If the cardiac impulse fails to follow a regular cir- cuit and divides along multiple pathways, a chaos of uncoordinated beats results, producing atrial fibril- lation. Fibrillation commonly occurs when the atrium is enlarged (usually because of heart disease). In ad- dition, it can occur in the absence of any apparent heart disease. The atrial rate shoots up to more than 350 beats per minute and the atria fail to pump blood effectively, quivering like “a can of worms” or “a bowl of jelly," as it has been variously described, The ventricular beat also becomes haphazard, producing a rapidirregular pulse. Although atrial fibrillation may cause the heart to lose 20 to 30 percent of its pumping effectiveness, the volume of blood pumped by the ventricles usually remains within the margin of safety, again because the atrioventricular node blocks out many of the chaotic beats. The ventricle may contract at a rate of only 125 to 175 beats per minute.
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting more than 7 million Americans and 33 million people worldwide (1). AF is characterized by an irregular pattern of atrial depolarization, resulting in rapid and disorganized atrial conduction and lack of effective atrial chamber contraction. The rhythm abnormality in patients with AF manifests with circulatory deficits and systemic thromboembolism that greatly increase mor- bidity and mortality. Because age is an independent risk factor for AF, its prevalence is expected to rise significantly as the population ages. AF has become a major clinical and economic burden, owing to the limitations and side effects associated with current AF thera- pies. Although AF most often manifests in the context of pre-exist- ing cardiac pathologies, such as hypertension and cardiomyopathy, idiopathic or lone AF forms have indicated a heritable component (2). Genome-wide association studies (GWAS) have to date identi- fied more than 100 AF-associated loci, including many transcrip- tion factor (TF) loci, suggesting that transcriptional control of atrialrhythm is an important mediator of AF risk (3, 4).
NeOAF makes the disease more complicated and makes treatment during sepsis or septic shock more challenging because of adverse cardiovascular effects including rapid heart rate, irregularrhythm, loss of atrial systole, and neu- rohormonal activation. In the acute phase, both tachycardia and loss of atrial systole caused by AF could reduce the car- diac output, further destablizing patients with sepsis. Subse- quently, the burden of NeOAF in patients with sepsis may result in acute heart failure [35, 36]. Moreover, atrial stasis and sepsis-related coagulopathy could lead to systemic embolization and an increased risk of ischemia stroke .
The electrocardiogram of a patient in AF does not have discernable, independent p- waves. Instead, the p-waves are replaced by fibrillatory waves that are rapid oscilla- tions that vary in shape and amplitude. Because of the irregular conduction of these atrial fibrillatory impulses to the ventricles, QRS complexes occur with varying R-R intervals. Overall, this results in a rapid, narrow complex, irregularrhythm without discernable p-waves (Fig. 1).
Cardiac disease is the leading cause of deaths worldwide. A proportion of them is caused by rhythm irregularities of the heart, such as atrial fibrillation. In the healthy heart, the cardiac contraction is produced by softly propagating non-linear electrical waves of exci- tation. Any disturbance in conduction or coordination of electrical signals can result in abnormal heart rhythms, so called arrhythmias. Bradycardia, tachycardia, heart block, and atrial and ventricular fibrillation are examples of arrhythmias. The stimulation of cardiac cells is instigated by a sudden change in the electrical potential across the cell membrane due to the transmembrane flux of charged ions. The release and propaga- tion of an electrical signal, which is ensured by controlled opening and closing of ions channels, is one of the most important functions of the cell. About fifty-two years ago, the first continuous mathematical model of cardiac cell designed to reproduce cell mem- brane action potentials is presented by Hodgkin and Huxley . Ever since, many complex models have been developed for cardiac cells inspired by their approach. Most of these models can be classified in three sets. 1) “First generation” of ionic models which are able to reproduce basic ionic currents such as the Beeler-Ruter (BR)  and Luo-Rudy-I (LR-I)  models. 2) “Second generation” of models, which in addition to a biophysi- cally detailed description of ion channel, pump and exchanger currents, also contain the intracellular ionic concentrations such as the DiFrancesco-Noble . 3) simplified models that only contain the minimum set of phenomenological currents necessary to repro- duce mesoescopic features of cell dynamics, e.g., conduction velocity (CV) restitution and action potential (AP) restitution [5,6]. Generally, simulations based on first and second generation models are computationally demanding, however it is often desirable to des- ignate the minimum key characteristics necessary to characterize a specific phenomenon and then proceed by using simplified models.
