Ischemic Heart Disease

1
 Definition

• A lack of oxygen and decreased or no blood

flow to the myocardium.

• Resulting from coronary artery narrowing or

obstruction.

2
 IHD may present as ….
• Acute coronary syndrome (ACS):
- Unstable angina
- Non–ST-segment elevation MI
- ST-segment elevation MI

• Chronic stable exertional angina.

• Ischemia without symptoms

• Coronary artery vasospasm (variant or Prinzmetal

angina).
3
 Pathophysiology

• The consequences of IHD usually result from

- increased demand in the face of a fixed

decrease in oxygen supply

4
 Pathophysiology
• The major determinants of myocardial oxygen demand
or consumption (MVO2) are
- Heart rate
- Contractility
- Intramyocardial wall tension during systole.
(most important)

• Indirect estimate of MVO2 is

- the double product (DP)
- (DP = HR × SBP).

• Alterations in MVO2 are important in producing

ischemia and for interventions intended to alleviate it.
5
 Pathophysiology
• The normal coronary system consists of large epicardial
or surface vessels (R1) and intramyocardial arteries and
arterioles (R2).

• Atherosclerotic lesions occluding R1 can lead R2 to

vasodilate to maintain coronary blood flow.

• With greater degrees of obstruction, R2 vasodilation is

insufficient to meet oxygen demand.

• Relatively severe stenosis (greater than 70%) may

provoke ischemia and symptoms at rest, whereas less
severe stenosis may allow a reserve of coronary blood
flow for exertion.
6
 Pathophysiology

• The diameter and length of obstructing lesions

and the influence of pressure drop across an
area of stenosis also affect coronary blood
flow and function of the collateral circulation.

7
 Clinical Presentation

• Many episodes of ischemia do not cause

symptoms of angina
(silent ischemia)

--- may be due to a higher threshold and

tolerance for pain.

8
 Clinical Presentation

• Patients often have a reproducible

- pattern of chest pain or other symptoms
- that appear after a specific amount of
exertion.

• Increased symptom frequency, severity, or

duration, and symptoms at rest
- suggest an unstable pattern that requires
immediate medical evaluation.
9
 Clinical Presentation
Symptoms may include:
• Sensation of pressure, heaviness, crushing, or
burning over the sternum or near it.

• This pain (substernal) often radiates to the left jaw,

shoulder, and arm.

• Chest tightness and shortness of breath may also

occur.

• The sensation usually lasts from 30 seconds to 30

minutes (from 5 to 20 minutes)
10
 Clinical Presentation
Precipitating factors include
• Exercise
• Cold environment
• Walking after a meal
• Emotional upset.
• Fright.
• Anger
• Sexual intercourse.

Relief occurs with rest and within 45 seconds to 5

minutes of taking nitroglycerin. 11
 Clinical Presentation
• Patients with variant or Prinzmetal angina
secondary to coronary spasm are more likely to
experience pain at rest and often the early
morning hours.

• Pain is not usually brought on by exertion or

emotional stress nor is it relieved by rest.

• ECG pattern is that of current injury with ST-

segment elevation rather than depression.

12
 Clinical Presentation
• Unstable angina is stratified into categories of low,
intermediate, or high risk for short-term death or
nonfatal MI.

• Common features of high-risk unstable angina include:

(1) Accelerating tempo of ischemic symptoms in the
preceding 48 hours.
(2) Pain at rest lasting more than 20 minutes
(3) Age greater than 75 years
(4) ST-segment changes
(5) Clinical findings of pulmonary edema, mitral
regurgitation, S3, hypotension, bradycardia, or
tachycardia. 13
 Diagnosis
Clinical history include

• The nature or quality of the chest pain

• Precipitating factors
• Duration
• Pain radiation
• The response to nitroglycerin or rest.

