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Deutsches Arzteblatt International May 2018Heart failure affects 1–2% of the population and is associated with elevated morbidity and mortality. Cardiac arrhythmias are often a result of heart failure, but they... (Review)
Review
BACKGROUND
Heart failure affects 1–2% of the population and is associated with elevated morbidity and mortality. Cardiac arrhythmias are often a result of heart failure, but they can cause left-ventricular systolic dysfunction (LVSD) as an arrhythmia-induced cardiomyopathy (AIC). This causal relationship should be borne in mind by the physician treating a patient with systolic heart failure in association with cardiac arrhythmia.
METHODS
This review is based on pertinent publications retrieved by a selective search in PubMed (1987–2017) and on the recommendations in current guidelines.
RESULTS
The key criterion for the diagnosis of an AIC is the demonstration of a persistent arrhythmia (including pathological tachycardia) together with an LVSD whose origin cannot be explained on any other basis. Nearly any type of tachyarrhythmia or frequent ventricular extrasystoles can lead, if persistent, to a progressively severe LVSD. The underlying pathophysiologic mechanisms are incompletely understood; the increased ventricular rate, asynchronous cardiac contractions, and neurohumoral activation all seem to play a role. The most common precipitating factors are supraventricular tachycardias in children and atrial fibrillation in adults. Recent studies have shown that the causal significance of atrial fibrillation in otherwise unexplained LVSD is underappreciated. The treatment of AIC consists primarily of the treatment of the underlying arrhythmia, generally with drugs such as beta-blockers and amiodarone. Depending on the type of arrhythmia, catheter ablation for long-term treatment should also be considered where appropriate. The diagnosis of AIC is considered to be well established when the LVSD normalizes or improves within a few weeks or months of the start of targeted treatment of the arrhythmia.
CONCLUSION
An AIC is potentially reversible. The timely recognition of this condition and the appropriate treatment of the underlying arrhythmia can substantially improve patient outcomes.
Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Cardiomyopathies; Humans; Prognosis; Tachycardia, Supraventricular; Ventricular Dysfunction, Left
PubMed: 29875055
DOI: 10.3238/arztebl.2018.0335 -
Academic Emergency Medicine : Official... Feb 2023The objective was to evaluate the comparative effectiveness and safety of pharmacological and nonpharmacological management options for atrial fibrillation/atrial... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
The objective was to evaluate the comparative effectiveness and safety of pharmacological and nonpharmacological management options for atrial fibrillation/atrial flutter with rapid ventricular response (AFRVR) in patients with acute decompensated heart failure (ADHF) in the acute care setting.
METHODS
This study was a systematic review of observational studies or randomized clinical trials (RCT) of adult patients with AFRVR and concomitant ADHF in the emergency department (ED), intensive care unit, or step-down unit. The primary effectiveness outcome was successful rate or rhythm control. Safety outcomes were adverse events, such as symptomatic hypotension and venous thromboembolism.
RESULTS
A total of 6577 unique articles were identified. Five studies met inclusion criteria: one RCT in the inpatient setting and four retrospective studies, two in the ED and the other three in the inpatient setting. In the RCT of diltiazem versus placebo, 22 patients (100%) in the treatment group had a therapeutic response compared to 0/15 (0%) in the placebo group, with no significant safety differences between the two groups. For three of the observational studies, data were limited. One observation study showed no difference between metoprolol and diltiazem for successful rate control, but worsening heart failure symptoms occurred more frequently in those receiving diltiazem compared to metoprolol (19 patients [33%] vs. 10 patients [15%], p = 0.019). A single study included electrical cardioversion (one patient exposed with failure to convert to sinus rhythm) as nonpharmacological management. The overall risk of bias for included studies ranged from serious to critical. Missing data and heterogeneity of definitions for effectiveness and safety outcomes precluded the combination of results for quantitative meta-analysis.
CONCLUSIONS
High-level evidence to inform clinical decision making regarding effective and safe management of AFRVR in patients with ADHF in the acute care setting is lacking.
Topics: Adult; Humans; Atrial Fibrillation; Atrial Flutter; Diltiazem; Metoprolol; Anti-Arrhythmia Agents; Heart Failure; Randomized Controlled Trials as Topic; Observational Studies as Topic
PubMed: 36326565
DOI: 10.1111/acem.14618 -
Annales de Cardiologie Et D'angeiologie Dec 2020In the pandemic caused by the SARS-CoV2 virus, arrhythmias were not in the foreground. However, the virus seems to affect many organs and the cardiac tropism is now well... (Review)
Review
In the pandemic caused by the SARS-CoV2 virus, arrhythmias were not in the foreground. However, the virus seems to affect many organs and the cardiac tropism is now well known. Knowledge in this area is still far from exhaustive, but several series published concerning patients with COVID-19 find a significant proportion of arrhythmias, some of which can potentially lead to a fatal outcome. These rhythm disorders are mainly supraventricular, such as atrial fibrillation (AF) or flutter but also ventricular disorders like ventricular tachycardias (VT) ventricular fibrillation (VF) and more rarely torsades de pointe (TdP). The causes are multiple, due to the multiorgan damage caused by the virus and potential drug interactions. In addition, the question of monitoring rhythm disorders that may emerge in the medium and long term after an infection remains to be explored.
Topics: Arrhythmias, Cardiac; COVID-19; Humans
PubMed: 33081916
DOI: 10.1016/j.ancard.2020.09.024