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Age years ; 61 13 62 Male sex n [%] ; 75 77 ; 66 59 ; 0.04 26.1 4.0 ns Body mass index kg m2 ; AF duration days ; 77 98 97 Previous cardioversion n [%] ; 53 55 ; 53 60 ; Class III AAD therapy n [%] ; 47 48 ; 47 53 ; LVEF 52 14 52 Underlying heart disease n [%] ; Coronary artery disease 19 20 ; 26 Hypertension 28 29 ; 18 Dilative cardiomyopathy 24 25 ; 11 Valvular disease 15 ; 23 Lone AF 11 ; Data are given as means standard deviation unless specified otherwise. AAD antiarrhythmic drug therapy amiodarone or sotalol AF atrial fibrillation; LVEF left ventricular ejection fraction on echocardiography; ns not significant.
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Predictive Value of QTd for Sustained Ventricular Tachyarrhythmias and Mortality in AVID Patients Treated with the ICD or with the Class III Antiarrhythmic Drugs Amiodarone or Sltalol Specific aims: The specific aim of this study is to determine the predictive value for future arrhythmic events of QT interval dispersion QTd ; on entry ECG in patients with malignant ventricular tachyarrhythmias in the AVID study undergoing therapy with either the ICD or class III antiarrhythmic drugs amiodarone or sotalol ; . A secondary objective is to evaluate the predictive value of changes in QTd and QT or QTc alone ; caused by antiarrhythmic therapy on these outcomes in the drug treatment arm. Background and significance: Prolongation of the QT interval has been found to predict an increased risk of ventricular arrhythmia and sudden death in patients with coronary artery disease 1, 2 ; , alcoholic cirrhosis 2, 3 ; , and in normal, apparently healthy individuals 4 ; . QTc prolongation as a risk factor for sudden death was also independent of age, history of myocardial infarction MI ; , heart rate, and drug use 2 ; . Another index of ventricular repolarization that may be even more useful as a predictor of risk is inter-lead variability in the QT interval QT dispersion, or QTd ; . This index reflects regional variation in ventricular repolarization 5, 6 ; , and may indicate a substrate predisposing to serious ventricular tachyarrhythmias 7-11 ; . Increased QT dispersion has been observed in patients with acute MI who develop ventricular tachyarrhythmias, compared with those with a benign course 12 ; . Similarly, QT dispersion is increased in patients with long QT syndromes at risk of ventricular arrhythmias 10 ; . Patients with hypertrophic cardiomyopathy who die suddenly have increased QT dispersion 13 ; . In patients with chronic heart failure, increased QT dispersion has recently been associated with a high risk of sudden death 14 ; . Certain therapies have been shown to affect QT dispersion. Moreno et al. has recently reported reduction in QT dispersion by successful thrombolytic therapy in acute MI 15 ; . Sotalll in one study was found to be associated with similar QT interval prolongation as congenital long QT syndrome, but QT dispersion was reduced after sotalol, whereas it was increased in the congenital long QT syndrome 10, 16 ; . In another study, sotalol given after MI increased QT interval compared with placebo ; , but decreased QT dispersion 10, 17 ; . In another study 11 ; , precordial QT dispersion was found to be a marker of torsade de pointes. A disparate effect of class IA antiarrhythmic agents versus amiodarone class III ; on QT dispersion was found. Whereas both drugs prolonged QT interval to the same degree, class IA therapy increased QTd in 9 patients with torsade de pointes, whereas in 29 patients without torsade, no increase in QTd was found. With amiodarone therapy in the same patients ; , no increase in QTd was observed in any patients, and none developed torsade. These findings suggest that QTd may be a predictor of torsade de pointes with antiarrhythmic therapy, and may be a better marker than QT prolongation. The cause and importance of the U wave during repolarization has been controversial. A recent study 18 ; suggests that the U wave may reflect afterdepolarization in a unique subpopulation of cells in subepicardial and mid myocardial.
