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Questions and Answers
What is the primary role of the R2 vessels during periods of low myocardial oxygen demand?
What is the primary role of the R2 vessels during periods of low myocardial oxygen demand?
- They regulate oxygen supply through vasodilation.
- They constrict to maintain low resistance. (correct)
- They are unaffected by changes in myocardial oxygen demand.
- They dilate to increase blood flow.
During which phase of the cardiac cycle does the heart primarily receive its perfusion?
During which phase of the cardiac cycle does the heart primarily receive its perfusion?
- During diastole only. (correct)
- Primarily during the isovolumetric contraction phase.
- During both systole and diastole equally.
- During systole only.
What physiological factors are responsible for the increase in coronary perfusion during exercise?
What physiological factors are responsible for the increase in coronary perfusion during exercise?
- Resulting reductions in diastolic pressures during systole.
- Increased myocardial oxygen demand and dilation of R2 vessels. (correct)
- Constrictive responses in the large coronary arteries.
- Decreased heart rate and increased blood viscosity.
Which statement accurately describes autoregulation in coronary blood flow?
Which statement accurately describes autoregulation in coronary blood flow?
What is the consequence of increased myocardial oxygen demand during stress?
What is the consequence of increased myocardial oxygen demand during stress?
What characterizes symptomatic angina pectoris?
What characterizes symptomatic angina pectoris?
What is a potential risk factor for all forms of atherosclerosis?
What is a potential risk factor for all forms of atherosclerosis?
Which of the following conditions is directly proportional to serum cholesterol concentrations?
Which of the following conditions is directly proportional to serum cholesterol concentrations?
What is the average risk of coronary artery disease (CAD) for women with type 2 diabetes?
What is the average risk of coronary artery disease (CAD) for women with type 2 diabetes?
What duration of chest pain is consistent with myocardial infarction?
What duration of chest pain is consistent with myocardial infarction?
Which of the following factors is a common trigger for angina?
Which of the following factors is a common trigger for angina?
What distinguishes asymptomatic ischemic heart disease (IHD) from symptomatic IHD?
What distinguishes asymptomatic ischemic heart disease (IHD) from symptomatic IHD?
What relationship does hypertension have with myocardial ischemia?
What relationship does hypertension have with myocardial ischemia?
What is the phenomenon called when coronary blood flow can increase significantly above resting levels?
What is the phenomenon called when coronary blood flow can increase significantly above resting levels?
What effect does atherosclerosis have on the resistance of the R1 vessels?
What effect does atherosclerosis have on the resistance of the R1 vessels?
What determines the primary factors affecting oxygen delivery to the heart muscle?
What determines the primary factors affecting oxygen delivery to the heart muscle?
How are plaques occupying less than 50% to 70% of the vessel's luminal diameter classified?
How are plaques occupying less than 50% to 70% of the vessel's luminal diameter classified?
What triggers angina by heightening norepinephrine levels?
What triggers angina by heightening norepinephrine levels?
What is the required condition for R2 vessels to maintain normal coronary flow when R1 vessels are obstructed?
What is the required condition for R2 vessels to maintain normal coronary flow when R1 vessels are obstructed?
What type of angina is specifically associated with coronary vasospasm?
What type of angina is specifically associated with coronary vasospasm?
What can happen to nonobstructive plaques if they occupy less than 50% to 70% of a vessel's diameter?
What can happen to nonobstructive plaques if they occupy less than 50% to 70% of a vessel's diameter?
What is a common side effect of non-DHP calcium channel blockers (CCBs)?
What is a common side effect of non-DHP calcium channel blockers (CCBs)?
When should non-DHP CCBs be avoided in treatment?
When should non-DHP CCBs be avoided in treatment?
For initial therapy in relieving symptoms, which options are recommended as alternatives to β-blockers?
For initial therapy in relieving symptoms, which options are recommended as alternatives to β-blockers?
Which class of evidence supports the use of ACE inhibitors in patients with stable ischemic heart disease and coexisting heart failure with an LVEF lower than 40%?
