A 58-Year-Old Man With New Onset Atrial Fibrillation

Correct Answer: A. Restore normal sinus rhythm by direct current cardioversion following a 4-week period of anticoagulation. If there is a recurrence, offer atrial electroanatomic mapping with catheter ablation for maintenance of sinus rhythm.

Discussion. Atrial fibrillation is the most common cardiac rhythm disturbance seen in clinical practice in the United States. Epidemiologic data and studies reveal incidence approaching 33% in adults older than 55 years of age.¹ The diagnosis is not a trivial one, as AF carries significant risks for stroke (associated with cardiac thromboemoli) and/or congestive heart failure (CHF) risk.1 Additionally, the ongoing significant and steadily progressive aging demographic of the US population makes AF a significant health issue going forward. Importantly, there are well-performed studies and ongoing trials improving our knowledge of pathophysiology and more effective therapy approaches.

As to pathophysiology, we now know in some detail the general pathologic anatomy and pathophysiology of AF. The initial pathology in an aging heart seems to arise in atrial myocytes, located in the regions where the pulmonary veins merge into the atria. These myocytes abnormally self-depolarize and initially create episodes of so-called “paroxysmal” atrial fibrillation (PAF), a condition causing classic symptoms of acute palpitations, shortness of breath with or without effort, and in severe situations, hypotension and CHF. As striking as these episodes can be, in this phase, either spontaneously or with relatively “easy” clinical maneuvers such as beta blockers, can be converted into normal sinus rhythm (NSR). However, in severe situations such as CHF or hypotension, cardioversion is required. Over time, with recurrence or chronicity of episodes, the somewhat mysterious cardiologic concepts of “remodeling” occurs in the effected atrial myocyte/pulmonary vein inflow areas and the AF becomes persistent.^1,2 This phase requires cardioversion to reverse and convert to NSR.² Finally, if the NSR is not maintained, then the condition of “long standing AF” is attained, which makes restoring NSR a much greater challenge. This phase is associated with demonstrable fibrosis in the atrial trigger areas, which results in the formation of re-entry “circus” pathways of conduction that sustain the arrhythmia.²

One of the significant fields of advancement in AF study is the ability to “map” the abnormal circuitry of the atrial pacemaker areas. Such electrophysiological studies can demonstrate, in vivo, the abnormalities discussed above. Thus, one can demonstrate triggering ectopic foci in the PAF population; triggers and “remodeling”/fibrosis in the persistent AF clinical population, and extensive fibrosis and electrical “remodeling” in the long standing, persistent AF population.² Besides demonstrating such anatomic, pathologic, and physiologic abnormalities in diagnosis of AF, such mapping has opened the doors to techniques that ablate the abnormal foci and circuitry in patients with AF to help convert to and maintain NSR.

Regarding the basic goals and strategies in AF management, Michaud and Stevenson¹ published an approach involving several phases:

1. Initial rate control during acute AF episode(s)
2. Ongoing stroke prevention
3. Management of risk factors for AF
4. Long-term strategies to reduce total “AF burden”

Before addressing phase 1, let’s discuss phases 2 and 3. In terms of stroke prevention, AF has long been known to confer significant stroke risk of 4% per year.³ Another well-described schema for stroke risk, the CHAD’s score, is a 9-point clinically based score that correlates with stroke risk in a specific patient, and states that anticoagulation is indicated when the CHAD’s point score is 2 or more.³ Currently, the direct-acting oral anticoagulants, e.g. Apixaban, have been shown to be as effective as traditional warfarin in stroke prevention as well as slightly safer regarding hemorrhage complications.⁴ An exception to anticoagulant treatment is when an AF episode is known to be < 48 hours and echocardiography is negative for presence of the thrombus in an acute AF cardioversion setting.¹ Attention to risk factors in AF to help maintain NSR involves weight loss when indicated, diagnosing and treating sleep apnea, metabolics control (e.g. lipids and diabetes) and reduction in ethyl alcohol or ethanol (ETOH) consumption. Of note, recent papers have demonstrated and proven after many decades of clinical lore that there can be proven to exist a rather direct correlation between ETOH intake/amount with AF episodes.^5,6