Ischemic chest pain may resemble pain arising from

a variety of noncardiac sources, and the
differential diagnosis of anginal pain from other
etiologies may be difficult based on history alone.
14
 Diagnosis
• The patient should be asked about existing personal risk
factors for coronary heart disease (CHD) including:
- Smoking, HTN, DM, dyslipidemia.

• Assess nonmodifiable risk factors:

- age, sex.

• Family history should be obtained that includes

- family history of atherosclerotic disease in first-
degree relatives
- Hypertension
- Familial lipid disorders
- DM
• Elevated HR or blood pressure can yield an increased DP
and may be associated with angina. 15
 Diagnosis
Recommended laboratory tests include:
• Hemoglobin (to ensure adequate oxygen-carrying
capacity),
• Fasting glucose (to exclude diabetes)
• Fasting lipoprotein panel
• Important risk factors in some patients may include
C-reactive protein; homocysteine level; evidence of
Chlamydia infection; elevations in lipoprotein (a),
fibrinogen, and plasminogen activator inhibitor.
• Cardiac enzymes should all be normal in stable angina.
• Troponin T or I, myoglobin, and creatinine kinase MB
may be elevated in unstable angina.
16
 Diagnosis
• The resting ECG is normal in about one-half of patients
with angina who are not experiencing an acute attack

• Typical ST or T-wave changes include

- S-T depression
- T-wave inversion
- S-T-segment elevation.

• Variant angina is associated with ST-segment elevation.

• Silent ischemia may produce elevation or depression.

17
 Diagnosis
• Exercise tolerance (stress) testing (ETT) is
recommended for patients with an
intermediate probability of CAD.

• Radionuclide angiocardiography is used to

measure ejection fraction (EF), regional
ventricular performance, cardiac output,
ventricular volumes, valvular regurgitation,
asynchrony or wall motion abnormalities, and
intracardiac shunts.
18
 Diagnosis

• Ultrarapid computed tomography.

• Coronary angiography (Cardiac

catheterization) may be performed in certain
circumstances… (is the most accurate test).

• Chest radiograph if the patient has HF

symptoms.
19
 Diagnosis

• Echocardiography is useful if the history or

physical findings suggest valvular pericardial
disease or ventricular dysfunction.

• In patients unable to exercise, pharmacologic

stress echocardiography (e.g., dobutamine,
dipyridamole, or adenosine) may identify
abnormalities that would occur during stress.

20
 Desired Outcome

• The short-term goals

- to reduce or prevent anginal symptoms that
limit exercise capability and impair quality of life.

• Longterm goals
- to prevent CHD events such as MI,
arrhythmias, and heart failure and to extend the
patient’s life.
21
 Treatment –
Nonpharmacologic Therapy
Risk-factor Modification

• Primary prevention: modification of risk factors

significantly reduce the prevalence of IHD.

• Secondary intervention : effective in reducing

subsequent morbidity and mortality.

22
 Treatment –
Risk-factor modification
Risk factors for IHD can be classified as:

• Non-modifiable (Unalterable): gender, age, family

history or genetic composition, environmental
influences, and, to some extent, diabetes mellitus.

• Modifiable (Alterable): smoking, hypertension,

hyperlipidemia, obesity, sedentary lifestyle,
hyperuricemia, psychosocial factors such as stress, and
the use of drugs (e.g., progestins, corticosteroids, and
calcineurin inhibitors “cyclosporine”).
23
 Treatment –
Nonpharmacologic Therapy

• Surgical revascularization options for select patients

include

coronary artery bypass grafting (CABG)

or
percutaneous coronary intervention (PCI) with or
without stent placement.

24
 β-Adrenergic Blocking Agents

• Decreased HR, contractility, and blood pressure

reduce MVO2 and oxygen demand in patients
with effort-induced angina.

• β-Blockers do not improve oxygen supply.

• In certain instances, unopposed α-adrenergic

stimulation may lead to coronary
vasoconstriction.
25
 β-Adrenergic Blocking Agents
• Improve symptoms in approximately 80% of patients
with chronic exertional stable angina

• Improve exercise duration and delay in the time at

which ST-segment changes and initial or limiting
symptoms occur.

