Changes in cardiac output, rhythm regularity, and symptom severity after electrical cardioversion of atrial fibrillation

Abstract

Objectives

Symptoms in atrial fibrillation (AF) range from none to disabling. The physiological correlates of AF symptoms are not well characterized. This study investigated the association between physiological parameters and symptom severity before and after electrical cardioversion (EC) of AF.

Design

We studied 44 patients with persistent AF (age 66.2 ± 7.9 years, 16% females) 4 ± 2 days before and 5 ± 2 days after EC. Physiological parameters included cardiac output (CO; non-invasive inert gas rebreathing), heart rate (HR), RR variability and resting and ambulatory blood pressure (BP). Symptoms and quality of life (QoL) were assessed by the modified European Heart Rhythm Association score (mEHRA), the Atrial Fibrillation Effect on Quality of Life (AFEQT) and the Symptom Checklist for frequency and severity of symptoms (SCL).

Results

28 of 44 patients were still in sinus rhythm (SR) at post EC evaluation. Those in SR had a decreased HR (-15.4 ± 13.1 bpm, p < 0.001), and an increased CO (+0.8 ± 0.7 L/min, p < 0.001) as compared to those with recurrent AF. Changes in CO after EC correlated with symptom improvement as scored by AFEQT (r = 0.36; p < 0.05), AFEQT symptoms subscore (r = 0.46; p < 0.01), SCL for frequency (r = 0.62; p < 0.01) and severity (r = 0.33; p < 0.05) of symptoms, and the mEHRA score (r = 0.50; p < 0.01). A decrease in RR variability showed similar correlations with these measures of symptom improvement.

Conclusions

Improvements in symptoms and quality of life experienced by patients after electrical conversion of atrial fibrillation are correlated with an increase in CO and a decreased RR variability.

Keywords:

• Atrial fibrillation
• electric cardioversion
• cardiac output
• symptoms
• quality of life

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Correction

Introduction

Atrial fibrillation (AF) is the most frequent sustained cardiac arrhythmia. The prevalence is above 3% in the general adult population and increases with age [1]. Many AF patients experience significant symptoms including palpitations, dizziness, shortness of breath and chest discomfort, but also psychological distress and anxiety [2,3], and AF is associated with a substantial quality of life (QoL) impairment [4].

Interestingly, while some patients experience AF symptoms as severe and disabling, others may be completely free of subjective symptoms, despite a substantial arrhythmia burden [5]. The reasons for this disparity are not well understood, and studies investigating the physiological mechanisms behind AF symptoms are scarce [6].

Adverse hemodynamic effects of AF, such as decreased cardiac output (CO), increased heart rate and RR variability, and changes in blood pressure (BP), are often mentioned as a possible cause of symptoms. In fact, some of the physiological changes during AF, such as the loss of atrial contraction with impaired ventricular diastolic filling, heart rate irregularity, extreme bradycardia or tachycardia during AF and related autonomic alterations, may all contribute to a reduced CO, thereby possibly adding to symptoms. However, to our knowledge, the relation between hemodynamic parameters such as CO, heart rate, heart rate irregularity, and symptoms in AF patients has not been sufficiently studied.

Therefore, this study was performed to assess the relationship between changes in different functional parameters, including CO, and symptoms as well as disease specific QoL in patients undergoing electrical cardioversion (EC) for symptomatic AF.

Methods

A larger study (Dnr. 2012/1272-31/4) [7], looking at 24h-BP after EC, was started in 2012 and was then expanded to include the present substudy (Dnr. 2014/2199-31/4). A power calculation showed that we needed 31 complete sets of data to have an 80% chance of demonstrating a significant change in CO based on the assumptions that EC could increase CO by 5% and that the standard deviation of changes in CO was 0.4 L. Therefore, we aimed to include 40–45 patients. Inclusion criteria were persistent AF and elective EC. Exclusion criteria were ongoing treatment with class I or III antiarrhythmic drugs or a known significant valvular heart disease, in order to diminish potential confounding factors influencing HR, SV or CO.

