Transcript Internal Medicine Board Review: Cardiology Acute Coronary

Internal Medicine Board Review:
Cardiology
Acute Coronary Syndrome
Christine Nardi
May 20, 2009
Hospitalizations in the U.S. Due to
ACS
Incidence rate of MI
has not
changed but survival has
Acute Coronary
Syndromes*
1.57 Million Hospital Admissions - ACS
UA/NSTEMI†
STEMI
1.24 million
0.33 million
Admissions per year
Admissions per year
*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69–171.
Acute Coronary Syndrome
• Clinical syndromes caused by acute myocardial
ischemia
– Unstable angina
• Angina at rest or new onset angina, accelerating symptoms
• No detectable increase of biomarkers
– Non-ST-elevation MI
• Angina at rest or new onset angina, accelerating symptoms
• Detectable release of biomarkers
– ST-elevation MI
• Clinical presentation of acute myocardial infarction with EKG
evidence of ST-segment elevation
Timing of Release of Various Biomarkers
After Acute Myocardial Infarction
Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3 rd ed. Rochester, MN:
Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80.
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.
Pathophysiology: unstable angina
and NSTEMI
• Spontaneous rupture of
lipid-laden, macrophage
rich atherosclerotic
plaques leading to
platelet activation and
thrombosis
• Leads to episodic
cessation of coronary
blood flow, ischemia and
pain
• Rarely, caused by
vasospasm (Prinzmetal’s
or cocaine)
Causes of UA/NSTEMI*
• Thrombus or thromboembolism, usually arising on disrupted or
eroded plaque
– Occlusive thrombus, usually with collateral vessels†
– Subtotally occlusive thrombus on pre-existing plaque
– Distal microvascular thromboembolism from plaque-associated
thrombus
– Thromboembolism from plaque erosion
• Non–plaque-associated coronary thromboembolism
• Dynamic obstruction (coronary spasm‡ or vascoconstriction) of
epicardial and/or microvascular vessels
• Progressive mechanical obstruction to coronary flow
• Coronary arterial inflammation
• Secondary UA
• Coronary artery dissection§
*These causes are not mutually exclusive; some patients have 2 or more causes. †DeWood MA, et al. N Engl J Med 1986;315:417–23. ‡May occur
on top of an atherosclerotic plaque, producing missed-etiology angina or UA/NSTEMI. §Rare. Modified with permission from Braunwald E. Circulation
1998;98:2219–22. Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Table 3.
Pathophysiology of STEMI
• Occlusive thrombus that
develops on a dissected
or ulcerative
atherosclerotic plaque,
resulting in complete
epicardial coronary artery
occlusion
• Moderately sized plaques
are more common than
those causing severe
stenosis
Evaluation
•
•
•
•
History
Physical exam
EKG
Cardiac biomarkers
Variables Used in the TIMI Risk Score
•Age ≥ 65 years
•At least 3 risk factors for CAD
•Prior coronary stenosis of ≥ 50%
0-2 low risk (5%)
3-4 intermediate risk
5-7 high risk (40%)
•ST-segment deviation on ECG presentation
•At least 2 anginal events in prior 24 hours
•Use of aspirin in prior 7 days
•Elevated serum cardiac biomarkers
The TIMI risk score is determined by the sum of the presence of the above 7 variables at admission. 1 point is given for each variable.
Primary coronary stenosis of 50% or more remained relatively insensitive to missing information and remained a significant predictor of
events. Antman EM, et al. JAMA 2000;284:835–42.
TIMI = Thrombolysis in Myocardial Infarction.
