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 ID: 775392
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Slide1
ST-Elevation Myocardial Infarction(STEMI)
Greg Johnsen, MD, FACC, FSCAI
Slide2Epidemiology 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
Slide3It 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%
Slide4Slide5Slide6In the USA
All of the Following Risk Factors
Are Decreasing Except?
Hypertension
Smoking
Hypercholesterolemia
Diabetes
Slide7Slide8Metabolic 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
Slide9Points 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
Slide10Vascular Injury and Atherosclerosis
Atherosclerosis
Chronic inflammatory process that develops in “response-to-injury”
metabolic environmental
genetic
physical infectious
Slide11Slide12Summary
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
Slide13Acute Myocardial Infarction (MI)
Reduction in myocardial perfusion which is sufficient to cause cell necrosis
Most Common Mechanism of Myocardial Infarcti
on
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
Slide14Other 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
Slide15Acute Coronary Syndrome
Unstable Angina
Non-ST-Elevation MI
(NSTEMI)
ST-Elevation MI
(STEMI)
Slide16Unstable AnginaNon-ST-segment elevation MI(NSTEMI)ST-segment elevation MI(STEMI)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).Characterized by clinical features of unstable angina in addition to elevated cardiac markers. Characterized by clinical features of myocardial infarction in addition to ST-segment elevation on a 12-lead EKG.
The Spectrum of Acute Coronary Syndromes
Slide17Slide18Slide19Slide20Characteristics of Plaques Prone to Rupture
Thin fibrous caps
Lipid, macrophage-rich
Smooth muscle poor
Slide21Slide22Slide23Slide24What 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
Slide25Triggers of Plaque Rupture
Emotional Stress
Physical Activity
Increased Sympathetic Tone
Slide26Triggers of Plaque Rupture
Heart Rate & Blood Pressure
Vasoconstriction
High Shear Stress
Physical and Emotional Stress
Infection
Inflammation
Slide27In 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 non-cardiac surgical procedures can predispose to STEMI
Slide28Risk Factors for ST-Elevation Myocardial Infarction & Cardiovascular Disease
Non-Modifiable Factors
Age
Male Gender
Family History of Cardiovascular Disease
Slide29Risk Factors for ST-Elevation Myocardial Infarction & Cardiovascular Disease
Modifiable Factors
Cigarette Smoking
Hyperlipidemia
Hypertension
Diabetes
Obesity
Physical Inactivity
Diet
hsCRP
Slide30Controversial Risk Factors for MI
Baldness
Gray Hair
Diagonal Earlobe Crease
(Frank’s Sign)
Slide31Symptoms 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.
Slide32Slide33Slide34Slide35Slide36Slide37Inferior Leads = II, III,
aVF
Right Coronary Artery or Left Circumflex Coronary Artery
Anterior Leads = V
1
– V
6
Left Anterior Descending Coronary Artery
Anterior Infarct = leads V
2
– V
5
Anteroseptal
Infarct = leads V
1
– V
4
Anterolateral
Infarct = leads V
3
–
V
6
,
I +
aVL
Lateral Leads = I +
aVL
, V
5
– V
6
Diagonal Branch Coronary Artery
Obtuse Marginal Branch Coronary Artery
Intermediate
Ramus
Branch
High Lateral Leads = I +
aVL
Low Lateral Leads = V
5
– V
6
Left Main Occulsion
ST elevation in aVR >1mm
ST elevation in aVR > V
1
Widespread ST depression in multiple leads most prominent in leads I, II, and V
4
– V
6
ST elevation in aVR may also be seen with proximal LAD occlusion and severe triple-vessel disease.
Slide39Slide40Slide41Slide42Reperfusion 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
Slide43Guidelines 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
Slide44Guidelines 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
Slide45Time
Is
Muscle
Slide46Slide47Slide48In 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.
Slide49Pre-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
Slide50Acute 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, 1
st
degree AV Block, evidence of low-output, asthma, and increased risk of
cardiogenic shock
Slide51In-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
Slide52Complications of ST-Elevation MI
Cardiogenic shock
Right Ventricular Infarction
Papillary Muscle Rupture
Ventricular Septal Rupture
Free Wall Rupture
Heart Block
Ventricular Fibrillation/Ventricular Tachycardia/Atrial
Fibrillation
Slide53Cardiogenic 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
Slide54Causes 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
Slide55Risk 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
Slide56Right 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 V
4
R, V
5
R or V
6
R
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
Slide57Acute 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
Slide58Ventricular 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
Slide59Free 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.
Slide60Peak 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
Slide61Higher 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
Slide62Higher 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
Slide63Higher 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
Slide64Higher 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
Slide65The 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……..
Slide66Slide6750 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
Slide68At 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.
Slide69Slide70Secondary Prevention10 Aspects of Treatment
Smoking
Diabetes
Blood Pressure Control
Antiplatelet agents/anticoagulants
Lipids
RAS Blockers
Physical Activity
Influenza Vaccine
Weight
Slide71Benefits 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.
Slide72Benefits 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
Slide73Benefits of Cardiac Rehabilitation
Improved health-related quality of life
Improved psychosocial symptoms and increased self-efficacy
Reduced hospitalization and use of medical resources
Return to work or leisure activities
Slide74Summary
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)
Slide75Summary
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.