94 Does chronic atrial fibrillation influence prognosis in patients with advanced systolic heart failure?

Introduction: Stable organized atrial tachyarrhythmias (ATs) /"rotors" that maintain AF have been identified in patients (pts) with paroxysmal atrial fibrillation (PAF) & persistent AF (PRAF) with no or minimal heart disease. Hypothesis: Biatrial ATs occur in AF pts with systolic heart failure (HF). Methods: We performed simultaneous contact catheter mapping of the RA & LA using 3 D non-contact mapping ) in 83 refractory AF pts during spontaneous AF episodes.Spontaneous atrial premature beats (APBs) & triggered ATs were analyzed. We also compared regional distribution of ATs & activation patterns in pts with & without HF. Results: 24 HF pts, mean age of 62±9 years, 75% male with mean left ventricular ejection fraction (LVEF) 45.5±9% and mean left atrial (LA) size 4.35±0.8 cm were mapped. They had 42 APBs that triggered 26 distinct organized stable ATs/"rotors". Each pt had 1 to 4 RA or LA regions showing triggering APBs (mean 1.75/pt) initiating AT. APBs arose predominantly from the RA or LA septum (45%) & superior LA/PV (24%) regions (Fig 1a). A biatrial distribution of the stable ATs/"rotors" occcurred in HF pts (Fig 1b) with few focal ATs. Compared to pts without HF (n=59), HF pts (n=24) trended to have more PRAF (83% vs 66%, p=0.18). 78 organized stable ATs/"rotors" were compared for regional distribution in PRAF pts with HF (n=16) & without HF (n=32). Stable ATs with focal LA/PV origin were uncommon in both groups (7% vs. 15%). LA ATs/"rotors" were similar (26% vs. 17%; p=0.58) as were typical RA flutter and atypical RA ATs/"rotors" in both groups (Fig 1c). Conclusions: 1. A majority of APBs initiating AF in HF pts originated from the septal and superior LA/PV regions. 2. While triggers are still frequently present with the LA/PV origin in HF pts, stable ATs/"rotors" had biatrial distribution & a lesser frequency of focal LA/PV ATs. 3. This spectrum of ATs/"rotors" was similar to PRAF pts without HF, potentially supporting similar ablative interventions in both pt groups.

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Rhythm Control of Persistent Atrial Fibrillation in Systolic Heart Failure: A Bayesian Network Meta-Analysis of Randomized Controlled Trials

International Journal of Heart Failure ◽

10.36628/ijhf.2021.0008 ◽

2021 ◽

Vol 3 ◽

Author(s):

Dibbendhu Khanra ◽

Saurabh Deshpande ◽

Anindya Mukherjee ◽

Siddhratha Mohan ◽

Hassan Khan ◽

...

Keyword(s):

Heart Failure ◽

Atrial Fibrillation ◽

Bayesian Network ◽

Randomized Controlled Trials ◽

Meta Analysis ◽

Systolic Heart Failure ◽

Persistent Atrial Fibrillation ◽

Rhythm Control ◽

Controlled Trials ◽

Randomized Controlled

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Abstract 304: Adaptive Sarcomeric Remodeling of Left Atrial Cardiomyocytes in Non-failing Non-valvular Atrial Fibrillation

Circulation Research ◽

10.1161/res.127.suppl_1.304 ◽

2020 ◽

Vol 127 (Suppl_1) ◽

Author(s):

Parth V Desai ◽

Thomas Martin ◽

Marisa Stachowski ◽

Maria Papadaki ◽

Jonathan A Kirk

Keyword(s):

Heart Failure ◽

Atrial Fibrillation ◽

Left Atrial ◽

Structural Changes ◽

Contractile Function ◽

Systolic Heart Failure ◽

Energy Utilization ◽

Valve Disease ◽

Hill Coefficient ◽

Contractile Apparatus

Contractile remodeling in sustained atrial fibrillation (AF) has been analyzed by limited studies whose results were confounded by either coexisting systolic heart failure or valve disease (valvular AF) or origin of tissue (right chamber instead of left, atrial appendage instead of main wall). We sought to assess the structural changes in contractile apparatus and its physiological implications on single cardiomyocyte mechanics in patients with non-failing non-valvular AF. We utilized left atrial wall tissue from rejected donor hearts from 5 subjects in sinus rhythm (SR) and 3 with AF (age 50, 2♀ vs 60, 1♀), all with no signs of cardiovascular or valvular disease. Isolated single skinned myocytes were mounted to a force transducer and length controller and set to an initial sarcomere length of 2.1 μm. Isometric active and passive forces were recorded using custom software during [Ca2+] solution switching (0.79 - 46.8 μM). Surprisingly, we found that isometric maximal calcium-activated force (Fmax) was almost two times higher in AF compared to SR patients (n: SR = 15 cells, AF = 9 cells, p < 0.0001). This was unexpected, as previous studies found that AF patients had depressed contractile function, although these were confounded by heart failure and valve disease. There were no differences in calcium sensitivity, hill coefficient, or cell cross-sectional area (CSA) between SR and AF. We next performed 1D SDS-PAGE electrophoresis to compare myosin heavy chain (MHC) isoforms. In SR patients, atrial expression of β-MHC was very low (14% of total MHC expression), but this was significantly elevated in AF patients (37%, p = 0.05). The observed rise in contractile force might be a compensatory adaptation to sustain ventricular filling in initial stages of non-valvular non-failing AF patients. Or it may be a maladaptive response to atrial unloading resulting in wasted energy utilization. The contribution of this cellular increase in contractility to whole organ function is unclear. There is strong evidence that fibrotic remodeling and inflammation play an important role in AF, but the clinical challenge is still significant. Conversely, there has been very little work done on the contractile apparatus in AF, and whether it may represent a possible therapeutic target.

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