• β-Blockade may allow angina patients previously

limited by symptoms to perform more exercise and
improve cardiovascular performance through a
training effect.
26
 β-Adrenergic Blocking Agents
 Ideal candidates for β-blockers include:
• Patients in whom physical activity is a prominent cause
of attacks.

• Patients with coexisting hypertension, supraventricular

arrhythmias, or postmyocardial infarction.

• Patients with anxiety associated with anginal episodes

 β-Blockers may be used safely in angina and heart

failure. 27
 β-Adrenergic Blocking Agents

Compared to CCB or Nitrates

• β-Blockers are first line in chronic angina requiring daily

maintenance therapy.

• β-Blockers are more effective

in reducing episodes of
- silent ischemia
- early-morning peak of ischemic activity

improving mortality after Q-wave MI.

28
 β-Adrenergic Blocking Agents

- For chronic exertional angina:

• β-Blockade is effective as monotherapy.

• Or in combination with nitrates and/or CCB.

• Reflex tachycardia from nitrates can be blunted with

β-blocker therapy, making this a useful combination.
29
 β-Adrenergic Blocking Agents

• Initial doses of β-blockers should be at the lower

end of the usual dosing range and titrated to
response.

30
 β-Adrenergic Blocking Agents

• Treatment objectives include

- lowering the resting HR to 50 to 60 beats/min

- limiting maximal exercise HR to about 100

beats/min or less.

- HR with modest exercise should be no more

than approximately 20 beats/min above resting HR
31
 β-Adrenergic Blocking Agents
Which β-blocker
• Longer half-lives
• Intrinsic sympathomimetic activity appears to be
detrimental in patients with rest or severe angina because
the reduction in HR would be minimized, therefore limiting
a reduction in MVO2.
• Cardioselective β-blockers may be used in some patients to
minimize adverse effects such as bronchospasm,
intermittent claudication, and sexual dysfunction.
• Combined nonselective α, β blocker (labetalol) may be
useful in some patients with marginal left ventricular (LV)
reserve.
32
 β-Adrenergic Blocking Agents
Adverse effects

• Hypotension
• Heart failure
• Bradycardia
• Heart block
• Bronchospasm
• Altered glucose metabolism
• Fatigue
• Malaise
• Depression

33
 β-Adrenergic Blocking Agents

• Abrupt withdrawal in patients with angina

- has been associated with increased severity
and number of pain episodes and MI.

• Tapering of therapy over several days should

minimize the risk of withdrawal reactions if
therapy is to be discontinued.

34
 Nitrates
 The action of nitrates is mediated:

• Indirectly through reduction of MVO2 secondary

to venodilation and arterial-arteriolar dilation,
leading to a reduction in wall stress from reduced
ventricular volume and pressure.

• Direct actions on the coronary circulation include

dilation of large and small intramural coronary
arteries, collateral dilation, coronary artery
stenosis dilation, and relief of spasm.
35
 Nitrates
 Pharmacokinetic characteristics

• Large first-pass metabolism.

• Short to very short half-lives (except for isosorbide

mononitrate “ISMN”)

• Large volumes of distribution

• High clearance rates.

• Interindividual variations in plasma concentrations.

36
 Nitrates
 Pharmacokinetic characteristics

• The half-life of nitroglycerin is 1 to 5 minutes regardless

of the route. ---- (the potential advantage of SR and
transdermal products).

• ISMN has a half-life of about 5 hours and may be given

once or twice daily, depending on the product chosen

• Isosorbide dinitrate (ISDN) is metabolized to ISMN.

37
 Nitrates

• Used to terminate an acute anginal attack.

• Sublingual, buccal, or spray nitroglycerin

products
- are preferred for alleviation of anginal
attacks
- because of rapid absorption.

38
 Nitrates
• Used to prevent effort- or stress-induced attacks

• Symptoms may be prevented by prophylactic oral or

chewable or transdermal products.