The DIONYSOS (Efficacy and Safety of Dronedarone Versus Amiodarone for the Maintenance of Sinus Rhythm in Patients With Atrial Fibrillation) trial investigated safety and efficacy of dronedarone compared with amiodarone for the maintenance of NSR in patients with persistent AF in a short-term study with a median treatment duration of 7 months. Inclusion criteria comprised patients with ECG- documented AF for more than 72 hours for whom cardiover- sion and antiarrhythmic treatment was indicated. Exclusion criteria were AFL, contraindication to oral anticoagulation or to amiodarone, and paroxysmal AF. The trial was conducted in a multinational, multicenter, double-blind, parallel-arm, placebo-controlled fashion. Patients (504) were random- ized either to a dronedarone 400 mg twice a day group (249 patients) or to an amiodarone group (255 patients), receiving 600 mg loading dose daily for 28 days, and a maintenance dose of 200 mg daily thereafter. Electrical cardioversion was performed between days 10 and 28 if the patient had not converted to NSR spontaneously.
Historically, because of the difficulty of using warfarin safely and effectively, many patients with cardioembolic stroke who should have been anticoagulated were instead given ineffective antiplatelet therapy (or no antithrombotic therapy). With the arrival of new oral anticoagulants that are not significantly more likely than aspirin to cause severe haemorrhage, everything has changed. Because antiplatelet agents are much less effective in preventing cardioembolic stroke, it is now more prudent to anticoagulate patients in whom cardioembolic stroke is strongly suspected. Recent advances include the recognition that intermittent atrial fibrillation is better detected with more prolonged monitoring of the cardiac rhythm, and that percutaneous closure of patent foramen ovale (PFO) may reduce the risk of stroke. However, because in most patients with stroke and PFO the PFO is incidental, this should be reserved for patients in whom paradoxical embolism is likely. A high shunt grade on transcranial Doppler saline studies, and clinical clues to paradoxical embolism, can help in appropriate selection of patients for percutaneous closure. For patients with atrial fibrillation who cannot be anticoagulated, ablation of the left atrial appendage is an emerging option. It is also increasingly recognised that high levels of homocysteine, often due to undiagnosed metabolic deficiency of vitamin B 12 , markedly increase the risk of stroke in atrial fibrillation, and that B vitamins (folic acid and B 12 ) do prevent stroke by lowering homocysteine. However, with regard to B 12 , methylcobalamin should probably be used instead of cyanocobalamin. Many important considerations for judicious application of therapies to prevent cardioembolic stroke are discussed.
After the end of one month, patients were evaluated for conversion to SR on the basis of a 12-lead ECG and 24 hour Holter. Patients who remained to be in AF were attempted for cardioversion to SR using electric DC shock. Electrical cardioversion was performed under deep sedation with intravenous diazepam or midazolam, the first synchronized DC shock was attempted with 100 J (biphasic); if it failed to restore SR, further shocks of 200 and 360 J were given. Regardless of rhythm, all the patients in the trial continued to receive amiodarone 200mg daily. Amiodarone was continued in the same dose in all patients for a total duration of six months from the time of inclusion. Patients were followed up at one, three and six months. At every follow up, a 12-lead ECG was recorded, 24 hour Holter was done to document the conversion to SR, intermittent AF and patients were evaluated for adverse effect of amiodarone. After three months of amiodarone therapy, and subsequently at next follow up, thyroid function test, chest X-ray, serum transaminase levels, pulmonary function test and a slit lamp examination for corneal opacities were done. Anti-coagulation was continued indefinitely in patients with AF and for minimum of three months who reverted to SR.
