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1919
Chapter 2
Coronary Artery Disease
Flavio de Souza Brito , Renato D. Lopes ,
and Matthew T. Roe
Chronic stable angina
Epidemiology
Coronary artery disease (CAD) is the single most frequent cause of death
worldwide, with over seven million deaths per year from CAD, accounting for
12.8 percent of all deaths. Chronic, stable angina is likely the most common
manifestation of CAD and is the lowest risk situation for patients with CAD, as
large randomized trials suggest that patients with stable angina have a favorable
prognosis, with a mortality rate of only 1.5 percent per year.
1,2
Pathophysiology
Stable angina occurs when there is regional myocardial ischemia caused by inad-
equate coronary perfusion through a fl ow-limiting coronary stenosis, and this
condition is usually induced by an increase in demand of oxygen to the myocar-
dium with increased physical activity. Complete reversibility of the symptoms
and repetitiveness of the episodes of angina over time (typically months to
years) are cardinal features of stable angina pectoris. However, as coronary
disease progresses and the luminal stenosis increase, stable angina can occur
with a lesser degree of activity or at rest; both situations are referred to as
unstable angina.
3,4
Classifi cation of angina pectoris
Classic or typical angina is usually described as a squeezing feeling in the
chest or heaviness, pressure, weight, vise-like aching, burning, and tightness.
It can present as symptoms that radiate to the shoulder, neck, jaw, inner arm,
and epigastrium, causing a band-like discomfort, and it is relatively predict-
able, lasting between 3 and 15 minutes. Usually, the symptoms are improved
when physical activity ceases or after nitroglycerin use that causes coronary
vasodilation. Atypical or noncardiac chest pain is more frequent in older,
female, and diabetic patients. In this case, the chest pain is usually pleuritic,
sharp, pricking, knife-like, pulsating, lancinating, and choking. It involves the
thorax, is positional, can occur in chest wall locations that are tender to
palpation, can be inframammary with radiation being highly variable and last-
ing seconds, minutes, hours, or all day. The severity of stable angina is typi-
cally assessed by the Canadian Cardiovascular Society Classifi cation scale
(Table 2.1).
3,4
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CHAPTER 2 Coronary Artery Disease
Anatomical and functional investigation
Functional imaging to assess inducible myocardial ischemia and anatomical tests
to confi rm the presence of obstructive coronary artery disease are often used
to further evaluate patients with stable or progressive angina. Although several
diagnostic testing modalities are available in clinical practice, the risk of exer-
cise, pharmacological stress agents, contrast agents, invasive procedures, and
cumulative ionizing radiation must be weighed to avoid unnecessary diagnostic
tests. Gender, symptoms, and associated risk factors should be assessed to
decide the best test for each individual patient.
Because of high availability and low costs, an exercise electrocardiogram is
the most common test used to confi rm the nature of suspected ischemic symp-
toms and to provide objective evidence of inducible ischemia, with sensitivity
and specifi city of 65 to 70 percent and 70 to 75 percent, respectively. Stress
echo and nuclear imaging have a Class IA indication (conditions for which there
is evidence or general agreement that a given procedure or treatment is useful
and effective and the data are derived from multiple randomized clinical tri-
als) in intermediate pretest likelihood and about the same estimated sensitivity
(80 to 85 percent) and specifi city (85 to 90 percent).
2,3,5
Multidetector com-
puted tomography coronary angiography, stress magnetic resonance imaging
and positron emission tomography receive Class IIa B indications (weight of
evidence/opinion is in favor of usefulness/effi cacy and data are derived from a
single randomized trial or nonrandomized studies) to intermediate-risk patients.
Patients with extensive ischemia on functional testing or high-risk fi ndings on
anatomical testing should be considered for coronary angiography—a Class IA
recommendation.
2,6
Management of stable angina
In terms of the management of stable angina, the American College of
Cardiology/American Heart Association (ACC/AHA) guidelines recommend
standard secondary prevention goals, such as smoking cessation; tight blood
pressure control, especially for patients with diabetes or chronic kidney
Table 2.1 Canadian Cardiovascular Society Classifi cation of Stable
Angina Severity
Class I
No angina with ordinary physical activity (e.g., walking, climbing stairs)
Angina with strenuous or prolonged exertion
Class II
Early-onset limitation of ordinary activity (e.g., walking rapidly or walking >2 blocks;
climbing stairs rapidly or climbing >1 fl ight); angina may be worse after meals, in cold
temperatures, or with emotional stress
Class III
Marked limitation of ordinary activity
Class IV
Inability to carry out any physical activity without chest discomfort
Angina occurs during rest
The classifi cation is from Sangareddi et al.
