REVIEW

Medical Therapy Versus Myocardial Revascularization in

Chronic Coronary Syndrome and Stable Angina
Prakash C. Deedwania, MD, Enrique V. Carbajal, MD
Division of Cardiology, Department of Medicine, Veterans Affairs Central California Health Care System, University of California, San
Francisco, School of Medicine, Fresno.

ABSTRACT

Coronary artery disease is a leading cause of death in the United States. Angina is encountered frequently
in clinical practice. Effective management of patients with coronary artery disease and stable angina should
consist of therapy aimed at symptom control and reduction of adverse clinical outcomes. Therapeutic
options for angina include antianginal drugs: nitrates, beta-blockers, calcium channel blockers, ranolazine,
and myocardial revascularization. Recent trials have shown that although revascularization is slightly
better in controlling symptoms, optimal medical therapy that includes aggressive risk factor modification
is equally effective in reducing the risk of future coronary events and death. On the basis of the available
data, it seems appropriate to prescribe optimal medical therapy in most patients with coronary artery
disease and stable angina, and reserve myocardial revascularization for selected patients with disabling
symptoms despite optimal medical therapy.
Published by Elsevier Inc. • The American Journal of Medicine (2011) 124, 681-688

KEYWORDS: Coronary artery disease; Medical therapy; Revascularization; Stable angina

Coronary artery disease remains the leading cause of death in
the United States and other developed countries.1,2 Stable an-
gina pectoris (angina) is the initial clinical manifestation of
coronary artery disease in a minority of patients. However,
many survivors of an acute myocardial infarction frequently
experience anginal symptoms.3 There are approximately 30
cases of angina for every hospitalized patient with myocardial
infarction.1 More than 10 million Americans have stable an-
gina. Angina can be disabling and frightening, and is associ-
ated with increased morbidity and mortality. Effective man-
agement of angina should lead to symptom control and
reduced risk of myocardial infarction and death.
Angina occurs as the result of an imbalance between
myocardial perfusion and oxygen demand. In most patients,
Funding: None.
Conflict of Interest: Dr Deedwania is a consultant/speaker for No-
vartis, Gilead, Servier, and Pfizer. Dr Carbajal has no conflicts of interest
associated with the work presented in this manuscript.
Authorship: Both authors had access to the data and played a role in
writing this manuscript.
Requests for reprints should be addressed to Prakash C. Deedwania,
MD, Professor of Medicine, UCSF, Chief, Cardiology Division, Veterans
Affairs Central California Health Care System, E224, 2615 E. Clinton Ave,
Fresno, CA 93703.
E-mail address: deed@fresno.ucsf.edu
myocardial ischemia occurs as the result of a flow-limiting
coronary atherosclerotic stenotic lesion. It is important to
recognize that whereas the high-grade stenotic lesions are
responsible for the impaired coronary blood flow, it is the
less stenotic (⬍50% stenosis) so-called vulnerable plaques
that seem to be responsible for most cases of acute coronary
syndrome. Therefore, the treatment of patients with stable
angina should aim not only at relief of symptoms but also at
stabilization of the vulnerable plaque to reduce risk of
coronary events.
There are multiple medical and revascularization mo-
dalities, including percutaneous coronary intervention
and coronary artery bypass grafting, available for treat-
ment of angina. However, current therapies are not uni-
versally effective in controlling symptoms, and most do
not reduce cardiovascular events (Table 1). Most patients
continue to experience anginal symptoms despite optimal
revascularization, and many require antianginal drugs.1,3
Persistence of symptoms is associated with impaired
quality of life.4 This review will discuss the role of
optimal medical therapy and myocardial revasculariza-
tion with percutaneous coronary intervention or coronary
artery bypass grafting in patients with coronary artery
disease and stable angina.

0002-9343/$ -see front matter Published by Elsevier Inc.

doi:10.1016/j.amjmed.2011.02.036
682 The American Journal of Medicine, Vol 124, No 8, August 2011

