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وقل رب وقل رب {{}}زدني علمازدني علما

DR Basem elsaid enanyLECTURER OF CARDIOLOGY

AIN SHAMS UNIVERSITY

Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells.

Myocardial infarction occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain normal operating function and hemostasis.

Ischemia at this critical threshold level for an extended time period results in irreversible myocardial cell damage or death.

From an anatomic or morphologic standpoint, the two types of MI are transmural and nontransmural.

A transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s

In a nontransmural MI, the area of ischemic necrosis is limited to either the endocardium or the endocardium and myocardium.

A more common clinical diagnostic classification scheme is also based on ECG findings as a means of distinguishing between two types of MI— one that is marked by ST elevation STEMI and one that is not NSTEMI

The distinction between an ST-elevation MI and a non-ST-elevation MI also does not distinguish a transmural from a non-transmural MI. The presence of Q waves or ST segment elevation is associated with higher early mortality and morbidity;

Age Gender Family history Hyperlipidemia Smoking Hypertension Diet Diabetes Obesity High plasma homocysteine levels

The most frequent mechanism:rupture or ulceration of a vulnerable atheroscleroticPlaque exposes the highly thrombogenicsubendothelium to circulating platelets andwhite blood cellsTissue factor activates the extrinsic coagulation Cascade (Factor VII, and also cleavage of factor IX, contribute to activation of intrinsic pathway) activated platelets release powerful promoters of vasoconstriction and platelet aggregation (thromboxane A2, serotonin, adenosine diphosphate, and platelet-activating factor) platelet adhesion and aggregation transient thrombosis or subtotal coronary artery occlusion with dynamic vasoconstriction.

If ischemia is neither severe nor prolonged(usually <20 min) and often recurs at rest, patientsare given a diagnosis of UA. However, if ischemialasts longer than 30 minutes (usually 1–2 hr) and is associated with elevated cardiac markers, a diagnosis of MI is made.

The severity of an MI is dependent on three factors:

1. The level of the occlusion in the coronary artery,

2. The length of time of the occlusion3. The presence or absence of collateral

circulation

The death of myocardial cells first occurs in the area of myocardium that most distal to the arterial blood supply—that is, the endocardium. As the duration of the occlusion increases, the area of myocardial cell death enlarges

Ischemia / infarction

chest pain

Diastolic Dysfunction Systolic Dysfunction

cardiac output

catecholamines

MVO2

wall tension

LV diastolic pressurepulmonarycongestionpO2

(heart rate, BP)

Acute infarction,

hours

Acute infarction,

hours to days

Acute infarction,

days to months

HOW TO DIAGNOSE STEMI

1-CLINICAL PICTURE 2-ECG3-BIOMARKERS

The degree of symptoms ranges from none at all to sudden cardiac death.

An asymptomatic MI is not necessarily less severe than a symptomatic event; but patients who experience asymptomatic MI's are more likely to be diabetic.

Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax or heavy weight or burning or stabbing

The pain is usually retrosternal in location, spreading frequently to both sides of the anterior chest, with predilection for the left side.

Radiation of chest pain into the jaw/teeth, shoulder, arm (sometimes ulnar aspect of the left arm producing a tingling sensation in the left wrist, hand, and fingers. ), and/or back

In some instances, the pain of AMI may begin in the epigastrium and simulate a variety of abdominal disorders, a fact that often causes <MI> to be misdiagnosed as “indigestion

Associated dyspnea or shortness of

breath Associated epigastric discomfort with

or without nausea and vomiting Associated diaphoresis or sweating

Syncope or near-syncope without other cause

Impairment of cognitive function without other cause

In patients with preexisting angina pectoris, the pain of infarction usually resembles that of angina with respect to location. However, it is generally much more severe, lasts longer, and is not relieved by rest and nitroglycerin.

In some patients, particularly the elderly, AMI is manifested clinically not by chest pain but rather by symptoms of <acute> left ventricular failure and chest tightness or by marked weakness or frank syncope.

AMI may occur at any time of the day, but most appear to be clustered around the early hours of the morning and/or are associated with demanding physical activity.

Approximately 50% of patients have some warning symptoms (angina pectoris or an anginal equivalent) prior to the infarct.

20 and 60 percent of nonfatal <MIs> are unrecognized by the patient and are discovered only on subsequent routine ECG or postmortem examinations.

Of these unrecognized infarctions, approximately half are truly silent.

The other half of patients with so-called silent infarction can recall an event characterized by symptoms compatible with <acute> infarction when leading questions are posed after the ECG abnormalities are discovered.

Unrecognized or silent infarction occurs more commonly in patients without antecedent angina pectoris and in patients with diabetes and hypertension.

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Pulse rate , may be normal,or bradycardia, tachycardia, or irregular pulses.

Up to 60% of patients with AMI present with diaphoresis.

Inspiratory rales and an S3 gallop are associated with left sided failure.

EKG 12 lead EKG ST elevation (>0.05

mV)

Localized change

Reciprocal changes (v1-v6,I and aVL S-T E ; II,III , aVF S-T D)

Progressive changes

<2hr hyperacute T waves

<4hr ST segment elevation

New elevation at the J point in 2+ contiguous leads

16-24hr ST back to baseline , T wave inversion

Weeks : Q waves usually persist

ST segment elevation V4R highly predictive of RV infarct

Higher in-hospital mortality Higher incidence of in-hospital

complications

Concordant ST segment elevation >1mv highly suggestive of AMI .

ST segment depression >1 mV in leads V1,V2,or V3 highly suggestive of AMI.

Discordant STsegment elevation >5mm suggestion of AMI.

Troponin: High sensitivity, high specificity for myocardial tissue

CK-MB: less tissue specific, but better specificity for irreversible injury

Myoglobin: for rapid diagnosis

ProteinMolecular mass (kD)

First detection

Duration of detection

Sensitivity

Specificity

Myoglobin 16 1.5–2 hours

8–12 hours +++ +

CK-MB 83 2–3 hours

1–2 days +++ +++

Troponin I 33 3–4 hours

7–10 days ++++ ++++

Troponin T 38 3–4 hours

7–14 days ++++ ++++

CK 96 4–6 hours

2–3 days ++ ++

ECHOCARDIOGRAPHY

Unfortunately, the presence of wall motion abnormalities on the echocardiogram may be due to an acute MI or previous (old) MI or other myopathic processes.

Thus, the usefulness of echocardiography in the diagnosis of MI is limited.

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