Many patients with organic heart disease can be broadly categorized into those with HF, CAD, or hypertension, although other types of heart disease can also be associated with AF. For patients with HF, safety data support the selection of amiodarone or dofetilide to maintain sinus rhythm. Patients with ischemic heart disease often require beta-blocker medication. Then sotalol, a drug with both beta-blocking activity and primary antiarrhythmic efficacy, is considered first unless the patient has HF. Amiodarone and dofetilide are considered secondary agents in this situation. The clinician may consider disopyramide, procainamide, or quinidine on an individual basis. In patients with hypertension without LVH, drugs such as flecainide and propafenone, which do not prolong repolarization and the QT interval, might offer a safety advantage and are recommended first. If these agents either prove ineffective or produce side effects, then amiodarone, dofetilide, and sotalol represent appropriate secondary choices. Disopyramide, procainamide, and quinidine are considered third-line agents in this situation. Hypertrophied myocardium is prone to proarrhythmic toxicity and development of the torsade de pointes type of ventricular tachycardia. Amiodarone is suggested as first-line therapy in patients with LVH (wall thickness greater than or equal to 1.4 cm) on the basis of its relative safety compared with several other agents. Because neither ECG nor echocardiography invariably detects LVH as defined by measurement of myocardial mass, clinicians face a conundrum. The selection of antiarrhythmic drugs for patients with a history of hypertension is compounded by the dearth of prospective controlled trials comparing the safety and efficacy of drug therapy for AF.
This study was approved by the University of Massachusetts Medical School Institutional Review Board. Between June of 2010 and May of 2011, 46 participants with persistent AF (duration of less than 12 months) undergoing a clin- ically indicated elective CV for AF and 41 age-matched controls were recruited. Written-informed consent was obtained prior to enrollment. Exclusion criteria were: history of prior cardiac surgery, history of atrial flutter, history of paced atrial or ventricular rhythm, history of aortic or mitral valvular prosthesis, history of significant (moderate or greater) mitral insufficiency or stenosis, history of atrial or ventricular thrombus, history of atrial septal defect, pregnancy, age less than 18, inability to give consent and failure of CV. Five participants were excluded from the study since they failed cardioversion. Control subjects were subjects who had undergone an echocardiogram for varied indications but had no history of AF. A standard 2-Dimensional (2D) transthoracic echocardiography (TTE) was performed prior to elective CV and was repeated within 24 h post-CV in sinus rhythm. CV was performed as per ACC/AHA/ESC guidelines with direct-current, synchronized shock in fasting subjects after intravenous sedation .
In some circumstances, conversion to sinus rhythm may be the best way to achieve rate control. Patients with ischemia or significant hemodynamic consequences of AF may be candidates for cardioversion. In general, direct current cardioversion is safe in patients who have been NPO for eight hours if the duration of their AF is less than 48 hours. Beyond this, in patients with severe ischemia or hemodynamic compromise, the risks of both anesthesia and thromboembolism must be considered. Chemical cardioversion can be considered in patients where anesthesia is either unavailable or unsafe. Ibutilide, a Class III antiarrhythmic, is the most commonly used agent for pharmacological conversion of AF. Ibutilide is a potassium channel blocker, prolongs the action potential and increases atrial refractoriness resulting in restoration of sinus rhythm. Potassium channel blockers also are associated with torsades de pointes. In one study, ibutilide was significantly more effective in converting patients with AF or flutter to normal sinus rhythm when com- pared to procainamide. 4 The dose of ibutilide
The present study is a substudy of the double blind, placebo-controlled Candesartan in the Prevention of Relapsing Atrial Fibrillation (CAPRAF) study . Briefly, 171 patients with AF were randomised to receive cande- sartan 8 mg once daily (n = 86) or placebo (n = 85) for 3 to 6 weeks before and then candesartan 16 mg once daily or placebo for 6 months after electrical cardioversion (Fig. 1). Patients with congestive heart failure or renal impairment were not included in the study. Cardioversion was deemed successful if sinus rhythm was established and maintained for at least 2 h (n = 134). Relapse of AF was defined as first electrocardiogram–recorded episode of AF. Blood samples were collected at baseline and at 6 months’ follow-up. CHA 2 DS 2 -VASc score was used to stratify patients ac-
Any abnormality in Rutuchakra (menstrual rhythm) leads to excessive and irregular uterine bleeding is known as Raktapradara or Dysfunctional Uterine Bleeding (DUB).The main ingredients of indi- genous compound churna are SHUNTHI and BHARANGI. SHUNTHI which is vata- kaphahara, di- pana, bhedana, raktashodaka, sophahara, possess significantly antioxidant properties, an effective supplement for heavy menstrual bleeding and act as raktapittahara and anti-inflammatory in action. Bharangi is kapha- vatahara, jvarahara, kasahara, raktadoshahara and amapacana. In present study 30 patients were selected that fulfilled the criteria of diagnosis and consented for the study. Af- ter completion of three consecutive cycles, treatment was withdrawn and net follow up was taken again after interval of one month to know any recurrence of sign/symptoms. The parameters selected for the study were Duration of menstrual flow, Amount of menstrual bleeding, consistency, inter- menstrual cycle, backache, pain in abdomen and haemogram.53.33% patients had moderately im- proved after third follow-up. The trial drugs are significant in the management of Raktapradara. Keywords: Raktapradara, SHUNTHI, Bharangi.