Current Therapeutic Approaches for Stable effective therapy for relief of anginal episodes. Often, long-
Angina acting nitrates are prescribed as prophylactic antianginal
The available therapeutic modalities for treatment of pa- drugs and are effective in nitrate responders. Because of
tients with angina include antianginal drugs and myocardial nitrate tolerance during long-term therapy, eccentric dosing
revascularization. Although until recently the antianginal providing a minimum of 10 to 12 hours nitrate-free interval
therapy primarily consisted of ni- is recommended.1,5,6 Nitrate ther-
trates, beta-blockers, and calcium apy has not been evaluated in cor-
channel blockers, newer drugs (ra- onary artery disease and stable an-
CLINICAL SIGNIFICANCE
nolazine, ivabradine) with unique gina regarding its impact on
mechanisms have now become ● Angina is a prevalent and challenging cardiovascular outcomes.
available. Despite the efficacy of condition for clinicians to manage.
antianginal drugs, many patients Beta-blockers
● Optimal medical therapy is equally ef-
are referred for revascularization, Beta-blockers are recommended
mainly because of a misguided be-
fective in reducing the risk of coronary as first-line therapy in coronary ar-
lief and bias that these procedures events and death. tery disease and stable angina.
reduce the risk of myocardial in- ● On the basis of the available data, it Treatment with beta-blockers has
farction or death. seems appropriate to prescribe optimal been associated with improved ex-
medical therapy in most patients with ercise tolerance and reduced fre-
Antianginal Drug Therapy quency and severity of an-
coronary artery disease and stable angina,
Nitrates, beta-blockers, and calcium gina.1,2,5,6,8 Beta-blockers work
and reserve myocardial revascularization by reducing myocardial oxygen
channel blockers (Table 2) tradi- for selected patients with disabling symp-
tionally have been used for angina demand by decreasing ventricular
1,2,5-10 toms despite optimal medical therapy. inotropy, heart rate, and maximal
relief. Although these drugs
are effective antianginal agents, velocity of myocardial fiber short-
data are lacking on the effect of ening. Beta-blockers reduce risk
such therapies on clinical outcomes, including myocardial in- of death (sudden and non-sudden) and myocardial infarc-
farction and death in patients with coronary artery disease and tion, primarily in survivors of myocardial infarction. How-
stable angina.1,5,6 Table 3 shows some of the important side ever, whether a similar benefit would occur in patients with
effects and limitations of antianginal agents in the treatment of angina without prior myocardial infarction is not known.
stable angina. No prospective randomized clinical trial has evaluated
the therapy with beta-blocker on clinical outcomes in stable
angina; limited data from the Atenolol Silent Ischemia
Nitrates
Study showed atenolol to be associated with a lower risk
Nitrates work primarily by venodilatation resulting in ve-
of major acute cardiac events.9 Beta-blockers are poorly
nous pooling of blood, which reduces ventricular volume,
cardiac work, and chamber size (Table 2). Nitrates are tolerated by many patients because of their side effects
systemic and coronary arterial vasodilators; however, to (Table 3).
what extent these effects account for their antianginal effi-
cacy is not well established (except in patients with coro- Calcium Channel Blockers
nary artery spasm). Sublingual nitroglycerine is the most Calcium channel blockers are potent coronary and systemic
arterial vasodilators that are highly effective in patients with
coronary artery spasm (Table 2). Calcium channel blockers
Table 1 Chronic CAD & Stable Angina: Revascularization and have become popular for treatment of angina primarily
Outcome
because of the lower incidence of side effects (Table 3).
Mortality MI However, their impact on cardiovascular outcomes in cor-
CASS 1981, 1990 ↔ ↔ onary artery disease and stable angina has not been system-
ECSS 1982, 1988 ↔2 ↔ atically evaluated in randomized controlled trials.
VACSS 1984, 1998 ↔ ↔
MASS-1 (p-LAD) 1999 ↔ ↔
TIME 2001 ↔ ↔ Newer Antianginal Drugs
RITA-2 2003 ↔ ↔ Although there has been a lack of development of newer
MASS-2 2007 ↔ §1, 2ⴱ antianginal drugs during the past 25 years, new drugs with
COURAGE 2007 ↔ ↔ a unique mechanism of action have been introduced for
BARI-2D 2009 ↔ ↔
treatment of stable angina. Of these, ranolazine and ivabra-
(↔) ⫽ No Effect, (2) ⫽ Decrease, (1) ⫽ Increase, (§) ⫽ Increased dine have undergone the most extensive evaluations and are
with PCI, (ⴱ) ⫽ Decreased with CABGS.
discussed next.
Deedwania and Carbajal Treatment of Stable Angina 683

Table 2 Pharmacologic Actions of Antianginal Drugs

Class Heart Rate Arterial Pressure Venous Return Myocardial Contractility Coronary Flow
␤-blockers 2 2 ↔ 2 ↔
DHP CCB 1ⴱ 2 ↔ 2 1
Non-DHP CCB 2 2 ↔ 2 1
Long acting nitrates 1/↔ 2 2 ↔ 1
Ranolazine† ↔ ↔ ↔ ↔ ↔
␤-blockers ⫽ Beta Blockers, DHP CCB ⫽ Dihydropyridine Calcium Channel Blocker, (ⴱ) ⫽ Except Amlodipine, (2) ⫽ Decrease, (↔) ⫽ No Effect,
(1) ⫽ Increase, (†) ⫽ Late Na⫹ Channel Blocker.