Selection of Initial Treatment Strategy: Initial
Invasive Versus Conservative Strategy
Invasive
Recurrent angina/ischemia at rest with low-level activities despite
intensive medical therapy
Elevated cardiac biomarkers (TnT or TnI)
angiography
New/presumably new ST-segment depression
Signs/symptoms of heart failure or new/worsening mitral regurgitation
High-risk findings from noninvasive testing
Hemodynamic instability
Sustained ventricular tachycardia
PCI within 6 months
Prior CABG
High risk score (e.g., TIMI, GRACE)
Reduced left ventricular function (LVEF < 40%)
Conservative Low risk score (e.g., TIMI, GRACE)
Patient/physician presence in the absence of high-risk features
Stress testing
UA/NSTEMI
Statin
ASA and/or
clopidogrel
B-blocker
Nitrate
Heparin/LMWH
TIMI 5-7
yes
GP IIb/IIIa inhibitor
TIMI 1-2
TIMI 3-4
Recurrent angina
Elevated trop
New ST depression
CHF
Prior CABG
PCI within 6 mo
Sustained VT
Hemodynamic
instability
no
Stress imaging
study
Positive
Or EF<40
normal
cath
Medical therapy
Short-Term Risk of Death/Nonfatal MI in Patients With UA/NSTEMI
Feature
High Risk
Intermediate Risk
Low Risk
≥ 1 of the
features
below must
be present:
No high-risk features, but must have
1 of the following:
No high- or intermediaterisk features but may
have any features below:
History
Accelerating
tempo of
ischemic sx
in preceding
48 h
Prior MI, peripheral or
cerebrovascular disease, or CABG;
prior ASA use
Character
of pain
Prolonged
ongoing (>
20 min) rest
pain
• Prolonged (> 20 min) rest angina,
• ↑ Angina frequency,
now resolved, w/ moderate/high
severity or duration
likelihood of CAD
• Angina provoked at
• Rest angina (> 20 min) or relieved
lower threshold
with rest or sublingual NTG
• New onset angina with
• Nocturnal angina
onset 2 wks to 2 mos
prior to presentation
• New-onset or progressive CCS
class III/IV angina in past 2 wks
w/o prolonged (> 20 min) rest pain
but with intermediate/high
likelihood of CAD
Short-Term Risk of Death/Nonfatal MI in Patients With UA/NSTEMI,
Continued
Feature High risk
Intermediate risk
Low risk
Clinical
findings
• Pulmonary edema, most
likely due to ischemia
• New/worsening MR
murmur
• S3 or new/worsening rales
• Hypotension, bradycardia,
tachycardia
• Age > 75 y
Age > 70 y
ECG
•Angina @ rest with
transient ST-segment
changes > 0.5 mm
•BBB, new/presumed new
•Sustained VT
• T-wave changes
• Pathological Q-waves/resting STdepression < 1 mm in multiple
lead groups (anterior, inferior,
lateral)
Normal or
unchanged
ECG
Cardiac
markers
↑ Cardiac TnT, TnI, or CK-MB
(e.g., TnT/TnI > 0.1 ng/mL)
Slightly ↑ cardiac TnT, TnI, or CKMB (e.g., TnT > 0.01, but < 0.1
ng/mL)
Normal
Estimation of the short-term risk of death and nonfatal cardiac ischemic events in UA/NSTEMI is a complex multivariable problem that cannot be
fully specified in a table such as this; this table is mean to offer general guidance & illustration rather than rigid algorithms. Braunwald E, et al.
AHCPR Publication No. 94-0602:1–154. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Table 7.
Long-Term Antithrombotic Therapy at Hospital
Discharge after UA/NSTEMI
UA/NSTEMI
Patient Groups at
Discharge
Medical Therapy
without Stent
ASA 75 to 162 mg/d indefinitely
(Class I, LOE: A)
Bare Metal Stent
Group
Drug Eluting
Stent Group
ASA 162 to 325 mg/d for at least 1
month, then 75 to 162 mg/d
indefinitely (Class I, LOE: A)
&
&
Clopidogrel 75 mg/d for at least 1
month and up to 1 year
(Class I, LOE:B)
Clopidogrel 75 mg/d at least 1
month (Class I, LOE: A) and up
to 1 year (Class I, LOE: B)
ASA 162 to 325 mg/d for at
least 3 to 6 months, then 75 to
162 mg/d indefinitely
(Class I, LOE: A)
&
Clopidogrel 75 mg/d for at
least 1 year (Class I, LOE: B)
Indication for
Anticoagulation?
Yes
Add: Warfarin (INR 2.0 to 2.5)
(Class IIb, LOE: B)
No
Continue with dual antiplatelet
therapy as above
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 11. INR = international normalized ratio; LOE = level of evidence.
