Heart Attack (Myocardial Infarction): Sign, Syptoms, types, Treatment:

Table of Contents

Myocardial infarction (Heart Attack):

It refers to localized area of cardiac necrosis due to ischemia. It affects man more than a women. Women are protected against MI during reproductive years, but postmenopausal hormone replacement therapy doesn’t protect women against MI.

Risk factors:

Aging, male gender, hypertension, smoking, DM, Hypercholesrolemia, Obesity, peripheral arterial disease, Family history.

Type of MI:

. Transmural infaction:

. Most common type.
. The artery is completely occlusive due to thrombus formation on disrupted plaque.
. Involves the whole thickness of the myocardium.
. All involves at least a portion of left ventricle.
. New Q waves develop in an ECG.
. ST segment elevation in ECG.

Subendocardial infaction:

. In this case the artery supply the area is not completely occlusive, though there is disruption of plaques with thrombus formation.
. Less common type.
Involves the inner third of the myocardium.
. Emcompasses the entire perfusion zone of the occluded artery.
. Q waves are absent.

PATHOGENESIS Of MI (Heart Attack):

Sudden disruption of atheromatous plaque.
Subendocardial collagen and necrotic plaque contents are exposed.
Platelets adhere to the exposed material and undergo aggregation , activation and released potent aggregates( thromboxane A2 & platelets factor 3 and 4 ).
Platelets aggregation and release of mediators stimulate vasospasm.
Within minutes the thrombus evolves to completely occluded the lumen of coronary vessels.
Occlusion of the coronary vessels result in cessation of aerobic glycolysis and initiation of anaerobic glycolysis leading to:
Inadequate production of ATP.
Accumulation of toxic product ( lactic acid).
The predominant mechanism of cell death is coagulation necrosis.

Biochemical changes:

Anaerobic glycolysis = second.
Loss of contractility = less than 2 min.
ATP reduces to 50% of normal = 10 min.
Irreversible cell injury = 20 – 40 min.
Micro- vascular cell injury = more than 1 hour.
Necrosis is complete = 6-12 hr.

Clinical features:

Chest pain;

Sudden onset of severe retrosternal chest pain lasting more than 30 – 45 minutes.
Pain is central and diffuse.
Pain is tight, squeezing and choking in character.
Pain is radiates to the left arm, jaw and neck.
Pain is aggravated by exertion and emotion.
Pain is not relived by nitroglycerine and rest.

Associated synptoms:

Breathlessness
Anxiety
Diaphoresis
Nausea and vomiting.

Cardiac enzyme in (Heart Attack):

	Elevated within	Peak	Return to normal
CK-MB	2-4 hr	24hr	72 hr
Troon in I & T	2-4 hr	28 hr	7-10 days
LDH	24 hr	3-6 days	8-14 days

Microscopic Morphology of MI:

Necrotic myocardium, acute inflammation ( 1- 3 days after MI ).
Wave of macrophages that remove necrotic myocardium ( 5- 10 days after MI ).
Formation of granulation tissue ( 1- 2 weeks after MI).
Scaring ( most advanced by the end of 6^th week ).

Localization of MI:

Distribution of coronary artery thrombosis;

. Left anterior descending = 45%
. Right coronary artery = 35%
. Left circumflex coronary artery = 15%
ECG consist of Q waves, ST segment elevation, T- waves inversion.
Inverted T waves = area of ischemia at the periphery of the infarct.
Elevated ST segment = injured myocardial cells surrounding the area os necrosis.
New Q waves = area of coagulation necrosis.
ECG diagnosis of MI can localized the affect site.

Area of infarction	ECG changes	Artery involved
Inferior wall MI	II, III, a VF	Right coronary
Anteroseptal MI	V1-V2	Left anterior descending
Anterolateral MI	V4-V6	Left circumflex
Lateral wall MI	I,ALL, V5, V6	Left circumflex
Posterior	V1-V4, ST segment, upright T waves	Posterior descending

Complication of MI;

Arrhythmia:

. Heart rate less than 60.

. No cannon A waves.

Third degree heart block;