Download clinical problems in cardiopulmonary disease

clinical problems in cardiopulmonary
disease
Management of a Patient With Angina
Pectoris*
Rabih R. Azar, MD, MSc; and David D. Waters, MD
(CHEST 2001; 119:287–289)
Key words: angina; angioplasty; coronary artery disease
Abbreviations: CAD ⫽ coronary artery disease; LDL ⫽ lowdensity lipoprotein
Case Presentation
56-year-old man consulted his physician comA plaining
of “pressure” in the central chest with
radiation into both arms. This symptom had been
present for approximately 1 year, was induced primarily by exertion, and was relieved promptly by
rest. It was nonprogressive in nature and did not
alter his lifestyle to any significant degree.
In the past, he had always enjoyed good health. He
had given up cigarette smoking 10 years previously
after having smoked one pack daily for 25 years. In
an evaluation 3 years ago, he was told that his
cholesterol was “slightly high.” He was overweight
with little recent change and considered his lifestyle
sedentary, seldom engaging in active exercise. He
was never told of hypertension or diabetes mellitus.
A physical examination disclosed a well-developed,
mildly obese man with a BP of 140/86 mm Hg, heart
rate of 82 beats/min and regular, height of 5 feet 8
inches, and a weight of 192 lb.
The results of an examination of the heart and lung
were normal, and the remainder of the general
examination was also normal.
The results of laboratory testing disclosed a normal CBC count and fasting blood glucose level. The
patient’s lipid profile disclosed the following levels:
total cholesterol, 232 mg/dL; high-density lipopro*From the University of California at San Francisco, CA.
Manuscript received May 4, 2000; revision accepted June 1,
2000.
Correspondence to: David D. Waters, MD, Division of Cardiology, San Francisco General Hospital, 1001 Potrero Ave, Room
5G1, San Francisco, CA 94110; e-mail: dwaters@
medsfgh.ucsf.edu
tein, 40 mg/dL; low-density lipoprotein (LDL), 166
mg/dL; and triglycerides, 170 mg/dL.
A treadmill examination then was performed. The
patient was able to achieve an exertional level of
approximately 7 metabolic equivalents (ie, 2.5 miles
per hour with a 12% grade). During the test, 1.5 mm
of horizontal ST-segment depression occurred at a
heart rate of 125 beats/min (76% of the expected
maximum heart rate). Shortly thereafter, chest pain
was noted, and the test was discontinued at a heart
rate of 130 beats/min.
The patient then was subjected to cardiac catheterization with coronary cineangiography, which provided the following information: the left ventriculogram showed a normally contracting chamber with
normal systolic and diastolic pressures. The left
anterior descending coronary artery disclosed a
short, high-grade lesion (90% narrowing) in an area
proximal to the first septal perforator branch. The
remainder of the left coronary system displayed
scattered luminal irregularities with an area of modest narrowing (30%) in the proximal portion of the
obtuse marginal branch of the left circumflex artery.
The right coronary artery harbored an area of 80%
narrowing (1 cm distal to the ostium). Distally, this
artery appeared free of significant disease. The two
high-grade lesions were considered to be amenable
to angioplasty procedures.
Questions for Consultants
1. What would be your overall management of
this patient?
2. Assuming that one chooses medical therapy
with rigorous lipid control, what circumstances
would you require in order to recommend an
alternate approach, such as angioplasty or coronary bypass surgery?
3. Would the severity of angina or the presence of
reduced left ventricular function influence your
therapeutic approach?
CHEST / 119 / 1 / JANUARY, 2001
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Comments by Consultants
Rabih R. Azar, MD, MSc, and David D. Waters,
MD
The patient is a 56-year-old man who presented
with chronic stable angina and a stress test suggesting at least moderate impairment in his exercise
tolerance due to ischemia. The fact that angina has
not limited his daily activity is related to his sedentary lifestyle. The other important elements to consider in the management of his condition are his risk
factors for coronary artery disease (CAD), the underlying left ventricular function, and the anatomy of
coronary atherosclerosis.
Our first step in managing this patient is to start
aspirin therapy (81 to 325 mg/d) and lipid-lowering
therapy, preferably with administration of a statin
agent. By inhibiting platelet aggregation, aspirin
decreases the incidence of future coronary events by
⬎ 50%, and this agent is a well-tolerated drug.
Cholesterol lowering improves endothelial function,
delays the progression of CAD, and, most importantly, leads to the stabilization of the atherosclerotic
plaques preventing future acute coronary syndromes. Our goal in lipid management would be to
lower the patient’s LDL levels to ⬍ 100 mg/dL.
Lipid lowering was shown to decrease significantly
the incidence of death and nonfatal myocardial
infarction in both primary and secondary prevention
trials with no significant serious side effects compared to placebo. Furthermore, in a recent prospective trial, aggressive LDL lowering (mean level, 77
mg/dL) with atorvastatin, 80 mg/d, was at least as
effective as angioplasty and usual care in reducing
ischemic cardiac events in patients with one- or
two-vessel CAD and normal left ventricular function.
