Myocardial Infarction

ByChiranjeevi PudiV Pharm D (2013-14)

CLASSIFICATION• Acute coronary syndromes include ST-elevation MI (STEMI) Non ST-elevation MI ( NSTEMI) Unstable Angina

PREVALENCE

• In the US, 1.3 million cases of nonfatal MI were reported in 2006• Incidence of 600 per 100,000 people• Increase in the proportion of NSTEMI compared

to STEMI• Approximately 500,000 to 700,000 deaths are

caused by heart disease

HISTORY The history is critical in making the diagnosis of

MI and sometimes provide only the only clues that lead to the diagnosis in the initial phase of presentation Chest Pain- anterior precordium tightness• Pain may radiate to jaw, neck and epigastrium• Dyspnea- angina equivalent, poor LV function• Nausea/abdominal pain with posterior MI• Anxiety

HISTORY• Nausea with and without vomiting• Diaphoresis or sweating• Syncope• Elderly present with MS changes, fatigue,

syncope or weakness• As many as half of MI are clinically silent

CAUSES• Most frequent cause is rupture of an

atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation• Coronary artery vasospasm• Ventricular hypertrophy• Hypoxia• Coronary artery emboli

RISK FACTORS FOR ATHEROSCLEROSIS• Age• Smoking• Hypercholesterolemia and triglyceridemia• Diabetes Mellitus• Poorly controlled hypertension• Family History• Sedentary lifestyle

PATHOPHYSIOLOGY

Mechanisms of Myocardial damage

The severity of an MI is dependent of three factors• The level of the occlusion in the coronary• The length of time of the occlusion• The presence or absence of collateral circulation

CARDIAC BIOMARKERS• Cardiac biomarkers are protein molecules

released into the blood stream from damaged heart muscle • Since ECG can be inconclusive , biomarkers are

frequently used to evaluate for myocardial injury• These biomarkers have a characteristic rise and

fall pattern

Troponin T and I• These isoforms are very specific for cardiac

injury• Preferred markers for detecting myocardial cell

injury• Rise 2-6 hours after injury Peak in 12-16 hours Stay elevated for 5-14 days

Creatinine Kinase ( CK-MB)• Creatinine Kinase is found in heart muscle (MB),

skeletal muscle (MM), and brain (BB)• Increased in over 90% of myocardial infraction• However, it can be increased in muscle trauma,

physical exertion, post-op, convulsions, and other conditions

CK-MB• Time sequence after myocardial infarction Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2 days• MB2 released from heart muscle and converted

to MB1.• A level of MB2 > or = 1 and a ratio of MB2/MB1

> 1.5 indicates myocardial injury

MYOGLOBIN• Damage to skeletal or cardiac muscle release

myoglobin into circulation• Time sequence after infarction Rises fast 2hours Peaks at 6-8 hours Returns to normal in 20-36 hours• Have false positives with skeletal muscle injury

and renal failure

CBC

•CBC is indicated if anemia is suspected as precipitant

•Leukocytosis may be observed within several hours after myocardial injury and returns to levels within the reference range within one week

C-reactive Protein (CRP)

• C- reactive protein is a marker of acute inflammation

• Patients without evidence of myocardial necrosis but with elevated CRP are at increased risk of an event

Release of cardiac markers after acute myocardial infarction (AMI)

CHEST X-RAY

• Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax)

• Chest radiography also reveals complications of myocardial infarction such as heart failure

ECG• An ECG can be used to detect patterns of

ischemia, injury, and infarctionIschemia • On the ECG, myocardial ischemia results in T-

wave inversion or ST segment depression in the leads facing the ischemic area. • The inverted T wave representative of ischemia is

symmetrical, relatively narrow, and somewhat pointed.

Injury• the injury process begins in the subendocardial layer

and moves throughout the thickness of the wall of the heart like a wave.• If the process is not interrupted, it eventually results

in a transmural MI.• On ECG, the hallmark of acute myocardial injury is

the presence of ST segment elevations.• With an acute injury, the ST segments in the leads

facing the injured area are elevated. • The elevated ST segments also have a downward

concave or coved shape and merge unnoticed with the T wave

(A)ST segment elevation without T-wave inversion.

(B) ST segment elevation with T-wave inversion. The elevated ST segments have a downward concave or coved shape and merge unnoticed with the T wave.

INFARCTION When myocardial injury persists, MI is the result. • During the earliest stage of MI, known as the hyperacute phase, the T

waves become tall and narrow. This configuration is referred to as hyperacute or peaked T waves.

• Within a few hours, these hyperacute T waves invert.• Next, the ST segments elevate, a pattern that usually lasts from several

hours to several days. • In addition to the ST segment elevations in the leads of the ECG facing the

injured heart, the leads facing away from the injured area may show ST segment depression.

• This finding is known as reciprocal ST segment changes. • Reciprocal changes are most likely to be seen at the onset of infarction, but

their presence on the ECG does not last long.• Reciprocal ST segment depressions may simply be a mirror image of the

ST segment elevations.