17
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CHAPTER 2 Coronary Artery Disease
disease, LDL-C reduction to less than 100 mg/dL or less than 70 mg for high-risk
patients; regular aerobic physical activity many days per week; and maintenance
of a body mass index (BMI) between 18.5 and 24.9 kg/m
2
.
5
Evidence-based med-
ications start with aspirin, since it signifi cantly reduces the risk of thrombotic
events in patients with coronary artery disease; and the dose usually recom-
mended for stable angina is 75 to 162 mg/day. Clopidogrel can be offered as
an alternative when aspirin is not tolerated or is contraindicated, and both
should be used after percutaneous coronary intervention (PCI) procedures.
7
Statin therapy should be prescribed in the absence of contraindications or doc-
umented adverse effects. Beta-blockers remain a pivotal treatment for stable
angina, most importantly in patients with a past history of myocardial infarction
(MI).The doses of beta-blockers should be titrated to achieve a heart rate less
than or equal to 60 beats per minute or even lower with stable, but severe
angina.
8
Calcium channel blockers are an alternative to beta-blockers or are
used in association and remain the reference treatment for vasospastic angina.
8
Short-acting nitrates provide effective symptomatic relief and can be used as
prophylaxis before physical exertion that might induce angina. With long acting
nitrates concerns relate to the risk of tolerance and the possibility of a rebound
effect, therefore a nitrate-free interval of 10 to 12 hours is important to reduce
tolerance.
7,8
Angiotensin-converting enzyme (ACE) inhibitors should be started
and continued indefi nitely in all patients with a left ventricular ejection frac-
tion less than or equal to 40 percent and in those patients with normal left
ventricular function but with hypertension, diabetes, or chronic kidney disease,
according to the fi ndings of the HOPE and EUROPA studies.
9–11
Trimetazidine,
ivabradine, and ranolazine can reduce angina-attack frequency and nitroglycerin
consumption, as well as increase exercise capacity, prolong time to the onset
of angina with exercise, and decrease ischemic ST-segment depression on the
ECG during treadmill exercise tests.
7,8
In summary, the lifestyle modifi cation
interventions and medications recommended for patients with stable angina
form a comprehensive secondary prevention strategy to reduce the risk of
future ischemic events and to control angina symptoms.
Choice of revascularization strategy
Depending on a given patient’s symptoms, functional capacity, and coronary
anatomy, stable angina can be treated with optimal medical treatment (OMT)
or combined with revascularization using PCI or coronary artery bypass graft-
ing (CABG). The COURAGE trial compared OMT alone to OMT + PCI in
patients with stable angina and signifi cant CAD on angiography. With close to
5 years of follow-up, there was no signifi cant difference in the composite out-
come of death or MI.
12
In the BARI 2D trial, OMT compared with initial revas-
cularization showed no differences in all-cause death or MI in patients with
stable angina and diabetes mellitus. However, CABG surgery for patients with
multi-vessel CAD signifi cantly decreased the rate of MI compared with OMT.
13
The SYNTAX trial showed that CABG, compared with PCI, was associated
with a lower rate of major adverse cardiac or cerebrovascular events at 1 year
(and even longer) among patients with stable angina and multi-vessel disease,
mainly in patients with high-risk coronary anatomical characteristics (extensive
and diffuse coronary lesions).
14
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CHAPTER 2 Coronary Artery Disease
The impact of ischemic burden on prognosis was studied in the COURAGE
trial nuclear substudy, and 100 patients with more than 10 percent ischemic
myocardium had a lower risk of death or MI with revascularization compared
with OMT. These results have prompted the much larger and defi nitive evalu-
ation of this treatment paradigm in the ISCHEMIA trial.
15
Recently, the FAME
2 study showed that fractional fl ow reserve (FFR), a technique to measure the
functional stenosis severity with the use of an intracoronary fl ow wire, before
PCI plus the best OMT, compared with the best OMT alone, substantially
decreased the need for urgent revascularization.