Patients scheduled for elective EC at the Karolinska University Hospital between February and December 2015 and March and June 2017 were consecutively included. Baseline data included information on cardiovascular risk factors, medical history and medication. Measurements of CO, cardiac index (CI), stroke volume (SV), heart rate (HR), RR variability, resting and ambulatory BP, symptoms and QoL were conducted approximately 4 ± 2 days before (pre-EC) and 5 ± 2 days after EC (post-EC). The study protocol adhered to the Declaration of Helsinki and was approved by the Swedish Ethical Review Authority (Dnr. 2012/1272-31/4 and 2014/2199-31/4). All subjects provided written informed consent prior to participation.

CO was measured by a non-invasive inert gas rebreathing method (Innocor^®, Innovision A/S, Odense, Denmark). A detailed description of this method has been published elsewhere [8]. In brief, patients inhaled a known volume of oxygen, 0.5% nitrous oxide (N2O), and 0.1% sulfur hexafluoride (SF6) over 5 breathing cycles. N2O and SF6 are inert gases out of which only N2O is soluble in blood allowing for determination of relative volumes of each gas in exhalation which approximates pulmonary blood flow and CO. Two measurements were performed after 5 min of rest in a sitting position (with 5 min in between for complete inert gas clearance) to establish a mean value. If the values differed >20% a third measurement was carried out. Values of CO, CI, volume of oxygen, volume of oxygen per kilogram, HR, SV, saturation, bolus dose, and maximal insoluble gas level were recorded. All tests were carried out by the same, experienced examiner.

A standard 12 lead ECG including a rhythm strip of 10 s (MAC 5500, GE Medical Systems Information Technologies, Milwaukee WI, USA) was recorded after 5 min of rest in supine position. Patients were kept blinded as to the underlying rhythm until all measurements had been carried out. RR variability was calculated as the standard deviation of the first 10 RR intervals.

Office BP was measured manually with an automatic oscillometric device (Omron 705IT Intelli Sense, Omron Healthcare Europe, Hoofddorp, the Netherlands). 24-hour ambulatory BP was measured with Spacelabs Healthcare monitors 90207 and 90217 (Medical Market I.N.T AB, Stockholm, Sweden) and analyzed with 92506 ABP Report Management System software). Office BP was measured in a standardized manner after 5 min at rest and 24-hour ambulatory BP measurements were made every 20th minute both during daytime (0600–2200 h) and night-time (2200–0600 h).

To evaluate the symptomatic burden of AF and QoL, three questionnaires were used before and after EC. First, the validated disease specific Atrial Fibrillation Effect on Quality of Life (AFEQT) questionnaire [9], second, the Symptoms Checklist (SCL) questionnaire for frequency and severity of symptoms [10], and third, the mEHRA score [11]. In brief, the AFEQT is a 20-item AF-specific measure of QoL evaluating domains of AF symptoms, impairment in social and physical activities, medical treatment concerns, and AF-specific treatment satisfaction. Responses are given on a 7-point rating scale and the total score ranges between 0 (severe symptoms and disability) and 100 (no symptoms or disability). Overall AFEQT scores have been shown to correspond with mild (score of approximately 71), moderate (score of approximately 58), and severe (score of approximately 42) QoL impairment [9]. Furthermore, AFEQT evaluates three functional subscores (symptoms, daily activities and treatment concerns) in the same manner. The SCL lists 16 symptoms commonly experienced by patients with AF and evaluates how often these symptoms were experienced and how severe each symptom was and item scores are then summed to produce a frequency score (0 to 64) and a severity score (0 to 48) [10]. The mEHRA score quantifies AF-symptoms based on their impact on daily activity (EHRA I, IIa, IIb, III, IV) [11].

