Background

With rapid improvements in technology and accumulation of clinical evidence, the implantable cardioverter defibrillator (ICD) has become a standard treatment for either primary or secondary prevention of sudden cardiac death. However, no analysis based on the perspective of emergency department has been reported, and managing patients with ICD remains a challenge to the emergency department doctors.

Methods

This study reviewed the emergency department visits of patients who received ICD implantation in a single university hospital from 1995 to 2004. The baseline demographic and laboratory data were compared between groups with the non‐parametric method of the Mann–Whitney U test for continuous data and the χ2 test for categorical data; p<0.05 was considered significant.

Results

81 patients (56 men and 25 women) were included in this study. 43% of patients had at least one emergency department visit during the follow‐up period, and a total of 86 emergency department visits were recorded. The most frequent aetiology of emergency department visits was ICD discharge (37 episodes; 43.1%) and the most frequent presenting symptom was electric shock sensation (25 episodes; 29.1%). Only 11 (12.8%) emergency department visits were because of non‐cardiac aetiologies. Patients with emergency department visits had significant lower left ventricular ejection fraction (mean (SD) 41.5 (19.8) v 55.2 (18.4) ejection fraction units; p = 0.005) and more use of warfarin (8.6% v 0%; p<0.05). Although most emergency department visits were device or arrhythmia related, the acute coronary syndrome and congestive heart failure still accounted for 27.9% of hospital returns in combination.

Conclusions

Defibrillator discharge, acute coronary syndrome and heart failure constitute most aetiologies of emergency department visits of patients with ICD. The risk factors include lower left ventricular ejection fraction and use of warfarin.

BACKGROUND

Significant cardiac neural and electrophysiologic remodeling occurs with hypercholesterolemia (HC). Whether simvastatin can reverse HC-induced remodeling is unclear.

OBJECTIVE

The purpose of this study was to determine the mechanisms underlying the antiarrhythmic effects of statins.

METHODS

Rabbits (N = 38) were fed HC chow (HC), standard chow (Control), HC chow followed by standard chow (Withdrawal), or HC chow and simvastatin (Statin) for 8 weeks. The hearts then were Langendorff-perfused for electrophysiologic studies. Nerves were identified by immunostaining of growth-associated protein-43 (GAP43) and tyrosine hydroxylase (TH). Action potential duration (APD) restitution in normal hearts with (N = 5) and without (N = 5) simvastatin therapy also was studied.

RESULTS

Serum cholesterol levels (mg/dL) were 1,855 ± 533 in HC, 50 ± 21 in Control, 570 ± 115 in Withdrawal, and 873 ± 112 in Statin groups (P <.001). Compared with HC (16,700 ± 5,342; 12,200 ± 3,878 µm2/mm2), the Statin group had significantly reduced GAP43-positive (10,289 ± 3,393 µm2/mm2, P = .03) and TH-positive (7,685 ± 2,959 µm2/mm2, P = .04) nerve density, respectively. APD was longer in HC rabbits than in controls (192 ± 20 ms vs 174 ± 17 ms; P <.03). Withdrawal and Statin groups had less APD prolongation than HC group. Statin group has less repolarization heterogeneity than HC group (P <.01). Statin therapy flattened the slope of APD restitution in normal hearts. Ventricular fibrillation was either induced or occurred spontaneously in 79% of hearts in HC, 20% in Control, and 66% in Withdrawal groups. However, there was no VF in hearts of Statin group (P <.001).

CONCLUSION

Simvastatin significantly reduced vulnerability to ventricular fibrillation via the mechanism of reduction of HC-induced neural and electrophysiologic remodeling.

The Brugada syndrome is characterized by ST segment elevation in the right precodial leads V1-V3 on surface ECG accompanied by episodes of ventricular fibrillation causing syncope or even sudden death. The molecular and cellular mechanisms that lead to Brugada syndrome are not yet completely understood. However, SCN5A is the most well known responsible gene that causes Brugada syndrome. Until now, more than a hundred mutations in SCN5A responsible for Brugada syndrome have been described. Functional studies of some of the mutations have been performed and show that a reduction of human cardiac sodium current accounts for the pathogenesis of Brugada syndrome. Here we reported three novel SCN5A mutations identified in patients with Brugada syndrome in Taiwan (p.I848fs, p.R965C, and p.1876insM). Their electrophysiological properties were altered by patch clamp analysis. The p.I848fs mutant generated no sodium current. The p.R965C and p.1876insM mutants produced channels with steady state inactivation shifted to a more negative potential (9.4 mV and 8.5 mV respectively), and slower recovery from inactivation. Besides, the steady state activation of p.1876insM was altered and was shifted to a more positive potential (7.69 mV). In conclusion, the SCN5A channel defect related to Brugada syndrome might be diverse but all resulted in a decrease of sodium current.