1.Diabetic polyneuropathy: mechanisms, prevention and treatment, are we doing too little, too late?
Philippine Journal of Anesthesiology 2001;13(1):45-54
Diabetic polyneuropathy affects millions of people with diabetes. Although, the symptoms may be highly unpleasant, management have concentrated mainly on the disease process and other more visible or devastating secondary complications like diabetic ulcers and cardiac arrhythmia. Glycemic control remains the most important aspect in the management of diabetes that can deter or decelerate subsequent development of diabetic polyneuropathy. However, concentration on this aspect alone veers away from control of symptoms that may improve quality of life of patients.
NEUROPATHY
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CARDIAC ARRHYTHMIA
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PAIN
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INJURY
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NERVE
3.Clinical Electrophysiological Studies on the Chronic Recurrent Sustained Ventricular Tachycardia.
Korean Circulation Journal 1984;14(2):243-251
Clinical electrophysiological studies(EPS) were done in seven patients with chronic recurrent sustained ventricular tachycardia(VT) in an attempt to delineate the reproducibility and to select the effective antiarrhythmic drugs for the prevention of the recurrence of VT. We could induce and terminate the sustained VT, and could select the effective antiarrhythmic drugs in all patient in the cardiac catheterization laboratory with EPS. With these effective antiarrhythmic drugs VT did not recur for the follow up period of 15 to 20 months. In view of the serious nature of the VT and the demonstrated benefits of EPS, we could conclude that patients with chronic recurrent sustained VT should undergo EPS.
Anti-Arrhythmia Agents
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Cardiac Catheterization
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Cardiac Catheters
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Follow-Up Studies
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Humans
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Recurrence
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Tachycardia, Ventricular*
5.Amiodarone-Induced ARDS after MVR: A case report.
Gi Bok LEE ; Eung Joong KIM ; Hyun Keun CHEE ; Yoon Cheol SHIN
The Korean Journal of Thoracic and Cardiovascular Surgery 2002;35(8):594-598
Amiodarone is an iodinated benzofuran derivative that has been proved effective in the control of supraventricular and ventricular arrhythmias refractory to other antiarrhythmic drugs. In patients treated with amiodarone, subsequent surgical intervention is a common clinical scenario, but unfortunately we do not have definite data about complications due to amiodarone after cardiac surgery. Some reports have shown that amiodarone treatment can be associated with a state of alpha-adrenergic and beta-adrenergic receptor blockade, which requires more pacing and epinephrine infusion for perioperative hemodynamic support. And some reports have also identified a severe form of ARDS in patients on amiodarone therapy which was associated with siginificant morbidity and mortality. We exprienced a patient who expired after mitral valve replacement due to amiodarone-induced ARDS; therefore, we report this case with a brief literature.
Amiodarone
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Anti-Arrhythmia Agents
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Arrhythmias, Cardiac
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Epinephrine
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Hemodynamics
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Humans
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Mitral Valve
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Mortality
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Thoracic Surgery
6.Ventricular Arrhythmia during Tracheal Intubation and Extubation under General Anesthesia Possibly Induced by Amisulpride: A Case Report.
Clinical Psychopharmacology and Neuroscience 2018;16(3):358-360
We are presenting the first documented case of amisulpride related ventricular arrhythmia during tracheal intubation and extubation under general anesthesia in an 48 year-old female with psychiatric history of chronic schizophrenia who was treated with amisulpride. This case suggests the threshold of perioperative arrhythmia is possibly decreased in patients with long-term antipsychotic medication. So, the potential risk of antipsychotics-induced perioperative arrhythmia should be evaluated, as well as heart rhythm monitoring, prophylactic use of antiarrhythmic drugs, and preoperative adjustment of antipsychotics should be considered.
Anesthesia, General*
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Anti-Arrhythmia Agents
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Antipsychotic Agents
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Arrhythmias, Cardiac*
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Female
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Heart
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Humans
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Intubation*
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Schizophrenia
9.Effect of antiarrhythmic peptide on ventricular arrhythmia induced by lysophosphatidic acid.
Qing ZHOU ; Tian-jie WANG ; Cun-tai ZHANG ; Lei RUAN ; Lian-dong LI ; Ren-de XU ; Xiao-qing QUAN ; Ming-ke NI
Chinese Journal of Cardiology 2011;39(4):301-304
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
10.Effect of nifekalant on acute electrical remodelling in rapid atrial pacing canine model.
Min TANG ; Shu ZHANG ; Qi SUN ; Wei HUA ; Cong-xin HUANG
Chinese Medical Journal 2006;119(24):2056-2061
BACKGROUNDNifekalant may prevent atrial fibrillation (AF) and possibly be useful in treatment of atrial tachyarrhythmia in patients with severe heart failure. This study investigated the electophysiologic effect of nifekalant on the acute atrial remodeling in rapid atrial pacing (RAP) model of canine.
METHODSTwelve mongrel dogs subjected to rapid stimulation (400 beats/min) at left atrial appendage (LAA) for 24 hours, were randomized into the control group (rapid pacing only, n = 6) and the nifekalant group (intravenous nifekalant therapy immediately after RAP, n = 6). Atrial electrophysiological parameters were measured in right atrium, coronary sinus, LAA, posterior wall of left atrium (PWLA) and left superior pulmonary vein (LSPV), before and after the RAP.
RESULTSIn the control group, the effective refractory periods (ERP) were shortened greatly at all sites, paced dogs had substantially shorter ERPs in the high right atrium, LAA, and LSPV, but fewer changes in the PWLA, the coefficient variation of ERP (COV ERP) was increased significantly. After rapid atrial stimulation, the inducibility of AF increased significantly [induction number: pre-RAP vs post-RAP, 1.00 +/- 0.89 vs 8.17 +/- 2.79, P < 0.01; duration of AF: pre-RAP vs post-RAP, (450.34 +/- 362.59) ms vs (9975.77 +/- 4376.99) ms, P < 0.01]. In the nifekalant group, although the ERPs were prolonged at all sites compared with those in pre-RAP state, only the value at LSPV differed significantly from that in pre-RAP state [pre-RAP vs post-RAP, (102.50 +/- 5.24) ms vs (132.51 +/- 5.20) ms, P < 0.01]; the COV ERP did not change statistically in this group. The inducibility of AF slightly increased but insignificantly after pacing [induction number: pre-RAP vs post-RAP, 0.83 +/- 0.75 vs 1.67 +/- 0.82, P = 0.19; duration of AF: pre-RAP vs post-RAP, (378.67 +/- 317.88) ms vs (1124.08 +/- 1109.77) ms, P = 0.06]. Conduction time values did not alter significantly in either of the two groups after RAP.
CONCLUSIONSIn canine RAP model, nifekalant inhibited ERP shortening and ERP heterogeneity increasing, decreased AF induction. Nifekalant can reverse acute electrical remodeling effect in this model.
Animals ; Anti-Arrhythmia Agents ; pharmacology ; Cardiac Pacing, Artificial ; Dogs ; Female ; Male ; Pyrimidinones ; pharmacology ; Refractory Period, Electrophysiological ; drug effects