• For long-term prophylaxis, Nitrates usually are used

in combination with β-blockers or CCB.

• The development of tolerance may be problematic.

39
 Nitrates
 Sublingual nitroglycerin

• 0.3 to 0.4 mg can relief pain in about

- 75% of patients within 3 minutes
- with another 15% becoming pain-free in 5 to 15
minutes.

• Pain persisting beyond 20 to 30 minutes after use of

two to three nitroglycerin tablets suggests ACS
- and the patient should be instructed to seek
emergency aid.
40
 Nitrates
 Adverse effects

• Postural hypotension ---- Excessive hypotension may

result in MI or stroke.
• Reflex tachycardia
• Headache (treated with acetaminophen)
• Flushing
• Occasional nausea.
• Rash (especially with transdermal nitroglycerin)
• Methemoglobinemia with high doses given for
extended periods.
42
 Nitrates
 Adverse effects

• Tolerance

- Both the onset and offset of tolerance to nitrates

occur quickly.

- One strategy to circumvent it is to provide a daily

nitrate-free interval of 8 to 12 hours.

43
 Nitrates
 Adverse effects

• Tolerance

- For example, ISDN should not be used more often than three
times a day to avoid tolerance.

- Intermittent (10 to 12 hours on, 12 to 14 hours off)

transdermal nitroglycerin therapy may produce modest but
significant improvement in exercise time in chronic stable
angina.

44
 Nitrates
• Nitrates may be combined with other drugs with
complementary mechanisms of action for chronic
prophylactic therapy.

 Combination therapy is generally used in:

• Patients with more frequent symptoms

• Patients with symptoms that do not respond to β- blockers

alone or CCB alone ==== (nitrates plus β- blockers or CCB)

• Patients intolerant of β-blockers or CCB.

• Patients having an element of vasospasm leading to

decreased supply ===== nitrates plus CCB. 45
Nitrates

46
 Calcium channel blockers (CCB)
 Dihydropyridine (nifedipine)

• Direct actions include vasodilation of systemic

arterioles and coronary arteries

• leading to a reduction of arterial pressure and

coronary vascular resistance.

• Have a potential to improve coronary blood flow by

inhibiting coronary artery vasomotion and
vasospasm. 47
 Calcium channel blockers (CCB)
Non-dihydropyridine (Verapamil and diltiazem)

• Depression of myocardial contractility and the

conduction velocity of the SA and AV nodes.

• They must be used with caution in patients with

preexisting conduction abnormalities or in
patients taking other drugs with negative
chronotropic properties.
48
 Calcium channel blockers (CCB)

• MVO2 is reduced with all CCB primarily because of

reduced wall tension secondary to reduced arterial
pressure.

49
 Calcium channel blockers (CCB)

• Overall, the benefit provided by CCB is related to

reduced MVO2 rather than improved oxygen
supply.

• In contrast to β-blockers

- CCBs may improve coronary blood flow

through areas of fixed coronary obstruction
- by inhibiting coronary artery vasomotion and
vasospasm.
50
 Calcium channel blockers (CCB)
 Good candidates for CCB include:

• Patients with contraindications or intolerance to β-blockers

• Coexisting conduction system disease (excluding the use of
verapamil and possibly diltiazem).
• Prinzmetal angina
• Peripheral vascular disease
• Concurrent hypertension
• Severe ventricular dysfunction.
- Amlodipine is probably the agent of choice in severe
ventricular dysfunction, and the other dihydropyridines
should be used with caution if the EF is less than 40%. 51
 Ranolazine

• Its mechanism may be related to reduction in

calcium overload in ischemic myocytes through
inhibition of the late sodium current.

• Ranolazine, a partial fatty acid oxidation inhibitor,

shifts ATP production from fatty acid to more
oxygen-efficient carbohydrate oxidation.

