Even though the relationship between antiarrhythmic drug usage and subsequent prostate cancer (PCa) risk has recently been highlighted, relevant findings in the previous literature are still inconsistent. In addition, very few studies have attempted to investigate the association between sodium channel blockers or potassium channel blockers for arrhythmia and the subsequent PCa risk. Therefore, this cohort study aimed to find the relationship between antiarrhythmic drug usage and the subsequent PCa risk using a population-based dataset. The data used in this study were derived from the Longitudinal Health Insurance Database 2005, Taiwan, China. We respectively identified 9988 sodium channel blocker users, 3663 potassium channel blocker users, 65 966 beta-blocker users, 23 366 calcium channel blockers users, and 7031 digoxin users as the study cohorts. The matched comparison cohorts (one comparison subject for each antiarrhythmic drug user) were selected from the same dataset. Each patient was tracked for a 5-year period to define those who were subsequently diagnosed with PCa. After adjusting for sociodemographic characteristics, comorbidities, and age, Cox proportional hazard regressions found that the hazard ratio (HR) of subsequent PCa for sodium channel blocker users was 1.12 (95% confidence interval [CI]: 0.84-1.50), for potassium channel blocker users was 0.89 (95% CI: 0.59-1.34), for beta-blocker users was 1.08 (95% CI: 0.96-1.22), for calcium channel blocker users was 1.14 (95% CI: 0.95-1.36), and for digoxin users was 0.89 (95% CI: 0.67-1.18), compared to their matched nonusers. We concluded that there were no statistical associations between different types of antiarrhythmic drug usage and subsequent PCa risk.
Adrenergic beta-Antagonists/adverse effects* ; Adult ; Age Factors ; Aged ; Anti-Arrhythmia Agents/adverse effects* ; Calcium Channel Blockers/adverse effects* ; Cohort Studies ; Comorbidity ; Databases, Factual ; Digoxin/adverse effects* ; Humans ; Incidence ; Male ; Middle Aged ; Potassium Channel Blockers/adverse effects* ; Prostatic Neoplasms/epidemiology* ; Retrospective Studies ; Socioeconomic Factors ; Sodium Channel Blockers/adverse effects* ; Taiwan/epidemiology*

An unusual grayish brown discoloration of the synovium was found during a knee arthroscopy of a 72-year-old man. He also had similar pigmentation affecting the skin on the legs, arms, hands, and face. It was found he had been taking 400 mg of amiodarone hydrochloride daily for last 7 years. Amiodarone is known to cause a slate grey pigmentation of skin and cornea, but we believe this is the first report of amiodarone-induced pigmentation of the synovium. The arthroscopist should be aware of the possibility of drug-related synovial pigmentation and include this in differential diagnosis.
Aged ; Amiodarone/*adverse effects/therapeutic use ; Anti-Arrhythmia Agents/*adverse effects/therapeutic use ; Arrhythmias, Cardiac/complications/drug therapy ; Arthroscopy ; Diagnosis, Differential ; Humans ; Knee Joint/surgery ; Male ; Pigmentation Disorders/*chemically induced/*diagnosis ; Skin/pathology ; Synovial Membrane/*pathology

No abstract available.
Aged, 80 and over ; Amiodarone/*adverse effects ; Anti-Arrhythmia Agents/*adverse effects ; Atrial Fibrillation/diagnosis/*drug therapy ; Drug-Induced Liver Injury/*etiology/radiography ; Female ; Humans ; Liver/*drug effects/radiography ; Predictive Value of Tests ; *Tomography, X-Ray Computed

No abstract available.
Amiodarone/*adverse effects ; Anti-Arrhythmia Agents/*adverse effects ; Female ; Humans ; Male

Amiodarone ; adverse effects ; Anti-Arrhythmia Agents ; adverse effects ; Arrhythmias, Cardiac ; drug therapy ; Corneal Diseases ; chemically induced ; Humans ; Male ; Middle Aged