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? Moricizine plus A-V nodal blocking drug * - 400 mg day ? ? Disopyramide plus A-V nodal blocking drug * - 300 mg day of ? disopyramide base ? Procainamide plus A-V nodal blocking drug * - 1, 500 mg day ? ? Combinations of above drugs ? * unless contraindicated General Precautions All patients should be evaluated carefully for potential proarrhythmia from any of the drugs. For patients with baseline, drug-free QTc of 0.46 seconds, quinidine, disopyramide, procainamide, moricizine, and sotalol should not be used. These drugs should be discontinued or the dose reduced if the QTc is 0.52 seconds. QT intervals should be evaluated as clinically appropriate, and the negative inotropic effects of drugs should be considered, particularly sotalol, propafenone, flecainide, and disopyramide. Care should be taken to evaluate bradycardia and hypokalemia in all patients given antiarrhythmic drugs. Caution regarding proarrhythmia must be exercised in using all antiarrhythmic drugs in the presence of organic heart disease and or LVH. AV nodal blocking drugs should be given as appropriate, unless contraindicated, especially with quinidine, disopyramide, flecainide, propafenone, moricizine, and procainamide. Such drugs will likely be less necessary with amiodarone and sotalol. Doses of AV node blocking drugs should be adjusted as appropriate to the patient's heart rate during atrial fibrillation. Only if the ventricular rate during atrial fibrillation is 80 beats per minute without drugs should an AV nodal blocking drug be omitted during therapy with quinidine, disopyramide, flecainide, propafenone, moricizine, and procainamide. Decisions regarding choice of rate-controlling medications beta blockers, calcium channel blockers, digitalis ; , and their dosages will be left to the physician at the local site. Antiarrhythmic serum or plasma drug levels should be used as clinically appropriate, but will not be required by the protocol. If a patient is refractory to AV nodal blockade with rate-controlling medications, AV node ablation can be performed. Use of antiarrhythmic drugs must be continued in order to maintain sinus rhythm. Precautions with Class I drugs Investigators should exercise caution in the administration of all Class I drugs to patients with left ventricular dysfunction manifest by a history of congestive heart failure, a low ejection fraction, or current clinical signs of CHF ; . Such patients should be considered for hospitalization and monitoring for initiation of treatment. Hospitalization should occur and olmesartan.
Procedures according to the guidelines of the Office of Laboratory Animal Welfare. Male Sprague-Dawley rats Taconic Farms, Germantown, NY ; weighing 180 to 200 g at the start of acute and inflammatory experiments or 90-110 g at the start of nerve ligation experiments, were used. Animals were group-housed and had free access to food and water at all times, except prior to oral administration of drugs when food was removed 12 hours before dosing. For comparison with compound-treated groups, animals treated with appropriate drug vehicle were included in each experiment. The volume of administration and all other experimental procedures and conditions for vehicle and compound-treated rats, were identical.
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All recordings were made from adult cats weighing between 1.5 and 4.4 kg. All animal care and experimental guidelines conformed to those established by the National Institute of Health and were approved by the Osaka University Animal Care and Use Committee.
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Recommendations given where other drug classes are ineffective, contraindicated or not tolerated amiodarone should be administered. B Antithrombotic therapy for persistent AF . Rate-control for permanent AF In patients with permanent AF, who need treatment for rate-control: beta-blockers or rate-limiting calcium antagonists should be the preferred initial monotherapy in all patients A digoxin should only be considered as monotherapy in predominantly sedentary patients. D GPP ; Factors indicating a high risk of AF recurrence include: a history of failed attempts at cardioversion structural heart disease mitral valve disease, left ventricular dysfunction or an enlarged left atrium ; a prolonged history of AF 12 months ; previous recurrences of AF. In patients with permanent AF, where monotherapy is inadequate: B to control the heart rate only during normal activities, beta-blockers or rate-limiting calcium antagonists should be given with digoxin to control the heart rate during both normal activities and exercise, rate-limiting calcium antagonists should be given with digoxin. Antithrombotic therapy for permanent AF In patients with permanent AF a riskbenefit assessment should be performed and discussed with the patient to inform the decision whether or not to give antithrombotic therapy. D GPP ; In patients with permanent AF where antithrombotic therapy is given to prevent strokes and or thromboembolism see section 1.8.6 ; : adjusted-dose warfarin should be given as the most effective treatment A adjusted-dose warfarin should reach a target INR of 2.5 range 2.0 to 3.0 ; A where warfarin is not appropriate, aspirin should be given at 75 to 300 mg day B where warfarin is appropriate, aspirin should not be coadministered with warfarin purely as thromboprophylaxis, as it provides no additional benefit. B Treatment for paroxysmal AF Rhythm-control for paroxysmal AF Where patients have infrequent paroxysms and few symptoms, or where symptoms are induced by known precipitants such as alcohol, caffeine ; , a `no drug treatment' strategy or a `pill-in-the-pocket' strategy should be considered and discussed with the patient. D GPP ; In patients with symptomatic paroxysms with or without structural heart disease12, including coronary artery disease ; a standard beta-blocker should be the initial treatment option. D GPP ; In patients with paroxysmal AF and no structural heart disease: where symptomatic suppression is not achieved with standard beta-blockers, either a Class Ic agent such as flecainide or propafenone ; D GPP ; or sotalol D GPP ; should be given where symptomatic suppression is not achieved with standard beta-blockers, Class Ic agents or sotalol, either amiodarone B or and losartan.