Statistics

Descriptive statistics, including mean and standard deviation, were used to present baseline characteristics and changes in hemodynamic variables before and after EC. Then the paired data sets, pre-EC and post-EC, enabled the use of paired Student’s t-tests for statistical evaluation. Pearson’s and Spearman’s correlations were calculated, where appropriate. Changes were considered statistically significant at p < 0.05. We also calculated a coefficient of variation of the CO measurements. Calculations were conducted in SPSS Statistics® version 25 (IBM Corp., Armonk, NY, USA) and Microsoft Office 365 Excel® 2016 (Microsoft Corp., Redmond, WA, USA).

Results

Fifty-four patients were recruited. Ten were excluded due to inadequate anticoagulation, spontaneous conversion to sinus rhythm (SR), or conversion to atrial flutter at the time of EC. Thus, 44 patients completed the study (Table 1). Measurements were conducted 4 ± 2 days pre-EC and 5 ± 2 days post-EC. Post-EC, sixteen patients (36%) had relapsed to AF (AF-AF group) and twenty-eight patients (64%) maintained SR (AF-SR group). Compared with patients who remained in SR, patients with AF relapse were younger, had a longer duration of AF, a lower HR pre-EC, and fewer were treated with aldosterone antagonists (Table 1).

Table 1. Baseline patient characteristics.

Baseline patient characteristics	All	AF-SR	AF-AF	p-value
Number	44 (100%)	28	16
Male sex	37 (84%)	23	14
Age (years)	66.5 (±7.9)	68.0 (±7.8)	63.8 (±7.5)	p < 0.05
Weight (kg)	89.7 (±16.6)	87.1 (±15.5)	94.3 (±18.1)
Body mass index	28.3 (±4.6)	28.4 (±4.8)	28.0 (±4.3)
Estimated AF duration (days)	94.6 (±77.0)	79.7 (±66.8)	120.5 (±88.6)	p < 0.05
Heart rate (beats per minute)	83.3 (±18.7)	90.3 (±19.5)	77.8 ± 14.9	p < 0.05
Alcohol (weekly standard units)	4.3 (±5.6)	3.9 (±3.7)	5.1 (±7.9)
Smokers	1 (2%)	0	1
Diabetes mellitus	4 (9%)	3	1
Cerebrovascular disease	6 (14%)	4	2
Cardiovascular disease	8 (18%)	7	1
Congestive heart failure	7 (16%)	6	1
Hypertension	26 (59%)	19	7
Betablocker	44 (91%)	24	16
ACE-I/ARB	21 (48%)	15	6
Diuretics	9 (20%)	6	3
Calcium channel blocker	10 (23%)	8	2
Aldosterone antagonist	23 (11%)	5	0	p < 0.05
Statins	18 (41%)	14	4
Insulin	1 (2%)	1	1

AF: atrial fibrillation; SR: sinus rhythm; ACE-I: angiotensin converting enzyme inhibitor; ARB: angiotensin receptor blocker.

Medication was kept stable after EC, as intended, with the exception of four patients in whom the betablocker dose was decreased (n = 1) or increased (n = 1), a low-dose calcium-inhibitor was started (n = 1) or digoxin was stopped and a betablocker started (n = 1).

Cardiac output

Pre-EC, patients had a CO of 3.6 ± 1.2 L/min at rest which, on average, increased by 0.8 ± 0.7 L/min (p < 0.001) for patients that maintained SR post-EC as compared to the group with AF relapse that had no change in CO (Figure 1, Table 2). The coefficient of variation of the CO measurements was 6.4%.

Figure 1. Changes in cardiac output for patients that (a) maintained sinus rhythm after electrical cardioversion, (b) remained in or relapsed to atrial fibrillation after electrical cardioversion. CO: cardiac output; Pre EC: before electrical cardioversion; Post EC: after electrical cardioversion.

Table 2. Hemodynamics and symptom scores (mean ± standard deviation) before (Pre-EC) and after (Post-EC) electrical cardioversion in (1) all patients, (2) AF-AF, those who relapsed to atrial fibrillation and (3) AF-SR, those who maintained sinus rhythm.