Therapy

The goals of therapy in AMI are the expedient restoration of normal coronary flow and the maximum salvage of functional myocardium

Antiplatelet Agents• Aspirin at least 160–162 mg on hospital day 1Followed by 75–162 mg daily starting hospital day 2

and continued indefinitely. • Interferes with function of cyclooxygenase and

inhibits the formation of thromboxane• Clopidogrel is also used which acts through a

blockade of ADP receptors on platelets• 300–600 mg loading dose on hospital day 1

followed by a maintenance dose of 75 mg PO qd starting on hospital day 2 Administer indefinitely in patients with an aspirin allergy.

Nitrates• Nitrates promote the release of nitric oxide from the

endothelium, which results in venous and arterial vasodilation• Vasodilatation reduces myocardial oxygen demand and preload

and afterload• 0.4 mg , repeated every 5 min × 3 doses• 5 to 10 mcg/min by continuous infusion titrated up to 75 to 100

mcg/min until relief of symptoms or limiting side effects headache or hypotension• most significant adverse effects - tachycardia, flushing,

headache, and hypotension. Nitrate• CI - sildenafil and vardenafil within the past 24 hours and

tadalifil within the past 48 hours.

Supplemental Oxygen• Because MI impairs the circulatory function of

the heart, oxygen extraction by the heart and other tissues may be diminished • Supplemental oxygen should be administered to

patient with symptoms and or signs of pulmonary edema or pulse oximetry readings less than 90%.

Unfractionated heparin• Forms a chemical complex with antithrombin III

inactivates both free thrombin and factor Xa• Recommended in patients with MI who undergo PTCA or

fibrinolytic therapy with alteplase

Low-molecular weight heparin• Direct activity against factors Xa and IIa• Proven to be effective in treating ACS that are

characterized by unstable angina or non ST- elevation MI• Their fixed doses are easy to administer and laboratory

testing to measure their therapeutic effect is not necessary makes them attractive alternative of un-fractionated heparin

Beta-blockers

• Recommended within 12 hours of MI symptoms and continued indefinitely• Reduces Myocardial mortality by decreasing

arrythmogenic death• Decrease the rate and force of myocardial

contraction and decreases overall oxygen demand

Thrombolytics• Thrombolytic drugs lyse coronary thrombi by

converting plasminogen to plasmin.• Thrombolytic therapy provides maximal benefit if

given within the first 3 hours after the onset of symptoms. • Significant benefit still occurs if therapy is given up to

12 hours after onset of symptoms.

Thrombolytics• As a class the plasminogen activators have been

shown to restore coronary blood flow in 50-80% of patients• Contraindication active intracranial bleeding,

CNS neoplasm, HTN, coagulopathy• Intracranial bleed risk major drawback

Glycoprotein IIb/IIIa Antagonists• Potent inhibitors of platelet aggregation• Use during PCI and in patients with high risk

features ACS have been shown to reduce the composite end points of death, reinfraction and the need for target lesion

Revascularization:

Percutanous Coronary Intervention

• Alternative if performed by skilled operator in an experienced center

• Standard is a “ door to balloon” time of 90 minutes• PCI can successfully restore coronary blood flow in 90 to 95%

of MI patients• PCI definitive survival advantage over fibrinolytics for MI

patients who are in cardiogenic shock

Stenting•A stent is introduced into a blood vessel on a balloon catheter and advanced into the blocked area of the artery

• the balloon is then inflated and causes the stent to expand until it fits the inner wall of the vessel, conforming to contours as needed

• the balloon is then deflated and drawn back

•The stent stays in place permanently, holding the vessel open and improving the flow of blood.

Angioplasty• a balloon catheter is passed through the guiding catheter to the area near the narrowing. A guide wire inside the balloon catheter is then advanced through the artery until the tip is beyond the narrowing.

• the angioplasty catheter is moved over the guide wire until the balloon is within the narrowed segment.

• balloon is inflated, compressing the plaque against the artery wall

• once plaque has been compressed and the artery has been sufficiently opened, the balloon catheter will be deflated and removed.

Bypass surgery healthy blood vessel is removed from leg, arm or chest

blood vessel is used to create new blood flow path in your heart

the “bypass graft” enables blood to reach your heart by flowing around (bypassing) the blocked portion of the diseased artery. The increased blood flow reduces angina and the risk of heart attack.

Lipid Management• All post MI patients should be on AMA step II

diet ( < 7% of calories from saturated fats)• Post MI patients with LDL > 100 mg/dl are

recommended to be on drug therapy to try to lower levels to <100 mg/dl• Recent data indicate that all MI patients should

be on statin therapy, regardless of lipid levels or diet

Long term Medications

• Most oral medications instituted in the hospital at the time of MI are continued long term• Aspirin, beta blockers and statin are continued

indefinitely• ACEI indefinitely in patients with CHF, ejection

fraction <.40, hypertension, or diabetes

Thank you!!