa receptor
antagonists, significant improvements were made in
patient outcomes during and after PCI.
Abciximab, a human-murine monoclonal antibody
fragment, was the first agent available. Subsequently
epitifibatide (cyclic heptapeptide) and tirofiban
(nonpeptide mimetic) have become available.These
agents, when administered IV during PCI and for 12
to 24 hours afterward, significantly decrease the risk
of death, acute MI, or need for repeat PCI.
Major adverse effects include bleeding and
thrombocytopenia.Therefore, hematocrit and platelet
counts should be monitored appropriately. Clearance
of both eptifibatide and tirofiban is renal, and dose
adjustments should take place accordingly.
In addition to appropriate use of the antiplatelet agents
(aspirin, clopidogrel, and GPIIb/IIIa inhibitors), patients
having PCI should also receive adequate antithrombin
therapy during the procedure. Available options include
unfractionated heparin the low-molecular-weight heparin
enoxaparin, and the direct thrombin inhibitor bivalirudin.
Any of the available agents may be initiated at the time of the
procedure, or may be continued with appropriate dose
adjustment if administered to the patient before PCI.
Antithrombin agents are typically discontinued immediately
after the PCI procedure unless acompelling separate
indication exists for therapeutic anticoagulation.
2-Coronary artery bypass graft
Coronary artery bypass grafting is a complicated surgical
procedure during which an atherosclerotic vessel is bypassed
using either a patient’s saphenous vein or internal mammary
artery. The graft (i.e., the saphenous vein or IMA) then
allows blood to flow past the obstruction in the native vessel.
Certain high-risk patient subgroups clearly have an improved
outcome with CABG. These include (a) patients with
significant left main coronary disease; (b) patients who have
three vessel disease, especially with LV dysfunction; (c)
patients who are refractory to medical treatment.
In patients who do not meet these criteria, either medical
treatment or PCI is a viable option.
Pharmacological TREATMENT
-Stable Exertional Angina Pectoris
Agents used in the treatment of patients with chronic stable
angina primarily affected either determinants of myocardial
oxygen supply, myocardial oxygen demand, or both. Within
this paradigm, β-blockers, calcium-channel blockers (CCBs),
and chronic nitrate therapy have demonstrated effectiveness
in the prevention of ischemic symptoms.
The selection of specific anti-ischemic pharmacotherapy for
patients with chronic stable angina should take into account
relevant patient characteristics as well as guideline
recommendations.
The current national guidelines recommend that all patients
be given the following unless contraindications exist: (a)
aspirin (b) β-blockers (c) angiotensin-converting enzyme
inhibitor (ACEI) to patients with CAD and diabetes , LV
systolic dysfunction,CKD (d) LDL lowering therapy with
CAD and LDL >130 mg/dL (e) nitroglycerin (f) calcium
antagonists .
β-BLOCKERS
β-Blockers effectively lower myocardial oxygen demand by
lowering heart rate, myocardial contractility, and
intramyocardial wall tension. The dose of β-blocker should
be titrated to a goal resting heart rate of 55 to 60 beats
per minute and therefore will be patient specific.
β-Blockers should be avoided in patients with primary
vasospastic angina and may worsen symptoms in patients with
reactive airway disease or peripheral arterial disease.The
most common side effects observed with chronic therapy
include bradycardia, hypotension,fatigue, and sexual
dysfunction. Other conditions that may prevent the use of β-
blocker therapy include severe bradycardia or atrioventricular
(AV) nodal conduction defects.
β-Adrenoreceptor blockade is effective in chronic exertional
angina as monotherapy and in combination with nitrates
and/or calcium channel antagonists. β-Blockers should be the
first-line drug in chronic angina that requires daily
maintenance therapy
because β-blockers are more effective in reducing episodes of
silent ischemia, reducing early morning peak of ischemic
activity, and improving mortality after Q-wave MI than
nitrates or calcium channel blockers . If β-blockers are
ineffective or not
tolerated, then monotherapy with a calcium channel blocker
or combination therapy if monotherapy is ineffective may be
instituted.
NITRATES
Nitrates are available in a number of different formulations
(Ssl,Oral,IV,Spray,Patch).Regardless of the formulation,
all nitrate options are effective at preventing or relieving
ischemic symptoms if used appropriately, including the use of
a nitrate-free interval. Nitrates can increase myocardial
oxygen
supply through vasodilation of the coronary arteries, as well
as reduce myocardial oxygen demand through the reduction
of
preload. Nitrates produce vasodilation through the
biotransformation
Long-acting nitrates are effective agents for the prevention of
anginal symptoms. Sublingual NTG is a vital agent to treat
and relieve acute anginal attacks.Common side effects of
nitrate therapy include hypotension, dizziness, and headache.
