Atrial premature beats are triggered from the atrial myocardium in a variety of situations and occur in a broad spectrum of the population. This includes patients without structural heart disease and those with any form of cardiac disease, independent of severity.


 Supraventricular premature beats represent premature activation of the atria from a site other than the sinus node and can originate from the atria or the atrioventricular node (called junctional premature beats), though the vast majority are atrial in origin.

Possible mechanisms responsible for spontaneous

●Reentry within the atrium [6] (see "Reentry and the development of cardiac arrhythmias")

●Abnormal automaticity [7] (see "Enhanced cardiac automaticity")

●Triggered activity [8] (see "Ventricular premature beats", section on 'Triggered activity')

Although the mechanisms responsible for APBs are not clear or well investigated, they are most likely due to abnormal automaticity. (See "Enhanced cardiac automaticity".)


ETIOLOGY —  APBs occur frequently in subjects with normal hearts as well as in persons with known cardiovascular disease.

●Idiopathic APBs – In patients without structural heart disease, APBs frequently originate from the pulmonary veins. APBs have long been observed to precede the degeneration of sinus rhythm into atrial fibrillation and are thus considered the main triggers of this common arrhythmia [9,10].

●Toxins or chemicals – Smoking, alcohol, and coffee are widely considered as potential precipitants of APBs [11-13].

•Smoking and alcohol are known to increase sympathetic tone, which may affect the frequency of APBs [11,12].

•Although there is a widespread belief that caffeine, particularly at high doses, is associated with palpitations and a number of arrhythmias, there is no evidence that it is proarrhythmic [14]. Caffeine has clear electrophysiologic effects on the atria, although the association with APBs is uncertain [13]. In a study of 1388 participants in the Cardiovascular Health Study, in which caffeine consumption was self-reported and patients underwent 24-hour ambulatory monitoring, there was no significant differences in the frequency of APBs between users and non-users of caffeine [15]. Nevertheless, there are patients who may be more sensitive to caffeine and note a relationship of palpitations to caffeine intake. Theophylline, another methylxanthine compound, also may increase APB frequency [16,17].

●Acute myocardial infarction – Patients with an acute myocardial infarction (MI) have an early increase in the frequency of APBs, with an incidence ranging from 25 to 81 percent [1,18,19]. One study noted a mean of 9 to 14 APBs per hour on day 1 post-MI, which decreased to one to two APBs per hour on day 10 post-MI [18].

●Coronary heart disease – Among patients with known or suspected coronary heart disease, APBs can be induced during exercise testing, but the prognostic importance of APBs during exercise testing remains unknown [20]. (See "Stress testing to determine prognosis of coronary heart disease", section on 'Atrial arrhythmias'.)

●Other heart diseases – The frequency of APBs appears to be increased in mitral stenosis, hypertrophic cardiomyopathy, and any condition that results in an elevation in pressure or dilatation of the right or left atrium including cardiomyopathy or valvular heart disease [21,22].

●Chronic obstructive pulmonary disease (COPD) – In patients with COPD, bronchodilator use has been identified as a significant risk factor for increased APBs [23].

APBs may occur in subjects with normal or abnormal hearts. Their presence may be increased by hypokalemia, digitalis toxicity, chronic lung disease, acute ischemia or myocardial infarction, excessive caffeine, nicotine or alcohol use, amphetamine use, stress, valvular heart disease, pericarditis, heart failure, hyperthyroidism, or inflammatory changes in the AV junction following heart surgery.




APBs are fairly ubiquitous, occurring commonly in both young and older adult subjects and in those with and without significant heart disease.

In a cross-sectional analysis of 1742 Swiss adults (50 years of age or older) from the general population who underwent Holter monitoring for 24 hours, 99 percent had at least one APB during the monitoring period [1]. In this Swiss cohort, the frequency of APBs steadily increased with age, with rates of 0.8, 1.4, and 2.6 APBs per hour among participants aged 50 to 55 years, 60 to 65 years, and 70 or more years, respectively [1]. Similar findings of greater APB frequency with advancing age have been reported in other cohorts as well [2-4].

The presence and frequency of APBs is dependent upon the presence of structural heart disease. APBs are particularly frequent in patients with mitral valve disease and in those with left ventricular dysfunction regardless of etiology. However, the high prevalence of APBs in the normal population makes such associations uncertain. (See 'Etiology' below.)

The wide range in the reported prevalence of APBs in different populations may be related to the day-to-day variability in their prevalence and frequency. Circadian variation in the frequency of APBs may also occur, but there is significant interpatient variation. In the Copenhagen Holter Study cohort, in which 638 persons (ages 55 to 75 years) underwent up to 48-hour Holter recording and were followed for a median 14 years, a circadian variation was observed in the group with frequent APBs (≥720/day; n = 66 persons), with the fewest APBs/hour observed during the night with a nadir at 6 AM and then reaching a peak value in the afternoon at 3 PM Runs of APBs in all subjects showed a similar circadian variation, while the risk of atrial fibrillation was equal in all time intervals throughout the day [5].

Junctional premature beats (JPBs) occur less commonly than both APBs and ventricular premature beats and are rarely seen in clinical practice. Their prevalence has not been well studied due in part to their scarcity as well as difficulty in making the correct diagnosis. In addition, many studies combine JPBs and APBs into one category of supraventricular premature beats.






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