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CLINICAL STATEMENTS AND GUIDELINES

January 2, 2024 Circulation. 2024;149:e1–e156. DOI: 10.1161/CIR.0000000000001193 e62

Joglar et al 2023 Guideline for the Diagnosis and Management of Atrial Fibrillation

and minimal toxicity make it a favorable option, often as an adjunct to conventional therapy (ie, atrioventricular nodal blockers). A meta-analysis including 6 RCTs (n=745 patients) investigated the effectiveness of intravenous magnesium in rate and rhythm control of rapid AF when administered in combination with standard rate-control methods (including beta blockers, diltiazem, verapamil, digoxin), as well as placebo. In the pooled analysis, intravenous magnesium was superior in achieving rate control (63% versus 40%; OR, 2.49 [95% CI, 1.80-3.45]) and modestly effective in rhythm conversion to sinus (21% versus 14%; OR, 1.75 [95% CI, 1.08-2.84]) compared with standard rate-control methods. Subgroup analysis showed the superiority of a lower dose (≤5 g) (24% versus 13%; OR, 2.10 [95% CI, 1.22-3.61]) compared with the higher dose (>5 g) (16% versus 13%; OR, 1.23 [95% CI, 0.65-2.32]) in rhythm control when compared with placebo.10

4 Intravenous amiodarone has been shown to be

effective in controlling ventricular rates in patients who are critically ill. In a retrospective study of 38 patients admitted to the intensive care unit, intravenous amiodarone was associated with a statistically significant decrease in heart rate without decrease in BP compared with intravenous diltiazem and digoxin.12 One study of 60 critically ill patients, predominantly with AF, with heart rate consistently >120 bpm randomized patients to 1 of 3 intravenous treatment regimens: diltiazem in a 25-mg bolus followed by a continuous infusion of 20 mg/h for 24 hours; amiodarone in a 300mg bolus; and amiodarone in a 300-mg bolus followed by 45 mg/h for 24 hours.13 A >30% rate reduction within 4 hours was not statistically different in either treatment arm, with less effective control more frequently observed in those receiving a bolus of amiodarone alone; thus overall, diltiazem allowed for significantly better heart rate control over 24 hours, but it also caused a significantly higher incidence of hypotension requiring discontinuation of the drug. 5.	 Limited data exist regarding the use of nondihydro-

pyridine calcium channel blockers in patients with HFrEF, due to the presumed limitation of negative inotropic effects. Two retrospective analyses highlight potential for increased morbidity when administered in this population. In a retrospective analysis of patients hospitalized with AF with rapid ventricular rate (RVR), diltiazem was associated with an increased risk of acute kidney injury within 48 hours of initiation of diltiazem in those patients with LVEF ≤50%, compared with those with normal EF (10% versus 3.6%; P=0.002).14 An additional retrospective analysis compared patients with HFrEF receiving either intravenous metoprolol or diltiazem. There was a higher incidence of worsening HF symptoms (increased oxygen requirement within 4 hours or initiation of inotropic support with 48 hours) in those patients receiving diltiazem (33% versus 15%; P=0.019). Neither analysis noted an increase in the in-hospital mortality rate, need for a higher level of care, or hypotension.

Figure 17. Acute Rate Control in AF With RVR. *Contraindicated in patients with moderatesevere LV dysfunction regardless of decompensated HF. Colors correspond to Table 2. AF indicates atrial fibrillation; AV, atrioventricular; HF, heart failure; LV, left ventricular; and RVR, rapid ventricular response.

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