BACKGROUND/AIMS: Amiodarone is one of the most widely used antiarrhythmic agents; however, amiodarone-induced pulmonary toxicity (APT) can be irreversible and sometimes fatal. The aim of this study was to evaluate the feasibility of chest computed tomography (CT) as a diagnostic tool for APT and to assess the utility of the CT APT score as an index for predicting the severity of APT. METHODS: Patients underwent amiodarone treatment for various reasons, most often atrial fibrillation, for more than 2 years, and those that received a cumulative dose > 100 g were enrolled. A total of 34 patients who underwent chest CT between December 2011 and June 2012 were enrolled, whether or not they had clinical symptoms. The APT CT score was defined as the number of involved regions in the lung, which was divided into 18 regions (right and left, upper, middle, and lower, and central, middle, and peripheral). The CT findings were evaluated according to the total dose and duration of amiodarone treatment and the results of a pulmonary function test. Clinical symptoms and outcomes were also evaluated according to APT CT scores. RESULTS: Seven patients had positive APT CT scores (interstitial fibrosis in five, organizing pneumonia in one, and mixed interstitial fibrosis and organizing pneumonia in one), and these patients exhibited significantly lower diffusion capacity for carbon monoxide in the lungs compared with patients without an increased APT CT score (70.2% +/- 6.9% vs. 89.7% +/- 19.4%; p = 0.011). Three of the seven patients experienced overt APT that required hospital admission. CONCLUSIONS: Chest CT is a useful diagnostic tool for APT, and the APT CT score might be a useful index for assessing the severity of APT.
Aged ; Amiodarone/*adverse effects ; Anti-Arrhythmia Agents/*adverse effects ; Atrial Fibrillation/diagnosis/*drug therapy ; Cross-Sectional Studies ; Cryptogenic Organizing Pneumonia/chemically induced/physiopathology/*radiography/therapy ; Feasibility Studies ; Female ; Forced Expiratory Volume ; Hospitalization ; Humans ; Lung/drug effects/physiopathology/*radiography ; Male ; Middle Aged ; Predictive Value of Tests ; Prospective Studies ; Pulmonary Diffusing Capacity ; Pulmonary Fibrosis/chemically induced/physiopathology/*radiography/therapy ; Respiratory Function Tests ; Risk Factors ; Time Factors ; *Tomography, X-Ray Computed ; Vital Capacity

BACKGROUND/AIMS: Most current knowledge regarding amiodarone toxicity derives from clinical trials. This study was performed to investigate the incidence and risk factors of overall adverse effects of amiodarone in real-world practice using a large sample size. METHODS: Between January 1, 2000 and March 10, 2012, a total of 930 consecutive patients who had been treated with amiodarone for arrhythmia were reviewed retrospectively. An amiodarone-associated adverse event was considered in cases of discontinuation or drug dose reduction due to an unexpected clinical response. RESULTS: The mean daily dose of amiodarone was 227 +/- 126 mg, and the mean duration was 490 +/- 812 days. During the mean follow-up duration of 982 +/- 1,137 days, a total of 154 patients (16.6%) experienced adverse effects related to amiodarone, the most common being bradycardia or conduction disturbance (9.5%). Major organ toxicities in the thyroid (2.5%), liver (2.2%), eyes (0.6%), and lungs (0.3%) were rare. All patients recovered fully without complications after amiodarone discontinuation or dose reduction. The only independent predictor of adverse effects was the duration of amiodarone treatment (odds ratio, 1.21; 95% confidence interval, 1.03 to 1.41; p = 0.016, per year). CONCLUSIONS: Low-dose amiodarone is well tolerated in a real-world clinical population. Further studies with a prospective design are needed to confirm this finding.
Aged ; Amiodarone/administration & dosage/*adverse effects ; Anti-Arrhythmia Agents/administration & dosage/*adverse effects ; Arrhythmias, Cardiac/drug therapy ; Atrioventricular Block/chemically induced/epidemiology ; Bradycardia/chemically induced/epidemiology ; Female ; Humans ; Incidence ; Male ; Middle Aged ; Republic of Korea ; Retrospective Studies ; Risk Factors