Headache often will resolve with continued therapy and may
be treated with acetaminophen.
Nitrate therapy may be used to terminate an acute anginal
attack, to prevent effort or stress-induced attacks, or for long-
term prophylaxis, usually in combination with β-blockers or
calcium channel
blockers
Sublingual nitroglycerin 0.3 to 0.4 mg will relieve pain in
approximately 75% of patients within 3 minutes, with
another 15% becoming pain free in 5 to 15 minutes.
Pain persisting beyond about 20 to 30 minutes following
the use of two or three nitroglycerin tablets is suggestive
of acute coronary syndrome and the patient should be
instructed to seek emergency aid. Patients should be
instructed to keep nitroglycerin in the original, tightly
closed glass container and to avoid mixing with other
medication, because mixing may reduce nitroglycerin
adsorption and vaporization.
Nitrates may be combined with other drugs for anginal
therapy including β-adrenergic-blocking agents and calcium
channel antagonists.These combinations are usually instituted
for chronic prophylactic therapy based on complementary or
offsetting mechanisms of action . Combination therapy is
generally used in patients with more frequent symptoms or
with symptoms that are not
responding to β-blockers alone (nitrates plus β-blockers or
calcium blockers), in patients intolerant of β-blockers or
calcium channel blockers, and in patients having an element
of vasospasm leading to
decreased supply (nitrates plus calcium blockers).
CALCIUM-CHANNEL BLOCKERS
Calcium-channel blockers are highly diverse compounds. They
differ markedly in chemical structure as well as specificity for
cardiac and peripheral tissue. Using these characteristics, it is
possible to classify calcium antagonists into several major types.
Both diltiazem and verapamil exert qualitatively similar effects
on myocardial and peripheral tissue. They slow conduction and
prolong the refractory period in the AV node. Ventricular refractory
period is not affected. Therefore, the antiarrhythmic utility of these
drugs is limited to controlling the ventricular rate in supraventricular
tachyarrhythmias
Both agents can depress myocardial contractility
and should be used with caution in patients with LV dysfunction
(systolic heart failure). They are moderate peripheral
vasodilators and potent coronary artery vasodilators.
Nifedipine is the prototype compound of the dihydropyridine
derivatives. Although amlodipine, felodipine, isradipine, and
nicardipine are second-generation dihydropyridines, only
nicardipine and amlodipine currently are approved for the
treatment
of chronic stable angina pectoris. In addition, amlodipine
is indicated for vasospastic angina.
In contrast to diltiazem or verapamil, the dihydropyridines do
not slow cardiac conduction and, therefore, have no
antiarrhythmic action. They are, however, more potent
peripheral vasodilators and may be associated with a reflex
increase in the heart rate.
Both dihydropyridine (DHP) and non-dihydropyridine (non-
DHP) CCBs produce an increase in myocardial oxygen supply
through vasodilation of the coronary arteries, as well as reduce
myocardial oxygen demand through lowering of
intramyocardial wall tension (by lowering systemic blood
pressure).
However, non-DHP CCBs would be expected to lower
myocardial oxygen demand to a greater degree because of
additional reductions in heart rate and contractility. Although
defined as being within
the same pharmacologic class, it is important to consider DHPs
and non-DHPs separately when considering their use in
patients with chronic stable angina.
The reductions in heart rate and contractility
with non-DHPs may be beneficial for some patients,
although detrimental in others such as patients with
compromised LV function or bradycardia at baseline
Conversely, DHP options such as amlodipine and felodipine
have been shown to be safe to use in patients with LV
dysfunction and to provide a reasonable option for the
prevention of ischemic symptoms in those patients. Side effects
of CCB therapy depend on the specific agent used. Use of non-
DHP CCBs may result in bradycardia, hypotension, and atria-
ventricular block. Patients receiving DHP CCBs may
experience reflex tachycardia, peripheral edema, headache, and
hypotension.
Good candidates for calcium channel blockers in angina include
patients with contraindications or intolerance of β-blockers,
coexisting conduction system disease (except for verapamil and
diltiazem), patients with Prinzmetal angina (vasospastic or
variable threshold angina), the presence of peripheral vascular
disease,
severe ventricular dysfunction (amlodipine is probably the
calcium channel blocker of choice and others need to be used
with caution if the ejection fraction is <40%), and concurrent
hypertension..
Ranolazine
Ranolazine is a new drug for angina that has a unique
mechanism of action which is unlike that of any other drug used
to alter the relationship between oxygen supply and demand.