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Diology centers throughout Canada. The investigational review board of each institution approved the study, and all patients gave written informed consent. Recruitment began in November 1996, randomization was concluded in February 1998, and follow-up was terminated in February 1999. Inclusion Criteria To be eligible, patients had to have had an episode of symptomatic atrial fibrillation within the preceding six months for which long-term antiarrhythmic drug therapy was planned. At least one episode of atrial fibrillation had to have lasted more than 10 minutes determined by history taking ; , and electrocardiographic confirmation was required. This criterion was chosen arbitrarily in an attempt to prevent the enrollment of patients with clinically inconsequential atrial tachyarrhythmias. Exclusion Criteria The exclusion criteria were as follows: atrial fibrillation known to have been present continuously for more than 6 months, myocardial infarction during the previous 6 months, cardiac surgery during the previous 30 days, moderate or severe cardiac disability New York Heart Association functional class III or IV ; , atrial fibrillation associated with an acute reversible condition, a serum creatinine concentration of more than 2.8 mg per deciliter 250 mol per liter ; , a serum alanine aminotransferase concentration more than 2.5 times the upper limit of normal, chronic lung disease requiring bronchodilator therapy, the WolffParkinsonWhite syndrome, previous long-term therapy lasting 4 weeks or more ; or intolerance of study drugs, untreated hypothyroidism, a corrected QT interval of more than 480 msec or an uncorrected QT interval of more than 500 msec in the absence of bundle-branch block, bradycardia defined as a heart rate of less than 50 beats per minute for a period of more than one minute while the patient was awake ; , second-degree or third-degree atrioventricular block or a sinus pause of more than two seconds without a permanent pacemaker, an age of less than 18 years, a need for antiarrhythmic therapy for arrhythmias other than atrial fibrillation, and any medical condition that would make survival for 1 year unlikely. In addition, premenopausal women who had not undergone tubal ligation or hysterectomy were excluded. Randomization, Therapy, and Follow-up Patients with atrial fibrillation lasting more than 48 hours had to undergo treatment with an anticoagulant agent at a dosage adjusted to achieve an international normalized ratio of 2 or more for a minimum of three weeks before randomization.31 After written informed consent was obtained, patients were randomly assigned to receive amiodarone or to receive sotalol or propafenone, in an open-label fashion. The patients assigned to sotalol or propafenone underwent a second randomization to determine whether they would receive sotalol or propafenone first. Loading doses of the drugs were administered and electrical cardioversion, if necessary, was performed within 21 days after randomization for the patients in both groups. Cardioversion was recommended if atrial fibrillation persisted after 14 days of loading doses of amiodarone and after 4 days of treatment with either sotalol or propafenone. If the first drug administered to a patient assigned to sotalol or propafenone was unsuccessful, the second agent was prescribed and cardioversion was reattempted. An electrocardiogram was transmitted by telephone on days 7 and 14, and patients were reevaluated in the clinic 21 days after randomization. Amiodarone was given at a dose of 10 mg per kilogram of body weight each day for 14 days, followed by 300 mg per day for 4 weeks, after which a daily maintenance dose of 200 mg was given. Sotalool was administered as follows: 160 mg every 12 hours to men 70 years of age or younger who had a creatinine concentration of 1.5 mg per deciliter 130 mol per liter ; or less and who weighed at least 70 kg; 80 mg every 8 hours to men who were older than 70, men who had a creatinine concentration of more than 1.5 mg per deciliter, men who weighed less than 70 kg, and and fenofibrate.
