Ebstein’s anomaly of the tricuspid valve
Jana Popelová, Erwin Oechslin, Harald Kaemmerer, Martin G St John Sutton, Pavel Žáček in Congenital Heart Disease in Adults, 2008
In asymptomatic females with good ventricular function, pregnancy may be well tolerated. There is a certain risk of right ventricular decompensation and arrhythmias in the presence of pregnancy-induced right ventricular volume overload. Atrioventricular nodal reentry tachycardia or atrial flutter may develop. A right-to-left shunt poses the patient at risk for paradoxical embolism. Hypoxemia poses a risk to the fetus. Pregnancy is contraindicated in significant cyanosis, serious arrhythmia and right-heart failure.
Cardiac arrhythmias in pregnant women: need for mother and offspring protection
Published in Current Medical Research and Opinion, 2020
Theodora A. Manolis, Antonis A. Manolis, Evdoxia J. Apostolopoulos, Despoina Papatheou, Helen Melita, Antonis S. Manolis
Ectopic beats (APCs and/or PVCs) during pregnancy are common, usually benign, and require no specific treatment, especially when asymptomatic and/or numerically limited10,11. Sustained arrhythmias in patients without any underlying SHD are likely to be atrioventricular (AV) nodal reentrant tachycardia (AVNRT) or pathway-related SVT (orthodromic AV reentrant tachycardia-AVRT), or idiopathic VT12,13. By contrast, in patients who have cardiomyopathy (CM), rheumatic, or other valve disease, or who have undergone corrective cardiac surgery for CHD, the mechanism is likely to be atrial or ventricular tachyarrhythmia (VTA) related to the pathological substrate11. A prior history of arrhythmias or SHD or a family history of sudden cardiac death (SCD) increases the risk of tachyarrhythmias during pregnancy.
Supraventricular tachycardia with the use of phentermine: case report and review of literature
Published in Postgraduate Medicine, 2021
Sundeep Kumar, Akhil Mogalapalli, Ruthvik Srinivasamurthy, Sayed T. Hussain, Philip L. Mar
AV nodal reentrant tachycardia (AVNRT) is a type of SVT originating from above the bundle of His. It results from a reentry circuit in or around the AV node, produced by two distinct pathways, designated as a slow and fast pathway. The slow-fast or typical AVNRT is the most common form of this arrhythmia. The circuit consists of anterograde conduction down the slow pathway with retrograde conduction up the fast pathway. Under normal circumstances (sinus rhythm), the impulse progresses down both pathways, but the impulse propagating down the fast pathway will reach the end of the AV node first, rendering the end of the slow pathway refractory before progressing into the bundle of His. AVNRT can occur because of differences in the rate of recovery for each pathway (refractory period). While the slow pathway conducts slower than the fast pathway, it ‘recharges’ or repolarizes faster than the fast pathway. Thus, this arrhythmia can be initiated if a critically timed premature atrial contraction sends an impulse down the slow pathway while the fast pathway is still refractory. In this scenario, when the impulse conducts down the slow pathway only, it can conduct retrogradely up the fast pathway once it reaches the end of the AV node if the fast pathway has recovered, setting up a reentry loop back down the slow pathway, all within the AV node, until something perturbs the cycle, such as carotid massage, Valsalva maneuvers, or IV adenosine [21].
Cardiac sarcoidosis – an expert review for the chest physician
Published in Expert Review of Respiratory Medicine, 2019
Jamie S. Y. Ho, Edwin R. Chilvers, Muhunthan Thillai
Historically, atrial arrhythmias were not considered to be a primary manifestation of CS [27]. However, recent studies suggest they are more common than previously thought [28] with a prevalence of between 5% and 30% [29]. One retrospective study showed that supraventricular arrhythmias were present in 32% of patients with CS, and the majority (95%) were symptomatic [30]. Atrial fibrillation was the most common atrial dysrhythmia (18%), followed by atrial tachycardia, atrial flutter and atrioventricular nodal reentry tachycardia. Left atrial enlargement was found to be the only variable investigated which was associated with supraventricular arrhythmias [30]. One autopsy study found that although 15–17% of patients with CS had atrial arrhythmias, only 2 of 15 patients revealed granulomas in the atrial wall, concluding that those atrial arrhythmias may be more likely secondary to ventricular dysfunction and atrial dilatation than direct atrial sarcoidosis [7]. However, there is evidence that the left atrial volume increase is not associated with increased filling pressure or diastolic dysfunction, thus supporting a primary atrial infiltration hypothesis. However, prospective studies on larger cohorts are needed to confirm this finding [29].
Related Knowledge Centers
- Bundle of His
- Cardioversion
- Palpitations
- Radiofrequency Ablation
- Supraventricular Tachycardia
- Tachycardia
- Atrium
- Atrioventricular Node
- Bundle of His
- Vagal Maneuver
- Medication