UA & NSTEMI Flashcards
Absolute contraindication to the use of nitrates
Hypotension
Recent use of PDE-5 inhibitor, sildenafil or vardenafil (w/in 24 hours) or tadalafil (w/in 48 hours)
Oral beta blockade targeted to a heart rate of ____
50-60 beats per minute
A syndrome of severe ischemic pain that usually occurs at rest and is associated with ST segment elevation. It is caused by focal spasm of an epicardial coronary artery with resultant transmural ischemia and abnormalities in left ventricular function that may lead to acute MI, ventricular tachycardia or fibrillation, and sudden cardiac death.
PRINZMETAL’S VARIANT ANGINA
- Coronary angiography demonstrates transient coronary spasm as the diagnostic hallmark of PVA.
The main therapeutic agent for PVA
Nitrates and calcium channel blockers
Which of the following best describes the primary pathophysiological cause of NSTE-ACS?
A. Myocardial oxygen supply exceeds demand due to coronary vasodilation
B. An imbalance between myocardial oxygen supply and demand due to one or more coronary artery processes
C. Sudden coronary artery occlusion leading to transmural infarction
D. Increased myocardial oxygen supply due to compensatory coronary vasodilation
Answer: B
Rationale: NSTE-ACS occurs due to an imbalance between myocardial oxygen supply and demand. This imbalance is caused by coronary artery processes such as plaque fissure with or without inflammation, plaque erosion, or epicardial/microvascular spasm rather than complete occlusion.
Which of the following is a key characteristic of “vulnerable plaques” responsible for ACS?
A. Thick fibrous cap with minimal lipid content
B. Central calcification with smooth edges
C. Eccentric stenosis with scalloped or overhanging edges and a narrow neck
D. Uniform concentric narrowing with a stable fibrous cap
Answer: C
Rationale: Vulnerable plaques in ACS often show eccentric stenosis with scalloped or overhanging edges and a narrow neck. They are composed of a lipid-rich core with a thin fibrous cap, making them prone to rupture.
Apart from coronary arterial thrombosis, which additional mechanism may contribute to NSTE-ACS without thrombosis?
A. Coronary artery aneurysm formation
B. Epicardial or microvascular spasm or increased myocardial oxygen demand
C. Coronary artery dissection leading to full occlusion
D. Coronary artery embolism from a distant source
Answer: B
Rationale: In some cases, NSTE-ACS occurs due to epicardial or microvascular spasm or increased myocardial oxygen demand in the presence of a fixed coronary obstruction, rather than thrombosis.
When should intravenous nitroglycerin be considered in a patient with NSTE-ACS?
A. If ischemic symptoms persist after three doses of sublingual nitroglycerin
B. As the first-line nitrate therapy in all patients
C. Only in patients with systolic blood pressure >150 mmHg
D. When there are no symptoms of ischemia but ACS is suspected
Answer: A
Rationale: IV nitroglycerin is recommended if ischemic symptoms persist after three sublingual doses of nitroglycerin, given 5 minutes apart. It is titrated to symptom relief while monitoring blood pressure.
Which of the following is an absolute contraindication to nitrate therapy in NSTE-ACS?
A. Tachycardia >100 bpm
B. Recent use of phosphodiesterase type 5 (PDE-5) inhibitors
C. Use of β-blockers
D. Mild hypertension
Answer: B
Rationale: Nitrates are contraindicated in patients who have recently taken PDE-5 inhibitors (e.g., sildenafil or vardenafil within 24 hours, tadalafil within 48 hours) due to the risk of severe hypotension.
Why are beta blockers considered a mainstay of anti-ischemic treatment in NSTE-ACS?
A. They cause coronary artery vasodilation
B. They increase myocardial oxygen supply by improving coronary perfusion
C. They reduce myocardial oxygen demand by decreasing heart rate and contractility
D. They have anticoagulant properties that help prevent coronary thrombosis
Answer: C
Rationale: Beta blockers reduce myocardial oxygen demand by slowing heart rate and decreasing contractility, which helps alleviate ischemia.
Which of the following is an absolute contraindication to beta-blocker therapy in NSTE-ACS?
A. Mild hypertension
B. Sinus tachycardia
C. High-degree atrioventricular (AV) block
D. History of stable angina
Answer: C
Rationale: Beta blockers should be avoided in patients with high-degree AV block, as they can worsen conduction abnormalities. They are also contraindicated in acute or severe heart failure, low cardiac output, and active bronchospasm.
Which patients may benefit from heart rate–slowing calcium channel blockers (e.g., verapamil, diltiazem) in NSTE-ACS treatment?
A. Patients with severe hypotension
B. Patients with acute decompensated heart failure
C. Patients with persistent ischemia despite full-dose nitrates and beta blockers
D. Patients with a heart rate below 50 beats per minute
Answer: C
Rationale: Calcium channel blockers are recommended for patients who continue to experience ischemic symptoms despite optimal beta-blocker and nitrate therapy or those who cannot tolerate either of these drugs.