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Index of Drugs RENAGEL .30 REQUIP .22 RESCRIPTOR .10 RESTASIS .44 RETIN-A liquid 0.05%.40 RETIN-A MICRO .40 RETROVIR inj .10 REVATIO.19 REVLIMID .35 REYATAZ .10 RHEUMATREX .35 RHINOCORT AQUA .39 RIBASPHERE .11 RIBAVIRIN .11 RIDAURA .35 rifampin.10 rifampin inj .10 RILUTEK .25 RISPERDAL .22 RISPERDAL CONSTA.22 RITALIN LA .23 RMS . 7 ROBAXIN inj.24 ROFERON-A .35 ROXICET oral soln. 7 ROXICODONE concentrate 20 mg ml . 7 ROXICODONE oral soln 5 mg 5 ml . 7 ROXICODONE tabs 5 mg. 7 RUBELLA VIRUS VACCINE .36 RYTHMOL SR .16 SAIZEN .29 salsalate . 6 SANCTURA.33 SANDIMMUNE .35 SANDOSTATIN LAR .30 SANTYL .43 SCOPOLAMINE inj .31 selegiline .22 selenium sulfide shampoo 2.5% .41 SENSIPAR .26 SEREVENT .38 SEROQUEL .22 sertraline .21 silver sulfadiazine .40 simvastatin .17 57 SINGULAIR. 38 SKELAXIN . 24 sodium polystyrene sulfonate . 36 SOLARAZE . 40 SOLIRIS. 34 SOLTAMOX oral soln . 12 SOLU-CORTEF inj . 29 SOLU-MEDROL inj 500 mg. 29 SOMAVERT . 30 SONATA . 23 SORIATANE . 41 sotalol . 16 SPIRIVA . 37 spironolactone . 16 spironolactone hydrochlorothiazide . 19 SPORANOX inj . 9 SPORANOX oral soln . 9 SPRYCEL . 14 STALEVO. 22 STRATTERA . 23 SUBOXONE. 24 SUBUTEX . 24 SUCRAID. 28 sucralfate . 33 sulfacetamide lotion 10% . 40 sulfacetamide oint, soln 10%. 43 sulfacetamide prednisolone phosphate 10% 0.25%. 44 SULFADIAZINE . 9 sulfamethoxazole trimethoprim. 11 sulfamethoxazole trimethoprim inj . 11 sulfasalazine. 32 sulfasalazine delayed-rel . 32 sulindac . 6 SUMYCIN susp 125 mg 5 ml . 9 SURMONTIL 100 mg . 21 SUSTIVA . 10 SUTENT . 14 SYMBICORT. 39 SYMLIN. 25 SYNAREL. 28 SYNTHROID. 30 SYPRINE . 26 TAMIFLU . 11 tamoxifen. 12 and atenolol.
Acute and delayed nausea and vomiting as predicted by physicians nurses MD RN ; versus as reported by patients receiving either highly Top ; or moderately Bottom ; emetogenic chemotherapy. Adapted from Grunberg et al.6.
Figure 3. Mean SD QT interval prolongation normalized for sotalol concentrations. A ; dQTcPOP; B ; dQTcF; C ; dQTcB in neonates 28 days ; , infants 2 years ; , and children and adolescents 15 years ; . p values according to ANOVA with Tukey's honestly significant difference test # ; and least significance difference test and atorvastatin.
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Before vta, no difference was observed between subgroups except for the mean hr: the mean hr of the sotalol subgroup was significantly lower than the mean hr of patients without aa drugs but similar to the -blocker subgroup value table 4 and perindopril and Buy sotalol.