16
Acute coronary syndromes
Overview
Acute coronary syndromes (ACS) refers to a continuum of biological events
progressing from plaque instability to plaque rupture, coronary thrombosis,
reduced coronary blood fl ow, myocardial ischemia, and ultimately myocardial
necrosis. It is a term used to encompass the spectrum of clinical disorders
caused by acute ischemic heart disease, including unstable angina (UA), non-ST-
elevation MI (NSTEMI), and ST-elevation MI (STEMI).
18,19
Epidemiology and prognosis
Nearly 1.4 million people are hospitalized annually with ACS in the United
States and registry data consistently show that NSTEMI is more frequent than
STEMI.
20
Hospital mortality is higher in patients with STEMI than among those
with NSTEMI (7 percent versus 3 to 5 percent, respectively), but at 6 months
the mortality rates are very similar in both conditions (12 percent and 13 per-
cent, respectively).
21
Long-term follow-up studies have shown that death rates
were higher among patients with NSTEMI compared with STEMI, with a two-
fold difference at 4 years.
21
These observed differences may be due to different
patient profi les, since NSTEMI patients tend to be older, with more comorbidi-
ties, especially diabetes and renal failure.
22,23
Pathophysiology
The most common cause of STEMI is an occlusive thrombus that develops at
the site of a ruptured or fi ssured atherosclerotic plaque, while in UA/NSTEMI
the microvascular embolization of platelet aggregates from nonocclusive throm-
bus at the site of atherosclerotic plaque rupture is the cause of myonecrosis.
19
Coronary atherosclerosis is the underlying condition for coronary events with
few exceptions. Events are rarely caused by coronary dissection, arteritis, myo-
cardial bridging, thromboembolism, or coronary vasospasm without obvious
coronary artery disease.
24
Plaque rupture is most commonly associated with
acute coronary events, and identifi cation of coronary atherosclerotic plaques
that are prone to rupture, called vulnerable plaques, is currently being investi-
gated intensely. Pathology and clinical studies revealed that the atherosclerotic
plaque type at the greatest risk of rupture is a thin-cap fi broatheroma, character-
ized by a large necrotic core covered by a thin layer of fi brous cap, but recent
observations using intravascular ultrasound (IVUS) suggest that identifying
plaques that are prone to rupture (i.e., vulnerable plaques) may be diffi cult.
25
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CHAPTER 2 Coronary Artery Disease
Clinical presentation
The most common presentation for STEMI is abrupt-onset angina symptoms
typically lasting for more than 30 minutes and occurring de novo in patients
without antecedent angina. Unstable angina can present as rest angina, new-
onset severe angina, or increasing severity and frequency of angina as previ-
ously described. Atypical presentations sometimes occur and symptoms with
these presentations include weakness, dyspnea, heart failure, and dizziness;
these symptoms are more common in women, patients with diabetes mellitus,
and the elderly.
19
The physical examination in a patient with ACS is usually
unremarkable. Patients with extensive myocardial ischemia may have exami-
nation fi ndings consistent with left ventricular dysfunction, such as a left ven-
tricular gallop (usually an S3), tachycardia, hypotension, and signs of peripheral
hypoperfusion.
25
Electrocardiogram
Findings that suggest a high likelihood of NSTEMI include ST-segment depres-
sion (more than 1 mm) or T-wave inversion in two or more contiguous pre-
cordial leads that occurs with symptoms and resolves when the patient is
asymptomatic.
25
ST-segment elevation in two contiguous leads (i.e., inferior
limb leads [II, III, and aVF], anterior precordial leads [V1–V4], lateral or antero-
lateral leads [I, avL, V4–V6]), a new or indeterminate left bundle branch block
(LBBB), or isolated ST-segment depression in the right precordial leads (i.e., V1
and V2) indicative of an acute posterior infarct are diagnostic for STEMI.
26
Cardiac biomarkers
The serologic detection of myonecrosis is necessary to differentiate unstable
angina from NSTEMI. Cardiac troponins (either I or T) are the preferred serum
cardiac biomarkers for detecting myonecrosis. Troponins are contractile pro-
teins found only in cardiac myocytes. When myonecrosis occurs, they are
released into the blood, where they can be detected within 4 to 6 hours of
symptom onset. Serum troponin may be undetectable early after myocardial
injury, however. Therefore, if clinical suspicion for ACS is high and the initial
serum troponin concentration is normal, a second measurement should be
obtained 4 to 8 hours later. The troponins are more sensitive and specifi c than
the total creatine kinase and creatine kinase MB and levels remain elevated for
1 to 2 weeks after an acute MI, whereas the creatine kinase MB returns to nor-
mal levels within 24 to 48 hours.
