Atrial fibrillation (AF) is the most common cardiac arrhythmia and is responsible for a majority of arrhythmia-related hospitalizations.¹ As the prevalence of AF continues to rise so does the number of related hospitalizations, morbidity, and mortality.² AF mechanisms include atrial ectopy, single localized reentry circuits, or multiple microreentrant circuits, all of which can be influenced by genotype, ischemic heart disease and inflammation. Other risk factors include hyperthyroidism, obstructive sleep apnea and congenital heart disease.^3-5 As the burden of AF begins to increase it is of utmost importance to identify all potential risk factors.

Multiple studies have demonstrated an association between seasonal variation and a variety of cardiac and non-cardiac disorders such as deep venous thrombosis, pulmonary embolism, aortic dissection, stroke, hypertension, congestive heart failure, angina, ventricular arrhythmias, myocardial infarction, and sudden cardiac arrest. Many of these diseases have been found to be more frequent in winter, with inverse correlations to outdoor temperature. Similar associations have been proposed for AF as well as AF related stroke.⁶

The primary purpose of this review is to summarize data regarding the association between seasonal variation and occurrence of AF paroxysms. Secondary aims of this review were to summarize data regarding additional associations to further investigate the primary association:

1) outdoor temperature and occurrence of AF paroxysms.

2) duration of daylight and occurrence of AF paroxysms.

3) barometric pressure and occurrence of AF paroxysms.

4) alcohol consumption and occurrence of AF.

5) seasonal variation and the occurrence of AF related stroke.

A systematic review of the literature was performed to identify manuscripts studying the association between various seasons and AF. This included the occurrence of AF paroxysms, AF related stroke, and AF related mortality. The overall association of AF with the seasons, any particular month, temperature, amount of daylight, and barometric pressure were all studied. The review was conducted using the PRISMA checklist.

In our analysis, a majority of studies demonstrated an association between seasonal variation and the occurrence of AF paroxysms. AF paroxysms were most frequent during winter and early spring and least frequent in the summer with peak months being February and April. The nadir of AF paroxysms was observed to be in the month of July. It is reasonable to imagine that stroke, a complication of AF, would be more frequent at times of greatest AF burden and thus studies investigating seasonal variation and AF related stroke were also reviewed which demonstrated highest frequency of AF related stroke during the winter and the lowest during summer. Mortality during AF hospitalizations also appears to be greatest in winter while inpatient mortality during AF related stroke hospitalizations does not appear to be affected by seasonal variation.^7-15,17,20

Several mechanisms have been proposed to explain the increased risk of AF paroxysms in winter with lower temperatures being the common denominator. Lower temperatures have been demonstrated to enhance sympathetic function by activation of central angiotensin or hypothalamic mineralocorticoid receptors, which can increase the risk of AF.^22-25 Blood pressure can also increase due to lower temperatures, which can ultimately lead to increased atrial pressure with subsequent atrial dilatation and pulmonary vein stretch leading to initiation and propagation of AF.^26-28 Endothelin I, renin, and angiotensin II levels may increase due to lower temperatures, which can also enhance arrhythmogenesis.^29-32 Cold temperatures may worsen atrial ischemia and promote glucose intolerance, both of which may increase the risk of AF paroxysms.¹⁵ Our review demonstrates equivocal results regarding the association between temperature and the occurrence of AF paroxysms.

