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4 Nonsinus Focal Atrial Tachycardia and MAT

See Figure 10 for the algorithm for acute treatment of suspected focal atrial tachycardia (AT) and Figure  11 for the algorithm for ongoing management of focal AT.

4.1 Focal Atrial Tachycardia

Focal AT is characterized as a fast rhythm from a discrete origin, discharging at a rate that is generally regular, and conducting in a centrifugal manner throughout the atrial tissue. Focal AT represents approximately 3% to 17% of the patients referred for SVT ablation.49,122,186 The demographics of focal AT in the adult population will continue to change as SVTs are increasingly ablated at a younger age. Focal AT can be sustained or nonsustained. The atrial rate during focal AT is usually between 100 and 250 bpm.186 Presence and severity of symptoms during focal AT are variable among patients. Focal AT in the adult population is usually associated with a benign prognosis, although AT-mediated cardiomyopathy has been reported in up to 10% of patients referred for ablation of incessant SVT.187,188 Nonsustained focal AT is common and often does not require treatment. The diagnosis of focal AT is suspected when the ECG criteria are met (Section 2). Algorithms have been developed to estimate the origin of the focal AT from the P-wave morphology recorded on a standard 12-lead ECG.189,190 In general, a positive P wave in lead V1 and negative P waves in leads I and aVL are correlated to ATs arising from the left atrium. Positive P waves in leads II, III, and aVF suggest that the origin of AT is from the cranial portion of either atria. Shorter P-wave duration is correlated to AT arising from the paraseptal tissue versus the right or left atrial free wall.191 The precise location of the focal AT is ultimately confirmed by mapping during EP studies when successful ablation is achieved.123–127,192–196 Focal AT has been localized to the crista terminalis, right or left atrial free wall or appendage, tricuspid or mitral annulus, paraseptal or paranodal areas, pulmonary veins, coronary sinus, and coronary cusps, but it originates more frequently from the right atrium than from the left atrium.197,198

The underlying mechanism of focal AT can be automatic, triggered activity, or microreentry, but methods to distinguish the mechanism through pharmacological testing or EP study are of modest value because of limited sensitivity and specificity.123,199,200 An automatic AT can be transiently suppressed by adenosine or by overdrive pacing and may be terminated by beta blockers, diltiazem, or verapamil. Whereas a triggered AT can be terminated by adenosine or overdrive pacing, its response to beta blockers, diltiazem, or verapamil may be variable. A microreentrant AT can be induced and terminated by programmed stimulation, but its response to adenosine, beta blockers, diltiazem, or verapamil may depend on the location of the microreentrant circuit; the tachycardia can be terminated by these drugs if the microreentrant circuit involves tissue around the sinus node,

Recommendations for Ongoing Management of IST COR LOE Recommendations I C-LD 1.  Evaluation for and treatment of reversible causes are recommended in patients with suspected IST.160,185

See Online Data Supplements 4 and 5. It is important to distinguish IST from physiological sinus tachycardia or focal AT from the high right atrium, which can have P-wave morphology similar to the sinus P wave. A careful history and physical examination, with further laboratory and imaging studies, are necessary to determine reversible causes of tachycardia, such as exogenous substances and drugs, infection, anemia, and hyperthyroidism. A focal AT would have sudden onset and termination, which would not be the case for IST. IIa B-R 1.  Ivabradine is reasonable for ongoing management in patients with symptomatic IST.168–176

See Online Data Supplements 4 and 5. In 1 small randomized crossover trial,168 ivabradine given at a dosage of 2.5 to 7.5 mg twice daily significantly reduced daytime heart rate from 98.4±11.2 at baseline to 84.7±9.0, compared with 98.6±11.1 on placebo (P<0.001), and improved exercise tolerance and symptoms in patients with IST. Similar findings have been observed in several additional nonrandomized observational studies.169–176 Furthermore, a significant number of patients in these studies reported complete resolution of symptoms, with persistent clinical benefit observed in some even after discontinuing the drug. In 1 observational study, ivabradine was more effective than metoprolol in reduction of the heart rate and amelioration of symptoms.170 The drug is well tolerated, with an excellent safety profile demonstrated in 2 large RCTs in patients with heart failure.166,167 Ivabradine can cause phosphenes, an enhanced brightness in a portion of the visual field; this side effect, which is usually transient, was reported in 3% of patients taking the drug in the SHIFT trial.167 IIb C-LD 1.  Beta blockers may be considered for ongoing management in patients with symptomatic IST.170,172

See Online Data Supplement 4 and 5. Beta blockers are modestly effective in lowering the heart rate and improving symptoms that are due to IST. In a small nonrandomized observational cohort, metoprolol succinate titrated to a target of 95 mg daily lowered the heart rate over 4 weeks from a baseline.172 In a small nonrandomized study comparing metoprolol with ivabradine, both agents reduced heart rate compared with baseline and improved exercise capacity.170 Although effectiveness of beta blockers is modest and hypotension may limit dose, the overall safety of beta blockers warrants their use for treatment of symptomatic patients. IIb C-LD 2.  The combination of beta blockers and ivabradine may be considered for ongoing management in patients with IST.172

See Online Data Supplement 4 and 5. Some patients with IST may have particularly refractory symptoms, and single-drug efficacy may be limited. In a small observational study, the addition of ivabradine (7.5 mg twice daily) to metoprolol succinate (95 mg daily) reduced the heart rate from baseline to a greater extent than did metoprolol alone.172 On combination therapy, symptoms related to IST were resolved in all patients, and the combined therapy was well tolerated. In the SHIFT and BEAUTIFUL studies, the majority of patients were taking the combination of ivabradine and a beta blocker, which was well tolerated.166,167 Nevertheless, patients who are considered for combination therapy should be monitored closely for the possibility of excess bradycardia. Ivabradine can cause phosphenes, an enhanced brightness in a portion of the visual field; this side effect was reported in 3% of patients taking the drug in the SHIFT trial.167

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