Abstract: Atrial fibrillation (AF) is the most common cardiac arrhythmia encountered in clinical practice. Although once considered a nuisance arrhythmia, recent clinical trial evidence suggests that the pres- ence of AF is an important independent predictor of mortality and morbidity. The primary goals of AF treatment are relief of symptoms and prevention of stroke. The value of anticoagulation with warfarin has been proven unequivocally. Control of ventricu- lar rate with atrioventricular nodal blocking agents—the so-called rate control strategy—is least cumbersome and sometimes the best approach. By contrast, efforts to restore and maintain sinus rhythm using antiarrhythmic drugs—the rhythm control approach—although tedious, may be ideal in patients who are young or highly symptomatic and in those with new-onset AF. The relative merits of both treatment strategies are discussed in this article, emphasizing the excellent clinical trial data that support each. (Curr Probl Cardiol 2011;36:87-120.)
The electric activity in GERD exhibited different patterns depending on the stage of the GERD. In score 1 GERD, an electroesophagram similar to that of healthy volunteers was recorded. This apparently denotes that the motile activity of the esophagus in score 1 is normal and that the esophageal peristaltic activity can probably clear the esophagus of the refluxed gastric contents. The irregular and diminished esophageal electric wave variables dis- played in score 2 GERD are presumably indicative of diminished motile activity and peristalsis of the esopha- gus with a resulting inhibited reflux clearance rate. The failure of adequate esophageal clearance is probably responsible for the clinical manifestations and investiga- tive results encountered in score 2 GERD. With progress of the condition to score 3, there is probably no motor or peristaltic esophageal activity as evidenced by the absence of the esophageal electric waves. In such case, we presume that there is no esophageal clearance.
Ventricular rhythm abnormalities are common during the early phase of acute MI with an incidence of ventricular fibrillation within first four hours, so called primary ventricular fibrillation, of 3-5% which declines rapidly thereafter. (29). Primary ventricular fibrillation is thought to be the result of micro entry mechanism in the infarct zone (30). Ventricular fibrillation is a major cause of death in those who die before receiving medical attention (31). Sustained VT which is hemodynamically stable should be treated with Intravenous lignocaine (bolus 1- 1.5mg/kg body weight along with maintenance infusion of 20- 50mg/kg). If it does not stop promptly electrical cardio version should be attempted. For VF, unsynchronized DC shock of 200 – 300W/sec is used.
these class IC drugs work promptly and with high efficacy. A cohort study including 268 patients with recent onset AF ( < 48 hours) assessed the safety and efficacy of the PiP strategy in patients without existing conduction abnormali- ties, structural heart disease, CHF, electrolyte disturbances, collagen vascular disease, or thromboembolic disease. This study revealed that patients who successfully converted to sinus rhythm and experienced no side effects after taking fle- cainide or propafenone orally in the ED were able to resolve their symptoms with the PiP at home within 2 hours 94% of the time. Among the 163 patients who experienced recur- rences after the first successful outpatient treatment with the PiP method, this approach was successful 84% of the time in resolving subsequent symptoms of arrhythmia. The most seri- ous side effect found was transient AFL with rapid ventricular rate. Over the 15 ± 5 months follow-up period, the number of ED visits and hospitalizations were significantly lower than prior to the year prior. 116 Another study on 122 patients with