Predictors of improvement in left ventricular systolic function after catheter ablation in patients with persistent atrial fibrillation complicated with heart failure.

AIMS: The current management of patients with atrial fibrillation (AF) and concomitant heart failure (HF) remains a significant challenge. Catheter ablation (CA) has been shown to improve left ventricular ejection fraction (LVEF) in these patients, but which patients can benefit from CA is still poorly understood. The aim of our study was to determine the predictors of improved ejection fraction in patients with persistent atrial fibrillation (PeAF) complicated with HF undergoing CA. METHODS AND RESULTS: A total of 435 patients with persistent AF underwent an initial CA between January 2019 and March 2023 in our hospital. We investigated consecutive patients with left ventricular systolic dysfunction (LVEF < 50%) measured by transthoracic echocardiography (TTE) within one month before CA. According to the LVEF changes at 6 months, these patients were divided into an improved group (fulfilling the '2021 Universal Definition of HF' criteria for LVEF recovery) and a nonimproved group. Eighty patients were analyzed, and the improvement group consisted of 60 patients (75.0%). In the univariate analysis, left ventricular end-diastolic diameter (P = 0.005) and low voltage zones in the left atrium (P = 0.043) were associated with improvement of LVEF. A receiver operating characteristic analysis determined that the suitable cutoff value for left ventricular end-diastolic diameter (LVDd) was 59 mm (sensitivity: 85.0%, specificity: 55.0%, area under curve: 0.709). A multivariate analysis showed that LVDd (OR = 0.85; 95% CI: 0.76-0.95, P = 0.005) and low voltage zones (LVZs) (OR = 0.26; 95% CI: 0.07-0.96, P = 0.043) were significantly independently associated with the improvement of LVEF. Additionally, parameters were significantly improved regarding the left atrial diameter, LVDd and ventricular rate after radiofrequency catheter ablation (all p < 0.05). CONCLUSIONS: The improvement of left ventricular ejection fraction (LVEF) occurred in 75.0% of patients. Our study provides additional evidence that LVDd < 59 mm and no low voltage zones in the left atrium can be used to jointly predict the improvement of LVEF after atrial fibrillation ablation.

Clinical Characterization of Arrhythmia-Induced Cardiomyopathy in Patients With Tachyarrhythmia and Idiopathic Heart Failure.

BACKGROUND: Arrhythmia-induced cardiomyopathy (AIC) is a known entity, but prospective evidence for its characterization is limited. OBJECTIVES: This study aimed to: 1) determine the relative frequency of the pure form of AIC in the clinically relevant cohort of patients with newly diagnosed, otherwise unexplained left ventricular systolic dysfunction (LVSD) and tachyarrhythmia; 2) assess the time to recovery from LVSD; and 3) identify parameters for an early diagnosis of AIC. METHODS: Patients were prospectively included, underwent effective rhythm restoration, and were followed-up at 2, 4, and 6 months to evaluate clinical characteristics, biomarkers, and cardiac imaging including cardiac magnetic resonance imaging. Patients with recurred arrhythmia were excluded from analysis. RESULTS: 41 of 50 patients were diagnosed with AIC 6 months after rhythm restoration. Left ventricular (LV) ejection fraction increased 2 months after rhythm restoration from 35.4% ± 8.2% to 52.7% ± 8.0% in AIC patients vs 37.0% ± 9.5% to 43.3% ± 7.0% in non-AIC patients. From month 2 to 6, LV ejection fraction continued to increase in AIC patients (57.2% ± 6.1%; P < 0.001) but remained stable in non-AIC patients (44.0% ± 7.8%; P = 0.628). Multivariable logistic regression analysis revealed that lower LV end-diastolic diameter at baseline could be used for early diagnosis of AIC, whereas biomarkers and other morphological or functional parameters, including late LV gadolinium enhancement, did not show suitability for early diagnosis. CONCLUSIONS: We observed a high prevalence of AIC in patients with otherwise unexplained LVSD and concomitant tachyarrhythmia, suggesting that this condition may be underdiagnosed in clinical practice. Most patients recovered fast, within months, from LVSD. A low initial LV end-diastolic diameter may constitute an early marker for diagnosis of AIC.

