UA & NSTEMI Flashcards
(33 cards)
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.
