ST-Elevation Myocardial Infarction - PowerPoint Presentation

Slide1

ST-Elevation Myocardial Infarction(STEMI)

Greg Johnsen, MD, FACC, FSCAI

Slide2

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

Slide3

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%

Slide4

Slide5

Slide6

In the USA

All of the Following Risk Factors

Are Decreasing Except?

Hypertension

Smoking

Hypercholesterolemia

Diabetes

Slide7

Slide8

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

Slide9

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

Slide10

Vascular Injury and Atherosclerosis

Atherosclerosis

Chronic inflammatory process that develops in “response-to-injury”

metabolic environmental

genetic

physical infectious

Slide11

Slide12

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

Slide13

Acute 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

Slide14

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

Slide15

Acute Coronary Syndrome

Unstable Angina

Non-ST-Elevation MI

(NSTEMI)

ST-Elevation MI

(STEMI)

Slide16

Unstable 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

Slide17

Slide18

Slide19

Slide20

Characteristics of Plaques Prone to Rupture

Thin fibrous caps

Lipid, macrophage-rich

Smooth muscle poor

Slide21

Slide22

Slide23

Slide24

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

Slide25

Triggers of Plaque Rupture

Emotional Stress

Physical Activity

Increased Sympathetic Tone

Slide26

Triggers of Plaque Rupture

Heart Rate & Blood Pressure

Vasoconstriction

High Shear Stress

Physical and Emotional Stress

Infection

Inflammation

Slide27

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 non-cardiac surgical procedures can predispose to STEMI

Slide28

Risk Factors for ST-Elevation Myocardial Infarction & Cardiovascular Disease

Non-Modifiable Factors

Age

Male Gender

Family History of Cardiovascular Disease

Slide29

Risk Factors for ST-Elevation Myocardial Infarction & Cardiovascular Disease

Modifiable Factors

Cigarette Smoking

Hyperlipidemia

Hypertension

Diabetes

Obesity

Physical Inactivity

Diet

hsCRP

Slide30

Controversial Risk Factors for MI

Baldness

Gray Hair

Diagonal Earlobe Crease

(Frank’s Sign)

Slide31

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.

Slide32

Slide33

Slide34

Slide35

Slide36

Slide37

Inferior 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

Slide38

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.

Slide39

Slide40

Slide41

Slide42

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

Slide43

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

Slide44

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

Slide45

Time

Is

Muscle

Slide46

Slide47

Slide48

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.

Slide49

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

Slide50

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, 1

st

degree AV Block, evidence of low-output, asthma, and increased risk of

cardiogenic shock

Slide51

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

Slide52

Complications 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

Slide53

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

Slide54

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

Slide55

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

Slide56

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 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

Slide57

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

Slide58

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

Slide59

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.

Slide60

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

Slide61

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

Slide62

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

Slide63

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

Slide64

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

Slide65

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……..

Slide66

Slide67

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

Slide68

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.

Slide69

Slide70

Secondary Prevention10 Aspects of Treatment

Smoking

Diabetes

Blood Pressure Control

Antiplatelet agents/anticoagulants

Lipids

RAS Blockers

Physical Activity

Influenza Vaccine

Weight

Slide71

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.

Slide72

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

Slide73

Benefits 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

Slide74

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)

Slide75

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.