Transcript Document

ST-Elevation
Myocardial Infarction
(STEMI)
Greg Johnsen, MD, FACC, FSCAI
Epidemiology of Acute Myocardial Infarction
Coronary Heart Disease
•Leading cause of death in high or middle income countries
•Leading cause of death in the USA
•Rates of death from CHD have declined in most high income
countries
•Rates of death from CHD have increased in the developing
world
•In 2004, CHD became the leading cause of death in India
It is estimated that 1.25 million Americans have an
acute MI each year.
ST-Elevation MI accounts for 30 – 40%
In the early 1960’s, prior to the era of
cardiovascular intensive care units, in-hospital
mortality was greater than 30%.
Today, in-hospital mortality is 6.5 – 7.5%
In the USA
All of the Following Risk Factors
Are Decreasing Except?
1. Hypertension
2. Smoking
3. Hypercholesterolemia
4. Diabetes
Metabolic Syndrome
NCEP ATP III Definition (3 or more)
•Abdominal Obesity
– WC ≥102 cm in men (40 in), ≥88 cm (35 in) women
•Serum TG ≥150mg/dL or drug TX
•Serum HDL
–Men ≤40 mg/dl, Women ≤50 mg/dl
•BP ≥130/85 mmHg or drug Tx
•Fasting glucose ≥100 mg/dL or drug Tx
Points to Remember
•CV deaths have decline markedly since the
1960s
•It continues to drop in men but not women
•CVD is the leading cause of death but shifting
from CAD to HF
•Prevalence of risk factors decreasing in US
except diabetes
Vascular Injury and Atherosclerosis
Atherosclerosis
•Chronic inflammatory process that develops in
“response-to-injury”
metabolic
environmental
genetic
physical
infectious
Summary
•Chronic inflammatory process that develops in
“response-to-injury”
•Lipoprotein accumulation and oxidation
•Monocyte and T-lymphocyte recruitment
•Leads to plaque progression
•Leads to endothelial dysfunction
Acute Myocardial Infarction (MI)
•Reduction in myocardial perfusion which is sufficient
to cause cell necrosis
Most Common Mechanism of Myocardial Infarction
•Thrombus formation in the coronary artery at the site
of a ruptured, eroded, or fissured atherosclerotic
plaque
•Ruptured plaque exposes the thrombogenic lipids in
the plaque to the blood which leads to activation of
platelets and clotting factors
•Coronary plaques most prone to rupture have a rich
lipid core and a thin fibrous plaque
Other Rare Causes of
Acute Myocardial Infarction
•Coronary artery embolism from a valvular vegetation or
intracardiac thrombus
•Cocaine use
•Coronary artery dissection
•Anemia
•Hypotension
•Coronary Spasm
Acute Coronary Syndrome
Unstable Angina
Non-ST-Elevation MI
(NSTEMI)
ST-Elevation MI
(STEMI)
The Spectrum of Acute Coronary Syndromes
Unstable Angina
Anginal pain with at least
one of the following
features:
• Of new onset and
severe.
• Occurs at rest or
with minimal
exertion
• Pain is worsening in
severity and length
of each episode
and length of each
episode (i.e.,
crescendo pattern).
Non-ST-segment elevation MI
(NSTEMI)
Characterized by clinical
features of unstable angina in
addition to elevated cardiac
markers.
ST-segment elevation MI
(STEMI)
Characterized by clinical
features of myocardial
infarction in addition to STsegment elevation on a 12lead EKG.
Characteristics of Plaques
Prone to Rupture
•Thin fibrous caps
•Lipid, macrophage-rich
•Smooth muscle poor
What accounts for the
disparity between degree of
coronary artery stenosis and
producing the acute
coronary syndromes?
The functional state of the atheroma, not merely
its size or the degree of luminal encroachment,
determines the propensity for development of
acute coronary syndromes
Triggers of Plaque Rupture
•Emotional Stress
•Physical Activity
•Increased Sympathetic Tone
Triggers of Plaque Rupture
• Heart Rate & Blood Pressure
• Vasoconstriction
• High Shear Stress
• Physical and Emotional Stress
• Infection
• Inflammation
In half of patients with STEMI, a precipitating factor or
prodromal symptoms can be identified
Unusually heavy exercise in habitually inactive patients
and emotional stress can precipitate STEMI
Accelerating angina and rest angina may culiminate in
STEMI
Respiratory infections, hypoxemia, cocaine use and noncardiac surgical procedures can predispose to STEMI
Risk Factors for ST-Elevation
Myocardial Infarction &
Cardiovascular Disease
Non-Modifiable Factors
Age
Male Gender
Family History of Cardiovascular Disease
Risk Factors for ST-Elevation
Myocardial Infarction &
Cardiovascular Disease
Modifiable Factors
Cigarette Smoking
Hyperlipidemia
Hypertension
Diabetes
Obesity
Physical Inactivity
Diet
hsCRP
Controversial Risk Factors
for MI
•Baldness
•Gray Hair
•Diagonal Earlobe Crease
(Frank’s Sign)
Symptoms of Acute Myocardial Infarction
•Substernal chest pressure, usually described as heavy,
squeezing, tightness, crushing and sometimes stabbing or
burning pain (Levine’s sign).