• Its antianginal effects do not depend on

reductions in HR or blood pressure
52
 Ranolazine
• Ranolazine is indicated for the treatment of
chronic angina.

• Can improve the exercise

• But they did not improve the primary efficacy

composite end point of cardiovascular death,
MI, or recurrent ischemia.

53
 Ranolazine
• It prolongs the QT interval ===
- it should be reserved for patients who have not
achieved an adequate response to other antianginal drugs.
- Baseline and follow up ECGs should be obtained to
evaluate effects on the QT interval.

• It should be used in combination with amlodipine, β-

blockers, or nitrates.

• Adverse effects are dizziness, headache, constipation, and

nausea.

• Metabolized by CYP3A4
54
 Treatment of stable exertional angina
pectoris

• The evidence-based drug therapy

recommendations of the American College of
Cardiology Foundation and American Heart
Association.

55
Treatment of stable exertional angina pectoris

• Guideline-directed medical therapy (GDMT) places a

strong emphasis on patient education.

• Lifestyle modifications include

- Daily physical activity
- Weight management
- Dietary therapy
- Smoking cessation
- Psychological interventions
- Limitation of alcohol intake
- Management of blood pressure and diabetes.
56
 Treatment of stable exertional angina pectoris

Risk Factor Modification

• Dyslipidemia: Moderate- or high-dose statin therapy in the

absence of contraindications or adverse effects, in addition
to lifestyle changes ====== Class I, level A

• For patients who do not tolerate statins, a bile acid

sequestrant, niacin, or both is reasonable ===== Class IIa,
level B

• Blood pressure: If blood pressure is 140/90 mm Hg or

higher, drug therapy should be instituted in addition to or
after lifestyle modifications ===== Class I, level A
• DM: For patients with DM, pharmacotherapy to achieve a
target A1C might be reasonable ===== Class IIb, level A 57
 Treatment of stable exertional angina pectoris
Medical Therapy to Prevent MI and Death
All patients should be given the following unless
contraindications exist:
• Aspirin (75-162 mg/day) continued indefinitely=== Class I,
Level A
• β-Blocker therapy started and continued for 3 years in
patients with normal LV function after MI or ACS === Class I,
Level B
• β-Blocker (carvedilol, metoprolol succinate, or bisoprolol) in
patients with LV systolic dysfunction (LVEF ≤40%) with HF or
MI, unless contraindicated ==== Class I, Level A
• ACE inhibitor in patients with HTN, DM, LVEF ≤40%, or CKD,
unless contraindicated. ARBs are recommended if intolerant
of ACE inhibitors ==== Class I, Level A
58
Treatment of stable exertional angina pectoris
Medical Therapy to Prevent MI and Death

All patients should be given the following unless

contraindications exist:

• Clopidogrel may be substituted for aspirin

when aspirin is absolutely contraindicated ===
Class I, Level B

59
 Treatment of stable exertional angina pectoris
Medical Therapy for Relief of Symptoms

• Sublingual nitroglycerin or nitroglycerin spray for

immediate relief of angina ==== Class I, level B

• β-Blockers as initial therapy for relief of symptoms ====

Class I, level B

• CCBs or long-acting nitrates for relief of symptoms

when β-blockers are contraindicated or cause
unacceptable side effects ==== Class I, level B

• CCBs or long-acting nitrates, in combination with β-

blockers, when initial treatment with β-blockers is
unsuccessful ==== Class I, level B 60
 Treatment of stable exertional angina pectoris
Medical Therapy for Relief of Symptoms

• Long-acting nondihydropyridine calcium antagonists

(verapamil, diltiazem) instead of a β-blocker as initial
therapy ==== Class IIa, level B

• Ranolazine can be useful as a substitute for β-blockers if

initial treatment with β-blockers causes unacceptable
adverse effects or is ineffective or contraindicated ====
Class IIa, level B

• Ranolazine combined with a β-blocker can be useful

when initial β-blocker treatment is unsuccessful ====
Class IIa, level B
61
 Treatment of stable exertional angina
pectoris
Therapies to be avoided include:

• Dipyridamole === Class III, Level B

Relatively weak antiplatelet agent on its own, and
chest pain may be aggravated in patients with
underlying CAD who are receiving dipyridamole.