[Septic cardiomyopathy-diagnosis and estimation of disease severity]. / Septische Kardiomyopathie ­ Diagnostik und Schweregradabschätzung.

BACKGROUND: The relevance of septic cardiomyopathy is frequently underestimated due to the complexity of the pattern of cardiac injury and the corresponding difficulties in quantifying the degree of functional impairment. AIM: Account of the methods for diagnosis and severity classification of septic cardiomyopathy. METHODS: Literature review and analysis of the main findings. RESULTS: Septic cardiomyopathy is characterized by both systolic and diastolic impairment of not only the left, but also the right ventricle, as well as by sinus-tachycardiomyopathy (≥ 90-95 beats/min) of variable degree. Sepsis-related organ failure assessment (SOFA) score, left ventricular ejection fraction (LVEF), ECG and cardiac biomarkers do not help in grading severity of septic cardiomyopathy. For that purpose either a sophisticated echocardiography diagnosis is mandatory, or the measurement of those global heart function parameters which take into account the dependency of cardiac output on afterload, in view of the pronounced vasodilatation in sepsis and septic shock, is needed. A suitable parameter on the basis of cardiac output measurement is afterload-related cardiac performance (ACP), which gives the percentage of cardiac output in a septic patient related to the cardiac output a healthy heart pumps when challenged by a fall in systemic vascular resistance to the same extent. The calculation of ACP shows that at least one in two septic patients suffers from impaired heart function and that mortality increases as severity increases. CONCLUSION: Simple parameters like LVEF are not apt for diagnosis nor for disease severity classification of septic cardiomyopathy. For that purpose either sophisticated echocardiography techniques or load-independent parameters-best validated-ACP measurements are appropriate.

Thrombus entrapment with left atrial appendage closure to facilitate early cardioversion in tachycardiomyopathy: a case report.

Background: The aetiological spectrum of heart failure with reduced ejection fraction is various. Tachycardiomyopathy is recognized as one of the cause, usually made retrospectively. In this clinical context, rhythm control with restoration of sinus rhythm is considered crucial to minimize ventricular function damage and allow contractility recovery. However, the presence of a thrombus in the left atrial appendage is a limiting factor, typically requiring anticoagulation until the thrombus resolves, at least 3 weeks, thus delaying the therapy. Case summary: We present a case of 65-year-old man with diagnosis of new-onset acute symptomatic heart failure with severe reduced ejection fraction (left ventricular ejection fraction 15%), in the context of a typical tachycardic atrial flutter and concomitant thrombus in the left atrial appendage confirmed by transoesophageal echocardiography. We successfully performed a thrombus entrapment procedure by means of percutaneous left atrial appendage closure, which allowed immediate restoration of sinus rhythm through cavotricuspid isthmus ablation. After the institution of the heart failure therapy, titrated up to the maximum tolerated dose, we observed a complete restoration of left ventricular function after 6 months. Discussion: Thrombus entrapment by means of left atrial appendage closure is a valid strategy that enables early cardioversion with arrhythmia ablation and rapid restoration of normal cardiac rhythm in severe heart failure with reduced ejection fraction, even in acute situations and typical atrial flutter.

A unique location of the accessory pathway in a child with permanent junctional reciprocating tachycardia.

Permanent junctional reciprocating tachycardia (PJRT) is a rare supra ventricular tachycardia (SVT) due to an accessory pathway (AP), characterized by slow and decremental retrograde conduction, which is predominantly seen in infants and children. Although the typical site of AP in PJRT is a right posteroseptal region around or just within the coronary sinus (CS), atypical sites of AP have been described. We report a rare case of PJRT in a 7-year-old girl with an AP located in the superio-paraseptal (Para-Hsian) region that was successfully ablated through a non-coronary sinus.

