The correct answer is: B. Folic acid, with or without vitamins B6 and B12, should not be used for secondary prevention in patients with NSTE-ACS.

According to Section 6.3.6., "Antioxidant Vitamins and Folic Acid: Recommendations," of the "2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes"¹:

CLASS III: NO BENEFIT
1. Antioxidant vitamin supplements (e.g., vitamins E, C, or beta carotene) should not be used for secondary prevention in patients with NSTE-ACS. (Level of Evidence: A)
2. Folic acid, with or without vitamins B6 and B12, should not be used for secondary prevention in patients with NSTE-ACS (Level of Evidence: A)
Although there is an association of elevated homocysteine blood levels and CAD, a reduction in homocysteine levels with routine folate supplementation did not reduce the risk of CAD events in 2 trials (the NORVIT [Norwegian Vitamin Trial] and the HOPE [Heart Outcomes Prevention Evaluation] study) that included post–MI or high-risk stable patients and produced poorer outcomes in another study. Additionally, in the NORVIT trial, there was a trend toward increased cardiovascular events (95% CI: 1.00 to 1.50; p¼0.05) in the cohort receiving the combination of folic acid, vitamin B6, and vitamin B12; the authors cautioned against using the treatment for secondary prevention (476). Similarly, experience in large clinical trials with antioxidant vitamins has failed to demonstrate benefit for primary or secondary prevention.

Regarding answer A, according to Section 4.3.3, "Fibrinolytic Therapy in Patients With Definite NSTE-ACS: Recommendation"¹:

CLASS III: HARM
1. In patients with NSTE-ACS (i.e., without ST-elevation, true posterior MI, or left bundle-branch block not known to be old), intravenous fibrinolytic therapy should not be used (Level of Evidence: A)
There is no role for fibrinolytic therapy in patients with NSTE-ACS. Fibrinolysis with or without subsequent PCI in patients with NSTE-ACS was evaluated by the Fibrinolytic Trialists and TIMI investigators. There was no benefit for mortality or MI. Intracranial hemorrhage and fatal and nonfatal MI occurred more frequently in patients treated with fibrinolytic therapy.

Regarding answer C, according to Section 6.3.5., "Hormone Therapy: Recommendation"¹:

CLASS III: HARM
1. Hormone therapy with estrogen plus progestin, or estrogen alone, should not be given as new drugs for secondary prevention of coronary events to postmenopausal women after NSTE-ACS and should not be continued in previous users unless the benefits outweigh the estimated risks. (Level of Evidence: A)
Although prior observational data suggested a protective effect of hormone therapy for coronary events, a randomized trial of hormone therapy for secondary prevention of death and MI (the HERS [Heart and Estrogen/Progestin Replacement] study) failed to demonstrate a beneficial effect. There was an excess risk for death and MI early after initiation of hormone therapy. The Women's Health Initiative included randomized primary prevention trials of estrogen plus progestin and estrogen alone. Both trials were stopped early owing to an increased risk related to hormone therapy that was believed to outweigh the potential benefits of further study. It is recommended that postmenopausal women receiving hormone therapy at the time of a cardiovascular event discontinue its use and that hormone therapy should not be initiated for the primary or secondary prevention of coronary events. However, there may be other permissible indications for hormone therapy in postmenopausal women (e.g., treatment of perimenopausal symptoms such as flushing or prevention of osteoporosis) if the benefits are believed to outweigh the increased cardiovascular risk. Postmenopausal women who are >1 to 2 years past the initiation of hormone therapy who wish to continue such therapy for another compelling indication should weigh the risks and benefits, recognizing the greater risk of cardiovascular events and breast cancer (combination therapy) or stroke (estrogen).

Regarding answer D, according to Section 7.10., "Cocaine and Methamphetamine Users"¹:

CLASS I
Patients with NSTE-ACS and a recent history of cocaine or methamphetamine use should be treated in the same manner as patients without cocaine- or methamphetamine-related NSTE-ACS. The only exception is in patients with signs of acute intoxication (e.g., euphoria, tachycardia, and/or hypertension) and beta-blocker use, unless patients are receiving coronary vasodilator therapy. (Level of Evidence: C)

CLASS IIa
Benzodiazepines alone or in combination with nitroglycerin are reasonable for management of hypertension and tachycardia in patients with NSTE-ACS and signs of acute cocaine or methamphetamine intoxication. (Level of Evidence: C)

CLASS III: HARM
Beta blockers should not be administered to patients with ACS with a recent history of cocaine or methamphetamine use who demonstrate signs of acute intoxication due to the risk of potentiating coronary spasm. (Level of Evidence: C) Cocaine exerts multiple effects on the cardiovascular system, which may precipitate ACS. Acute cocaine exposure results in increased BP, heart rate, endothelial dysfunction, and platelet aggregation, all of which may precipitate ACS. Cocaine's direct vasoconstrictor effect can produce coronary vasospasm. Long-term use of cocaine results in progressive myocyte damage and accelerated atherosclerosis. ACS in patients with a history of cocaine use should be treated in the same manner as patients without cocaine use. The exception is in patients with ACS in the presence of acute cocaine intoxication. Because cocaine stimulates both alpha- and beta-adrenergic receptors, administration of intravenous beta blockers may result in unopposed alpha stimulation with worsening coronary spasm. Evidence suggests it is safe to administer intravenous beta blockers in patients with chest pain and recent cocaine ingestion, although information is lacking about the effects of beta-blocker administration during the acute stages of cocaine intoxication. Intravenous beta blockers should be avoided in patients with NSTE-ACS with signs of acute cocaine intoxication (euphoria, tachycardia, and/or hypertension). In these patients, benzodiazepines alone or in combination with nitroglycerin have been useful for management of hypertension and tachycardia owing to their effects on the central and peripheral manifestations of acute cocaine intoxication. Methamphetamine abuse is becoming increasingly common in the United States owing to the ease of manufacturing and the lower cost of methamphetamines compared with cocaine. Methamphetamines may be ingested orally, inhaled, or used intravenously. Methamphetamine affects the central nervous system by simultaneously stimulating the release and blocking the reuptake of dopamine and norepinephrine. Like cocaine, methamphetamine exerts multiple effects on the cardiovascular system, all of which may precipitate ACS. The acute effects of methamphetamine are euphoria, tachycardia, hypertension, and arrhythmias. MI may result from coronary spasm or plaque rupture in the presence of enhanced platelet aggregation. Long-term use of methamphetamine has been associated with myocarditis, necrotizing vasculitis, pulmonary hypertension, and cardiomyopathy. Because methamphetamine and cocaine have similar pathophysiological effects, treatment of patients with ACS associated with methamphetamine and cocaine use should theoretically be similar.

References

1. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;64:e139-e228.