Now, to address the ever-narrowing path connecting rate/rhythm control, or phase 1. It is an accepted fact now that AF rhythm control is favored as both an acute and long-term strategy for most patients with AF.⁷ What continues to evolve, however, is when and how to do so. Of course, in the hyperacute setting of symptomatic AF, rate control with rapid acting drugs (e.g. betablockers, calcium channel blockers) is indicated. If NSR is not quickly attained this followed by electronic cardioversion. Interestingly, the earlier use of atrial mapping and ablation techniques earlier during treatment rather than trying to maintain NSR pharmacologically is still evolving. This is due to significant toxicity burden in patients maintained long term with the “best” antiarrhythmic, amiodarone. Further, there is efficacy failure in the 50% range with betablockers alone.^8,9

The techniques of atrial mapping and subsequent ablations are evolving into front-line therapy in AF. In atrial mapping using cardiac catheter techniques, an electroanatomical map is created that will demonstrate abnormal electrical behavior and signals (hot spots of depolarization, abnormal reentry circuits), which can then be ablated.

Two recent studies similarly report the increased efficacy of cryoablation techniques as initial therapy in AF.10,11 Andrade and colleagues¹⁰ studied 303 patients with symptomatic paroxysmal untreated AF with half receiving traditional pharmacology management while half had atrial mapping and ablation. They were followed (using implantable cardiac monitoring as well as usual clinical means) for 1 year. The ablation group outperformed the pharmacologic group regarding decreased symptomatic AF (11% vs 26%) and time in AF. Serious adverse effects were essentially equal (3.2% vs 4%) between the two groups.¹⁰

Wazni and colleagues¹¹ performed a similar study involving 203 patients, with “success” defined as freedom from initial failure after a 90-day electrical blanking period for ablation or time for drug dose adjustment to steady state.¹¹ Again, at the 1-year follow-up period, ablation outperformed pharmacology with a 75% success rate compared with 45% in the pharmacology group. This efficacy had a toxicity cost of two serious events (one angiomyolipoma at 7 days and one pericardial effusion within 30 days) in the ablation group. Total adverse events were equivalent, however, with 14% in both groups.¹¹

An accompanying editorial¹² was appropriately cautious in stating that these studies showed superiority in lower recurrence rates of AF, quality of life and “AF burden” but not yet in mortality and stroke as follow-up was only 1 year. It should be noted, as it was in the editorial, that the study groups were rather “young” (mean age 58 and 61 years) and in otherwise in good cardiac health such that these results may not be as robust in a more general AF population; and that appropriate local skill, experience, and expertise is a must for accurate mapping and safe ablatomy.¹² Still, the editorial concludes that there is consensus in the use of catheter mapping isolation and ablation in “selected patients” with paroxysmal AF at first line therapy.¹²

Indeed, the presented patient fits into this category of age, and good cardiovascular and general health, such that answer A is the best choice. Answers B and D are suboptimal because using rate control only in this setting seems too conservative and after 1-year ablation has less efficacy. Conversely, answer C, total ablation of the AV node with subsequent pacing, has significant downstream toxicity (e.g. late CHF) and is too aggressive.

Patient Follow-Up. The patient presents with an elegant and accurate time frame of symptomatology. As he had experienced some form of symptoms (palpitation with exercise) sporadically in the previous week, out of caution, a 4-week course of Apixiban (5mg twice a day) was prescribed along with a beta blocker to bring his cardiac rate < 100/min. His home halter monitor showed him going in and out of AF. Echocardiogram showed normal valves, with an ejection fraction of 58%, and no structural cardiac abnormalities. Blood testing for troponins and thyroid statins were within normal range.