Duration of daylight has also been proposed as a mechanism to explain the increased risk of AF paroxysms in winter. Yamashita et al. have demonstrated circadian variation in the expression of potassium channels, particularly that decreased exposure to sunlight can lead to alterations in cardiac ion channels such that action potentials shorten, increasing the risk of reentrant arrhythmias such as AF.³³ The role of Vitamin D, a vitamin whose synthesis is dependent upon exposure to sunlight, in the setting of this particular association has also been investigated and it appears that Vitamin D does not mediate this phenomenon. Vitamin D does not appear to have a role in this interaction.¹⁷

Barometric pressure may be another factor mediating the effects of seasonal variation on the occurrence of AF paroxysms. Gluszak et al. demonstrated that barometric pressure, specifically low pressure fronts, increases the risk of AF paroxysms. Interestingly, risk was greatest 24 to 48 hours before the actual change in barometric pressure.⁷ This temporal finding was consistent with previously reported findings from a study by Delyukov et al. that demonstrated negative effects of changes in barometric pressure on cardiovascular function preceding arrival of the atmospheric front by 3 to 24 hours.³⁴ The timing of the effects of low pressure fronts on physiologic changes may be due to alterations in the electrical field that occur before arrival of the atmospheric front.

Alcohol consumption may also play a part in the increased occurrence of AF paroxysms in the winter. Kupari et al. investigated and found a positive correlation between alcohol sales and the occurrence of AF paroxysms. Actual alcohol consumption, however, was not directly assessed in this study and alcohol sales were used a surrogate.¹² This association remains unclear.

Other factors that may contribute to the association between seasonal variation and the occurrence of AF paroxysms include the increased burden of respiratory infections and chronic obstructive pulmonary disease in the winter, which can trigger AF. These factors, although possible AF triggers, may also confound the association between seasonal variation and occurrence of AF paroxysms as asymptomatic AF may be detected more frequently in the winter due to an increased number of hospitalizations for these other reasons. Additionally, heart failure and sepsis, which are also more frequent in winter, may attribute to the greater risk of AF in winter.⁶

The risk of AF-related stroke peaks during winter season and nadirs in summer. This is likely due to previously documented seasonal variations in fibrin, fibrinogen, and factor VII.^35,36 Additionally, cold temperatures increase erythrocyte and platelet count, increasing blood viscosity and subsequent risk of thrombus formation.³⁷ Whether prescription of therapy or compliance rates with treatment have any role remains unclear. This association is important to note as care providers should stress the importance of monitoring and controlling blood pressure, activity level, and avoiding infections in those with already known AF as the winter season approaches. Those with hypertension should be advised to ensure compliance with current therapy and blood pressure should be closely monitored. All patients should be encouraged to maintain appropriate activity levels and exercise during the winter, a season often associated with decrease in activity. Those with AF should be particularly encouraged to obtain the influenza vaccination during winter as this has been demonstrated to reduce cardiovascular and all-cause mortality and may help prevent infection induced AF.³⁸ Notwithstanding, patients with AF need to be counseled on the fore-mentioned things allround the year but especially in winter season.

The strengths of reviewed studies include the large sample size of some of these studies, particularly those based on registry data. Some of the included studies also studied not only the seasonal variation and occurrence of AF paroxysms but also investigated potential factors mediating this association such as temperature, duration of daylight, and barometric pressure. Limitations of reviewed studies include that all but 1 study captured only those hospitalized for AF or those who had AF while hospitalized for other reasons. This allows for missing “milder” or asymptomatic cases. Additionally, some studies were not able to distinguish between incident and prevalent cases. Some reviewed studies also only included AF that was coded as the primary diagnosis and may have ignored cases with AF coded as the secondary or tertiary diagnosis. The use of discharge records also brings into question the reliability of discharge diagnosis, which may not always be accurate. Caution should also be exercised in determining causality due to the retrospective nature of majority of these studies.

Our study has the inherent limitations of a systematic review. We did not have access to patient level data, hence some important endpoints like medication adherence and other comorbidities could not be assessed. Due to lack of similar definitions across studies, quantitative analysis could not be performed. We are unable to make firm conclusions on most endpoints due to very low number of studies for those endpoints. Large prospective studies are needed to further clarify this potential association.

There is an association between seasonal variation and the occurrence of AF paroxysms with the greatest risk being during winter and early spring and the nadir being in summer.

Temperature, duration of daylight, and barometric pressure are thought to mediate this seasonal fluctuation in AF occurrence.

None.