Cardio-Thyrotoxicosis Syndrome: A Review of Thyrotoxic Cardiovascular Disease.

Thyrotoxicosis, an endocrine disorder characterized by elevated serum thyroid hormone levels of tri-iodothyronine (T3) and/or thyroxine (T4), can impact cardiovascular health in several ways. The cardiovascular system is often severely targeted by the thyrotoxic state, and the term "Cardio-thyrotoxic syndrome" has been proposed to encompass the various cardiovascular disease states resulting from thyrotoxicosis. In this review, we discuss various cardiovascular disorders resulting from the effects of thyrotoxicosis. It is important to keep a high index of suspicion for thyroid disorder in the setting of new atrial fibrillation, heart failure, and tachycardia-induced cardiomyopathy. Management of cardio-thyrotoxicosis involves control of heart rate and blood pressure and treatment of acute cardiovascular complications. Thyroid-specific therapy to achieve a euthyroid state will not only improve but even potentially reverse cardiovascular abnormalities.

Atrial arrhythmias and heart failure: A "modern view" of an old paradox.

BACKGROUND: Heart failure (HF) and atrial arrhythmias (AAs) are two clinical conditions that characterize the daily clinical practice of cardiologists. In this perspective review, we analyze the shared etiopathogenetic pathways of atrial arrhythmias, which are the most common cause of atrial arrhythmias-induced cardiomyopathy (AACM) and HF. HYPOTHESIS: The aim is to explore the pathophysiology of these two conditions considering them as a "unicum", allowing the definition of a cardiovascular continuum where it is possible to predict the factors and to identify the patient phenotype most at risk to develop HF due to atrial arrhythmias. METHODS: Potentially eligible articles, identified from the Electronic database (PubMed), and related references were used for a literature search that was conducted between January 2022 and January 2023. Search strategies were designed to identify articles that reported atrial arrhythmias in association with heart failure and vice versa. For the search we used the following keywords: atrial arrhythmias, atrial fibrillation, heart failure, arrhythmia-induced cardiomyopathy, tachycardiomyopathy. We identified 620 articles through the electronic database search. Out of the 620 total articles we removed 320 duplicates, thus selecting 300 eligible articles. About 150 titles/abstracts were excluded for the following reasons: no original available data, no mention of atrial arrhythmias and heart failure crosstalk, very low quality analysis or evidence. We excluded also non-English articles. When multiple articles were published on the same topic, the articles with the most complete set of data were considered. We preferentially included all papers that could provide the best evidence in the field. As a result, the present review article is based on a final number of 104 references. RESULTS: While the pathophysiology of AACM and Heart Failure with reduced ejection fraction (HFrEF) has been studied in detail over the years, the causal link between atrial arrhythmias and heart failure with Preserved Ejection Fraction (HFpEF) has been often subject of interest. HFpEF is strictly related to AAs, which has always been considered significant risk factor. In this review we described the pathophysiological links between atrial fibrillation and heart failure. Furthermore, we illustrated and discussed the preclinical and clinical predicting factors of AF and HFpEF, and the corresponding targets of the available therapeutic agents. Finally, we outlined the patient phenotype at risk of developing AF and HFpEF (Central Illustration). CONCLUSIONS: In this review, we underline how these two clinical conditions (AF and HFpEF) represent a "unicum" and, therefore, should be considered as a single disease that can manifest itself in the same phenotype of patients but at different times. Furthermore, considering that today we have few therapeutic strategies to treat these patients, it would be good to make an early diagnosis in the initial stages of the disease or intervene even before the development of signs and symptoms of HF. This is possible only by paying greater attention to patients with predisposing factors and carrying out a targeted screening with the correct diagnostic methods. A systemic approach aimed at improving the immuno-metabolic profile of these patients by lowering the body mass index, threatening the predisposing factors, lowering the mean heart rate and reducing the sympathetic nervous system activation is the key strategy to reduce the clinical impact of this disease.

