Increases in the content of lipoproteins within regions of the intima.

Bind to constituents of the extracellular matrix

Lipoproteins that accumulate in the extracellular space of the intima of arteries

Lipoproteins undergo oxidative modifications

Predisposing Factors

Age: 55 years old

Genetic Factor: (+) heart disease - paternal side

(+) stroke - maternal uncle side

(+) hypertension - first line of

blood in the family

Personality features: Type “A” Personality

Precipitating Factors

Sedentary Lifestyle

Obesity: 171 lbs.

High Blood Pressure: 160/ 84 mmHg

History of hypercholesterolemia

Diet

Caffeine Consumption: 3 cups/ day

Oxidative modification of sequestered lipoproteins

Rise of hydroperoxides, lysophospholipids, oxysterols, and aldehydic breakdown products of fatty acids and phospholipids

Breakdown of peptide backbone as well as derivatization of certain amino acid residues

Activation of pro-inflammatory lipids

Activation of the monocyte, macrophages, lymphocytes

Monocytes attach to the endothelium and migrate to intima

Build up made of fat, cholesterol, calcium, and other cellular waste in the inner lining of the coronary artery

Plaque formation

Disruption or rupture of a vulnerable plaque

Platelets initiate thrombosis at the site of a ruptured plaque

A mural thrombus forms at the site of plaque disruption / site of vascular injury

Thrombotic occlusion of the coronary artery

Acute coronary syndrome

Decreased blood flow in the blood vessel

Decreased oxygen supply, increased demand for oxygen -- tachycardia

Cells are deprived from oxygen Shortness of breath

Restlessness

Myocardial ischemia

Anaerobic metabolism

Lactic acid formation

Cells send pain signals to the brain nausea & heartburn/ feeling of indigestion

Prolonged oxygen deprivation

inability to produce ATP aerobically.

Cells fail to meet their metabolic needs

Progressive occlusion of the plaque in the artery

Increased myocardial contraction Tachycardia

The brain is overloaded with escalating pain signals coming from the heart chest pain

Sodium-potassium pump suspends where the sodium ions and water begin to fill in eventually causing them to lyse.

With lysis, cells release of intracellular potassium store and intracellular enzymes which injure neighboring cells.

Intracellular proteins gain access to general circulation and interstitial space resulting to interstitial edema and swelling around

myocardial cells

Initiation of inflammatory reactions where platelets accumulate, release of clotting factors.

Degranulation of mast cell begins resulting to the release of histamine pain radiating to shoulders

and various prostaglandins. Some may have vasoconstrictive

properties and may stimulate clotting.

Cell death.

Reference: Harrison’s principle of Medicine

ACUTE MYOCARDIAL INFARCTION

Necrosis of the heart muscle

Alters conduction, increases

automaticity and promotes triggered

activity related to

after-depolarizations.

Presence of sinus tachycardia,

premature ventricular

contraction (PVC),

Massive muscle loss.

Left ventricular failure and cardiogenic shock Presence of s4, fine

crackles on the lungs,

shortness of breath