What is the recommended target heart rate when using oral beta blockers in NSTE-ACS patients?
A. 40–50 beats/min
B. 50–60 beats/min
C. 60–70 beats/min
D. 70–80 beats/min
Answer: B
Rationale: The goal of beta-blocker therapy in NSTE-ACS is to reduce heart rate to 50–60 beats per minute to minimize myocardial oxygen demand while avoiding excessive bradycardia.
Which lipid-lowering strategy is recommended early after NSTE-ACS, particularly before percutaneous coronary intervention (PCI)?
A. Low-dose statin therapy
B. Intensive statin therapy with atorvastatin 80 mg or rosuvastatin 40 mg daily
C. Ezetimibe monotherapy
D. PCSK9 inhibitors as the initial treatment
Answer: B
Rationale: High-intensity statin therapy with atorvastatin 80 mg or rosuvastatin 40 mg daily is recommended early after ACS and before PCI to reduce periprocedural myocardial infarction and prevent future cardiovascular events.
For NSTE-ACS patients with inadequate LDL-C response to high-intensity statins, which additional lipid-lowering agents may be considered?
A. Fibrates
B. Omega-3 fatty acids
C. Ezetimibe and/or PCSK9 inhibitors (alirocumab, evolocumab)
D. Niacin
Answer: C
Rationale: If LDL-C reduction is insufficient (<50% decrease despite high-intensity statin therapy), ezetimibe and/or PCSK9 inhibitors (alirocumab, evolocumab) may be added to further lower LDL-C and reduce future cardiovascular risk.
Which P2Y12 receptor blocker is an inactive prodrug requiring metabolic activation?
A. Clopidogrel
B. Prasugrel
C. Ticagrelor
D. Cangrelor
Answer: A
Rationale: Clopidogrel is a prodrug that requires activation by the liver enzyme CYP2C19 to exert its antiplatelet effects. This metabolic activation step contributes to variability in patient response.
Compared to clopidogrel, which P2Y12 inhibitor achieves a more rapid onset and higher level of irreversible platelet inhibition but increases bleeding risk?
A. Prasugrel
B. Ticagrelor
C. Cangrelor
D. Dipyridamole
Answer: A
Rationale: Prasugrel is a thienopyridine that provides faster and more potent irreversible platelet inhibition than clopidogrel, reducing ischemic events but increasing bleeding risk.
Ticagrelor differs from prasugrel and clopidogrel in that it:
A. Requires activation by the CYP2C19 enzyme
B. Is a reversible platelet P2Y12 inhibitor
C. Has no effect on platelet function
D. Is only effective after PCI
Answer: B
Rationale: Unlike clopidogrel and prasugrel, which cause irreversible P2Y12 receptor inhibition, ticagrelor reversibly inhibits platelet function, allowing faster recovery of platelet activity after discontinuation.
Which P2Y12 inhibitor is contraindicated in patients with a history of stroke or transient ischemic attack (TIA) due to increased bleeding risk?
A. Clopidogrel
B. Prasugrel
C. Ticagrelor
D. Cangrelor
Answer: B
Rationale: Prasugrel is contraindicated in patients with a history of stroke or TIA because it significantly increases the risk of bleeding, particularly intracranial hemorrhage.
How long should dual antiplatelet therapy (DAPT) be continued in NSTE-ACS patients without an indication for long-term anticoagulation?
A. 1 month
B. 3 months (preferably 12 months)
C. 6 months
D. Lifetime
Answer: B
Rationale: DAPT should be continued for at least 3 months, but preferably 12 months, to balance the risk of thrombosis versus bleeding.
What is the primary cause of Prinzmetal’s variant angina (PVA)?
A. Fixed atherosclerotic coronary obstruction
B. Focal spasm of an epicardial coronary artery
C. Microvascular dysfunction
D. Increased myocardial oxygen demand due to tachycardia
Answer: B
Rationale: PVA is caused by focal spasm of an epicardial coronary artery, leading to transmural ischemia and potential complications such as ventricular arrhythmias and acute MI.
Coronary angiography demonstrates transient coronary spasm as the diagnostic hallmark of PVA. Hyperventilation and intracoronary acetylcholine have been used to provoke focal coronary stenosis on angiography or to provoke rest angina with ST-segment elevation to establish the diagnosis.
Which of the following is a known trigger for coronary artery spasm in PVA?
A. Increased vagal tone
B. Adrenergic vasoconstrictors, leukotrienes, or serotonin
C. Hyperthyroidism
D. Autoimmune inflammation
Answer: B
Rationale: The exact cause of coronary artery spasm in PVA is not well defined, but it is thought to be linked to hypercontractility of coronary arterial smooth muscle, triggered by adrenergic vasoconstrictors, leukotrienes, or serotonin.