In addition to medical therapy, we would recommend revascularization of the left anterior descending artery and the right coronary artery. We recommend this because the patient has at least a
moderately limited exercise capacity and a large
amount of myocardium at risk. Studies comparing
bypass surgery to medical therapy alone have shown
a survival benefit for surgery in patients with twovessel CAD involving the proximal left anterior
descending artery. For this patient, we would favor
angioplasty with stenting over bypass surgery. In
patients without diabetes mellitus and with a preserved left ventricular function, the Bypass Angioplasty Revascularization Investigation trial has shown
that both revascularization strategies are equally
effective in terms of survival and freedom from
myocardial infarction. The two coronary lesions seen
in this patient seem easily amendable to percutaneous revascularization. Angioplasty is much less aggressive than bypass surgery, but the likelihood for
repeat interventions is higher because of restenosis.
However, coronary stenting has significantly decreased this complication. Angioplasty is not superior
to medical therapy for the prevention of myocardial
infarction and death, but it is better in angina control
and in improving exercise capacity. This is important
for our patient who is mildly obese, has a sedentary
lifestyle, and is still relatively young. We would
recommend that he starts a progressive exercise
program and loses weight following angioplasty.
If the patient refuses revascularization, we would
start him on a ␤-blocker (in addition to aspirin and
aggressive lipid lowering) with careful monitoring of
his underlying symptoms. Any evidence of the progression of symptoms or further deterioration in
exercise capacity should urge reconsideration of
coronary revascularization. Should he develop left
ventricular dysfunction, our recommendation for
revascularization would be even stronger. In the
absence of myocardial infarction, left ventricular
dysfunction suggests a severe reduction in coronary
blood flow resulting in myocardial hibernation. This
condition usually improves after revascularization.
Left ventricular dysfunction is also an independent
predictor of reduced survival. While multivessel
angioplasty was shown to be equal to bypass surgery
in terms of improving survival and the incidence of
nonfatal myocardial infarctions, patients with impaired left ventricular function were excluded from
these trials. This would lead us to recommend bypass
surgery as a first choice in a revascularization strategy in a patient with left ventricular dysfunction.
Editor’s Comment
This case exemplifies the various options presently
available to the clinician for the management of
stable CAD. In comparison with earlier standard
medical management, several trials have demonstrated the efficacy of vigorous cholesterol reduction
in reducing atheroscleric events and prolonging survival in patients who already have manifested ischemic cardiac or cerebrovascular disease. As Dr.
Waters’ group has demonstrated,1 aggressive lipid
lowering with atorvastatin in patients with stable
coronary disease who have one or two major coronary vessels involved is at least as effective as the
traditional mechanical interventions (ie, angioplasty
or bypass operations) in the prevention of subsequent ischemic events and in prolonging survival.
These findings apply at the least to patients who are
asymptomatic or have mild to moderate angina
pectoris and who have normal or only mildly decreased resting left-ventricular systolic function
(ejection fraction, ⱖ 40%). In comparison with med-
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Clinical Problems in Cardiopulmonary Disease
ical therapy, mechanical interventions result in more
immediate and complete relief of anginal symptoms
in this group of patients, despite providing no survival benefit. In past comparisons with medical
therapy, coronary bypass surgery has been found to
prolong survival in patients who have triple-vessel
coronary artery disease combined with impaired left
ventricular function, as well as in such patients who
have involvement of the proximal left anterior descending coronary artery, even with normal left
ventricular function or an absence of triple-vessel
disease.2,3 Equivalent outcomes have been reported
when surgery is compared with angioplasty in such
groups of nondiabetic patients.4 In the light of the
aggressive lipid lowering produced by modern drugs,
singly or in combination, time-honored indications
for surgery or angioplasty are in a state of flux and
may no longer be valid. Thus, in a patient such as
this, one could make a strong case for initial therapy
with a statin-type cholesterol-lowering drug combined with vigorous risk factor control, reserving
mechanical interventions for patients who fail to
respond or who show further progression of cardiac
symptoms. How contemporary medical therapy
would compare with mechanical interventions (an-
gioplasty or surgery) in the presence of left-ventricular dysfunction, triple-vessel coronary disease, or
more severe symptoms is largely unknown and awaits
the results of long-term trials. In the meantime,
however, one might anticipate that the aggressive
lowering of lipid levels would at least complement
angioplasty or surgery in such patients, presumably
by stabilizing untreated atherosclerotic lesions.
References
1 Pitt B, Waters D, Brown WV, et al. Aggressive lipid-lowering
therapy compared with angioplasty in stable coronary artery
disease. N Engl J Med 1991; 341:70 –76
2 Yusuf S, Zucker D, Peduzzi P, et al. Effect of coronary artery
bypass graft surgery on survival: overview of 10 year results
from randomized trials by the Coronary Artery Bypass Graft
Surgery Trialists Collaboration. Lancet 1994; 344:563–570
3 American College of Cardiology/American Heart Association
Task Force on Assessment of Diagnostic and Therapeutic
Cardiovascular Procedures (Subcommittee on Coronary Artery Bypass Graft Surgery). Guidelines and indications for
coronary artery bypass graft surgery. J Am Coll Cardiol 1991;
17:543–589
4 Lincoff AM, Topol EJ. Interventional catheterization techniques. In: Braunwald, E, ed. Heart disease. 5th ed. Philadelphia, PA: WB Saunders, 1997; 1366 –1403
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