Ranolazine A subanalysis of the MERLIN-TIMI 36 trial provided

Recently, ranolazine was approved by the Food and Drug
Administration (FDA) for treatment of angina.11,12 Al-
though the precise mechanism of action of ranolazine is not
established, it is thought to be related to selective late
sodium channel blockade. The findings from several clinical
trials suggest that antianginal effect of ranolazine is differ-
ent than that of conventional antianginal medications be-
cause it is not a coronary vasodilator and does not reduce
myocardial oxygen demand (no effect on heart rate, blood
pressure, preload, or inotropy)13-15 (Table 2).
During the past decade, several randomized controlled
trials in patients with coronary artery disease and inducible
ischemia on treadmill exercise test showed that ranolazine
used as monotherapy or as an add-on therapy with tradi-
tional antianginal drugs improves anginal symptoms and
performance during exercise testing. Although ranolazine
was initially approved for clinical use only in patients with
persistent anginal symptoms despite traditional antianginal
drugs, the FDA recently approved its unrestricted use in all
patients with stable angina after its safety was demonstrated
in a large cohort of high-risk patients with acute coronary
syndrome in the Metabolic Efficiency With Ranolazine for
Less Ischemia in Non-ST-Segment Elevation Acute Coro-
nary Syndromes (MERLIN-TIMI 36) study.11,12
additional data supporting antianginal efficacy of ranola-
zine.12 This subanalysis of patients with a history of chronic
angina before the acute coronary syndrome12 demonstrated
that treatment with ranolazine was associated with a signif-
icant improvement in anginal symptoms, decreased need for
additional antianginal drugs, and improved exercise perfor-
mance (Figure 1). In addition, ranolazine was associated
with a significantly lower risk of the primary combined end
point at the 1-month follow-up (23.3% vs 19.8%, respec-
tively, P ⫽ .039) and at 12 months (29.4% vs 25.2%, re-
spectively, P ⫽ .017). This risk reduction was primarily due
to reduction in recurrent ischemia at 1 month (17.2% vs
13.7%, respectively, P ⫽ .015) and 12 months (21.1% vs
16.5%, respectively, P ⫽ .002).12
Available data indicate that ranolazine is safe, well tol-
erated, and effective even in patients who continue to ex-
perience angina despite treatment with conventional anti-
anginal drugs.11-15 Furthermore, because of the lack of
hemodynamic effects, ranolazine can be used safely in pa-
tients with bradycardia and hypotension (Tables 2 and 3).
On the basis of data from MERLIN-TIMI 36 and other
randomized controlled trials, ranolazine can be used safely
in patients with diabetes, chronic obstructive pulmonary
disease, and left ventricular dysfunction/heart failure, and in