Compared to patients with NSTE-ACS, patients with PVA are more likely to:
A. Be older and have multiple coronary risk factors
B. Have a history of cigarette smoking but fewer other coronary risk factors
C. Present with exertional angina rather than rest pain
D. Exhibit persistent ST-segment depression on ECG
Answer: B
Rationale: PVA patients tend to be younger and have fewer coronary risk factors than those with NSTE-ACS, except for cigarette smoking, which is a common risk factor.
Which diagnostic test is commonly used to provoke coronary spasm and confirm PVA in patients without obstructive coronary disease?
A. Exercise stress testing
B. Dobutamine stress echocardiography
C. Hyperventilation or intracoronary acetylcholine testing
D. Cardiac MRI
Answer: C
Rationale: Hyperventilation or intracoronary acetylcholine administration can induce coronary spasm, helping confirm the diagnosis in patients with suspected vasomotor abnormalities.
Which of the following medications is the mainstay of treatment for Prinzmetal’s variant angina (PVA)?
A. Beta blockers and aspirin
B. Nitrates and calcium channel blockers
C. ACE inhibitors and loop diuretics
D. Clopidogrel and warfarin
Answer: B
Rationale: Nitrates and calcium channel blockers are the primary therapeutic agents for PVA because they relax coronary smooth muscle and prevent vasospasm. Beta blockers and aspirin are generally not preferred, as they may worsen ischemic episodes.
Why is aspirin generally not recommended for patients with Prinzmetal’s angina?
A. It increases platelet aggregation
B. It can worsen ischemic episodes due to effects on prostacyclin synthesis
C. It has no role in coronary artery disease
D. It causes vasospasm directly
Answer: B
Rationale: Aspirin may increase the severity of ischemic episodes in PVA by altering prostacyclin synthesis, making coronary arteries more sensitive to vasospastic stimuli.
Which of the following medications has shown benefit in reducing major adverse cardiovascular events in PVA, despite an unclear mechanism?
A. Statins
B. Beta blockers
C. Direct thrombin inhibitors
D. Loop diuretics
Answer: A
Rationale: Statins have been shown to reduce the risk of major adverse cardiovascular events in PVA patients, although the exact mechanism is not well established.
What is the main concern in patients with Prinzmetal’s variant angina who experience ischemia-associated ventricular fibrillation?
A. Increased risk of bradyarrhythmia
B. Need for percutaneous coronary intervention
C. Indication for an implantable cardioverter-defibrillator (ICD)
D. Increased stroke risk
Answer: C
Rationale: Patients with PVA who develop ventricular fibrillation despite maximal medical therapy should receive an implantable cardioverter-defibrillator (ICD) to prevent sudden cardiac death.
Which of the following statements regarding the prognosis of PVA is true?
A. PVA has a poor prognosis, with a 50% mortality rate at 5 years
B. Many patients experience frequent angina episodes in the first 6 months, followed by symptom improvement
C. All PVA patients have a high risk of MI
D. Patients with mild or no fixed coronary obstruction have a higher risk of cardiac death
Answer: B
Rationale: Many patients with PVA go through an active phase with frequent angina episodes within the first 6 months, but symptoms and cardiac events tend to decrease over time. The 5-year survival rate is excellent (90–95%), though about 20% may experience MI.
Which of the following is a contraindication to the use of nitrates in patients with NSTE-ACS?
A. Recent use of a beta blocker
B. Systolic blood pressure >90 mmHg
C. Right ventricular infarct
D. Heart rate >100 beats per minute
✅ Answer: C
Rationale: Nitrates can lead to severe hypotension in patients with right ventricular infarction due to their preload-reducing effect. Other contraindications include recent use of a PDE-5 inhibitor, hypotension, and severe aortic stenosis.
A beta blocker should be avoided in which of the following conditions?
A. PR interval <0.12 seconds
B. Severe reactive airway disease
C. Sinus tachycardia
D. ST-segment depression without symptoms
✅ Answer: B
Rationale: Beta blockers should be avoided in patients with severe reactive airway disease, as they may cause bronchospasm. Other contraindications include high-degree AV block, bradycardia, hypotension, shock, or severe heart failure (Killip class III/IV).
Which of the following patients would be a good candidate for a calcium channel blocker in the acute phase of NSTE-ACS?
A. A patient with left ventricular dysfunction
B. A patient with vasospastic angina
C. A patient with hypotension (BP <90 mmHg)
D. A patient with pulmonary edema
✅ Answer: B
Rationale: Calcium channel blockers (e.g., diltiazem or verapamil) are recommended in patients with vasospastic angina or those with contraindications to beta blockers. However, they should be avoided in hypotension, pulmonary edema, and left ventricular dysfunction due to their negative inotropic effects.
Which of the following drugs should be avoided in a patient who recently took sildenafil?
A. Beta blockers
B. Nitrates
C. Calcium channel blockers
D. Morphine
✅ Answer: B
Rationale: Nitrates should never be used in patients who recently took a PDE-5 inhibitor (sildenafil, vardenafil, tadalafil), as this can cause severe hypotension and cardiovascular collapse.