Emerging concepts in heart failure management and treatment: focus on tachycardia-induced cardiomyopathy.

Tachycardia-induced cardiomyopathy is an entity characterized by reversible dysfunction of the left ventricle, which can be induced by different types of arrhythmia such as atrial fibrillation, atrial flutter, incessant supraventricular tachycardia and ventricular arrhythmia (more frequent causes). Correct identification of the causative arrhythmia and normalization of the heart rate (e.g through medical treatment, electrical cardioversion, ablation) can lead to recovery of left ventricular function. Tachycardia-induced cardiomyopathy should be suspected in patients with tachycardia and left ventricular dysfunction (heart failure setting), especially when there is no history of previous heart disease. Its usual phenotype is that of non-ischaemic/non-valvular dilated cardiomyopathy and it can occur in both children (main cause: permanent junctional reciprocating tachycardia) and adults (main cause: atrial fibrillation). With proper treatment, most cases recover within a few months, though there is a risk of relapse, especially when the causal arrhythmia reappears or its control is lost. This is a narrative review that comprehensively addresses the pathophysiology, clinical manifestations, and therapeutic management of tachycardia-induced cardiomyopathy. This article is part of the Emerging concepts in heart failure management and treatment Special Issue: https://www.drugsincontext.com/special_issues/emerging-concepts-in-heart-failure-management-and-treatment.

Taquicardia ventricular asociada a mutación en el gen de ankirina B / Ventricular tachycardia associated to a mutation in the ankyrin B gen

Resumen Se presenta el caso de una mujer de 14 años, con taquicardiomiopatía secundaria a taquicardia ventricular. Se evidenció la presencia de una variante de significado incierto en el gen ANK2, por lo que se consideró un posible síndrome de ankirina B. La paciente fue tratada con éxito a través de ablación con radiofrecuencia. Tras dicho procedimiento, tuvo recuperación completa de su función ventricular izquierda y resolución de los complejos ventriculares prematuros y los episodios de taquicardia ventricular.

Abstract We report a case of a 14-year-old with tachycardiomyopathy due to ventricular tachycardia. A variant of uncertain significance of the ANK2 gene was identified, which is suggestive of a possible ankyrin-B syndrome. The patient underwent a successful radiofrequency ablation. After the procedure, the patient completely recovered her left ventricular function and there was resolution of the premature ventricular complexes and ventricular tachycardia.

Tachycardiomyopathy entails a dysfunctional pattern of interrelated mitochondrial functions.

Tachycardiomyopathy is characterised by reversible left ventricular dysfunction, provoked by rapid ventricular rate. While the knowledge of mitochondria advanced in most cardiomyopathies, mitochondrial functions await elucidation in tachycardiomyopathy. Pacemakers were implanted in 61 rabbits. Tachypacing was performed with 330 bpm for 10 days (n = 11, early left ventricular dysfunction) or with up to 380 bpm over 30 days (n = 24, tachycardiomyopathy, TCM). In n = 26, pacemakers remained inactive (SHAM). Left ventricular tissue was subjected to respirometry, metabolomics and acetylomics. Results were assessed for translational relevance using a human-based model: induced pluripotent stem cell derived cardiomyocytes underwent field stimulation for 7 days (TACH-iPSC-CM). TCM animals showed systolic dysfunction compared to SHAM (fractional shortening 37.8 ± 1.0% vs. 21.9 ± 1.2%, SHAM vs. TCM, p < 0.0001). Histology revealed cardiomyocyte hypertrophy (cross-sectional area 393.2 ± 14.5 µm2 vs. 538.9 ± 23.8 µm2, p < 0.001) without fibrosis. Mitochondria were shifted to the intercalated discs and enlarged. Mitochondrial membrane potential remained stable in TCM. The metabolite profiles of ELVD and TCM were characterised by profound depletion of tricarboxylic acid cycle intermediates. Redox balance was shifted towards a more oxidised state (ratio of reduced to oxidised nicotinamide adenine dinucleotide 10.5 ± 2.1 vs. 4.0 ± 0.8, p < 0.01). The mitochondrial acetylome remained largely unchanged. Neither TCM nor TACH-iPSC-CM showed relevantly increased levels of reactive oxygen species. Oxidative phosphorylation capacity of TCM decreased modestly in skinned fibres (168.9 ± 11.2 vs. 124.6 ± 11.45 pmol·O2·s-1·mg-1 tissue, p < 0.05), but it did not in isolated mitochondria. The pattern of mitochondrial dysfunctions detected in two models of tachycardiomyopathy diverges from previously published characteristic signs of other heart failure aetiologies.

