Laboratory
Findings
| At
the time of presentation with AMI: |
| TC: |
174 mg/dL
|
| HDL-C: |
40 mg/dL
|
| LDL-C: |
110 mg/dL
|
| VLDL-C: |
24 mg/dL
|
| Hs-CRP: |
0.587 mg/dL
(significantly higher than normal)
|
Guidelines
for the Case Patient
According to ATP III, the case patient's LDL-C
goal before his MI would have been <160 mg/dL; after
the MI, however, his LDL-C target drops to <100 mg/dL.
To view a presentation by Dr Nissen on the synergistic
roles of invasive and noninvasive therapies, please
click on CME
Activities and view our CD-ROM, "Exploring the Continuum
of CHD Risk." |
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56-Year-Old Male With Ruptured Atherosclerotic Plaque Distant
From the Culprit Lesion of an AMI
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Paul
Schoenhagen, MD |
|
Steven
E. Nissen, MD |
The following case was provided by Paul Schoenhagen, MD,
and Steven E. Nissen, MD. Dr Schoenhagen is a Fellow, Cardiovascular
Medicine, at the Cleveland Clinic Foundation. Dr Nissen, an
NLEC Faculty Member, is Vice Chairman, Cardiology Department,
the Cleveland Clinic Foundation; Professor of Medicine, Clinical
Cardiology, at the Cleveland Clinic Campus of Ohio State University;
and Medical Director of the Cleveland Clinic Cardiovascular
Coordinating Center.
Disclosure Information for Dr Schoenhagen: None.
Disclosure Information for Dr Nissen: Consultant or Research
Study: Pfizer Inc; Merck & Co., Inc. AstraZeneca; Sankyo Pharma
Inc.; Takeda Pharmaceuticals North America, Inc., Guidant; Aventis;
Fournier; Boston Scientific; Pharmacyclics; Celltech; Esperion.
A 56-year-old male presented to the
emergency room several hours after the onset of fluctuating
substernal chest pain. His electrocardiogram showed ST elevations
in the anterior leads, but Q waves were already present, consistent
with an evolving anterolateral myocardial infarction (MI) (Figure
1). The patient was immediately taken to the cardiac catheterization
laboratory. Coronary angiography showed complete occlusion of
the left anterior descending (LAD) coronary artery, which was
reopened during subsequent intervention with excellent final
results (Figure 2). The patient had no previous history
of coronary artery disease (CAD). He quit smoking 40 years ago
and had no history of hypertension or hyperlipidemia. There
was no family history of CAD. His angiogram showed an additional
suspicious site in the proximal LAD, which was further evaluated
with intravascular ultrasound (IVUS).
IVUS
Findings
Examination of the proximal LAD revealed a ruptured plaque several
centimeters proximal to the acute myocardial infarction "culprit
lesion" site (Figures 3 and 4). This site did not represent
a clinically significant stenosis and ordinarily would not be
considered for intervention.
Discussion
The presentation of this patient exemplifies a common dilemma
in the treatment and prevention of major coronary events.
The patient is relatively young, and his risk-factor profile
includes only a remote history of smoking. His first symptom
of CAD is an unheralded AMI. Recent studies show that most
acute coronary events are caused by the sudden rupture of
vulnerable plaques.1,2 These
lesions are most often mildly stenotic before rupture, and
it is the formation of thrombus following plaque rupture that
occludes the vessel. Unfortunately, AMI and sudden coronary
death are the initial manifestations of CAD in more than 50%
of patients.3
Despite contemporary treatments, the prognosis
in such patients remains guarded, particularly when inflammatory
markers such as high-sensitivity C-reactive protein (hs-CRP)
are elevated. Emerging data regarding CRP suggest that the
systemic inflammatory state associated with active atherosclerosis
is one of the factors influencing outcome. With this background,
it should not be surprising that additional ruptured plaques
are frequently found in patients presenting with stable and
unstable coronary syndromes. In our patient, there is dramatic
evidence of an additional plaque rupture in the proximal LAD
(Figures 3 and 4).
A recent angiographic study by Goldstein
et al has found evidence of additional complex angiographic
lesions in almost 30% of patients presenting with AMI.4
Similarly, an angioscopic study from Japan showed additional
vulnerable lesions in a large percentage of patients presenting
with AMI.5 These findings
help explain the very high risk of recurrent MI and death
in patients during the first year following an acute coronary
syndrome. Atherosclerotic disease burden is often substantial
in both symptomatic and asymptomatic patients. Necropsy studies
have shown that atherosclerotic lesion development begins
in childhood and that advanced lesions are frequently found
in young adults.6 In a recent
intravascular ultrasound study, our group has shown that atherosclerotic
lesion can be found in more than 80% of people in the age
group of the presented patient.7
Importantly, early lesion development is
associated with vessel expansion (positive remodeling) rather
than with luminal stenosis; therefore, it is not appreciated
during stress testing or angiography.8
Recent studies show that positive remodeling is more frequent
in patients presenting with AMI, indicating that vulnerable
lesions are usually not highly stenotic.9,10
These findings demonstrate that current
diagnostic tools show only the tip of an "atherosclerotic
iceberg"11 (Figure 5).
In the future, systemic markers (genetic, inflammatory) and
imaging techniques (IVUS, CT, MRI) may allow assessment of
plaque burden and vulnerability.12-15
It is interesting to note that the presented patient had an
elevated hs-CRP on admission (see Laboratory Findings).
Treatment
It is now evident from prospective clinical trials,
such as the Myocardial Ischemia Reduction with Aggressive
Cholesterol Lowering Study, that lipid-lowering treatment
of even mildly elevated LDL-C levels can substantially reduce
the incidence of clinical events following an acute coronary
syndrome.16 Our case patient
was treated with high-dose (80 mg) atorvastatin to lower the
risk of a recurrent coronary event.
For the clinician, there are several important
consequences:
 |
The treatment of the culprit lesion in the patient presenting
with AMI is only the first step in a continuum of care.
Because of the systemic nature of CAD, the subsequent
treatment directed at additional lesions is important
in order to both prevent recurrent events and affect long-term
outcome.17 Currently,
this treatment consists of aggressive lipid modification—as
demonstrated by the MIRACL study—as well as control
of other risk factors. The hospital physicians, the cardiologist,
and the primary care physician share responsibility for
ensuring the appropriate follow-up of these patients.18
|
|
The case presentation also shows the limitations
of current treatment guidelines. Based on his conventional
risk-factor profile, the patient would not have been a
candidate for intensified preventive interventions despite
his significant, but unrecognized, disease burden (see
Guidelines for the Case Patient). Future guidelines
will likely include additional patient groups based on
emerging risk factors. However, until clinical evidence
is available, the practitioner should aggressively follow
current guidelines. 
|
References
| |
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| 16. |
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