25
In the patient suspected of having a STEMI,
the presence of elevated serum cardiac biomarkers confi rms the presence of
myonecrosis. However, because they are not detectable in the blood until 2 to
4 hours after the onset of MI, reperfusion therapy should not be delayed in a
patient with suspected STEMI until elevated serum marker concentrations are
documented.
26
General management of ACS
Aspirin should be administered to ACS patients as soon as possible after
hospital presentation and continued indefi nitely in patients who tolerate it.
Compared with placebo, aspirin (initial dose of 162 to 325 mg followed by 75
to 162 mg daily) reduces the risk of death or recurrent MI by 50 percent in
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CHAPTER 2 Coronary Artery Disease
this patient population.
27
A second antiplatelet agent is always neccessary in
ACS management—P2Y12 inhibitors or a GP IIb/IIIa inhibitor should be used
according to the correct indication in different clinical scenarios.
In the TRITON-TIMI 38 study, prasugrel, a new thienopyridine P2Y12 inhibi-
tor with rapid onset of action, was compared with clopidogrel in patients with
UA/NSTEMI and STEMI who were scheduled to undergo PCI. Prasugrel signifi -
cantly reduced the rate of cardiovascular death, nonfatal MI, or nonfatal stroke
by an approximate 20 percent relative reduction. This benefi t in ischemic
events, however, was accompanied by an increase in major bleeding (2.4 per-
cent) when compared with clopidogrel (1.8 percent) as well as increases in
life-threatening and fatal bleeding. Following this trial, prasugrel was also com-
pared with clopidogrel in patients with UA/NSTEMI treated medically without
planned revascularization in the TRILOGY ACS trial. In this study, prasugrel
was not superior to clopidogrel over 2.5 years of follow-up.
28,29
Another potent, oral, direct-acting, and reversible P2Y12 inhibitor, ticagre-
lor, was compared with clopidogrel in the PLATO trial. In this trial, patients
with ACS with or without ST-segment elevation were randomized to receive
ticagrelor or clopidogrel early after presentation. Ticagrelor signifi cantly
reduced the rate of death from vascular causes, MI, or stroke without a signifi -
cant increase in major bleeding.
30
Statin therapy promotes plaque stabilization and restores endothelial func-
tion. In patients with ACS, intensive lipid lowering with atorvastatin (80 mg)
reduces the incidence of death, MI, or recurrent ischemia, even in those with
LDL levels of less than 100 mg/dL.
31
The evidence for the benefi cial effects of beta-blockers is from early stud-
ies in STEMI and stable angina patients, but a recent large clinical outcomes
study showed no benefi t from early use of high doses of intravenous and oral
beta-blockers for patients with acute MI (most of whom had STEMI).
32
Oral
administration of beta-blockers is currently preferred with low initial doses and
avoidance in patients with relatively low blood pressure or heart rates, those
with heart failure, and those with a history of signifi cant bronchospasm.
19
A systematic overview of trials of ACE inhibition early in STEMI indicated
that this therapy is safe, well tolerated, and associated with a small but sig-
nifi cant reduction in 30-day mortality, with most of the benefi t observed in
the fi rst week. Opinions still differ as to whether to give ACE inhibitors to all
patients or only to high-risk patients (those with signs of heart failure or left
ventricular dysfunction).
19,23
Oral or intravenous nitrate treatment is indicated
to relieve angina; intravenous nitrate treatment is recommended in patients
with recurrent angina and/or signs of heart failure.
22
Calcium channel blockers
are only recommended for symptom relief in patients already receiving nitrates
and beta-blockers and in patients with contraindications to beta-blockade.
Unstable angina/NSTEMI
Risk stratifi cation and prediction scores
All patients with suspected UA/NSTEMI should be classifi ed according to their
risk of short-term death or nonfatal MI (Table 2.2). In addition to providing
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CHAPTER 2 Coronary Artery Disease
prognostic information, risk categorization helps to guide initial management
decisions, including the decision to perform angiography with the provisional
use of revascularization. It is equally important to identify patients at low risk
in whom potentially hazardous and costly invasive and medical treatments
provide little benefi t or in fact may cause harm.