The lower frequency found in these studies after long-term oral verapamil is in contrast, to an increase in both atrial rate and dispersion of atrial refractoriness immediately after a 10 minute verapamil infusion 67 ; . In this study performed by Ramanna and colleagues 67 ; in 15 patients with chronic AF 1 year ; no measurements were obtained, however, after a longer treatment period e.g. after 1 or 7 days ; . An acute frequency increase may therefore not preclude a chronic frequency decrease. Differences in the study protocols may contribute to the different findings. For instance, the observed increase in fibrillatory frequency after acute verapamil infusion 67 ; might be mediated by an increased sympathetic tone following hemodynamic alterations 30 ; . From previous investigations it is known that this autonomic change contributes to higher atrial rates 14, 40 ; . Furthermore, verapamil could suppress pulmonary vein foci and or excert favourable long-term effects on the reversal of morphological remodeling 62 ; . EFFECTS OF ANTIARRHYTHMIC DRUGS ON FIBRILLATORY FREQUENCY Several studies have investigated the impact of acute antiarrhythmic drug administration on atrial rates in human AF. Procainamide 12, 71, 76, ; , propafenone 10, 12 ; , disopyramide 3 ; , flecainide 10 ; , cibenzoline 21 ; , sotalol 39 ; and ibutilide 13, 83 ; have all been found to reduce the average frequency of fibrillatory activity. These findings are in concordance with one single study 17 ; analyzing the effects of orally administered antiarrhythmic drugs in 12 patients by applying the introduced technique Figure 4 ; . More recently, our group has found that short-term 3 days ; oral flecainide 200 mg d ; leads to a greater frequency reduction 1.80.6 Hz vs. 1.00.6 Hz ; than oral amiodarone 1200 mg d ; Bollmann, unpublished data.
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Mitral stenosis is typically a consequnece of childhood rheumatic fever but congenital disease is well recognised. It is associated with a tapping apex beat, a loud S1, Openning snap and Mid diastolic rumble with pre-systolic accentuation in those in sinus rhythm. The opening snap is characteristically lost with heavy valvular calcification. In particular Mitral stenosis is poorly tolerated in pregnancy due to volume overload. It is well characterised by doppler echocardiography. A 68 year-old woman with atrial fibrillation is admitted for DC cardioversion. The procedure resulted in successful restoration of sinus rhythm. Which one of the following drugs would be most likely to maintain sinus rhythm following this procedure? Available marks are shown in brackets 1 ; amiodarone 2 ; digoxin 3 ; diltiazem 4 ; sotalol 5 ; verapamil!
Dofetilide was as efficacious as sotalol in preventing the induction of sustained ventricular tachycardia, which was achieved in one third of the patients. There was no concordance in the response to the two drugs. During the acute phase dofetilide was significantly better tolerated than sotalol. However, during longterm treatment, which was not randomized, both drugs were well tolerated. This study is based on the use of electrophysiological testing as a guide for selecting antiarrhythmic drug therapy in ventricular tachyarrhythmias, a.
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Ablation in larger diameter ostial pulmonary vein PV ; segments may decrease the risk for PV stenosis and yield a higher success rate because of the more complete isolation of arrhythmogenic tissue. We report on a series of consecutive patients who underwent PV ablation performed by circumferential mapping, an ablation end point of the isolation of all PVs, and radiofrequency energy delivery guided by continuous intracardiac ultrasound ICUS ; designed to achieve ostial PVleft atrial LA ; disconnection, including the isolation of common PV trunks. Patients were referred after they had not had success with 2 antiarrhythmic drugs. Patients with permanent AF for 1 year were excluded. Patients with persistent AF were cardioverted and treated with dofetilide 52% ; , amiodarone 23% ; , or sotalol 13% ; for 1 month before and after ablation; 57% were in normal sinus rhythm at the time of ablation. FIGURE 1. ICUS image of a left common PV with subsidiary branches. The echocardiographic linear image in the opening of the common segment is the LASSO mapping catheter. A duodecapolar Du o - Dec, Daig Corporation, Minnetonka, Minnesota ; catheter was looped in the right atrium and the distal end advanced into the coronary sinus. Two long sheaths SL1, Daig Corporation ; were passed into the left atrium by a double transseptal puncture of the fossa ovalis, perfused with heparinized saline solution flow rate 100 cm3 hour ; , and used to introduce the 4-mm tip ablation catheter Biosense Webster, Inc., Diamond Bar, California ; and the 10- or 20-pole circumferential mapping catheter LASSO, Biosense Webster, Inc. ; . After a bolus of intravenous heparin 5, 000 U, a continuous infusion maintained an activated clotting time of 250 seconds.