Table 3 Side Effects, Precautions and Contraindications of Antianginal Drugs

Calcium Channel
Beta Blockers Nitrates Blockers Ranolazine
Side effects ● Hypotension ● Hypotension ● Hypotension ● Dizziness
● Syncope ● Syncope ● Flushing ● Headache
● Sexual dysfunction ● Headache ● Dizziness ● Constipation
● Fatigue ● Tolerance ● Edema ● Nausea
● Depression ● Fatigue
Precautions/ ● Bradycardia ● Left ventricular outflow ● Bradycardia ● Use with QT prolonging drugs
contraindications ● AV conduction tract obstruction ● AV conduction ● Significant liver disease
problems ● Erectile dysfunction problems ● Contraindicated with strong CYP3A4
● Sick sinus (concomitant use of ● Sick sinus inhibitors (ketoconazole,
syndrome PDE5 inhibitors). syndrome clarithromycin, or nelfinavir) and
● Peripheral vascular ● Heart failure CYP3A inducers (rifampin,
disease ● LV dysfunction phenobrab)
● COPD
684
Figure 1 Effect of ranolazine compared with placebo on
angina and recurrent ischemia in patients with a history of
chronic angina who have presented with an acute coronary
syndrome. Reproduced with permission from Wilson S, Scirica
B, Braunwald E, et al. Efficacy of ranolazine in patients with
chronic angina observations from the randomized, double-
blind, placebo-controlled MERLIN-TIMI (Metabolic Effi-
ciency With Ranolazine for Less Ischemia in Non-ST-Segment
Elevation Acute Coronary Syndromes) 36 Trial. J Am Coll
Cardiol. 2009;53:1510-1516. CI ⫽ confidence interval; HR ⫽
hazard ratio.
patients requiring a phosphodiesterase 5 inhibitor, such as
sildenafil.12,15
Ivabradine
Ivabradine is a newer drug that has been evaluated in pa-
tients with coronary artery disease and stable angina.16-18
Ivabradine is a specific inhibitor of the I-f channels in the
sinoatrial node and considered as a pure heart rate-lowering
agent in patients with sinus rhythm. Ivabradine does not
have an effect on blood pressure, myocardial inotropy, in-
tracardiac conduction, or ventricular repolarization.16-18
Ivabradine is effective in reducing myocardial ischemia and
controlling anginal symptoms in patients with stable angina
who are in sinus rhythm, primarily by reducing heart
rate.16-19 Several clinical trials have evaluated the role of
ivabradine as monotherapy and as an add-on therapy, and
showed effectiveness in controlling anginal symptoms and
improving the exercise performance.16-19 In addition, the
data from a large randomized clinical trial in patients with
stable coronary artery disease and left ventricular systolic
dysfunction showed that treatment with ivabradine was as-
sociated with reduced incidence of coronary artery disease-
related outcomes in the subgroup of patients with a resting
heart rate of ⱖ 70 beats/min.19 A recent randomized con-
trolled trial in patients with systolic heart failure and heart
rate ⬎ 70 beats/min also showed significant survival benefit
with ivabradine.20 Although, ivabradine is not yet approved
by the FDA in the United States, when approved it will be
an additional choice for antianginal therapy in patients with
coronary artery disease and stable angina.
The American Journal of Medicine, Vol 124, No 8, August 2011
Combination Therapy
Combination therapy is often necessary to achieve adequate
symptom control in many patients with stable angina. Ideal
combination therapy should provide maximum symptom
relief with few adverse effects. Current guidelines recom-
mend that combination therapy should use a beta-blocker
with nitrate or a calcium channel blocker on the basis of a
patient’s underlying comorbid conditions. Such a combina-
tion may allow the clinician to use lower doses of each
agent to achieve symptom control with minimal side effects.
Ranolazine has been found to be a useful combination in
patients who remain symptomatic despite use of traditional
antianginal drugs.
Other Drugs in Patients with Stable Angina
and Chronic Coronary Artery Disease
On the basis of the results of several randomized controlled
trials demonstrating vasculoprotective effects of renin-ang-
iotensin-aldosterone system blockers and statins, these
drugs also are routinely recommended for patients with
coronary artery disease and stable angina in an effort to
reduce the risk of myocardial infarction and death. The
following section provides a brief overview in this regard.
Angiotensin-Converting Enzyme Inhibitors
On the basis of the well-demonstrated vasculoprotective
effects of angiotensin-converting enzyme inhibitor in 2 ran-
domized controlled trials, the Heart Outcomes Prevention
Evaluation (HOPE) trial21 and the European trial on reduc-
tion of cardiac events with perindopril in stable coronary
artery disease (EUROPA),22 angiotensin-converting en-
zyme inhibitors are recommended for most patients with
stable coronary artery disease. In the HOPE trial,21 com-
pared with placebo, treatment with ramipril was associated
with lower major acute cardiac events (P ⬍ .0001) and
significantly fewer cardiovascular revascularizations
(18.3% vs 16%, P .002). The EUROPA study22 evaluated
the effect of another angiotensin-converting enzyme inhib-
itor, perindopril, on clinical outcomes in patients with stable
coronary artery disease and angina and showed that, com-
pared with placebo, perindopril resulted in a relatively small
but significantly lower risk (9.9% vs 8%, respectively) of
the composite end point (myocardial infarction, cardiovas-
cular death, or resuscitated arrest). A meta-analysis of 6
studies,23 including the HOPE and EUROPA, revealed that,
compared with placebo, therapy with an angiotensin-con-
verting enzyme inhibitor was associated with a modest,
statistically significant favorable effect resulting in reduced
rates of cardiovascular death, all-cause mortality, and non-
fatal myocardial infarction.
On the basis of these findings, an angiotensin-converting
enzyme inhibitor should be considered in patients with
stable coronary artery disease who are at high risk of car-
diovascular events. In patients who are intolerant to angio-
tensin-converting enzyme inhibitors (primarily because of
severe cough), an angiotensin receptor blocker can be used.
Deedwania and Carbajal Treatment of Stable Angina
Lipid-Lowering Therapy
A number of studies during the last 2 decades have shown
that lipid-lowering therapy with statins reduces not only the
risk of major acute cardiac events but also the need for
revascularization and decreases signs and symptoms of
myocardial ischemia.24-28 Several randomized controlled
trials have specifically evaluated the role of lipid-lowering
therapy with statin as anti-ischemic therapy in patients with
stable coronary artery disease and have shown that lipid-
lowering therapy is associated with antianginal and anti-
ischemic effects.29-32 On the basis of these findings, statin
therapy is indicated for all suitable patients with stable
coronary artery disease and angina.
Role of Myocardial Revascularization
Myocardial revascularization has been evaluated and com-
pared with medical therapy in patients with coronary artery
disease and stable angina. Revascularization includes coro-
nary artery bypass grafting and percutaneous coronary in-
tervention with or without stent deployment. Although re-
vascularization provides relief of anginal symptoms, it only
abolishes anginal episodes in a minority of patients. A
significant proportion of patients continue to experience
anginal symptoms after revascularization.32 Furthermore,
revascularization procedures are often performed in asymp-
tomatic patients with the intent of reducing the incidence of
coronary events and cardiac death in patients with stable
coronary artery disease. However, little data exist to support
such benefit.
Comparison of Revascularization with Medical
Therapy
During the past 4 decades, several studies32-56 have com-
pared the impact of pharmacologic therapy versus revascu-
larization in patients with coronary artery disease and stable
angina. In general, these studies have shown that revascu-
larization is usually more effective in symptom control
compared with conventional antianginal drug therapy.
However, it is important to note that since the earlier time
when many of the previous trials were conducted, the med-
ical therapy for patients with stable angina has improved
considerably with the routine use of beta-blockers, anti-
platelet agents, angiotensin-converting enzyme inhibitors,
and lipid-lowering therapy (particularly with statins); thus,
the result of earlier trials might not be applicable and per-
tinent today. Recent randomized controlled trials using
these drugs have shown that medical therapy is effective in
controlling symptoms, and when aggressive risk factor
modification is implemented, such strategy is as effective as
revascularization in reducing the risk of major acute cardiac
events in patients with coronary artery disease and stable
angina.33,55,56
On the basis of the angiographic profiles considered to
confer higher risk to various subgroups in the Veterans
Administration Coronary Artery Bypass Surgery Coopera-
tive Study, European Coronary Surgery Study, and Coro-
685
nary Artery Surgery Study studies, recommendations for
treatment with coronary artery bypass grafting were put into
practice guidelines for patients with coronary artery disease
and stable angina who had similar high-risk angiographic
features. Of the several high-risk subgroups identified by
angiography, only the subgroup with proximal left anterior
descending involvement has been evaluated in a prospective
manner in the Medicine, Angioplasty, or Surgery Study 1
and showed no significant difference in hard clinical end
points between revascularization strategy and medical
therapy.51,52
Strategies Comparing Invasive versus
Optimum Medical Therapy
Several studies have evaluated the role of coronary artery
bypass grafting, percutaneous coronary intervention, and
medical therapy in patients with stable coronary artery dis-
ease. These include the Asymptomatic Cardiac Ischemia
Pilot,35,36 the Medicine, Angioplasty, or Surgery Study
trials,51,52,55 the Clinical Outcomes Utilizing Revasculariza-
tion and Aggressive Drug Evaluation trial,32 and the Bypass
Angioplasty Revascularization Investigation 2 Diabetes
trial.56 Overall, the results of these studies have shown that
except for better symptom control with revascularization,
there is essentially no significant difference in hard clinical
events between medical therapy and revascularization strate-
gies in patients with stable coronary artery disease (Table 1).
Two recently completed major randomized controlled
trials conducted by the National Heart, Lung, and Blood
Institute have carefully compared revascularization with
optimal medical therapy consisting of aggressive anti-is-
chemic therapy plus comprehensive risk factor modification
Figure 2 The estimated 4.6-year rate of the composite pri-
mary outcome of death from any cause and nonfatal myocar-
dial infarction was 19.0% in the PCI group and 18.5% in the
medical-therapy group. Adapted with permission from Boden
W, O’Rourke R, Teo K, et al. Optimal medical therapy with or
without PCI for stable coronary disease. COURAGE Trial
Research Group. N Engl J Med. 2007;356:1503-1516. CI ⫽
confidence interval; PCI ⫽ percutaneous coronary intervention.
686 The American Journal of Medicine, Vol 124, No 8, August 2011