•In STEMI, sudden onset of chest pain often associated with
shortness of breath, diaphoresis, weakness, nausea and
vomiting.
•The pain sometimes radiates to the C7 – T4 dermatomes
(left arm, shoulders, jaw, neck, back and epigastrium).
Radiation to both arms is a strong predictor of acute MI.
•In 20% of patients (diabetics, elderly, postoperative or
female) chest pain may be absent.
Inferior Leads = II, III, aVF
Right Coronary Artery or Left Circumflex Coronary Artery
Anterior Leads = V1 – V6
Left Anterior Descending Coronary Artery
Anterior Infarct = leads V2 – V5
Anteroseptal Infarct = leads V1 – V4
Anterolateral Infarct = leads V3 – V6, I + aVL
Lateral Leads = I + aVL, V5 – V6
Diagonal Branch Coronary Artery
Obtuse Marginal Branch Coronary Artery
Intermediate Ramus Branch
High Lateral Leads = I + aVL
Low Lateral Leads = V5 – V6
Left Main Occulsion
•ST elevation in aVR >1mm
•ST elevation in aVR > V1
•Widespread ST depression in multiple leads most
prominent in leads I, II, and V4 – V6
ST elevation in aVR may also be seen with proximal LAD
occlusion and severe triple-vessel disease.
Reperfusion Goals in ST-Elevation MI
(PCI = Percutaneous Coronary Intervention)
Primary PCI: Door to Balloon Time less than 90 minutes
Primary PCI: First medical contact to device time less than
90 minutes
Primary PCI: When transferred from a different hospital:
First medical contact to device time less than 120 minutes
Fibrinolytic therapy: Door to needle time less than 30
minutes
Guidelines for Primary PCI in STEMI
Class I
•Primary PCI should be performed within 12 hours of onset of
STEMI
•Primary PCI should be performed within 90 minutes of first
medical contact as a systems goal when presenting to a hospital
with PCI capability
•Primary PCI should be performed within 120 minutes of first
medical contact as a systems goal when presenting to a hospital
without PCI capability
•Primary PCI should be performed in patients with STEMI who
develop severe heart failure or cardiogenic shock and are suitable
for revascularization as soon as possible
Guidelines for Primary PCI in STEMI
Class IIa
•Primary PCI is reasonable in STEMI if there is clinical or
ECG evidence of ongoing ischemia between 12 and 24
hours after symptom onset
•PCI is reasonable in patients with STEMI and clinical
evidence for fibrinolytic failure or infarct artery reocclusion
Time
Is
Muscle
In 2006, the American College of
Cardiology launched the D2B Alliance, a
campaign to reduce systems delay in
the care of STEMI.
As a result, median door to balloon
times were reduced 32 minutes from 96
minutes to 64 minutes between 2005
and 2010.
Pre-hospital ECG Transmission to STEMI
Receiving Hospital
Reduces Door-to-Balloon Time
•Chart review of STEMI patients between January 1st,
2010 to November 25, 2010.
•Mean door-to-balloon time with a pre-hospital ECG
was 53 minutes.