Atrial fibrillation-induced tachycardiomyopathy and heart failure: an underappreciated and elusive condition.

Many patients with persistent, chronic, or frequently recurring paroxysmal atrial fibrillation (AF) may develop a tachycardiomyopathy (TCM) with left ventricular (LV) dysfunction and heart failure (HF), which is reversible upon restoration and maintenance of sinus rhythm, when feasible, or via better and tighter ventricular rate (VR) control. Mechanisms involved in producing this leading cause of TCM (AF-TCM) include loss of atrial contraction, irregular heart rate, fast VR, neurohumoral activation, and structural myocardial changes. The most important of all mechanisms relates to optimal VR control, which seems to be an elusive target. Uncontrolled AF may also worsen preexisting LV dysfunction and exacerbate HF symptoms. Data, albeit less robust, also point to deleterious effects of slow VRs on LV function. Thus, a J-shaped relationship between VR and clinical outcome has been suggested, with the optimal VR control hovering at ~ 65 bpm, ranging between 60 and 80 bpm; VRs above and below this range may confer higher morbidity and mortality rates. A convergence of recent guidelines is noted towards a stricter rather than a more lenient VR control with target heart rate < 80 bpm at rest and < 110 bpm during moderate exercise which seems to prevent TCM or improve LV function and exercise capacity and relieve TCM-related symptoms and signs. Of course, restoring and maintaining sinus rhythm is always a most desirable target, when feasible, either with drugs or more likely with ablation. All these issues are herein reviewed, current guidelines are discussed and relevant data are tabulated and pictorially illustrated.

Rate of atrial fibrillation and flutter induced tachycardiomyopathy in a cohort of hospitalized patients with heart failure and detection of indicators for improved diagnosis.

Background: Atrial fibrillation (AF) and atrial flutter (AFL) induced tachycardiomyopathy (TCM) has been known to cause reversible heart failure (HF) for many years. However, the prevalence of the disease is unknown, and diagnosis is challenging. Therefore, the aim of the present study was (1) to assess the rate of AF/AFL induced TCM and (2) to identify indicators for diagnosis. Methods: Consecutively, all patients with a diagnosis of HF who were hospitalized in our department within 12 months were reviewed. For the main analysis, all patients with HF with reduced ejection fraction (HFrEF) and AF or AFL were included. AF/AFL induced TCM was diagnosed when there was at least a 10% improvement in left ventricular ejection fraction under rhythm or rate control within 3 months. Patients with HFrEF with AF/AFL but without TCM served as control group. Results: A total of 480 patients were included. AF/AFL induced TCM occurred in 26 patients (5.4%) and HFrEF with AF/AFL in 53 patients (11%). Independent indicators of AF/AFL induced TCM were age<79 years [Odds ratio 5.887, confidence interval (CI) 1.999-17.339, p < 0.001], NT-pro-BNP <5,419 pg/mL (Odds ratio 2.327, CI 1.141-4.746, p = 0.004), and a resting heart rate >112 bpm (Odds ratio 2.503, CI 1.288-4.864, p = 0.001). Conclusion: Approximately 5% of all patients hospitalized for HF suffer from AF/AFL induced TCM. Improved discrimination of AF/AFL induced TCM to HFrEF with AF/AFL is possible considering age, NT-pro-BNP level, and resting heart rate >112 beats/minute. Based on these parameters, an earlier diagnosis and improved therapy might be possible.