on risk of death and myocardial infarction.32,56 The Clinical
Outcomes Utilizing Revascularization and Aggressive Drug
Evaluation trial compared the clinical efficacy of percuta-
neous coronary intervention plus optimal medical therapy
versus optimal medical therapy alone in patients with stable
coronary artery disease.32 Optimal medical therapy con-
sisted of therapy with a beta-blocker and, when needed,
diltiazem and aggressive management of risk factors for
coronary artery disease. During the median follow-up of 55
months, the optimal medical therapy and the optimal med-
ical therapy plus percutaneous coronary intervention groups
had similar rates of the primary combined (death and non-
fatal myocardial infarction) outcome (18.5% vs 19.0%, re-
spectively) (Figure 2). As expected, a significantly greater
proportion of patients in the percutaneous coronary inter-
vention group were angina-free at 12 months (57% vs 50%,
respectively, P ⫽ .005); however, this benefit was lost at 3
years (59% vs 56%, respectively).57
The Bypass Angioplasty Revascularization Investigation
2 Diabetes trial56 in patients with diabetes, coronary artery
disease, and classic angina compared the effects of prompt
revascularization by discretionary coronary artery bypass
grafting or percutaneous coronary intervention with medical
therapy alone on clinical outcomes. During the 5-year fol-
low-up, there was no difference between the medical ther-
apy and revascularization groups on the risk (13.5% vs
13.2%, respectively) of the primary outcome (all cause-
death), the risk of myocardial infarction (11.6% vs 10.0%,
respectively), or the risk of stroke (2.8% vs 2.6%, respec-
tively) (Figure 3).
According to the older and newer recent revasculariza-
tion trials in patients with stable coronary artery disease
discussed, compared with medical treatment, revasculariza-
tion results in similar rates of hard clinical outcomes in the
main groups. The consistent benefit of revascularization
compared with medical treatment seems to be a more strik-