	All	All	p-value	AF-AF	AF-AF	p-value	AF-SR	AF-SR	p-value
	Pre-EC	Post-EC		Pre-EC	Post-EC		Pre-EC	Post-EC
Number	44	–	–	16	–	–	28	–	–
Cardiac output (L/min)	3.6 ± 1.2	4.1 ± 1.4	<0.001	3.9 ± 1.2	3.9 ± 1.3	ns	3.5 ± 1.2	4.3 ± 1.5	<0.001
Stroke volume (mL)	49.2 ± 19.1	67.6 ± 32.9	<0.001	48.7 ± 16.7	50.0 ± 21.5	ns	49.5 ± 20.7	77.6 ± 34.3	<0.001
Heart rate (beats per minute)	82.4 ± 17.6	72.1 ± 20.1	0.0023	90.3 ± 19.5	91.8 ± 16.7	ns	77.8 ± 14.9	60.3 ± 10.3	<0.001
RR interval (s)	0.77 ± 0.19	0.92 ± 0.25	<0.001	0.73 ± 0.18	0.68 ± 0.11	ns	0.79 ± 0.20	1.06 ± 0.19	<0.001
RR variability (standard deviation)	0.17 ± 0.08	0.06 ± 0.06	<0.001	0.17 ± 0.07	0.13 ± 0.05	0.008	0.17 ± 0.08	0.02 ± 0.02	<0.001
Systolic BP (mmHg)	121 ± 14	123 ± 14	ns	118 ± 15	117 ± 17	ns	123 ± 13	126 ± 11	ns
Diastolic BP (mmHg)	77 ± 10	74 ± 11	ns	75 ± 12	78 ± 13	ns	78 ± 10	71 ± 9	0.002
Systolic BP 24h (mmHg)	117 ± 14	119 ± 14	ns	116 ± 14	115 ± 13	ns	117 ± 14	122 ± 14	0.01
Diastolic BP 24h (mmHg)	77 ± 9	74 ± 10	0.005	78 ± 11	76 ± 10	ns	76 ± 9	72 ± 10	0.006
AFEQT (total score)	56.5 ± 21.6	71.2 ± 19.0	<0.001	55.4 ± 19.6	58.4 ± 19.6	ns	57.1 ± 23.1	78.7 ± 14.3	<0.001
AFEQT (symptoms subscore)	73.9 ± 22.7	85.8 ± 17.6	0.006	80.0 ± 15.2	73.4 ± 20.1	ns	70.4 ± 25.7	92.9 ± 11.2	<0.001
SCL (frequency of symptoms score)	32.9 ± 8.6	26.9 ± 9.3	<0.001	32.5 ± 7.7	32.6 ± 10.1	ns	33.1 ± 9.2	23.5 ± 7.0	<0.001
SCL (severity of symptoms score)	15.7 ± 8.4	9.0 ± 8.3	<0.001	16.3 ± 7.8	13.0 ± 9.6	ns	15.4 ± 8.9	6.7 ± 6.5	<0.001
mEHRA score; mean (score)	2.6 ± 0.6	1.8 ± 0.8	<0.001	2.5 ± 0.6	2.2 ± 0.7	0.022	2.7 ± 0.6	1.6 ± 0.7	<0.001

EC: electrical cardioversion; AF: atrial fibrillation; SR: sinus rhythm; BP: blood pressure; AFEQT: atrial fibrillation effect on quality of life; SCL: symptoms checklist; mEHRA: modified European Heart Rhythm Association score; Pre EC: before electrical cardioversion; Post EC: after electrical cardioversion. IQR: inter quartile range; ns: non-significant (p-value ≥ 0.1).

