Predictive Factors of Therapy-Related Cardiovascular Events in Patients with Lymphoma Receiving Anthracyclines.

BACKGROUND: Cancer-therapy-related cardiac dysfunction (CTRCD) is a growing concern for public health, with a growing incidence due to improved survival rates of patients with hematological malignancies due to diagnostic and therapeutic advances. The identification of patients at risk for CTRCD is vital to developing preventive strategies. METHODS: A single-center retrospective cohort study was conducted between 1 January 2017 and 15 February 2023. Medical records of patients with lymphoma treated with first-line anthracyclines were reviewed. Demographic data, cardiovascular risk factors, biomarkers of myocardial damage, and echocardiographic information were collected. RESULTS: A total of 200 patients were included. The incidence of CTRCD was 17.4% (35/200). Patients with CTRCD were older than those without CTRCD, with a mean age of 65.17 years vs. 56.77 (p = 0.008). Dyslipidemia (DL) (31.4% vs. 13.4% p = 0.017) and previous cardiovascular disease (40% vs. 13.3%; p < 0.001) were more frequent in the group who developed an event. Mean baseline NT-proBNP levels in the subgroup with cardiovascular events were 388.73 kg/L ± 101.02, and they were 251.518 kg/L ± 26.22 in those who did not (p = 0.004). Differences in Troponin I levels were identified during and after treatment without exceeding the laboratory's upper reference limit. Patients were followed for a median of 51.83 months (0.76-73.49). The presence of a CTCRD event had a negative impact on overall mortality from any cause (HR = 2.23 (95% CI: 1.08-2.93); p = 0.031). CONCLUSIONS: Early identification of risk factors is crucial to manage patients at risk for CTRCD.

Dapagliflozin Improved Cardiac Function and Structure in Diabetic Patients with Preserved Ejection Fraction: Results of a Single Centre, Observational Prospective Study.

Sodium-glucose cotransporter inhibitors (SGLT2i) have demonstrated a reduction in cardiovascular events in diabetes and heart failure (HF). The mechanisms underlying this benefit are not well known and data are contradictory. The purpose of this study is to analyse the effect of dapagliflozin on cardiac structure and function in patients with normal ejection fraction. Between October 2020 and October 2021, we consecutively included 31 diabetic patients without prior history of SGLT2i use. In all of them, dapagliflozin treatment was started. At inclusion and during six months of follow-up, different clinical, ECG, analytical, and echocardiographic (standard, 3D, and speckle tracking) variables were recorded. After a follow-up period of 6.6 months, an average reduction of 18 g (p = 0.028) in 3D-estimated left ventricle mass was observed. An increase in absolute left ventricle global longitudinal strain (LV-GLS) of 0.3 (p = 0.036) was observed, as well as an increase in isovolumetric relaxation time (IVRT) of 10.5 ms (p = 0.05). Moreover, dapagliflozin decreased the levels of plasma creatin-kinase (CK-MB) and atrial natriuretic peptide (ANP). In conclusion, our data show that the use of SGLT2i is associated with both structural (myocardial mass) and functional (IVRT, LV-GLS) cardiac improvements in a population of diabetic patients with normal ejection fraction.

Long-term outcomes of ivabradine in inappropriate sinus tachycardia patients: appropriate efficacy or inappropriate patients.

BACKGROUND: Inappropriate sinus tachycardia (IST) is characterized by persistent and disproportional elevation of heart rate (HR). Ivabradine has been successfully used in some patients. METHODS: Twenty-four patients (18 women, 41 ± 13 year olds) were diagnosed with IST according to current guidelines criteria. Patients were treated with 5-7.5 mg of ivabradine twice a day. Twenty-four-hour Holter recordings and the SF-36 Health Survey were performed at 6 months to evaluate both HR control and clinical status. RESULTS: Holter recordings before and after 6 months on treatment showed a significant reduction in the average maximal HR of 155 ± 18 beats/min versus 132 ± 16 beats/min, mean HR of 97 ± 6 beats/min versus 79 ± 8 beats/min (mean daytime HR of 103 ± 8 beats/min vs 84 ± 10 beats/min) and minimal HR of 58 ± 12 beats/min versus 48 ± 7 beats/min (Wilcoxon analysis, P < 0.05). The SF-36 mean score showed a significant improvement on ivabradine treatment (57 ± 23 vs 76 ± 20), with a better physical and mental status scores (56 ± 25 vs 74 ± 22 and 58 ± 24 vs 78 ± 18, respectively) (Wilcoxon analysis, P < 0.001). Mean dose of ivabradine was 5.8 ± 1.4 mg. No episodes of severe bradycardia or syncope were reported. After 1 year, patients were asked to stop treatment to reevaluate the situation. Twenty patients were on treatment and only 10 patients accepted to stop ivabradine. Only two patients (20%) remained on IST criteria. CONCLUSIONS: IST patients treated with ivabradine showed both HR normalization and quality-of-life improvement maintained in the long-term follow-up. Stopping ivabradine after 1 year unexpectedly showed that HR remained in the normal limits in 80% of the patients.

Characterization of gap junction remodeling in epicardial border zone of healing canine infarcts and electrophysiological effects of partial reversal by rotigaptide.

BACKGROUND: The border zone of healing myocardial infarcts is an arrhythmogenic substrate, partly the result of structural and functional remodeling of the ventricular gap junction protein, Connexin43 (Cx43). Cx43 in arrhythmogenic substrates is a potential target for antiarrhythmic therapy. METHODS AND RESULTS: We characterized Cx43 remodeling in the epicardial border zone (EBZ) of healing canine infarcts 5 days after coronary occlusion and examined whether the gap junction-specific agent rotigaptide could reverse it. Cx43 remodeling in the EBZ was characterized by a decrease in Cx43 protein, lateralization, and increased Cx43 phosphorylation at serine (S) 368. Rotigaptide partially reversed the loss of Cx43 but did not affect the increase in S368 phosphorylation, nor did it reverse Cx43 lateralization. Rotigaptide did not prevent conduction slowing in the EBZ, nor did it decrease the induction of sustained ventricular tachycardia by programmed stimulation, although it did decrease the EBZ effective refractory period. CONCLUSIONS: We conclude that partial reversal of Cx43 remodeling in healing infarct border zone may not be sufficient to restore normal conduction or prevent arrhythmias.

Cardiac anatomy for the interventional arrhythmologist: I.terminology and fluoroscopic projections.

Cardiac anatomy is complex and its understanding is essential for the interventional arrhythmologist. The first difficulty is the terminology used to describe the location of sites of mapping and ablation. For many years, electrophysiologists have named these positions following the conventional electrocardiographical vocabulary, or the terminology used by surgeons performing arrhythmic surgery. This traditional nomenclature, however, failed to take note of the crucial principle of considering the location of the heart in the human body as viewed in its erect position. In other words, it had failed to use an attitudinally appropriate terminology. Almost 10 years ago, a new attitudinal nomenclature was proposed for the right and left atrioventricular junctions. In this first of a series of reviews of cardiac anatomy as seen by the interventional arrhythmologist, we discuss the role of attitudinally appropriate terminology, and relate this to the projections used for cardiac fluoroscopy, fluorography, and angiography. Throughout our series of reviews, we will illustrate the value of The Visible Human Slice and Surface Server in facilitating the understanding of the fluoroscopic anatomy. (PACE 2010; 497-507).