ISCHEMIC HEART DISEASE

Ischemic heart disease (IHD) o Smoking

- Inadequate supply of blood and oxygen o Hypertension
- Imbalance between myocardial oxygen supply and demand o DM
- MOST COMMON CAUSE: atherosclerotic disease of epicardial - Disturb normal functions:
coronal artery o Control of vascular tone  inappropriate constriction
o Maintenance of antithrombotic surface  thrombus
EPIDEMIOLOGY AND GLOBAL TRENDS formation
Associated w/: o Control of inflammatory cell adhesion  abnormal
- Genetic factors interactionis
- High-fat and energy-rich diet - Vulnerable vessel + Vulnerable blood  hypercoagulability +
- Smoking hypofibrinolysis
- Sedentary lifestyle Atherosclerosis develops at irregular rates in different segments 
Risk factors: segmental reduction in cross-sectional area
- Obesity - Predilection at sites of ↑ turbulence – branch points
- Insulin resistance - Stenosis  reduces the diameter by 50%  limitation to ↑ flow
- Type 2 DM to meet MVO2
IHD – likely to become most common cause of death by 2020 o Reduced by 80% - blood flow at rest may be reduced 
further minor decreases cause ischemia at rest
PATHOPHYSIOLOGY - Segmental atherosclerotic narrowing – most commonly by
For any given level of demand for O2, myocardium will control supply formation of a plaque  subject to rupture or erosion of cap
of oxygen-rich blood to prevent underperfusion o Plaque contents upon exposure:
- Determinants of Myocardial O2 demand (MVO2)  platelets – activated and aggregate
o Heart rate  coagulation cascade is activated
o Contractility - Location – influences quantity of myocardium rendered ischemic
o Wall tension (stress) and severity
Adequate supply requires: Satisfactory O2-carrying capacity of blood o Left main coronary artery and proximal LAD – hazardous
- Determined by: o Collateral vessels – if narrowing develops gradually
o inspired O2 Worsening  distal resistance vessels dilate
o pulmonary function - Pressure gradient develops
o Hemoglobin - Resistance vessels maximally dilated  blood follow becomes
o Adequate level of coronary blood flow  phasic dependent on pressure in coronary artery distal to obstruction
 Majority during diastole - Ischemia – precipitated by ↑ in MVO2 precipitated by:
Coronary resistance to flow occurs across 3 sets of arteries o Physiologic vasomotion
- Large epicardial arteries (R1) o Loss of endothelial control
- Prearteriolar vessels (R2) Major determinant
o Pathologic spasm (Pinzmetal’s)
of coronary
- Arterioral and intramyocardial vessels
resistance
(R3) EFFECTS OF ISCHEMIA
Normal coronary circulation is dominated by MVO2 Coronary atherosclerosis – nonuniform ischemia
- Met by ability to vary its resistance (blood flow) - Regional disturbances  Segmental hypokinesia, or bulging
- Normal: R2 & R3 demonstrate capacity for dilation in response to: (dyskinesia)  ↓ pump function
o Exercise and emotional stress (metabolic regulation) - Poor perfusion of subendocardium – more intense ischemia
o Blood pressure (autoregulation) Ischemia of large portions of ventricle  transient LV failure
- Atherosclerosis: ↓ lumen  limits ↑ perfusion w/ ↑ demand - If papillary muscle is involved  mitral regurgitation (MR) occur
o Reduction severe: ↓ basal state - Transient – angina pectoris
Blood flow also can be limited by: - Prolonged – myocardial necrosis and scarring
- Spasm (Pinzmetal’s angina) Normal myocardium – metabolizes fatty acids (FA) & glucose to CO2
- Thrombi and water
- Coronary emboli - Severe deprivation
- Aortitis o FAs cannot be oxidized
- Congenital abnormalities – L anterior descending coronary artery o Glucose  lactate
from pulmonary artery (infants) o ↓ intracellular pH and stores of high-energy phosphates
Myocardial ischemia: o ↓ ATP  impaired cell membrane function  leakage of K
- ↑ MVO2 when coronary blood flow is limited and uptake of Na + Ca
- d/t left ventricular hypertrophy d/t aortic stenosis - Reversible damage: <=20 minutes of total occlusion w/o collaterals
- severe anemia or presence of carboxyhemoglobin – rarely cause ECG: inversion of T-waves
ischemia but lowers threshold to ischemia - More severe: displacement of ST segment
- Microvascular angina – abnormal constriction or failure of normal Transient T-wave Transient ST- ST-segment
dilation inversion segment depression elevation
non-transmural, patchy More severe
CORONARY ATHEROSCLEROSIS intramyocardial subendocardial transmural ischemia
Epicardial coronary arteries – major site ischemia ischemia
- Major risk factors: Electrical instability
o ↑ LDL - Isolated ventricular premature beats
o ↓ HDL - Ventricular tachy or ventricular fibrillation
ISCHEMIC HEART DISEASE