RR variability and other physiological variables

As expected, RR variability decreased after EC in patients that remained in SR (from 0.17 ± 0.08 to 0.02 ± 0.02, p < 0.001) and the HR decreased (from 77.8 ± 14.9 to 60.3 ± 10.3, p < 0.001). Patients that had relapsed to AF did not have a decrease in HR, however, their RR’ variability surprisingly also decreased, although to a lesser extent (from 0.17 ± 0.07 to 0.13 ± 0.05, p = 0.008) (Table 2). There was an increase in systolic BP as well as a decrease in diastolic BP post-EC in the AF-SR group according to 24h ambulatory BP measurements (+5 ± 14 mmHg systolic, p < 0.01, and −4 ± 10 mmHg diastolic, p < 0.01, respectively). Systolic office BP remained unchanged before and after EC but there was a decrease in diastolic office BP (−7.4 ± 10.9 mmHg, p < 0.01) in patients with SR post-EC.

Symptoms and QoL

There was an improvement in QoL for patients that maintained SR as scored by the total AFEQT score (−19.8 ± 21.4, p < 0.01) and the AFEQT symptoms subscore (−22.5 ± 25.7, p < 0.001) (Table 2). Also, symptom frequency (−10.2 ± 9.9, p < 0.001) and symptom severity (−6,6 ± 9,2, p < 0.05) according to SCL, decreased amongst patients that maintained SR (Table 2). Furthermore, symptomatic burden according to mEHRA also decreased (−1.1 ± 1.0, p < 0.01) amongst patients that maintained SR (Table 2).

Specific symptoms

According to AFEQT, the symptoms that decreased most amongst patients that maintained SR were palpitations (−40%), irregular heartbeat (−49%), pause in heart activity (−50%) and dizziness (−40%). Furthermore, patients that maintained SR were less restricted in their recreational pastimes (−42%), social activities (−42%), and physical activity at the post-EC evaluation. They experienced decreased fatigue (−44%), shortness of breath (−44%), inability to exercise (−43%), inability to walking uphill or upstairs (−44%) and inability to perform vigorous activities (−40%). According to SCL, the symptoms that decreased most in frequency amongst patients that maintained SR were irregular heartbeat (−51%), and fatigue (−40%).

Correlations

In patients that maintained SR the level of CO increase was correlated to an improvement in QoL, a decrease in symptomatic burden as scored by the AFEQT total score, the AFEQT symptoms subscore, the SCL score for frequency and severity of symptoms, and the mEHRA score (Table 3, Figure 2).

Figure 2. Correlations between changes in cardiac output and symptoms scores as scored by (a) total atrial fibrillation quality of life score, (b) atrial fibrillation quality of life score symptom subscore, (c) symptom checklist for frequency of symptoms, (d) symptom checklist for severity of symptoms. CO: cardiac output; AFEQT: atrial fibrillation quality of life score; SCL: symptom checklist score of frequency and severity of symptoms.

Table 3. Correlations between change in symptom- and quality of life scores and change in hemodynamic variables before and after electrical cardioversion of atrial fibrillation.

	Cardiac output	Heart rate	RR variability	Systolic blood pressure (office)	Diastolic blood pressure (office)	Systolic blood pressure (24h)	Diastolic blood pressure (24h)
AFEQT total score (r)	0.36*	0.12	0.44**	0.07	0.10	0.21	0.13
AFEQT symptoms subscore (r)	0.46**	0.36*	0.47**	0.02	0.25	0.22	0.13
SCL frequency of symptoms score (r)	0.62**	0.29	0.49**	0.05	0.11	0.35*	0.11
SCL severity of symptoms score (r)	0.33*	0.24	0.42**	0.07	0.02	0.30	0.03
mEHRA score (rho)	0.50**	0.32*	0.41**	0.16	0.34*	0.37*	0.09

AFEQT: atrial fibrillation quality of life score; SCL: symptom checklist score; mEHRA: modified European heart rhythm association score. *=p < 0.05, **=p < 0.01.

Decreased heart rate was correlated to an improvement in QoL as scored by the AFEQT symptoms subscore and an improvement in the mEHRA score (Table 3).

Decreased rhythm irregularity, as measured by RR variability, was also correlated to an improvement in QoL and a decrease in symptomatic burden as scored by the AFEQT total score, the AFEQT symptoms subscore, the SCL score for frequency and severity of symptoms, and the mEHRA score (Table 3).