•Mean door-to-balloon time without a pre-hospital ECG
was 77 minutes. (p = .0003)
Catheterization and Cardiovascular Interventions 2011; 77:S1
Acute Treatment of ST-Elevation MI
• 4 Aspirin 81mg chewed
• Plavix 600mg
• Heparin 5,000 units IV
• Morphine IV as needed for pain control
• Nitrates (NTG – sublingual and IV) – Contraindicated in RV Infarct,
Hypotension and severe bradycardia (HR less than 50)
• Metoprolol IV – Contraindicated in CHF, Hypotension bradycardia, 1st
degree AV Block, evidence of low-output, asthma, and increased risk of
cardiogenic shock
In-Hospital Treatment of ST-Elevation MI
• Aspirin
• Plavix, Effient, or Ticagrelor (Brilinta)
• Beta Blocker (Metoprolol or Carvedilol)
• High Dose Statin (Atrovastatin)
• ACE Inhibitor (Lisinopril) for LVEF less than 40% and or
pulmonary congestion
• Aldosterone Antagonist (Aldactone) for CHF
Complications of ST-Elevation MI
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Cardiogenic shock
Right Ventricular Infarction
Papillary Muscle Rupture
Ventricular Septal Rupture
Free Wall Rupture
Heart Block
Ventricular Fibrillation/Ventricular Tachycardia/Atrial
Fibrillation
Cardiogenic Shock
(7% of Acute MI)
• Decreased cardiac output with insufficient tissue
perfusion in the presence of adequate intravascular
volume
• Clinical signs: oliguria, cool, cyanotic extremeties,
altered mental status
• Hemodynamics; systolic BP less than 90, cardiac
index less than 2.2 and pulmonary capillary wedge
pressure greater than 15
Causes of Cardiogenic Shock
• Severe LV Dysfunction
• Extensive RV Infarction
• Mechanical Complications
• Acute MR due to papillary muscle rupture or dysfunction
• Ventricular Septal Defect
• Free wall rupture
Risk Factors for the
Development of Cardiogenic Shock
• Elderly (Age greater than 70)
• Diabetes
• Anterior Infarction
• Prior MI
• 3 Vessel or Left Main Coronary Artery Disease
• Early Use of Beta Blockers in Large Infarcts
Right Ventricular Infarction
• Usually occurs in association with inferior infarction
• Clinical findings include shock with clear lungs, elevated jugular venous
pressure, Kussmaul sign, and pulsus paradoxus
• EKG: ST elevation in right-sided leads V4R, V5R or V6R
• Hemodynamics: Elevated Right Atrial Pressure > 12
Normal to low pulmonary pressures
Pulmonary capillary wedge pressure < 15
• Management: volume expansion with normal saline IV,
prompt reperfusion; nitroglycerin is contraindicated
Acute Mitral Regurgitation
Papillary muscle Rupture (90% associated with inferior infarction)
• Acute Pulmonary Edema/Cardiogenic Shock
• Murmur of MR may be minimal or absent
• Diagnosis with Echocardiogram/Transesophageal Echocardiogram
• Treatment with Intra-aortic Balloon Pump, Nitroprusside and/or
Dobutamine, Mitral Valve Surgery ASAP
Ventricular Septal Defect
(55% due to inferior infarction, 45% due to anterior infarction)
• Acute onset of biventricular CHF or cardiogenic shock
• Holosystolic murmur and a precordial thrill
• Diagnosis with Echocardiogram
• Treatment with Intra-aortic Balloon Pump, Nitroprusside and/or
Dobutamine, eventual surgery
• Very high mortality
Free Wall Rupture
• LAD, Diagonal or Left Circumflex Coronary Artery Myocardial
Infactions. More frequent in elderly patients with a history of
hypertension.
• Usually presents as a catastrophic event – PEA due to
tamponade. Syncope and cardiogenic shock are also common.
May have pleuritic chest pain, nausea or restlessness.
• Diagnosis with pericardial effusion seen on echocardiogram.
• Treatment with emergency surgery, intra-aortic balloon pump.
Peak Time Periods for MI
• 6 a.m. – 12 Noon
• Monday is the most common day of the week
• Top 3 peak days for MI are Christmas day, the day after Christmas, and
New Years Day
• Spikes in incidence during major sporting events (Superbowl or World
Cup)
• Spikes in incidence with natural disasters (earthquakes, hurricanes,
etc.)
