Impact of low-voltage zones on the left atrial anterior wall on the reduction in the left atrial appendage flow velocity in persistent atrial fibrillation patients

Hori, Yoshiaki; Nakatani, Naoki; Fukuda, Reiko; Ukaji, Tomoaki; Sato, Hirotsugu; Koshikawa, Yuri; Inami, Shu; Ishikawa, Takahiro; Kobayashi, Shigeto; Sakai, Yoshihiko; Tanaka, Isao

doi:10.1007/s10840-019-00532-z

Cited by 10 publications

(12 citation statements)

References 31 publications

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“…Hori et al observed that the presence of LVA on the anterior wall was associated with a low ≤ 0.2 m/s LAA emptying velocity in LSPSAF patients, with further reduction if LVA was located in the close proximity to the LAA orifice. The progression of atrial remodelling was considered to be a major contributing factor to this phenomenon, in addition to an ascending aorta being in direct contact with the anterior wall [17].…”

Section: Influence Of Laa Flow Velocities On the Voltage-defined La Rmentioning

confidence: 99%

Left and right atrial appendage functional features as predictors for voltage-defined left atrial remodelling in patients with long-standing persistent atrial fibrillation

et al. 2021

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It was hypothesised that left atrial (LA) fibrosis identified by the presence of low-voltage areas (LVA) may influence the mechanical and electrical function of the left (LAA) and right (RAA) atrial appendage among the long-standing persistent atrial fibrillation (LSPAF) population. 140 consecutive patients underwent voltage mapping of LA with a multielectrode catheter following pulmonary vein isolation and restoration of sinus rhythm with cardioversion. Echocardiography determined LAA peak outflow and inflow velocities and intracardiac catheter-based mean LAA and RAA AF cycle length (AFCL) were obtained during AF before ablation. The impact of flow velocities and AFCL on the prevalence and location of LVA was further evaluated. LVA were detected in 54% of the patients. 14% of the patients presented severe global LVA burden > 20% of the total LA surface area. 29% of the patients presented a disseminated pattern of remodelling as 3 out of 5 LA segments were affected. LAA AFCL, RAA AFCL, LAA flow velocities did not predict the absolute presence of LVA. However LAA AFCL > 155 ms predicted disseminated LVA pattern and LAA AFCL > 165 ms severe LVA incidence. LAA AFCL > 155 ms was predictive for existence of LVA within antero-septal LA segments whilst LAA emptying velocity ≤ 0.2 m/s within lateral wall. Moreover RAA AFCL > 165 ms was strongly related to the presence of LAA AFCL > 15 ms and > 165 ms. LAA and RAA functional assessment was predictive of the presence of advanced stages of voltage-defined LA fibrosis and its regional distribution among LSPAF population

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Section: Influence Of Laa Flow Velocities On the Voltage-defined La Rmentioning

confidence: 99%

Left and right atrial appendage functional features as predictors for voltage-defined left atrial remodelling in patients with long-standing persistent atrial fibrillation

et al. 2021

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“…Also, another study has shown a significant association between LVA and clinically manifest and subclinical silent cerebral ischemia detected on cerebral delayed‐enhancement MRI in 200 patients with AF undergoing ablation, even after adjustment for CHA2DS2‐VASC score 99 . This may be attributed to a reduced LA appendage flow velocity with the presence of LVZ, particularly on the LA anterior wall, which could subsequently lead to thrombus and cardioembolic complication 100 …”

Section: Identification Of Atrial Fibrosismentioning

confidence: 99%

Atrial fibrosis and substrate based characterization in atrial fibrillation: Time to move forwards