• Low-intensity anticoagulation with warfarin, in

addition to aspirin, is recommended but bleeding
would be increased === Class IIb, Level B
62
 Treatment of stable exertional angina
pectoris
American College of Cardiology and American Heart Association
Evidence Grading System.

Recommendation Class:
• I = Conditions for which there is evidence or general agreement that
a given procedure or treatment is useful and effective.
• II = Conditions for which there is conflicting evidence or a divergence
of opinion about the usefulness/efficacy of a given procedure or
treatment.
• IIa = Weight of evidence/opinion is in favor of usefulness or efficacy.
• IIb = Usefulness/efficacy is less well established by
evidence/opinion.
• III = Conditions for which there is evidence or general agreement
that a given procedure or treatment is not useful/effective and in
some cases may be harmful. 63
 Treatment of stable exertional angina
pectoris
American College of Cardiology and American Heart Association
Evidence Grading System.

Level of Evidence:

• A = Data derived from multiple randomized clinical trials with large

numbers of patients.

• B = Data derived from a limited number of randomized trials with

small numbers of patients, careful analyses of nonrandomized
studies, or observational registries.

• C = Expert consensus was the primary basis for the

recommendation.
64
 Treatment of stable exertional angina
pectoris
When angina occurs more frequently than once a day
• Chronic prophylactic therapy should be instituted.

• β-Blockers may be preferable because of less frequent

dosing and other desirable properties (e.g., potential
cardioprotective effects, antiarrhythmic effects, lack of
tolerance, antihypertensive efficacy).

• The appropriate dose should be determined by the goals

outlined for HR and DP.

• An agent should be selected that is well tolerated by

individual patients at a reasonable cost.
65
 Treatment of stable exertional angina
pectoris
When angina occurs more frequently than once a day

• Patients most likely to respond well to β-blockers are those

with
- a high resting HR
- a relatively fixed anginal threshold (i.e., their
symptoms appear at the same level of exercise or
workload on a consistent basis).

66
 Treatment of stable exertional angina
pectoris

• Nitrate therapy should be the first step in managing acute

attacks of chronic stable angina if the episodes are
infrequent (e.g., a few times per month).

67
 Treatment of stable exertional angina
pectoris
For prophylaxis when undertaking activities that
predictably precipitate attacks.

• Nitroglycerin 0.3 to 0.4 mg sublingually may be used

about 5 minutes prior to the time of the activity.

• Nitroglycerin spray may be useful when inadequate

saliva is produced to rapidly dissolve sublingual
nitroglycerin or if a patient has difficulty opening the
tablet container.
• The response usually lasts about 30 minutes.
68
 Treatment of stable exertional angina
pectoris
• CCB are as effective as β-blockers and are most useful in
patients who have a variable threshold for exertional
angina.

• CCB may provide better skeletal muscle oxygenation,

resulting in decreased fatigue and better exercise tolerance
== specially “dihydropyridine”.

• Patients with conduction abnormalities and moderate to

severe LV dysfunction (EF <35%) should not be treated with
verapamil or diltiazem
- whereas amlodipine may be used safely in many of
these patients.
69
 Treatment of stable exertional angina
pectoris

• Verapamil and Diltiazem have significant effects on the

AV node and can produce heart block in patients with
preexisting conduction disease or when other drugs
with effects on conduction (e.g., digoxin, β-blockers) are
used concurrently.

• Nifedipine may cause excessive HR elevation, especially

if the patient is not receiving a β-blocker, and this may
offset its beneficial effect on MVO2.

