STEMI/ACUTE CORONARY SYNDROME

Abhishek Jha

DEFINITIONS

Myocardial infraction also know as heart attack when disruption of blood supply occur to part of the heart damaging heart muscles.

Heart muscle death

Blockage/ obstructions of coronary arteries by clot formations

SYMPTOMS

Chest pain = typical radiate pain-Pain radiate to back , neck vertebra , jaws, left hand and five fingers

High intensity pain, severe pain under sternum

Squeezing or heaviness, shortness of breath

Nausea, vomiting, weakness, Diaphoresis, syncope

RISK FACTOR

Age (more than 45 yrs)

Smoking and alcohol and poor diet

High blood pressure

High cholesterol

Diabetes

Obesity

Stress

Lack of physical activity

PATHOPHYSIOLOGICAL

There is disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade or occlusion of the artery.

Plaque rupture is believed to be triggering mechanism for the development of clot , at the site that can occlude blood flow resulting myocardial infractions

Irreversible damage to the myocardium can begin as early as 20 to 40 minutes after interruption of blood flow.

The dynamic process of infarction may not be completed, however, for several hours.

Necrosis of tissue appears to occur in a sequential fashion about 5-6 hours

Reimer and associates demonstrated that cellular death occurs first in the subendocardial layer called Subendocardial infraction and spreads like a “wavefront” throughout the thickness of the wall of the heart called Transmural infraction.

a substantial amount of myocardial tissue can be salvaged if flow is restored within 6 hours after the onset of coronary occlusion.

The cellular changes associated with an MI can be followed by:= The development of infarct extension (new myocardial necrosis)= Infarct expansion (a disproportionate thinning and dilation of the infarct zone)= Ventricular remodeling (a disproportionate thinning and dilation of the ventricle).

LOCATIONS OF THE INFRACTIONS

1.MIs can be located in the

> Anterior> Septal > Lateral> Posterior>Inferior walls of left ventricle

INVESTIGATIONS/DIAGNOSIS 1st Test – ECG = ST Elevations

Blood test, Cardiac Marker (CKMB levels) {(+ve in MI) or (-ve in case of angina)}

Cardiac Troponin

History

ECG

Very specific and a good test, particularly helpful if positive:

– Should be done within 10 minutes of arrival on anyone with suspected ACS

– Observation

ST elevation

- In the normal ECG, the ST segment should not be elevated more than 1 mm in the standard leads or more than 2 mm in the precordial leads. With an acute injury, the ST segments in the leads facing the injured area are elevated. It occur due to premature repolarization.

. Pathological Q wave

-They are the result of absence of electrical activity. A myocardial infarction can be thought of as an electrical 'hole' as scar tissue is electrically dead and therefore results in pathologic Q waves. Pathologic Q waves are not an early sign of myocardial infarction, but generally take several hours to days to develop. Once pathologic Q waves have developed they rarely go away

HISTORY

Character of pain

Onset and durations

Locations and radiation

Aggravating and relieving factors

Autonomic symptoms

Patients with MI describe as heaviness, squeezing, chocking or smothering sensation. Or sensations as someone were crush my chest.

Substernal pain can radiate to neck, left arm, back or jaws

Pain of MI is more often prolonged and unrelieved by rest or sublingual nitroglycerin

Gastrointestinal complaints are related to severity of pain and resulting vagal stimulations.

PHYSICAL EXAMINATIONS Patients usually appear restless and in distressand skin is warm and moist

Breathing may be labored and rapid, fine crackles or rhonchi may be heard when auscultating the lung

When the patient placed in the left lateral decubitus position, abnormalities of the precordial pulsations can be felt. These abnormalities includes a lack of point of maximal impulse or the presence of diffuse contractions .

On auscultations, the first heart sound may be diminished as a result of dec contractility

A fourth heart sound is heard in almost all patients with MI, Whereas a third heart sound is detected in only about 10% to 20 % of patients

Transient systolic murmurs may be heard

After about 48 to 72 hrs , many patients acquire a pericardial friction rub

CARDIAC MARKER

Creatine kinase –MB (CKMB)

CK-MB appears in the serum in 6 to 12 hours, peaks between 12 and 28 hours, and returns to normal levels in about 72 to 96 hours.

Serial samplings are performed every 4 to 6 hours for the first 24 to 48 hours after the onset of symptoms

Myoglobin Myoglobin is an oxygen-binding protein found in skeletal and cardiac muscle. Myoglobin’s release from ischemic muscle occurs earlier than the release of CK

The myoglobin level can elevate within 1 to 2 hours of acute MI and peaks within 3 to 15 hours.

Because myoglobin is also present in skeletal muscle, an elevated myoglobin level is not specific for the diagnosis of MI. consequently, its diagnostic value in detecting an MI is limited

Troponin (troponin T and troponin I):

Troponin I levels rise in about 3 hours, peak at 14 to 18 hours, and remain elevated for 5 to 7 days.

Troponin T levels rise in 3 to 5 hours and remain elevated for 10 to 14 days

TREATMENT

Time is Muscle: Every 10 minute delay to Percutaneous Coronary Intervention (PCI) results in a 1% change in mortality.

Fibrinolytic agent -streptokinase-PA

Aspirin and anti-platlet drugs

beta-blockers- metoprolol, carvidalol

ACE inhibitors

Coronary artery bypass graft

Thank You