• Recent studies have shown an increased risk of MI after angry outbursts
Higher Risk of MI in the Morning
• Surge of stress hormone (cortisol) in the morning
• Surge of “fight or flight” (Catecholamines) in the morning
• Higher Blood Pressure and Heart Rate
• Platelets are more adhesive to the vessel wall in the morning
• Natural fibrinolytic system in the body is less active in the
morning
Higher Risk of MI in the Winter
(Multiple Factors Account for This)
• Blood vessels constrict and the blood clots more readily in cold weather
• Shoveling snow is a frequent trigger of MI
• In Australia, peak MI incidence is in June
• Florida, Southern California, and Hawaii also have a peak incidence of
MI in the winter months
Higher Risk of MI in the Winter
(Multiple Factors Account for This)
•
Inflammation can trigger a MI by making the coronary plaques less
stable
•
The Flu and respiratory infection cause significant inflammation
•
The Flu season peaks in the winter months in concert with peak
incidence of MI in winter
•
People eat more, exercise less, smoke more, have more stress, and
gain more weight during the holiday season
Higher Risk of MI in the Winter
(Multiple Factors Account for This)
• Shorter days with less UV radiation which leads to lower Vitamin D levels
• Less sunlight and shorter days lead to depression and seasonal affective
disorder
• People with depression are at an increased risk for developing heart
disease
• Blood pressure and weight both increase in the winter
The Perfect Storm for a Heart Attack
It is Monday morning, the day after Christmas. You are
suddenly awakened at 6:00 a.m. to the shaking and rattling of an
Oklahoma earthquake. Because of the surprise of the
earthquake, you forget to take your aspirin, plavix, lipitor,
metoprolol and metformin. You are angry and depressed because
you have just recovered from the flu and you have gained 10
pounds, and you have to go back to work at a high stress job.
You have a fight with your father-in-law because he is invading
your space and getting on your nerves. For comfort, you eat a
large piece of pecan pie and drink a large glass of eggnog for
breakfast, and then you smoke a cigarette. At 7:00 a.m., you go
out into the freezing cold to shovel a foot of snow off of your
driveway and it is a full moon. We all know what happens
next……..
•50 patients with recent STEMI were randomized into two
groups.
•24 enrolled in a 6 month exercise-based cardiac rehab
program (Group T)
•26 were discharged with generic instructions for maintaining
physical activity and correct lifestyle (Group C)
•All patients had an exercise myocardial perfusion study and
a cardiopulmonary exercise within 3 weeks after STEMI and
at 6 months
European Journal of Preventive Cardiology 2012 Dec; 19 (6) 1410 - 1419
At follow up, the cardiac rehab group (Group T) had:
• a significant reduction of stress-induced ischemia
(p < 0.001)
• improvement in resting and post-stress wall motion
(p < 0.005)
• improvement in peak oxygen consumption (p < 0.001)
At follow up, the generic instructions group (Group C) had no
change in myocardial perfusion parameters, LV function, and
cardiopulmonary indexes.
Secondary Prevention
10 Aspects of Treatment
 Smoking
 Diabetes
 Blood Pressure Control
 Antiplatelet agents/anticoagulants
 Lipids
 RAS Blockers
 Physical Activity
 Influenza Vaccine
 Weight
Benefits of Cardiac Rehabilitation
• 20 – 30% reduction in all-cause mortality rates
•Decreases mortality at up to 5 years post participation
•Reduced symptoms (angina, dyspnea, fatigue)
•Reduction in non-fatal recurrent myocardial infarction
over a median follow-up 12 months.
Benefits of Cardiac Rehabilitation
• Improves adherence with preventive medications
• Increased exercise performance
• Improved lipids (total cholesterol, HDL, LDL, and
triglycerides)
• Improved knowledge about cardiac disease and its
management
• Enhanced ability to perform activities of daily living
Benefits of Cardiac Rehabilitation
• Improved health-related quality of life
• Improved psychosocial symptoms and increased selfefficacy
• Reduced hospitalization and use of medical resources
• Return to work or leisure activities
Summary
•In the USA, cardiovascular deaths have declined markedly since the 1960s.
•Rates of death from CHD have declined in most high income countries but
are increasing in the developing world.
•In the USA, the prevalence of risk factors are all decreasing except for
diabetes.
•Atherosclerosis is a chronic inflammatory process that develops in “response
to injury”.
•Most commonly, STEMI occurs secondary to plaque rupture or plaque erosion
with total occlusion of the coronary artery with thrombus.
•Coronary plaques prone to rupture have a thin fibrous cap with a lipid rich
core with a lot of inflammation (T - lymphocytes and macrophages)
Summary
•Triggers of plaque rupture include emotional stress, physical activity and
increased sympathetic tone.
•Higher risk of mortality and complications in STEMI with a late presentation,
inadequate reperfusion or delayed reperfusion.
•Higher incidence of MI on Mondays, 6 a.m. to 12 Noon, in the winter, around
the holidays, and during flu season.
•Higher incidence of MI during natural disasters and with people who have a
history of depression and angry outbursts.
•Cardiac Rehab has been show to reduce myocardial ischemia.
•Cardiac Rehab leads to a 20 – 30% reduction in all cause mortality and a
reduction in non-fatal recurrent myocardial infarction.