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Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes Ling-Ping Lai, Jiunn-Lee Lin, Wen-Pin Lien, Yung-Zu Tseng, and Shoei K. Stephen Huang J. Am. Coll. Cardiol. 2000; 35; 1434-1441 This information is current as of July 27, 2008.
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This meta-analysis supports the present recommendation that indicates -blockers as a first-line medication for prevention of postoperative AF.65 Sotalol and amiodarone are also effective and can be considered as appropriate alternatives. A most important measurable clinical benefit, other than AF prevention itself, is reduction in LOS by one half of a day. This could lead to a significant cost savings.
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1. Was this act legal? medical legal issues associated with embalming Doctor Bruno RIOU Now a university professor and hospital practitioner in the emergency department at the Piti-Salptrire Hospital. He was the on-call emergency anaesthetist on the night of 30 August 1997 and assisted in the emergency surgery on the Princess of Wales. Interviewed by Operation Paget officers at the Piti-Salptrire Hospital - Statements 131, 131A and 58M Operation Paget Officer's Statement ; Professor Riou was on-call at the hospital on Saturday night Sunday morning. He accepted the request from Dr Marc Lejay, Control dispatcher of the Service d'Aide Mdicale d'Urgence SAMU ; , the French ambulance service, to admit the Princess of Wales to the Piti-Salptrire Hospital emergency department and was present when she arrived. Professor Riou was part of the team that carried out the emergency surgery on the Princess of Wales. He officially pronounced her dead at 4am. In line with French procedures, Professor Riou believes that he signed a certificate that contained a declaration that there was a medical legal obstacle associated with the body. This was because the death was due to an accident and could not be attributed to natural causes. It did not mean that Professor Riou believed that there were suspicious circumstances or a crime involved. A pathologist appointed by the Public Prosecutor's office, Professor Dominique Lecomte, carried out an external examination of the Princess of Wales' body ninety minutes after her death. She declared that there were no suspicious circumstances relating to the injuries found on the body and that they were consistent with injuries from a road traffic collision. Professor Riou, as a medical professional, was authorised to certificate the death. He completed a document `Accidental Death Certificate Template' Statement 58M ; . This form confirmed that there was now no medical legal obstacle to embalming. Professor Riou confirmed that no pregnancy test was carried out on the Princess of Wales and no sample of urine taken. He stated: `No, we never do a pregnancy test as a matter of routine for multiple trauma patients, since in any case X-rays and scans will have to be done. Pregnancy tests are sometimes done in emergency departments when the question of X-rays is being considered.'.
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Processing as discussed in the previous section was used to calculate ventricular ejection time from the ICG waveform as well as from PCG signal. The recordings were done in normal conditions and post exercise relaxation condition at intervals of 5 min. The number of ensemble averaging cycle for ICG waveform was taken as 8. Table 1 Estimated values mean, s.d. ; of Zo, -dz dt ; max, and Tlvet from ICG and PCG, for 5 subjects under resting condition. The number in parentheses indicates the s.d.
Silva JR, Guariento ME, Fernandes GA, et al. Impact of long-term administration of amiodarone on the thyroid function of patients with Chagas' disease. Thyroid. 2004; 14: 371-7 - Sim I, McDonald KM, Lavori PW, et al. Quantitative overview of randomized trials of amiodarone to prevent sudden cardiac death. Circulation. 1997; 96: 2823-9 - Singh SN, Fletcher RD, Fisher SG, et al. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure. N Engl J Med. 1995; 333: 77-82 - Singh BN, Singh SN, Reda DJ, et al; Sotalol Amiodarone Atrial Fibrillation Efficacy Trial SAFE-T ; Investigators. Amiodarone versus sotalol for atrial fibrillation. N Engl J Med. 2005; 352: 1861-72.
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