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several weeks. He says that approximately a year ago the pain would occasionally occur when he was mowing his yard but now the pain sometimes occurs while he is sitting in a chair at night reading a book. The pain which is localized over the sternum, lasts much longer now than it did a few months ago. What type of disease does this individual have at present ?
Etiology of IHD
1. Reduced coronary blood flow (90% 0f cases) a- Disease of the coronary: mostly due to atherosclerosis associated with thrombosis or vasospasm. Other uncommon causes include emboli from IE, vasculitis, vasospasm, coronary ostial narrowing as in syphilis. b- severe tachycardia (shortening of diastole) C- Aortic valve disease as stenosis or regurge D- severe hypotension as in shock.
Etiology of IHD
2. Increased myocardial demand.eg tachycardia, myocardial hypertrophy. 3.Hypoxia due to diminished oxygen transport eg severe anemia, advanced lung disease, and cyanotic congenital heart disease.
Pathogenesis of ischemic injury:Hypoxia: is the most important factor leading to ATP depletion, increase cytosolic calcium and shift to anaerobic respiration resulting into either reversible cell injury (cloudy swelling and fatty change) or irreversible cell injury (necrosis)
Failure to remove waste products (metabolites) e.g., accumulation of metabolites may explain the pain of muscle ischemia.
I.
ANGINA PECTORIS
A clinical syndrome characterized by intermittent or episodic chest pain or discomfort caused by:
transient and reversible myocardial ischemia which is not severe enough to cause death of myocardial muscles.
PAIN
crushing , squeezing, constricting or knife like. It may radiate to the back , neck or left arm.
Angina pectoris
Stable Angina
It is associated with chronic fixed atherosclerotic narrowing of the coronaries.
Unstable Angina
It is precipitated by fissuring or disruption of the fixed atherosclerotic plaque with superadded thrombosis or vasospasm but the lumen is still opened.
Variant Angina
It is associated with coronary artery spasm near an advanced atherosclerotic plaque .
No Myocardial Necrosis
MI - Types
Transmural
Full thickness
Sub-endocardial
Inner 1/3 to half of ventricular wall Decreased circulating blood volume( shock, Hypotension, Lysed thrombus)
Circumferential
Transmural infarct
Subendocardial infarct
wavy fibers
Neutrophilic infiltrate
coagulative necrosis
1 -2 weeks
>3 weeks
Morphology: *Enlarged heart due to hypertrophy and dilatation of all chambers. *Atherosclerotic coronary narrowing. *Multiple areas of fibrous scar due to healed myocardial infarction. *Thickened endocardium covered by thrombi
Clinical picture:
1. Progressive congestive heart failure in patients with previous attacks of angina &/ or MI. 2. Arrythmias are common. 3. Death caused by - Arrythmias - CHF. - Acute myocardial infarction
Mechanism: Lethal cardiac arrythmias especially ventricular fibrillation. Morphology: Complicated coronary atherosclerotic plaque recent or old MI or scarring.