The bidirectional interaction between atrial fibrillation and heart failure: consequences for the management of both diseases.

Atrial fibrillation (AF) and heart failure (HF) are both highly prevalent diseases and are accompanied by a significant disease burden and increased mortality. Although the conditions may exist independently, they often go hand in hand as each is able to provoke, sustain, and aggravate the other. In addition, the diseases share a risk profile with several coinciding cardiovascular risk factors, promoting the odds of developing both AF and HF separately from each other. When the diseases coexist, this provides additional challenges but also opportunities for the optimal treatment. The recommended management of the comorbidities has been much debated in the past decades. In this review, we describe the pathophysiological coherence of AF and HF, illustrate the current knowledge on the management of them as comorbidities of each other and look forward to future developments in this field.

Radiofrequency ablation for fascicular ventricular tachycardia causing tachycardiomyopathy and brief literature review.

A 10-years-old boy presented with a history of effort intolerance and palpitations for 4 months. His electrocardiogram showed wide complex tachycardia suggestive of fascicular ventricular tachycardia (VT). The echocardiogram showed moderate-to-severe left ventricular systolic dysfunction without any structural lesion. The tachycardia was unresponsive to adenosine and direct current cardioversion. It responded to oral verapamil. The electrophysiology study confirmed the tachycardia as left posterior fascicular VT. The tachycardia was successfully ablated guided by Purkinje potential on three-dimensional mappings. He showed improvement in ventricular functions before discharge. He is doing well on short-term follow-up.

Incessant Focal Atrial Tachycardia Leading to Tachycardiomyopathy.

A 22-year-old man presented with severe left ventricular (LV) dysfunction and progressive heart failure. The 12-lead electrocardiogram showed short runs of supraventricular tachycardia suggestive of focal atrial tachycardia. The patient underwent successful radiofrequency ablation. There was a complete recovery of symptoms and LV function at six months of follow-up. We discuss the importance of identifying tachycardiomyopathy as a reversible cause of heart failure.

Catabolic/Anabolic Imbalance Is Accompanied by Changes of Left Ventricular Steroid Nuclear Receptor Expression in Tachycardia-Induced Systolic Heart Failure in Male Pigs.

BACKGROUND: Steroid hormones play an important role in heart failure (HF) pathogenesis, and clinical data have revealed disordered steroidogenesis in male patients with HF. However, there is still a lack of studies on steroid hormones and their receptors during HF progression. Therefore, a porcine model of tachycardia-induced cardiomyopathy corresponding to HF was used to assess steroid hormone concentrations in serum and their nuclear receptor levels in heart tissue during the consecutive stages of HF. METHODS AND RESULTS: Male pigs underwent right ventricular pacing and developed a clinical picture of mild, moderate, or severe HF. Serum concentrations of dehydroepiandrosterone, testosterone, dihydrotestosterone, estradiol, aldosterone, and cortisol were assessed by enzyme-linked immunosorbent assay. Androgen receptor, estrogen receptor alpha, mineralocorticoid receptor, and glucocorticoid receptor messenger RNA levels in the left ventricle were determined by qPCR.The androgen level decreased in moderate and severe HF animals, while the corticosteroid level increased. The estradiol concentration remained stable. The quantitative real-time polymerase chain reaction revealed the downregulation of androgen receptor in consecutive stages of HF and increased expression of mineralocorticoid receptor messenger RNA under these conditions. CONCLUSIONS: In the HF pig model, deteriorated catabolic/anabolic balance, manifested by upregulation of aldosterone and cortisol and downregulation of androgen signaling on the ligand level, was augmented by changes in steroid hormone receptor expression in the heart tissue.