19,22,31
Validated and simple-
to-use risk prediction scores for UA/NSTEMI, such as the TIMI risk score,
the GRACE risk score, the PURSUIT risk score, and recently the ACTION
Registry-GWTG risk score, have similar discriminatory value and may also be
useful in guiding the selection of management strategies for patients with UA/
NSTEMI
34,36,37
(Table 2.3).
Management of NSTEMI
Aspirin should be administered to UA/NSTEMI patients as soon as possible
after hospital presentation and continued indefi nitely in patients who tolerate
it. (ACC/AHA—2012 Class I/Level of evidence [LOE]: A).
22
A P2Y12 inhibitor
should be added to aspirin as soon as possible and maintained over 12 months.
Table 2.2 Short-Term Risk of Death or MI in Unstable Angina
High Risk Intermediate Risk Low Risk
At least one feature
must be present:
• Prolonged (>20 min)
ongoing rest pain
• Angina at rest
with dynamic ST
depression >0.5 mm
or new bundle
branch block
• Angina with new
or worsening MR
murmur
• Angina with S3, new
or worsening rales,
or pulmonary edema
• Angina with hypo-
tension, bradycardia,
or tachycardia
• Age >75 years
• Elevated cardiac
troponins
(>0.1 ng/mL)
• Sustained ventricular
tachycardia
No high-risk features
but must have one of
the following:
• Prolonged (>20 min)
rest angina, now
resolved, with
moderate or
high likelihood of
coronary heart
disease
• Rest angina (<20 min)
relieved with
rest or sublingual
nitroglycerin
• Angina with dynamic
T-wave changes
>2.0 mm or abnormal
Q waves
• Aspirin use prior to
hospitalization
• Prior MI or CABG
• Peripheral
vascular disease or
cerebrovascular
disease
• Slightly elevated
cardiac troponins
(>0.01 ng/mL but
<0.1 ng/mL)
• Age >70 years
No high-or
intermediate-risk
features but may have
any of the following:
• New-onset angina
or progressive CCS
class III or IV angina
without prolonged
(>20 min) chest pain
but with moderate
or high likelihood of
coronary heart disease
• Normal or unchanged
ECG during chest
discomfort
• Cardiac markers not
elevated
Adapted from ACC/AHA Guideline Update for management of patients with Unstable Angina or
Non-ST-Elevation Myocardial Infarction, March 2002.
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CHAPTER 2 Coronary Artery Disease
Table 2.3 Risk Scores for UA/STEMI
TIMI GRACE PURSUIT ACTION-
Registry- GWTG
• Age >65 years
• >3 CAD risk
factors
• Known CAD
(>50% stenosis
• Prior aspirin
• >2 anginal
episodes in
prior 24 hours
• ST deviation
>0.5 mm of
presenting
ECG
• Elevated
cardiac markers
• Age
• Heart rate
• Systolic BP
(mmHg)
• Creatinine
(mg/dL)
• Killip class
• Cardiac arrest
at admission
• Elevated
cardiac
markers
• ST-segment
deviation
• Age
• Sex
• Worst
CCS class
in previous
6 weeks
• Signs of heart
failure
• ST depression
on presenting
ECG
• Age
• Creatinine
(mg/dL)
• Systolic BP
(mmHg)
• Troponin
• Heart rate
• Heart failure or
shock
• ST-segment
changes
• Prior peripheral
arterial disease
Adapted from references 36 and 37.
Ticagrelor, prasugrel, and clopidogrel (platelet P2Y12 inhibitors) are recom-
mended for all patients at moderate-to-high risk of ischemic events. According
to the CURRENT–OASIS 7 trial, in patients with ACS, there was no signifi cant
difference between a 7-day double-dose regimen of clopidogrel (600 mg load-
ing dose followed by 150 mg for 6 days, followed by standard dosing) and stan-
dard-dose clopidogrel (300 mg loading followed by daily 75 mg) with respect to
the primary outcome of cardiovascular death, MI, or stroke, although in those
receiving PCI, stent thrombosis was reduced. There was also no signifi cant dif-
ference between aspirin doses of 300 to 325 mg daily and doses of 75 to 100
mg daily with respect to the same outcome.