Which class of evidence supports the use of ACE inhibitors in patients with stable ischemic heart disease and coexisting heart failure with an LVEF lower than 40%?
What should be administered if β-blocker treatment is unsuccessful for initial therapy?
What should be administered if β-blocker treatment is unsuccessful for initial therapy?
For which of the following patient scenarios is the use of ACE inhibitors strongly recommended?
For which of the following patient scenarios is the use of ACE inhibitors strongly recommended?
Which treatment has been recognized for its antianginal properties for over a century?
Which treatment has been recognized for its antianginal properties for over a century?
What is a potential beneficial mechanism of ACE inhibitors mentioned in the guidelines?
What is a potential beneficial mechanism of ACE inhibitors mentioned in the guidelines?
What is required for organic nitrates to become active compounds?
What is required for organic nitrates to become active compounds?
What does Class II evidence indicate regarding ACE inhibitors for patients with stable ischemic heart disease?
What does Class II evidence indicate regarding ACE inhibitors for patients with stable ischemic heart disease?
Which treatment option should be added to β-blockers if initial treatment fails?
Which treatment option should be added to β-blockers if initial treatment fails?
What does Class III evidence indicate about the use of certain procedures or treatments for stable ischemic heart disease?
What does Class III evidence indicate about the use of certain procedures or treatments for stable ischemic heart disease?
What is the primary purpose of calcium channel blockers (CCBs) in pharmacotherapy?
What is the primary purpose of calcium channel blockers (CCBs) in pharmacotherapy?
Which of the following conditions does NOT warrant the recommendation of ACE inhibitors?
Which of the following conditions does NOT warrant the recommendation of ACE inhibitors?
Which assessment would classify a recommendation as Class I for the use of ACE inhibitors?
Which assessment would classify a recommendation as Class I for the use of ACE inhibitors?
Which of the following is a characteristic of Class II evidence in the context of ACE inhibitors for ischemic heart disease?
Which of the following is a characteristic of Class II evidence in the context of ACE inhibitors for ischemic heart disease?
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Study Notes
Coronary Flow Reserve
- During exercise, coronary blood flow can increase 4 to 5 times the resting rate.
- This increased flow is called coronary flow reserve.
Factors Affecting Coronary Flow Reserve
- Speed of task performance affects oxygen demand increase.
- Mental and emotional stress can trigger angina by increasing norepinephrine and decreasing vagal activity.
- Cold exposure and low blood sugar can also contribute to increased heart rate and potential angina.
Atherosclerotic Plaque & Coronary Flow
- Plaque forms in the large epicardial vessels (R1).
- As plaque grows, resistance in R1 vessels increases.
- Healthy R1 vessels offer minimal resistance to flow.
- Atherosclerosis progression increases R1 resistance.
- Autoregulation compensates for increased R1 resistance by vasodilation in the smaller endocardial vessels (R2) to maintain flow.
- Plaque occupying less than 50-70% of the vessel's diameter is considered non-obstructive and rarely causes ischemia or angina.
- Non-obstructive plaque can rupture, leading to acute coronary syndrome (ACS).
- Plaque occupying 70% or more of the luminal diameter is considered obstructive.
- Obstructive plaque requires full R2 vessel dilation to maintain normal coronary flow.
Myocardial Oxygen Supply
- The heart muscle's oxygen delivery is determined by several factors including:
- Coronary blood flow
- Heart rate and systole
- Oxygen extraction and carrying capacity
- Coronary collateral circulation
- Coronary vasospasm and Prinzmetal's angina
Resistance Vessels & Autoregulation
- Smaller endocardial vessels (R2) are resistance vessels that regulate flow based on myocardial oxygen demand (MVO2).
- R2 vessels constrict when MVO2 is low (at rest) and dilate when MVO2 is high (during exercise or stress).
- This process is called autoregulation.
- Vasodilators are released to increase coronary blood flow in response to increased MVO2.
Myocardial Perfusion
- Most tissues and organs are perfused during systole.
