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.

BACKGROUND: The reduction in the left atrial appendage (LAA) flow velocity is related to the presence of emboli in atrial fibrillation (AF) patients. The LAA is located on the left superior side of the left atrial (LA) anterior wall, and we investigated the relationship between the reduction in the LAA flow velocity (LAAFV) and low voltage zones (LVZs < 0.5 mV) on the LA anterior wall. METHODS: In 146 persistent AF patients, LAAFV measurements, by transesophageal echocardiography, and catheter ablation were performed. LA mapping was performed before ablation during sinus rhythm, and the locations of any anterior-LVZs were documented. RESULTS: Eighty-one patients had a documented LVZ on the LA anterior wall, and those with an LVZ had a significantly lower LAAFV compared to those without (anterior-LVZ(+) vs. anterior-LVZ(-) = 26 ± 11 vs. 34 ± 10 cm/s, p < 0.001), while no significant difference was observed when compared to the other LVZ regions. A low-LAAFV (≦ 20 cm/s) was observed in 36 patients, and the CHADS2-vasc score and existence of an anterior-LVZ were associated with a low-LAAFV. In patients with anterior-LVZs, the distance between the anterior-LVZ and LAA orifice correlated with a low LAAFV (r = 0.534, p < 0.001) as compared to the surface area of the anterior-LVZ (r = - 0.288, p = 0.009). CONCLUSIONS: In persistent AF patients, an LVZ on the LA anterior wall was associated with a low LAAFV. In addition, an anterior-LVZ located near the LAA orifice was further related to a reduction in the LAAFV.

Influence of the left atrial contact areas on fixed low-voltage zones during atrial fibrillation and sinus rhythm in persistent atrial fibrillation.

BACKGROUND: Atrial low-voltage zones (LVZ) are suggested as important factors for maintaining persistent atrial fibrillation (PsAF). The relationship between LVZs and left atrial (LA) contact areas (CoAs) is still unclear. OBJECTIVE: To assess whether CoA regions were involved in atrial substrate properties maintaining PsAF. METHODS: A total of 50 patients with PsAF (36 long-lasting) were analyzed. Three representative CoA detection areas (ascending aorta-anterior-LA, descending aorta-left pulmonary vein antrum, and vertebrae-posterior-LA) were registered on the mapping geometry. Electrograms during AF and sinus rhythm (SR) were acquired, and the fractionated electrograms (CFE; < 80milliseconds) and voltages were analyzed regarding the CoAs. RESULTS: After SR conversion, 76% (38/50) had a significant LVZ (>5% of the total LA surface area). Patients with long-lasting PsAF versus PsAF had larger CoA areas (7.7 ± 3.0 vs. 4.5 ± 2.5cm2 , P < 0.05) and overlapped-LVZs (8.2 [3.2-11.0] vs. 2.1 [0.7-3.7] cm2 , P = 0.0126) between the SR-LVZs (<0.5 mV) and AF-LVZs (<0.2 mV). Overlapped-LVZs were frequently observed in CoA regions (anterior 76.4%; LIPV antrum 78.8%, and vertebrae 39.2%), and those LVZs had smaller unipolar voltages than those distant from the CoA regions (0.64 ± 0.16 vs. 2.5 ± 1.5 mV, P < 0.0001). SR-LVZ targeted ablation, including of CoA regions, rendered AF termination (n = 8, 21%), and 88% of the sites were not located immediately above, but adjacent to, the overlapped-LVZs. Significant AF slowing (6.0 ± 0.6 to 5.6 ± 0.6 Hz; P < 0.05) accompanied by unintentional CFE elimination (9.8-1.8 cm2 ; P < .0001) was achieved in patients without termination. CONCLUSION: Our data suggested that external structures in contact with the LA are involved in the creation of localized diseased myocardium necessary for PsAF maintenance.

[A case of severe hypokalemia caused by a Chinese herbal remedy (Yokukansan) in an 81-year-old woman with dementia].

An 81-year-old woman had been visiting 2 hospitals for hypertension and dementia, prior to admission to our emergency room for nausea, hypertension, severe hypokalemia (K 1.29 mEq/l) and abnormal electrocardiography findings. She had been taking a Chinese herbal remedy (Yokukansan, 7.5 g/day) for the behavioral and psychological symptoms of dementia (BPSD) for 6 months before admission. On admission, she presented with metabolic alkalosis with hypokalemia, a high urinary excretion of potassium, low plasma rennin activity and hypoaldosteronism. We diagnosed pseudoaldosteronism caused by the Chinese herbal remedy Yokukansan (which includes licorice). Discontinuation of Yokukansan and the administration of potassium supplements normalized her serum potassium level within 2 weeks. However, we could not successfully control her BPSD by drugs such as tiapride hydrochloride or risperidone. BPSD is a serious problem in an aging society, with the ever-increasing incidence of dementia. The use of Yokukansan has recently been receiving attention as a new treatment modality for BPSD. Because this agent has relatively few adverse effects compared with typical antipsychotic agents, the use of Yokukansan is continuing to increase sharply. Pseudoaldosteronism, if caused by Yokukansan, may cause death by severe hypokalemia, but the early identification of hypokalemia is sometimes difficult because drug-induced hypokalemia is not dose-dependent. We think it is important to create awareness of the possible adverse effects of Yokukansan, such as hypertension and electrolyte abnormalities to make the most of this commonly used drug for the treatment of BPSD among dementia patients.