38
The 2012 ACC/AHA guidelines
suggest clopidogrel (Class I/LOE: B), ticagrelor (Class I/LOE: B), and prasugrel
(Class I/LOE: B—only at the time of PCI) for patients with defi nite UA/NSTEMI
at medium or high risk and in whom an initial invasive strategy is selected.
In patients in whom an initial conservative strategy is selected, clopidogrel or
ticagrelor (loading dose followed by daily maintenance dose) should be added
to aspirin and anticoagulant therapy as soon as possible after admission and
administered for up to 12 months. (Class I/LOE: B).
22,39,40
Anticoagulation is recommended for all patients in addition to antiplatelet
therapy. In comparison with unfractionated heparin (UFH), enoxaparin has a
more predictable anticoagulant effect and a lower incidence of thrombocytope-
nia and does not require serum monitoring. In patients with ACS treated with
a conservative strategy, enoxaparin is superior to UFH in preventing in-hospital
death or MI with similar rates of bleeding complications. In patients treated
invasively, enoxaparin therapy is associated with a higher rate of bleeding than
UFH, with a similar rate of death or MI. In conservatively treated patients at
high risk for bleeding, fondaparinux is the preferred antithrombotic agent, but
because of an excess of catheter-related thrombosis, it is infrequently used
in patients in whom an early invasive approach is planned. Bivalirudin is an
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CHAPTER 2 Coronary Artery Disease
acceptable antithrombotic option for patients treated with an invasive strategy,
particularly those considered at high risk for having a bleeding complication,
but is not recommended to patients conservatively treated.
19,22,34,41,42
An intra-
venous GP IIb/IIIa inhibitor is an option in patients in whom an invasive strategy
is planned before PCI (ACC/AHA—2012 Class I/LOE: A—intravenous eptifi -
batide and tirofi ban are preferred) or at the time of PCI (ACC/AHA—2012
Class I/LOE: B). Abciximab should not be administered to patients in whom PCI
is not planned (ACC/AHA—2012 Class III/LOE: A).
22,43
Early invasive versus conservative approach to revascularization
(and timing of intervention)
Many publications have assessed the effects of a routine invasive versus con-
servative or selective invasive approach in the short and long term, but there
is no clear evidence regarding very early angiography for UA/NSTEMI patients
managed invasively versus delayed angiography.
22
The TIMACS trial was a mile-
stone in this issue because it showed that early intervention (coronary angiog-
raphy 24 hours or less after randomization) did not differ greatly from delayed
intervention (coronary angiography 36 hours or more after randomization) in
preventing the primary outcome, but it did reduce the rate of the composite
secondary outcome of death, MI, or refractory ischemia and was superior to
delayed intervention in high-risk patients.
44
A recent meta-analysis, based on
the FRISC-2, ICTUS, and RITA-3 studies comparing a routine invasive versus
a selective invasive strategy, showed benefi t for early invasive management
through 1 year.
45
Therefore, in the high-risk patients for developing recurrent
ischemia or infarction despite intensive medical therapy, an early invasive strat-
egy is usually recommended; cardiac catheterization is performed (within 24 to
48 hours of admission) and coronary revascularization is accomplished percuta-
neously or surgically, if indicated. Clinical factors that favor an invasive approach
include old age, diabetes, previous MI, ST-segment depression, recurrent angina
at rest despite maximal medical therapy, elevated cardiac biomarkers, signs and
symptoms of heart failure, hemodynamic instability, sustained ventricular tachy-
cardia, recent percutaneous coronary intervention, history of coronary bypass
surgery, and depressed left ventricular systolic function.
22,23
Patients at very
high risk, such as those with ischemic pain that is refractory to the usual anti-
ischemic therapy, as well as those with hemodynamic or electrical instability
should have arteriography performed immediately, with a view to proceeding
with coronary revascularization within 2 hours of presentation (urgent invasive
strategy). It is important to state that early invasive management ensures only
early angiography and that revascularization decisions after early angiography
are complex and individualized based upon patient comorbidities and medical
history, coronary anatomy, and other aspects.
44
STEMI
Reperfusion therapy (PCI and fi brinolytic therapy)
It is well established that use of rapid reperfusion therapy with primary PCI
or fi brinolysis reduces infarct size, preserves left ventricular function, and
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