Ranolazine reduces calcium overload in the ischemic myocyte
through inhibition of the late sodium current (INa). Myocardial
ischemia produces a cascade of 45complex ionic exchanges that
can result in intracellular acidosis, excess cytosolic Ca2+,
myocardial cellular dysfunction, and, if sustained, cell injury
and death. Activation of the adenosine triphosphate-dependent
K+ current during ischemia results in a strong efflux of K+ ions
from myocytes. Sodium channels are activated on
depolarization, leading to a rapid influx of sodium into the cells.
The inactivation of INa has a fast component that lasts a few
milliseconds and a slowly inactivating component that can last
hundreds of milliseconds.
Ranolazine is a relatively selective inhibitor for late INa. In
isolated ventricular myocytes in which the late INa was
pathologically augmented, ranolazine prevented or reversed the
induced mechanical dysfunction, as well as ameliorated
abnormalities of ventricular repolarization.
Ranolazine does not affect heart rate, inotropic state, or
hemodynamic state or increase coronary blood flow.
Ranolazine is extensively metabolized via CYP450 3A and
potent inhibitors of 3A increase the plasma concentration by a
factor of about three. Ketoconazole, Erythromycin, diltiazem
and verapamil should not be co-administered with ranolazine.
Ranolazine is indicated for the treatment of chronic angina and
because it prolongs the QT interval, it should be reserved for
patients who have not achieved an adequate response with
other antianginal agents. Contraindications include preexisting
QT interval prolongation, hepatic impairment,and
concurrent QT interval-prolonging drugs. In controlled trials,
the most common adverse reactions are dizziness, headache,
constipation and nausea. Ranolazine should be started at 500
mg twice daily and increased to 1,000 mg twice daily as needed
based on symptoms.
ANTIPLATELET THERAPY
Antiplatelet therapy has occupied a central place in the treatment
of patients with CAD for many years. Aspirin (ASA) therapy has
been demonstrated to reduce the incidence of MI and sudden
cardiac death in patients with chronic stable angina. Aspirin’s
clinical efficacy in chronic stable angina, coupled with its minimal
cost and demonstrated efficacy after MI, have made it the
gold standard for antiplatelet monotherapy in patients withCAD.
Current national guidelines from the American College of Cardiology
(ACC)/AHA recommend an ASA dose of 75 to 162 mg
daily for the prevention of MI and death in patients with CAD.
Clopidogrel represents a suitable alternative antiplatelet
agent to prevent MI and death in chronic stable angina
patients unable to take ASA. clopidogrel should be
administered at a dosage of 75 mg/day. Given the different
mechanisms of antiplatelet effect, combining aspirin with
clopidogrel would be expected to provide additional
protection from MI and death in patients with CAD as
compared to monotherapy. But, dual antiplatelet therapy in
patients with CAD is currently limited to those who have had
a recent ACS or recent percutaneous coronary intervention
(PCI) plus stent placement.
-Variant Angina Pectoris (Prinzmetal
Angina)
Prinzmetal, in his original description of variant angina
pectoris, noted the waxing and waning course of this
syndrome associated with ST-segment elevation and that it
most commonly resolves without progression to MI. Patients
who develop variant angina are usually younger, have fewer
coronary risk factors but more commonly smoke than
patients with chronic stable angina.
The exact cause of variant angina is not well
understood, but may be an imbalance between
endothelium-produced vasodilator factors
(prostacyclin, nitric oxide) and vasoconstrictor
factors (e.g., endothelin, angiotensin II) as well as an
imbalance of autonomic control characterized by
parasympathetic dominance or inflammation may
also play a role.More recently there have been a
number potential common adrenoreceptor
polymorphisms that may predispose patients to
developing vasospasm.
All patients should be treated for acute attacks and
maintained on prophylactic treatment for 6 to 12
months following the initial episode. Nitrates have
been the mainstay of therapy for the acute attacks of
variant angina and coronary artery spasm for many
years. Most patients respond rapidly to sublingual
nitroglycerin or isosorbide dinitrate; however,
intravenous and intracoronary nitroglycerin may be
very useful for patients who do not respond to
sublingual preparations. Because calcium antagonists
may be more effective, have few serious adverse
effects in effective doses, and can be given less
EVALUATION OF THERAPEUTIC OUTCOMES
Improved symptoms of angina, improved cardiac
performance and improvement in risk factors may all be
used to assess the outcome of treatment of IHD and
angina. Symptomatic improvement in exercise capacity
(longer duration) or fewer symptoms at the same level of
exercise is subjective evidence that therapy is working.
Once patients have been optimized on medical therapy,
symptoms should improve over 2 to 4 weeks and remain
stable until their disease progresses. Coronary angiography
may be used to assess the extent of stenosis or re-stenosis
after angioplasty or CABG.
THANKS