Figure 3 Rates of survival and freedom from major cardiovascular events. There was no significant
difference in rates of survival between the revascularization group and the medical-therapy group (A)
and between the insulin-sensitization group and the insulin-provision group (B). The rates of major
cardiovascular events (death, myocardial infarction, or stroke) also did not differ significantly between
the revascularization group and the medical-therapy group (C) or between the insulin-sensitization group
and the insulin-provision group (D). Reproduced with permission from Frye R, August P, Brooks M, et
al. A randomized trial of therapies for type 2 diabetes and coronary artery disease. BARI 2D Study
Group. N Engl J Med. 2009;360:2503-2515.
Deedwania and Carbajal Treatment of Stable Angina
ing, albeit temporary, improvement in anginal discomfort.
On the basis of these data, it does not seem appropriate to
refer most patients with stable coronary artery disease and
angina for revascularization unless they have disabling
symptoms despite optimal medical therapy.
CONCLUSIONS
There are many therapeutic options available for the treat-
ment of anginal symptoms in patients with stable coronary
artery disease. These options include antianginal drugs:
nitrates, beta-blockers, calcium channel blockers, and rano-
lazine, as well as myocardial revascularization procedures.
Although combination therapy is often necessary for symp-
tomatic relief, there has been no evaluation of the effects of
combination antianginal therapy on hard clinical end points.
Recent trials have shown that although revascularization is
initially more effective in controlling symptoms, when used
along with aggressive risk factor modification, optimal
medical therapy is equally effective in reducing the risk of
future coronary events and death. There is a need for more
definitive outcome studies that examine the role of existing
therapies (including aggressive and comprehensive risk fac-
tor modification) and newer antianginal agents with the
state-of-the-art revascularization procedure in high-risk pa-
tients with stable coronary artery disease, chronic angina,
and demonstrable myocardial ischemia. Until prospective
randomized controlled trials can demonstrate the superiority
of myocardial revascularization in reducing the risk of myo-
cardial infarction and death in certain high-risk cohorts, it
seems prudent to prescribe optimal medical therapy in most
patients with stable coronary artery disease and angina and
reserve myocardial revascularization for the select few who
have uncontrollable and disabling symptoms despite receiv-
ing optimal medical therapy (including aggressive risk fac-
tor management) for a reasonable period of time.
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