http://www.macoalition.org/documents/ACCP_8_published.pdf

Antithrombotic Therapy in Atrial Fibrillation: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)

Background—Transient atrial contractile dysfunction (“atrial stunning”) follows conversion of atrial fibrillation (AF) to sinus rhythm and has significant clinical implications; however, the underlying mechanisms are poorly understood. We investigated the hypothesis that rapid atrial activation (as during AF) impairs cellular contractility and affects cellular Ca2+ handling. Methods and Results—Edge detection and indo 1 fluorescence techniques were used to measure unloaded cell shortening and intracellular Ca2+ transients in atrial myocytes from control (Ctl) dogs and dogs subjected to atrial pacing at 400 bpm for 7 (P7) or 42 (P42) days. Atrial tachycardia reduced fractional cell shortening (0.1 Hz) from 7.3±0.4% (Ctl) to 4.3±0.3% and 2.0±0.3% in P7 and P42 dogs, respectively (P<0.01 for each). Resting [Ca2+]i was not altered in paced dogs, but the systolic Ca2+ transient was significantly reduced. Furthermore, cells from paced dogs showed slowed relaxation and use-dependent decreases of Ca2+ transients ...

Cellular Mechanisms of Atrial Contractile Dysfunction Caused by Sustained Atrial Tachycardia

https://www.annalsthoracicsurgery.org/article/S0003-4975(98)00230-6/pdf

Radiofrequency and cryoablation of atrial fibrillation in patients undergoing valvular operations.

Evaluation of transesophageal echocardiography before cardioversion of atrial fibrillation and flutter in nonanticoagulated patients

A 60-year-old dentist presents to the emergency room with palpitations for 3 hours. The ECG shows atrial flutter (AFl) with atrioventricular (AV) conduction varying from 2:1 to 4:1. He has known hypertension for which he takes 10 mg of enalapril daily. In the last 2 years he was seen twice because of AFl and on both occasions 1 mg of ibutilide IV resulted in the return of sinus rhythm with 1:1 AV conduction. Catheter ablation of the arrhythmia is discussed with the patient, to which he agrees and curative AFl ablation is scheduled in 4 weeks.

### History

In 1906, Einthoven made an electrocardiographic recording of AFl.1 In 1913, Lewis called attention to the typical saw tooth pattern and the negative deflections of the atrial waves in leads II and III.2

During the next 50 years, there was much discussion about whether AFl was caused by a rapidly firing atrial focus or is the result of a large circus movement involving the atria. After mapping atrial activation with endocardial and esophageal recordings, Puech et al3 concluded that the flutter cycle in the human heart involved activation of the whole right atrium. Stimulation studies by Waldo et al4 revealed that in postoperative AFl the arrhythmia was based on a reentry mechanism involving a large atrial area. They demonstrated the presence of an excitable gap that allowed the speeding up of the flutter rate during atrial pacing and termination of the arrhythmia by pacing.

### Mechanism and Types of Macroreentrant Tachycardias

With the use of endocardial activation mapping and stimulation studies, several investigators have shown that different types of macroreentrant atrial tachycardias are possible. As indicated in Figure 1, the circuit is usually located in the right atrium. In the circuit, a critical component of slow conduction is frequently present, often located in the isthmus of …

Contemporary Management of Atrial Flutter

It is often suggested but never proven that atrial function is not affected during atrial flutter, nor after its conversion to normal sinus rhythm. To evaluate this hypothesis, a prospective study was performed in 22 patients (age range 20 to 88 years) with atrial flutter. Diastolic transmitral flow was analyzed with echo-Doppler before and after conversion. After randomization, conversion was attempted with overdrive pacing or up to two 50 J shocks. If the initial method was unsuccessful, a 200 J shock was administered. All patients were converted to sinus rhythm with this protocol. Shortly after conversion (at 1 and 6 hours), atrial contribution to ventricular filling was absent in 4 of 22 patients. In the remaining 18 patients, atrial contribution to ventricular filling was small. Atrial contribution to transmitral flow improved from 20 to 27% within 24 hours (p 1 week. The findings suggest that stasis in the atria can remain temporarily present after successful conversion of atrial flutter to sinus rhythm.

Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion.

Internal cardioversion was attempted in three patients with chronic atrial fibrillation, refractory to conventional external direct current shocks. Endocardiac shocks were delivered between the proximal electrode on a multipolar USCI pacing catheter and a back paddle. This is positioned with the tip proximal of the bundle of His, and the proximal ring electrode floating in the right atrium. Two patients were converted with 200 Joules, one needed 400 Joules. Two of our three patients were chronically maintained in sinus rhythm after the initial conversion, one had recurrence within 24 hours.

Intracardial shock for the conversion of chronic atrial fibrillation

Atrial stunning lasts more than one week after conversion of atrial flutter

A 35-year-old woman with frequent attacks of paroxysmal supraventricular tachycardia and psychiatric background was submitted to ablation of AV-nodal tachycardia. Before ablation, tachycardia with a cycle length of 455 ms was easily induced with regular atrial stimulation or with one extrastimulus. Radiofrequency current (35 Watts) was applied on a site, localized between the His bundle and the ostium of the coronary sinus. The local electrogram showed an atrial activation 20 ms before the atrial activation at the His bundle site during tachycardia. Application terminated AV-nodal tachycardia within 2.5 seconds. Two back-up applications were given during sinus rhythm. At the control study, conduction over the slow pathway was abolished, and the fast conduction remained intact with a Wenckebach 2:1 block point at 180 beats/min. She remained free of recurrences with a follow-up of more than 3 months. The possibility of selective ablation of the slow pathway in AV-nodal tachycardia is discussed.

Radiofrequency ablation of a slow pathway in AV-nodal tachycardia.

ABSTRACT Background/Aim To provide longitudinal data on the evolution of lipid levels and the intake of lipid-lowering therapies in patients with stable coronary artery disease. Methods Single-centre retrospective study with inclusion of 350 patients with a first coronary artery event in 2014 or earlier and outpatient cardiac clinic follow-up in 2015 and 2019. Lipid levels were collected within a time frame of 3 months of their visits. This retrospective study protocol (2020.086) was approved by the ethical committee and by the Data Privacy Officer of AZ Maria Middelares Ghent. For this type of study, formal consent is not required, following local law and regulations. Results Average LDL levels were 82 (±26) mg/dl in 2015 and 70 (±24) mg/dl in 2019 (p < 0.001). Most patients included were already on statin treatment before inclusion in the trial (94%), with a significant increase in high-intensity statin use (45% vs. 58%) after a 5-year follow-up. At the same time, we observed a significant increase in ezetimibe use (in combination with statin therapy or in monotherapy) (8% vs. 22%) during follow-up. LDL ≤70 mg/dl was 34% in 2015 and 53% in 2019. LDL ≤55 mg/dl was 13% in 2015 and 28% in 2019. Conclusion This study shows significant intensification of lipid-lowering therapy use during follow-up, and a significant lipid level lowering after 5-year follow-up, in an outpatient cardiac clinic follow-up. Further improvement in lipid control is still desirable, especially after the European Society of Cardiology recommend stricter lipid levels in the 2021 Prevention Guidelines.

Changes in lipid lowering medication and lipid levels over time in patients with stable coronary artery disease

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