Furthermore, increased systolic 24-hour ambulatory BP was correlated to the SCL score for frequency of symptoms, and the mEHRA score (Table 3).

Discussion

Although many AF patients experience significant symptoms, the physiological correlates of AF-symptoms are not well understood. The main finding of this study was that AF patients maintaining SR after EC experienced improvements in symptoms and QoL which were correlated to an increase in CO and rhythm regularity. This finding may contribute to a better understanding of physiological correlates of AF-related symptoms.

Early studies investigating changes in CO after EC report conflicting findings. Many methods can be used to measure CO and no significant changes in CO have been reported 0–24 h after EC using the indicator dilution technique [12], right heart catheterization [13], Fick and indicator-dilution [14], or arterial cannulation and Pressure Recording Analytical Method (PRAM) monitoring [15]. Non-invasive CO measurement by inert gas rebreathing has been validated against invasive methods and has a high precision [16]. For the purpose of measuring CO during atrial fibrillation, the sampling period of approximately 15 s is an advantage compared with methods averaging only a few cardiac cycles as it is less sensitive to beat-to-beat variations in SV [8]. The coefficient of variation in this study was 6.4% which is deemed acceptable and which is in line with previous findings by our research group (6.8% and 6.0%) [8] and others (6.9%) [17].

Charles and Upshaw reviewed 11 studies in 136 patients which evaluated CO with different methods from immediately after up to one month after EC and concluded that a majority of patients experience an improved CO (average +25%) [18]. CO changes were initially small (0–34%) but increased after 3 days (28–56%) [18]. Thus, it seems essential that changes in CO are studied at least 72 h after EC. The delay in CO improvement is likely linked to atrial stunning which occurs in 38–80% of cases and lasts 48–72 h after EC [19].

The decrease in CO associated with AF may result from different mechanisms. First, the absence of an atrial contraction leads to suboptimal ventricular filling and stroke volume [20] especially in patients with diastolic dysfunction [21]. Second, irregular cardiac activation itself may contribute to a reduced CO. Third, a lower CO may be a result of the tachycardia and this may be particularly problematic in patients with diastolic dysfunction [21].

The effect on QoL when converting AF to SR has been studied before, though often with non-validated and general questionnaires [10, 22]. Our results are consistent with the finding of Sandhu et al. who did use the disease-specific AFEQT questionnaire 3 months after EC for AF. [23]. The improvement in QoL for patients maintaining SR, on average 5 days after EC, in our study was from 56.1 (±23.3, p < 0.01) to 78.7 (±14.3, p < 0.01) on a scale of 0–100, reflecting moderate and mild impairment respectively. The average improvement was by 19.8 points (±21.4, p < 0.01) and Dorian et al. related a change in over 19 points in the AFEQT QoL score to a moderate improvement in global QoL [24]. The disease specific and validated AFEQT questionnaire has been shown to be internally consistent (Cronbach alpha coefficient >0.88), and sensitive to the severity of AF and changes over time [9, 25]. We also used the disease specific and reliable SCL (Cronbach alpha coefficient >0.87) evaluating both frequency and severity of symptoms [10]. Additionally, we used the mEHRA score which is established in clinical guidelines [11]. All three scores showed a reduction in symptoms and improved QoL in patients with SR.

To our knowledge, this is the first study to suggest that the changes in symptoms and QoL after EC, are correlated with hemodynamic changes in CO and RR variability. In this study, patients who maintained SR experienced an average increase in CO by 23%. Furthermore, the CABANA trial demonstrated that catheter ablation of AF, compared to drug therapy, resulted in improved QoL as measured by AFEQT [26]. Interestingly, we only found mild correlations between symptom improvement and changes in HR and BP in this relatively small study and the strongest physiological correlates were CO and RR variability. Frykman et al. demonstrated that AF episodes that caused patients to seek care had a higher ventricular rate [27], but in contrast, Clark et al. have shown that rhythm irregularity in itself, regardless of heart rate, causes adverse hemodynamic consequences [28].

