Atrial fibrillation case studies

The therapy of atrial premature contractions (APC) depends on the patient s symptoms. Asymptomatic APC need not be treated. However, asymptomatic APC may be associated with an increased risk of atrial fibrillation. In such cases, suppression of APC may be useful in prolonging the time to the onset of atrial fibrillation. /3-blockers or Class la/Ic agents may be effective for suppression of APC. The use of Class Ic agents, such as fiecainide, may achieve almost complete suppression of APC, but the risk-benefit ratio of these agents has not been studied. 

Case study level 3 - Atrial fibrillation - see page 23... 

Nattel S, Opie L (2006). Controversies in atrial fibrillation. Lancet 367 262-272 Ngeh J, Gupta S, Goodbourn C et al. (2003). Chlamydia pneumoniae in elderly patients with stroke (C-PEPS) a case-control study on the seroprevalence of Chlamydia pneumoniae in elderly patients with acute cerebrovascular disease. Cerebrovascular Diseases 15 11-16... 

In 40 patients with atrial fibrillation, some with severe heart disease (including cardiogenic shock in eight and pulmonary edema in 12), amiodarone 450 mg was given through a peripheral vein within 1 minute, followed by 10 ml of saline 21 patients converted to sinus rhythm, 13 within 30 minutes and another 8 within 24 hours (21). There were two cases of hypotension, but in those that converted to sinus rhythm there was a slight increase in systolic blood pressure. There were no cases of thrombophlebitis. Efficacy is hard to judge from this study, because it was not placebo-controlled. 

Qf 136 patients with atrial fibrillation treated with either amiodarone (n = 96) or propafenone (n = 40), 15 developed subsequent persistent atrial flutter, nine of those taking amiodarone and six of those taking propafenone (58). In all cases radiofrequency ablation was effective. It is not clear to what extent these cases of atrial flutter were due to the drugs, although the frequency of atrial flutter in previous studies with propafenone has been similar. Atrial enlargement was significantly related to the occurrence of persistent atrial flutter in these patients. 

The adverse effects of propafenone in placebo-con-trolled trials in patients with atrial tachydysrhythmias have been reviewed (16). The following effects were reported after single intravenous oral doses to produce conversion of atrial fibrillation to sinus rhythm. Non-cardiac adverse effects included mild dizziness. Mild hypotension was also noted, but only required withdrawal of propafenone in one of 29 patients in one study. There have been prodysrhythmic effects in several studies, including atrial flutter with a broad QRS complex, which can occur in up to 5% of cases in some cases atrial flutter can have a rapid ventricular response due to 1 1 atrioventricular conduction, which has been attributed to slowing of atrial conduction and reduced refractoriness of the atrioventricular node. Other prodysrhythmic effects in a few patients included sinus bradycardia with sinus pauses and effects on atrioventricular conduction. 

The use of propafenone in atrial fibrillation (SEDA-23, 202) has been studied in a randomized, double-bhnd, placebo-controUed trial in 55 patients (17). The dose of propafenone was chosen according to body weight 450, 600, and 750 mg for those weighing 50-64, 65-80, and over 80 kg respectively. Propafenone converted atrial fibrillation to sinus rhythm significantly more quickly than placebo, and most patients given propafenone had converted by 6 hours. However, by 24 hours there was no significant difference between the two groups. Four patients had hypotension after propafenone, in three cases transiently. The patient with sustained hypotension had poor left ventricular systolic function, but it responded promptly to the administration of fluids and electrical cardioversion. In one patient with transient hypotension there was a brief episode of sinus bradycardia and in another an isolated sinus pause. 

Cardiovascular Effects. No studies were located regarding cardiovascular effects in hiunans after inhalation exposure to 1,1-dimethylhydrazine. Data regarding the adverse effects of hydrazine on the cardiovascular system in humans are limited to a single case study. Atrial fibrillation, enlargement of the heart, and degeneration of heart muscle fibers were noted in a worker exposed to an undetermined concentration of hydrazine once a week for 6 months (Sotaniemi et al. 1971). It is uncertain whether these effects are directly attributable to hydrazine exposure. 

Sitges M, Teijeira VA, Scalise A, et al. Is there an anatomical substrate for idiopathic paroxysmal atrial fibrillation A case-control echocardiographic study. Europace 2007 9 294—8. 

As in the case of the CYPllBl gene, many CY-P11B2 variants have now been defined from chn-ical studies. For review, see [2071]. The many variants [2072, 2073] have been related to a number of diseases, including congenital hypoal-dosterism [2074], salt-wasting syndrome [2075], adenoma [2076, 2077], treatment for diabetic nephropathy [2078], high-altitude pulmonary edema [2079,2080], metabolic syndrome [2081], hypertension [2082-2095], stroke [2096], atrial fibrillation [2097], and other cardiovascular risks [2098]. 

Cardiovascular The use of glucocorticoids is associated with increased risks of myocardial infarction, stroke, and heart failure, but data are limited on the risk of atrial fibrillation and atrial flutter. In a case-control study patients with a first hospital diagnosis of atrial fibrillation or flutter were identified in Northern Denmark p "]. For each case 10 population controls matched by age and sex were selected. 

Christiansen CF, Christensen S, Mehnert F, Cummings SR, Chapurlat RD, Sprensen HT. Glucocorticoid use and risk of atrial fibrillation or fiutter. A population-based, case-control study. Arch Intern Med 2009 169(18) 1677-83. 

Atrial fibrillation Atrial fibrillation (AF) is characterised by a disorganised electrical activity in the atrium, which leads to an inefficient atrial contraction. This scenario is well known to increase the risk of stroke by 25% in women aged over 65 years. The primary end point of the WHI randomised, placebo-controlled hormone trials was CFID. The effort to link WHI participants to their Medicare claims records has allowed the identification of 581 additional AF cases that had not been previously identified. This new piece of data enhances the power to study novel outcomes. Once participants who suffered from AF at baseline were excluded, in the oestrogen plus progestagen trial there... 

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