Management of STEMI
• PCI
– Higher vessel patency,
lower reinfarction and
stroke rates,
immediate risk
stratification
– Should be performed if
presenting within 12
hours of symptom
onset if a skilled PCI
lab is available
• Fibrinolytic therapy
– Highly available, ease
of use
– If no contraindications
and no PCI available,
fibrinolytics should be
administered within 30
minutes from arrival to
ED (if symptoms
started within the last
12 hours)
Absolute Contraindications to
Fibrinolytics
•
•
•
•
•
•
•
Prior intracranial hemorrhage
Known structural cerebral vascular lesion (AVM)
Known malignant intracranial neoplasm
Ischemic stroke without 3 months
Suspected aortic dissection
Active bleeding (excluding menses)
Significant closed-head injury or facial trauma
within 3 months
Mortality Predictors in STEMI
•
•
•
•
•
•
Age > 65 years
Clinically evident heart failure
Diabetes
Renal failure
Previous myocardial infarction
Time of presentation (reperfusion less
successful 12 hours after symptom onset)
Complications during STEMI
• Hypotension
– Hypovolemia, increased vagal tone, low CO, hypoxia,
rhythm disturbances
• Pulmonary congestion
– O2, nitrates, morphine, diuretics when appropriate
• RV infarction
– Hypotension, elevated JVP, inferior STEMI,
bradcardia
– ST-elevation in V4R
– Treatment: fluids, temporary pacemaker
Complications after STEMI
• Occur in 0.1% of STEMI patients 2-7 days after
infarction
–
–
–
–
Ventricular septal defect
Papillary muscle rupture (acute MR)
Left ventricular free wall rupture (tamponade)
pericarditis
• New systolic murmur (VSD or MR)
• Diagnosed with echo or Swan-Ganz catheter
– VSD: O2 saturation step-up
– Tamponade: equalization of diastolic pressures in all
heart chambers
Key Points
• Intermediate and high risk patients with UA or
NSTEMI benefit from an early invasive strategy
with angiography
• Early management of UA or NSTEMI includes
ASA, heparin, nitrates, b-blocker, GP IIb/IIIa
inhibitor, clopidogrel and statin
• LMWH (enoxaparin) is a suitable alternative to
unfractionated heparin for patients with acute
coronary syndrome or STEMI and those
undergoing early PCI
Key Points
• Clinical predictors of mortality in patients with
acute STEMI are time to presentation after
symptom onset, age>65, heart failure, DM, renal
failure and previous MI
• Immediate reperfusion, preferable with PCI,
should be performed for any STEMI
• Most patients with STEMI should be started
early on oral b-blocker
• STEMI patients with anterior infarction,
pulmonary congestion, or a LVEF<40% should
be started on an ACE inhibitor
Differential Diagnosis
•
•
•
•
•
Aortic dissection
Pulmonary embolus
Perforating ulcer
Tension pneumothorax
Esophageal rupture (Boerhaave’s
syndrome)
Key Points
• In patients with STEMI, successful fibrinolysis is
suggested by resolution of chest pain and STsegment elevation and/or transient ventricular
arrhythmias early after reperfusion.
• In patients with STEMI, reperfusion arrhythmias
usually do not require therapy.
• Immediate coronary angiography is not indicated
unless recurrent ischemia, persistent ST
elevation or hemodynamic instability (including
CHF) occurs.
Key Points
• Patients with STEMI should undergo
coronary reperfusion in the most
expeditious manner
• STEMI patients who cannot be reperfused
by direct coronary intervention within 90 to
120 minutes should receive fibrinolytic
therapy if there are no contraindications
Key Points
• Ascending aortic dissection may involve
the coronary arteries, most commonly the
RCA
• Ascending aortic dissection may lead to
disruption of the aortic valve, leading to
aortic regurgitation
Key Points
• Glycoprotein receptor blockade is
indicated for patients with acute coronary
syndrome who will undergo coronary
angiography and intervention
Key Points
• Medical therapy for acute, recent myocardial infarction
includes B-blocker, aspirin, ACE-inhibitor and statins
• This is an uncomplicated (based on the absence of
further symptoms and EKG changes) anterior STEMI
• Late fibrinolysis is not beneficial for most patients and
may be associated with an increase of transformation to
a hemorrhagic zone of infarction
• A glycoprotein IIb/IIIa blocker in addition to aspirin and
heparin is indicated for patients with continuing ischemia,
elevated troponin level or other high-risk features
including angina at rest with ST changes and CHF
Key Points
• In patients with chest pan and intermediate risk of CAD,
non-invasive testing is indicated
• Patients with chest pain and low coronary artery disease
risk with a normal EKG and a normal exercise EKG can
be discharged without coronary angiography
• Immediate coronary angiography would be appropriate if
there were high risk markers:
–
–
–
–
Elevated enzymes
Hypotension
Decreased LVEF
New EKG changes in a patient with unstable angina or NSTEMI
Key Points
• Right ventricular infarction is a cause of
hypotension following inferior infarction
and typically requires appropriate volume
infusion
• Right ventricular infarction should be
suspected as a cause of hypotension
when findings of right heart failure
coincides with an absence of evidence of
pulmonary congestion
Key Points
• Papillary muscle rupture and ventricular
septal defect are recognized mechanical
complications that occur early after
myocardial infarction
• Both papillary muscle rupture and
ventricular septal defect present with
hypotension and acute dyspnea