As expected, HR and RR’ variability decreased and SV increased after EC. To improve CO, SV needs to increase enough to offset the decrease in HR. After cardioversion, restoration of ventricular filling by atrial contribution and by reduction of heart rate could produce an increase in stroke volume. This could explain the increase in systolic as well as possibly the decrease in diastolic BP. However, this is if the cardiac afterload and systemic resistances are unchanged. In a larger study, we recently found a significant increase in systolic BP after conversion from AF to SR while diastolic BP only slightly decreased rendering mean arterial pressure almost unchanged [29]. This may reflect activation in the sympathetic nervous system and in the Renin-Angiotensin- Aldosterone-System but also difficulties to obtain reliable measures of BP in patients with an irregular pulse. Surprisingly, RR’ variability also decreased in patients that relapsed to AF, without a corresponding increase in CO. It would be of interest to investigate if stress, psychological factors, and sympathetic activation also have an effect on the irregularity of AF.

There are several limitations to this study. One limitation is the relatively small sample size which made it inappropriate to study specific subgroups. There may also be a risk of selection bias since the study only included patients scheduled for elective EC, and thus does not enable us to draw conclusions about patients with particularly severe or mild symptoms. Furthermore, the study in not controlled, in the sense that a control group not subjected to EC was not included. Thus, we can only draw conclusions on correlations and not casual relationships. However, a strength is that measurements were conducted on the same patients both before and after EC, so patients functioned as their own controls. It is not possible to completely exclude confounding factors that may explain some of the observed correlations. There is a risk of the placebo effect affecting the symptom scores, although patients were kept blinded to the underlying rhythm as they filled out the questionnaire. There is also a risk that changes in medication, as described above, or diet could have affected both the cardiac output and the symptom scores, however, we consider this to be a low risk considering the short time between measurements and few alterations in medications. Another limitation is that echocardiographic data was not available in all patients, although information on a clinical history of heart failure was available and is presented in Table 1 and inert gas rebreathing has been shown to be accurate and reproducible in patients with advanced heart failure [30]. It is also worth mentioning that the baseline comorbidities of the included patients were modest, and that measurements were carried out at rest and not during exercise. The follow-up time was short which we attempted to balance by using several different measurements for symptoms and QoL which all fell out as significant. The AFEQT specifically has been validated by evaluating symptoms over an average of 4 weeks while we evaluated post EC-symptoms over an average of 5 days. However, patients were carefully instructed how to use the AFEQT and results were well in line with other measures of symptoms and QoL which all correlated to increased CO after EC. Furthermore, the recorded CO values in this study were generally low raising the possibility that CO was systematically underestimated. It is known that pulmonary shunting, indicated by an arterial oxygen saturation (SaO₂) below 95%, is leading to an error in the CO estimate of the rebreathing method [31]. Yet, in this study, mean SaO₂ was 98% at inclusion and only 2 patients had SaO₂ values slightly below 95%.

Conclusions

This study shows that the decrease in symptomatic burden and improvement in QoL, seen in AF patients after cardioversion is correlated to an increase in CO and a decrease in RR variability, thus providing significant and meaningful physiological correlates to the symptomatic improvement. Future studies are needed to confirm these findings and establish causal relationships, to understand why AF is asymptomatic in a substantial proportion of patients, to understand the hemodynamic effects of restoring SR with EC and how this is related to clinical outcomes such as symptoms and QoL.

Disclosure statement

Frieder Braunschweig has received speaker or consultancy fees by Biotronik, Medtronic, Abbott, Boston Scientific, Boehringer, Novartis, Pfizer and Orion.

Correction Statement

This article was originally published with errors, which have now been corrected in the online version. Please see Correction (http://dx.doi.org/10.1080/14017431.2024.2331901)

Additional information

Funding

This study was supported by the Swedish Heart and Lung Foundation.