China
Africa
Explore chapters and articles related to this topic
Fetal arrhythmias
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Júlia Hajdú, Valéria Váradi, Zoltán Papp
There are studies on infants with CAVB who developed late-onset dilated congestive cardiomyopathy despite early and adequate institution of cardiac pacing. At the time of clinical presentation, many infants have symptoms or signs of an upper respiratory tract infection, otitis media, or gastrointestinal infection. Myocardial biopsy or histologic examination of the explained heart revealed the following: myocyte hyper-trophy, interstitial fibrosis, and myocyte degradation in two subjects. An active inflammatory infiltrate was not detected. An upper respiratory/gastrointestinal infection might have reactivated a previously dormant inflammatory process. The increased rate that followed pacemaker implantation may have provoked a form of tachycardia-induced cardiomyopathy (38). The mortality rate is as high as 25%, and many patients require cardiac transplantation.
Nitric Oxide and Cardiac Contraction: Clinical Studies
Published in Malcolm J. Lewis, Ajay M. Shah, Endothelial Modulation of Cardiac Function, 2020
Coronary endothelial NO release could not only affect left ventricular performance acutely at the time of tachycardia or exercise but could also chronically influence diastolic left ventricular distensibility. Chronic exercise augments endothelium-mediated dilatation of epicardial coronary arteries in conscious dogs (Wang, Wolin and Hintze, 1993). A paracrine myocardial action of augmented coronary endothelial release of NO as a result of chronic exercise could explain the increase in left ventricular diastolic distensibility observed in athlete’s heart (Shapiro, 1992), which rapidly reverses once training is stopped. A similar mechanism could be operative in the early stages of tachycardia-induced cardiomyopathy, because chronic pacing at high heart rate has been shown to increase coronary endothelial release of NO (Hintze et al., 1989) and because tachycardia-induced cardiomyopathy is also characterised by a reversible increase in left ventricular diastolic distensibility. Elevated left ventricular wall stress, as observed in the remodeling process after myocardial infarction (Mc Kay et al., 1986; Pfeffer and Braunwald, 1990) or during left ventricular volume overload (Ross, 1985), raises coronary blood flow. The resultant increase of endothelial NO release could influence left ventricular distensibility and explain regional left ventricular dilatation of non-infarcted portions in ischemic cardiomyopathy and global left ventricular dilatation in volumeoverload cardiomyopathy.
Supraventricular rhythms
Published in Andrew R Houghton, David Gray, Making Sense of the ECG, 2014
Non-sustained episodes of focal atrial tachycardia are commonly seen on ambulatory ECG monitoring, and are often asymptomatic. Sustained atrial tachycardia can lead to a tachycardia-induced cardiomyopathy, and it is particularly important not to misdiagnose the rhythm as sinus tachycardia in such cases.
Is heart rate in post-hematopoietic stem cell transplant patients clinically relevant?
Published in Postgraduate Medicine, 2022
Angel Lopez-Candales, Pankaj Mathur, J Paul Mounsey, Muthu Veeraputhiran
Even when managing IST by simply controlling symptoms and reducing HR, which might not be at all related but in fact challenging in cancer patients, the most important clinical aspect of recognizing an abnormal resting HR is identifying the trigger. Which physiological or psychological trigger(s) are involved in this abnormal response? [11,13] Although most of the IST patients are generally healthy [11,13], the occurrence of IST among cancer patients in general, particularly post HSCT, has not been characterized, and this remains as an area of uncertainty. Albeit IST rarely results in cardiomyopathy [11,13], persistent elevation of the resting HR or an inappropriate increase in HR with minimal physical activity is known to alter left ventricular systolic and diastolic function [18]. More specifically, excessive HR was shown to reduce upright cardiac output in young healthy controls aged 13–23 years [18], so we can only speculate what tachycardia might do in older patients, in those post HSCT, and those with coexisting cardiac conditions or those exposed to certain drugs [19]. Finally, it is also important to remember that it is not uncommon for tachycardia-induced cardiomyopathy to occur months to years after the initial onset of ST [16,17].
Cryoablation versus antiarrhythmic therapy for initial treatment of atrial fibrillation: a systematic review and meta-analysis
Published in Expert Review of Cardiovascular Therapy, 2021
Mitra Patel, Khalid Changal, Neha Patel, Ahmed Elzanaty
Atrial fibrillation (AF) is a common arrhythmia that affects approximately 2% of the overall population [1]. In asymptomatic people, rate control is usually the preferred mode of control to prevent tachycardia-induced cardiomyopathy; however, many of these studies were performed in patients with long-standing AF [2]. In a certain population of asymptomatic patients and in symptomatic patients, it is more beneficial to convert to and maintain normal sinus rhythm [3]. The Early Rhythm-control in patients with Atrial Fibrillation (EAST-AFNET 4) trial showed that a rhythm-control strategy is superior to usual cardiac care in improving cardiovascular outcomes at 5 years among patients with a recent diagnosis of AF [4]. In this population, guidelines state that the initial use of antiarrhythmic therapy to maintain sinus rhythm far exceeds a rate control route. Unfortunately, these medications can have variable efficacy accompanied by a plethora of potential side effects [3]. An alternative option, catheter ablation, has been shown to be superior to antiarrhythmic therapy in maintaining sinus rhythm and improving quality of life in these patients [4,5].
Current pharmacotherapeutic strategies for cardiac arrhythmias in heart failure
Published in Expert Opinion on Pharmacotherapy, 2020
Ashish Correa, Yogita Rochlani, Wilbert S. Aronow
AF accounts for over one-third of all hospitalizations for cardiac dysrhythmias and is the most commonly encountered sustained arrhythmia in medical practice [13,18]. AF is more prevalent among patients with HF compared to the general population, and this prevalence steadily rises with worsening degrees of HF [19–21], to the point that over 50% of the patients with advanced HF also have AF [6,22]. The increased prevalence of AF in HF patients can be explained in part by the fact that they share many risk factors. However, it has also been shown that AF can predispose to both the development and the progression of HF and vice-versa. AF can exacerbate HF due to rapid ventricular response, reduced diastolic left ventricular filling time, loss of atrial systolic kick and increased mitral regurgitation. Further, AF is the most common cause of tachycardia-induced cardiomyopathy, which can cause HF and hasten its progression. HF, in turn, can cause or trigger AF due elevated filling pressures, dysregulation of intracellular calcium, neurohormonal activation and atrial dilation [18]. A similar relationship exists between HF and atrial flutter, though rate control is generally much harder to achieve with flutter, and cardioversion and catheter ablation tend to be of greater importance.