Quah

Dharmaprani

Tiver

et al. 2021

Cardiovasc electrophysiol

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Atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia in clinical practice. However, current therapeutic interventions for atrial fibrillation have limited clinical efficacy as a consequence of major knowledge gaps in the mechanisms sustaining atrial fibrillation. From a mechanistic perspective, there is increasing evidence that atrial fibrosis plays a central role in the maintenance and perpetuation of atrial fibrillation. Electrophysiologically, atrial fibrosis results in alterations in conduction velocity, cellular refractoriness, and produces conduction block promoting meandering, unstable wavelets and micro‐reentrant circuits. Clinically, atrial fibrosis has also linked to poor clinical outcomes including AF‐related thromboembolic complications and arrhythmia recurrences post catheter ablation. In this article, we review the pathophysiology behind the formation of fibrosis as AF progresses, the role of fibrosis in arrhythmogenesis, surrogate markers for detection of fibrosis using cardiac magnetic resonance imaging, echocardiography and electroanatomic mapping, along with their respective limitations. We then proceed to review the current evidence behind therapeutic interventions targeting atrial fibrosis, including drugs and substrate‐based catheter ablation therapies followed by the potential future use of electro phenotyping for AF characterization to overcome the limitations of contemporary substrate‐based methodologies.

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“…LVZs were identified as areas with a bipolar peak-to-peak voltage amplitude of less than 0.5 mV. [4][5][6][7]10,11 In addition, the ascending aorta was reconstructed by means of the 3D mapping system and merged with the LA voltage map. The electroanatomical maps were merged with the CT images that had been obtained.…”

Section: Electrophysiologic Study With 3d Voltage Mappingmentioning

confidence: 99%

Formation of low‐voltage zones on the anterior left atrial wall due to mechanical compression by the ascending aorta

Hayashida

Nagashima

Kurokawa

et al. 2021

Cardiovasc electrophysiol

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Background: Although low-voltage zones (LVZs) in the left atrium (LA) are considered arrhythmogenic substrates in some patients with atrial fibrillation (AF), the pathophysiologic factors responsible for LVZ formations remain unclear.Objective: To elucidate the anatomical relationship between the LA and ascending aorta responsible for anterior LA wall remodeling. Methods:We assessed the relationship between existence of LVZs on the anterior LA wall and the three-dimensional computed tomography image measurements in 102 patients who underwent AF ablation.Results: Twenty-nine patients (28%) had LVZs grearer than 1.0 cm 2 on the LA wall in the LA-ascending aorta contact area (LVZ group); no LVZs were seen in the other 73 patients (no-LVZ group). The LVZ group (vs. no-LVZ group) had a smaller aorta-LA angle (21.0 ± 7.7°vs. 24.9 ± 7.1°, p = .015), greater aorta-left-ventricle (LV) angle (131.3 ± 8.8°vs. 126.0 ± 7.9°; p = .005), greater diameter of the noncoronary cusp (NCC; 20.4 ± 2.2 vs. 19.3 ± 2.5 mm; p = .036), thinner LA wall-thickness adjacent to the NCC (2.3 ± 0.7 vs. 2.8 ± 0.8 mm; p = .006), and greater cardiothoracic ratio (percentage of the area in the thoracic area, 40.1 ± 7.1% vs. 35.4 ± 5.7%, p < .001).The aorta-LA angle correlated positively with the patients' body mass index (BMI), and the aorta-LV angle correlated negatively with the body weight and BMI. Conclusion:Deviation of the ascending aorta's course and distention of the NCC appear to be related to the development of LA anterior wall LVZs in the LAascending aorta contact area. Mechanical pressure exerted by extracardiac structures on the LA along with the limited thoracic space may contribute to the development of LVZs associated with AF.

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Impact of low-voltage zones on the left atrial anterior wall on the reduction in the left atrial appendage flow velocity in persistent atrial fibrillation patients

Cited by 10 publications

References 31 publications

Left and right atrial appendage functional features as predictors for voltage-defined left atrial remodelling in patients with long-standing persistent atrial fibrillation

Left and right atrial appendage functional features as predictors for voltage-defined left atrial remodelling in patients with long-standing persistent atrial fibrillation

Atrial fibrosis and substrate based characterization in atrial fibrillation: Time to move forwards

Formation of low‐voltage zones on the anterior left atrial wall due to mechanical compression by the ascending aorta

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