Acute amiodarone toxicity after a single dose of intravenous amiodarone is very rarely seen. We report the case of a 64-year-old Chinese man who presented with atrial fibrillation and fluid overload due to congestive cardiac failure. He was treated with a single bolus dose of intravenous amiodarone, after which he developed elevated serum transaminases, coagulopathy, thrombocytopenia and acute renal failure. His parameters returned to normal after 25 days and his recovery was uneventful.
Acute Kidney Injury ; chemically induced ; Amiodarone ; adverse effects ; Anti-Arrhythmia Agents ; adverse effects ; Atrial Fibrillation ; drug therapy ; Blood Coagulation Disorders ; chemically induced ; Heart Failure ; complications ; drug therapy ; Humans ; Male ; Middle Aged ; Thrombocytopenia ; chemically induced ; Transaminases ; blood ; Treatment Outcome

OBJECTIVETo investigate the effect and potential mechanism of lysophosphatidic acid (LPA) and antiarrhythmic peptide (AAP10) on rabbit ventricular arrhythmia.

METHODSTwenty-four rabbits were randomly divided into three groups (n = 8 each): control group, LPA group and AAP10 + LPA group. Using arterially perfused rabbit ventricular wedge preparations, transmural ECG and action potentials from both endocardium and epicardium were simultaneously recorded in the whole process of all experiments with two separate floating microeletrodes. The incidence of ventricular arrhythmia post S1S2 stimulation was recorded. Protein levels of nonphosphorylated Cx43 and total Cx43 were evaluated by Western blot. The distribution of nonphosphorylated Cx43 was observed by confocal immunofluorescence microscopy.

RESULTSCompared with the control group, the QT interval, endocardial action potential duration, transmural repolarization dispersion (TDR) and incidence of ventricular arrhythmia were significantly increased and nonphosphorylated Cx43 expression was significantly upregulated in the LPA group. Compared with the LPA group, cotreatment with AAP10 can reduce the QT interval, endocardial action potential duration, TDR and incidence of ventricular arrhythmia (25.0% vs 62.5%, P < 0.01) and downregulate nonphosphorylated Cx43.

CONCLUSIONSLPA could promote the arrhythmia possibly by upregulating nonphosphorylated Cx43 and subsequent gap junction transmission inhibition. Gap junction enhancer AAP10 could attenuate the pro-arrhythmic effect of LPA probably by downregulating myocardial nonphosphorylated Cx43 expression.

Animals ; Anti-Arrhythmia Agents ; pharmacology ; Arrhythmias, Cardiac ; chemically induced ; metabolism ; physiopathology ; Connexin 43 ; metabolism ; Lysophospholipids ; adverse effects ; Oligopeptides ; pharmacology ; Rabbits

An 82-yr-old man was presented with fever and cough accompanied by generalized erythematous rash. He had taken mexiletine for 5 months, as he had been diagnosed with dilated cardiomyopathy and ventricular arrhythmia. Laboratory studies showed peripheral blood eosinophilia and elevated liver transaminase levels. Chest radiographs showed multiple nodular consolidations in both lungs. Biopsies of the lung and skin lesions revealed eosinophilic infiltration. After a thorough review of his medication history, mexiletine was suspected as the etiologic agent. After discontinuing the mexiletine and starting oral prednisolone, the patient improved, and the skin and lung lesions disappeared. Subsequently, mexiletine was confirmed as the causative agent based on a positive patch test. Drug-induced hypersensitivity syndrome is a severe adverse reaction to drugs and results from treatment with anticonvulsants, allopurinol, sulfonamides, and many other drugs. Several cases of mexiletine-induced hypersensitivity syndrome have been reported in older Japanese males with manifestation of fever, rash, peripheral blood eosinophilia, liver dysfunction without other organ involvement. Here, we report a case of mexiletine-induced hypersensitivity syndrome which presented as eosinophilic pneumonia in a Korean male.
Aged, 80 and over ; Anti-Arrhythmia Agents/*adverse effects ; Arrhythmias, Cardiac/drug therapy ; Cardiomyopathy, Dilated/drug therapy ; Drug Hypersensitivity/*diagnosis/etiology ; Exanthema/pathology ; Humans ; Lung/pathology/radiography ; Male ; Mexiletine/*adverse effects ; Pulmonary Eosinophilia/*chemically induced/*diagnosis ; Syndrome ; Tomography, X-Ray Computed