The patient underwent successful electrical cardioversion at day 29. He continues to take beta blockers. At 3 months, he did not experience any AF episodes. He is back to his normal daily and recreational activities. He is amenable to atrial mapping and ablation but wants to see how long he can maintain NSR without it. Considering his relatively young age and quite vigorous lifestyle, the plan is to follow him and if there is recurrence, then proceed to ablation at that time.

What’s The Take Home? Atrial fibrillation remains the most common cardiac arrhythmia encountered in practice, with incidence as high as 37% among people aged 55 and older.¹ The disorder has been subclassified into (1) paroxysmal AF characterized by abrupt onset and relatively easy spontaneous correction to normal sinus rhythm (NSR) at least temporarily; (2) persistent AF, which is not so easily reversible and requires electrical cardioversion to restore NSR; and (3) longstanding persistent AF, which is AF that has been chronically present for a year or more.¹

As a global entity, AF has significant morbidity/mortality of its own, e.g. shortness of breath, exercise intolerance, uncomfortable palpitations, and significant stroke risk from cardiac embolization as well as mortality/morbidity added background risk for CHF and early mortality. Its pathogenesis is complex and involves abnormal atrial muscle triggering foci with subsequent remodeling and fibrosis which facilitate re-entry pathways and chronicity.

The keystones of therapy involve attempts to convert the patient to NSR as quickly and as safely possible, to maintain NSR as long as possible, and to prevent cardiac embolization and stroke with the outstanding anticoagulants now available. The current trend is evolving toward more early and aggressive methods to accomplish this. The order of battle in AF therapeutics is rhythm over rate control and invasive techniques such as radiofrequency/cold balloon ablative techniques to the pulmonary vein/atrial areas over medical/chronic use of anti-arrhythmic drugs. Indeed, earlier interventions are now favored for ablative techniques.

AUTHOR
Ronald N. Rubin MD^1,2

AFFILIATIONS
¹Lewis Katz School of Medicine at Temple University, Philadelphia, PA
²Department of Medicine, Temple University Hospital, Philadelphia, PA

CITATION
Rubin RN. A 58-Year-Old Man With New Onset Atrial Fibrillation. Consultant. 2024;64(11):eXX. doi: 10.25270/con.2024.11.000002

DISCLOSURES
The author reports no relevant financial relationships.

CORRESPONDENCE:
Ronald N. Rubin, MD, Temple University Hospital, 3401 N. Broad Street, Philadelphia, PA 19140 (blooddocrnr@yahoo.com)

References

1. Michaud GF, Stevenson WG. Atrial fibrillation. N Eng J Med. 2021;384: 353-361.
2. Al Housari M, Miragha V, Terasawa M, et al. Pulmonary vein remodeling between atrial fibrillation subtypes: a matched comparison cardiac computer tomography based study between patients with paroxysmal and persistent atrial fibrillation. Amer J Card. 2023;207:100-107
3. MDCalc. CHADS₂ score for atrial fibrillation stroke risk. Accessed November 20, 2024. https://www.mdcalc.com/calc/40/chads2-score-atrial-fibrillation-stroke-risk.
4. Voskoboinik K, Kalman JM, DeSilva, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Eng J Med. 2020; 383:1305-1316.
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9. Roy D, Talajic M, Dorian P, et al. Amiodarone to prevent recurrence of atrial fibrillation. N Eng J Med. 2000; 342: 913-920.
10. Andrade JG, Wells GA, Deyell MW, et al. Cryoablation or drug therapy for initial treatment of atrial fibrillation. N Eng J Med. 2021; 384: 305-315.
11. Wazni OM, Dandamudi G, Sood N, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Eng J Med. 2020; 383: 1305-1316.
12. Gillis AM. A Sober reality? Alcohol, abstinence, and atrial fibrillation. N Engl J Med. 2020;382(1):83-84. doi:10.1056/NEJMe1914981