· a narrowing of one or more coronary arteries from atherosclerotic disease which limits myocardial blood flow. Increasing degrees of stenosis first limit reserve flow, then reduce flow at rest, and finally may totally occlude the vessel.
A. The normal coronary artery layers
· Endothelium
· Intima
· Internal elastic lamina
· Media
· External elastic lamina
· Adventitia
B. Lesions of atherosclerosis
· Fatty streak begins in childhood
· Lipid laden macrophages and T-lymphocytes with smooth muscle cells cause focal intimal thickening
· More smooth muscle cells and connective tissue form in the intima
· Eccentric fibrous plaque develops, which is white and elevated
· Lipid deposition in cells and connective tissue
· A luminal fibrous cap forms
· Zone of necrotic tissue beneath the cellular area
· Rupture and thrombosis of a plaque is the probable cause of most unstable angina and acute myocardial infarction
· Acute ischemia commonly develops in vessels with less than 50% stenosis
· More severe stenoses also occlude, but may not have acute ischemia due to protective collaterals
· Hemorrhage may occur suddenly within a plaque
· Platelet aggregation, vessel stenosis, and coronary spasm all play a role in acute narrowing/occlusion
· Plaque regression occasionally occurs
· Development of collaterals important in restoring regional perfusion
· CAD usually involves proximal portions of the 3 major arteries, particularly at branch points
· The LAD and RCA are more often involved than the CX
· 40% of patients studied for symptoms will have significant stenoses in all 3 vessels
· 95% of patients with 1 completely occluded artery will have a significant stenosis in at least one other artery
· 10-20% of patients with significant disease will have L main involvement
· Diffuse distal disease unsuitable for CAB is uncommon
A. Coronary angiography
· Severity of lesions and size of distal vessels may be underestimated
· 75% reduction in cross-section = 50% diameter reduction (moderate)
· 90% reduction in cross-section = 67% diameter reduction (severe)
· Ejection fraction should be considered with heart size, as the heart size can be normal even in severe LV dysfunction
B. Tests of LV function
· Resting LV function depends on the amount of myocardium devoid of scar
· Exercise LV function reflects loss of coronary flow reserve, and is typically depressed when compared to resting function
· Global LV function usually visually estimated on angiography as ejection fraction
· Can also be evaluated by CASS score, which is the sum of five segmental scores
· Segmental LV wall function assessed by local wall motion or thickening during cardiac cycle
A. Progression of Stenoses
· Rate of progression is highly variable
· Young age, hyperlipidemia, and presence of PVD denote more rapid progression of coronary stenoses
· 50% of patients will develop new significant lesions within 2 years
B. Progression of LV Dysfunction
· As areas of ischemia become more extensive, global LV systolic function will fall during exercise testing
· LVEDV will increase from the decreased systolic function
· LV diastolic function also falls from impaired myocardial relaxation during early diastole
· All factors ultimately result in increased LVEDP
· LV dysfunction at rest is usually from myocardial scarring
· Myocardial stunning or hibernation can cause resting LV dysfunction as well
A. Stable angina
· Chest pain on exertion is a common event with progression of coronary stenoses
· Graded exercise testing helps quantify the degree of reduction in flow reserve
· Angina typically becomes more severe with time, although some patients do not progress
B. Unstable angina
1. Definitions:
· Severe and persisting angina with EKG evidence of ischemia and minor CK-MB changes
· Severe class IV angina within 2 months of onset
· Severe angina lasting more than 15 minutes occuring within 10 days of presentation
· Severe angina within 2 weeks of acute myocardial infarction
2. Plaque fissure and/or rupture is the probable cause of unstable angina
3. These patients have increased tendency to develop myocardial infarction
C. Acute myocardial infarction
· Severe proximal LAD disease is prone to cause acute MI
· 30% of patients studied will have an acute MI within 5 years
· Probability of acute MI is increased by number of previous MIs and number of vessels involved
· Thrombolytics have reduced current hospital mortality to less than 10%
· Death usually the result of acute cardiac failure or sudden ventricular arrhythmia
D. Death
· The majority of patients with CAD ultimately die from cardiac causes
· Most common cause is acute or subacute cardiac failure
· 20% of patients have sudden death
· 10-year survival is about 60%
· Severity of reduction of regional coronary flow reserve
· Number of myocardial regions with reduced flow reserve
· Nature of plaque and internal thrombolytic/fibrinolytic state
· Amount and distribution of scar
· Hemodynamic instability
· Ischemic instability
· Ventricular electrical instability
· Older age
· Diabetes
· Hypertension
· Hyperlipidemia
· COPD
· Chronic renal disease
· Smoking
· Previous CVA
| Number of vessels with stenoses | 5-year survival |
| 1 (any) | 90-95% |
| 1 (RCA) | 96% |
| 1 (LAD) | 92% |
| 1 (prox LAD) | 90% |
| 2 | 88% |
| 3 | 70% |
| Left main | 40-60% |