70
 Treatment of stable exertional angina
pectoris
• Chronic prophylactic therapy with long-acting forms of
nitroglycerin (oral or transdermal), ISDN, ISMN, and
pentaerythritol trinitrate may also be effective.
• But development of tolerance is a limitation == 8h free
• Monotherapy with nitrates should not be first-line
therapy unless β-blockers and calcium channel
antagonists are contraindicated or not tolerated.
• The choice among nitrate products should be based on
experience, cost, and patient acceptance.
71
 Treatment of stable exertional angina
pectoris
• Aspirin 75 to 162 mg daily should be continued
indefinitely in the absence of contraindications.

• Clopidogrel 75 mg daily is an alternative for patients

unable to take aspirin due to allergy or intolerance.

• The combination of aspirin (75–162 mg daily) and

clopidogrel 75 mg daily may be reasonable in certain
high-risk patients.

• Dipyridamole therapy is not recommended.

72
 Treatment of stable exertional angina
pectoris
Conditions that exacerbate or provoke angina
• Medications:
- Vasodilators - Excessive thyroid replacement
-Vasoconstrictors

• Other medical problems:

-Profound anemia -Uncontrolled hypertension
-Hyperthyroidism - Hypoxemia

• Other cardiac problems:

- Tachyarrhythmias - Bradyarrhythmias
- Valvular heart disease - Hypertrophic
cardiomyopathy
73
74
75
 Treatment of coronary artery spasm

• All patients should be treated for acute attacks

and maintained on prophylactic treatment for
6 to 12 months after the initial episode.

• Aggravating factors such as

- alcohol or cocaine use and cigarette
smoking
should be stopped.
76
 Treatment of coronary artery spasm

Acute attack

• Nitrates are the mainstay of therapy, and most

patients respond rapidly to sublingual
nitroglycerin or ISDN.

• IV and intracoronary nitroglycerin may be

useful for patients not responding to
sublingual preparations.
77
 Treatment of coronary artery spasm
Chronic treatment

• CCB may be more effective, have few serious adverse

effects, and can be given less frequently than nitrates.

• Some authorities consider CCB the agents of choice for

variant angina.

• Nifedipine, verapamil, and diltiazem are all equally effective

as single agents for initial management.

• Combination therapy with nifedipine plus diltiazem or

nifedipine plus verapamil is reported to be useful in
patients unresponsive to single-drug regimens.
78
 Treatment of coronary artery spasm

• Patients unresponsive to CCB alone may have nitrates

added.

• β-Blockers have little or no role in the management of

variant angina as they may induce coronary
vasoconstriction and prolong ischemia (unopposed
alpha receptors).

79
 Evaluation of outcome
For Exercise induced angina

• Subjective measures of drug response include

- the number of painful episodes

- amount of rapid-acting nitroglycerin consumed

- patient reported alterations in activities of daily

living (e.g., time to walk two blocks, number of stairs
climbed without pain).

80
 Evaluation of outcome
For Exercise induced angina

• Objective clinical measures of response include

- HR

- blood pressure

- the DP as a measure of MVO2

- resolution of ECG changes at rest, during exercise,

or with ambulatory ECG monitoring (especially if there
is ST-segment deviation).
81
 Evaluation of outcome
For Exercise induced angina

• Once patients have been optimized on medical therapy

- symptoms should improve over 2 to 4 weeks

and remain stable until the disease progresses.

82
 Evaluation of outcome
• Monitoring for major adverse effects:
- headache and dizziness with nitrates
- fatigue and lassitude with β-blockers
- and peripheral edema, constipation, and dizziness
with CCB.

• ETT

• Blood monitoring of lipid profiles, fasting plasma

glucose, thyroid function tests, hemoglobin/hematocrit,
and electrolytes.
83
 Evaluation of outcome
For variant angina

Reduction in symptoms and nitroglycerin consumption

as documented by a patient diary can assist the
interpretation of objective data obtained from
ambulatory ECG recordings (ST-segment depression and
elevation)

• Additional evidence is a reduced number of attacks of

angina requiring hospitalization, and the absence of MI
and sudden death
84