- The heart is uniquely perfused during diastole, the myocardial relaxation phase.
- Two factors contribute to this:
- Ventricular pressure during systole increases coronary circulation pressure above perfusion requirements, preventing flow.
- Diastole allows for pressure reduction, enabling coronary flow.
Diastole & Myocardial Perfusion
- During a cardiac cycle, the myocardium spends twice as much time in diastole compared to systole.
- This reduced perfusion time significantly limits oxygen supply.
Angina Pectoris
- Pain usually has a substernal component, but can also be felt on the right or left side of the chest, upper back, or epigastrium.
- Pain can radiate to the jaw, neck, or arm.
- Angina is typically triggered by exertion, emotional upset, or events increasing myocardial oxygen demand.
- Anginal pain is transient, lasting between 2 and 30 minutes.
- Pain lasting longer than 30 minutes may indicate myocardial infarction, and pain lasting less than 2 minutes is unlikely to be due to ischemia.
Symptomatic vs. Asymptomatic Angina
- Symptomatic angina is characterized by chest discomfort due to angina pectoris or acute myocardial infarction.
- Asymptomatic angina, also called silent IHD, occurs without angina or anginal equivalents.
Risk Factors for Coronary Artery Disease (CAD)
- Positive Family History: Runs in families due to shared genetic, environmental, and lifestyle factors.
- Smoking: Consistent use increases risk.
- Hypertension: Risk increases directly with blood pressure.
- Hypercholesterolemia: Risk increases directly with serum LDL cholesterol concentrations.
- Diabetes Mellitus: Potent risk factor for all forms of atherosclerosis.
- Men with type 2 diabetes have a 2-4 fold greater annual risk of CAD.
- Women with type 2 diabetes have a 3-5 fold greater risk.
- Hemostatic Factors: May contribute to plaque formation and rupture.
Angina Relief Pharmacotherapy
- Initial therapy for angina relief:
- β-blockers (LOE B)
- Alternative initial therapy when β-blockers are contraindicated or have side effects:
- Calcium channel blockers (verapamil or diltiazem) (LOE B)
- Long-acting nitrates (LOE B)
- If β-blocker treatment is unsuccessful:
- Add calcium channel blockers + long-acting nitrates (LOE B)
- If β-blocker treatment is unsuccessful for initial treatment:
- Add ranolazine in combination with β-blockers (LOE A)
Calcium Channel Blockers (CCBs)
- Common side effects vary between dihydropyridine (DHP) and non-DHP classes.
- Non-DHP CCBs can cause bradycardia, hypotension, atrioventricular block, and LV depression.
- Non-DHP CCBs are not recommended for those with contraindications or intolerance to β-blockers.
- Non-DHP CCBs are a substitute for β-blockers in cases of contraindication or side effects.
Nitrates
- Organic nitrates have antianginal properties.
- They require biotransformation into active compounds.
ACE Inhibitors
- Recommended for specific subgroups with stable ischemic heart disease (SIHD), including:
- Coexisting heart failure or asymptomatic LV dysfunction (LVEF below 40%).
- Hypertension.
- Diabetes.
- Beneficial mechanisms include:
- Regression of left ventricular hypertrophy and vascular hypertrophy.
- Prevention of atherosclerosis progression.
ACC/AHA Evidence Grading System
- Class I: Evidence or general agreement that procedure or treatment is useful and effective.
- Level of Evidence (LOE) A: Multiple randomized clinical trials with large numbers of patients.
- Level of Evidence (LOE) B: Limited randomized clinical trials with smaller numbers of patients, careful analysis of non-randomized studies or observational registries.
- Class II: Conflicting evidence or diverging opinions on effectiveness.
- Level of Evidence (LOE) a: Weight of evidence or opinion favors usefulness/efficacy.
- Level of Evidence (LOE) b: Less well-established evidence for usefulness/efficacy.
- Class III: Evidence or general agreement that procedure or treatment is not useful or effective
- No level of evidence provided.
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