Ischemic Heart Disease

Question 1

What are the risk factors for development of coronary atherosclerosis?

Answer 1

Major: Smoking, Hypertension, Dyslipidemia (elevated cholesterol)
Questionable: Diabetes, Obesity, Inflammation, Psychological stress, sedentary lifestyle
Not-treatable: Male, age, genetics

Question 2

Understand distinguishing features of the coronary circulation

Answer 2

• Myocardium depends on AEROBIC metabolism (can’t do the whole lactic acid thing), no ATP reserve
• Heart, even at rest, extracts almost ALL O2 from blood. Only way to increase supply is to increase blood flow rate
• LV is perfused in diastole only (systole compresses vessels)

Question 3

Principle determinants of myocardial oxygen supply and demand

Answer 3

Supply:

• Myocardial O2 delivery = coronary blood flow rate x O2 content of arterial blood
• Rate
  
  • perfusion pressure: as pressure drops, arterioles dilate to maintain flow (impaired in CAD)
  • perfusion time: 1/hr
  • vascular resistance (Nitro & Ca chan bockers dilate)
• Content: compromised by anemia (less Hgb) or hypoxemia (less saturation)

Demand:

• HR: more contractions = more ATP needed
• Wall tension:
• Inotropic state

Question 4

Understand key elements of pathophysiology and treatment of stable coronary heart disease.

Answer 4

Treatment, supply:

• Prevent diastolic hypotension
• Maximize diastolic time w/ B blockers
• Decrease coronary resistance w/ vasodilators like Nitro & Ca chan blockers
• Prevent reduction in O2 content (anemia, hypoxemia)

Treatment, demand:

• Lower BP to lower wall tension
• Lower HR (B blocker, ca chan blocker)
• Lower wall tension by reducing LV cavity size (lower preload (diuretics, nitrates)
• Lower inotropic state to lower contractility (B blocker, Ca chan blocker)

Question 5

Understand key elements of pathophysiology and treatment of unstable coronary heart disease (unstable angina or myocardial infarction).

Answer 5

• Inflammation in arterial wall weakens fibromuscular cap
• Plaque ruptures, lipid core is exposed = highly thrombogenic
• Oxidized LDL drives in Macs & lymphocytes which become foam cells. They secrete factors that degrade the fibrous cap, e.g. MMP, cytokines

Question 6

Diagnosis of coronary artery disease.

Answer 6

• Hx: CP, dyspnea, risk factors
• PE: CHF, signs of atherosclerosis in vascular beds (bruit in carotids, BPs down extremities
• EKG: ST depression, inv T, Q
• Stress test: Exercise to induce ischemia (75% sensitive)
  , Echo, nuclear perfusion, ultrafast CT (to see calcification)
• Coronary angiography = gold standard. Good for lumen but not wall structure
• Fractional flow reserve: administer adenosine to dilate vessel as much as possible. measure pressure before and after blockage. If distal/prox < 0.75, stenosis is significant

Question 7

Treatment with medications.

Answer 7

Stable

• Nitrates, B blocker, Ca chan blocker
• Anti-hypertensive
• Statin
• Aspirin, clopidogrel
• ACE-i or ARB for LV dysfunction (CHF)

Question 8

Approaches to coronary angioplasty and stents.

Answer 8

Balloon:

• Might expose the plaque, so pt needs to be on anti-coags to avoid thrombus formation
• Might cause restenosis too (like a keloid),