bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased prevalence of coronary atherosclerosis in cancer survivors: a matched cross-sectional study with coronary CT angiography
Authors: Polomski E A S , Heemelaar J C , De Ronde M E S , Al Jaff A A M , Mertens B J A , Van Dijkman P R M , Jukema J W , Antoni M L 
Published: October 2024

Abstract

Background
Cancer and atherosclerosis share many risk factors. Although cardiovascular disease is highly prevalent among cancer survivors, it is unknown whether coronary atherosclerosis is present at a younger age in patients with a history of cancer.

Purpose
The purpose of this study is to evaluate the prevalence of coronary atherosclerosis in different age groups of patients with a history of cancer compared to matched controls.

Methods
Consecutive patients with a history of cancer aged &gt;30 years who underwent evaluation for coronary artery disease with coronary computed tomography angiography (CCTA) between 2010 and 2023 were included in this cross-sectional study. Patients with a history of cancer were matched 1:2 to a control population without oncological history using propensity score matching. Patients were matched on age, gender, body mass index, hypercholesterolemia, hypertension, diabetes, use of statins and smoking status. The presence of atherosclerosis in the main coronary arteries was compared between the groups.

Results
The study population consisted of 313 patients with an oncological history and 626 matched control patients. The median age during CCTA scan was 59.4 [50.4-67.5] years and 66.1% of the patients were female. Coronary atherosclerosis was observed in 258 (82.4%) patients with a history of cancer compared to 461 (73.6%) control patients with a risk ratio of 1.12 [95% CI: 1.04-1.20], p&lt;0.01. Mainly younger patients with a history of cancer aged between 30-59 years had a significant increased prevalence of coronary atherosclerosis with a risk ratio of 1.18 [1.04-1.33] compared to healthy controls (p=0.02). In our study population, thoracic radiotherapy was not associated with an increased prevalence of coronary atherosclerosis. Calcified plaques were observed more frequently in patients with a history of cancer (14.4% vs. 9.3% respectively, p=0.018).

Conclusion
Patients with a history cancer have a higher prevalence of coronary atherosclerosis as observed on CCTA compared to matched patients without cancer. This effect was most pronounced in younger patients aged 30-59 years. There is an unmet need to define strategies for cardiovascular disease monitoring and prevention in this growing patient population of patients with a history of cancer.Presence of coronary atherosclerosisRadiotherapy and atherosclerosis
The impact of peptide receptor radionucleotide therapy with Lutetium-177 DOTATATE on cardiac metastases in neuroendocrine tumors
Authors: Scalia I , Sonbol B , Farina J M , Pereyra M , Wang Y , Bekaii-Saab T S , Yang M , Connolly H M , Pellikka P A , Herrmann J , Halfdanarson T R , Starr J S , Luis A S , Arsanjani R , Ayoub C 
Published: October 2024

Abstract

Background
Cardiac metastasis from neuroendocrine tumors (NET) is rare and has been thought to potentially result in life threatening sequalae. Peptide receptor radionucleotide therapy (PRRT), such as Lutetium-177 (Lu-177) DOTATATE, has been validated as effective treatment for patients with NET who have progressed on somatostatin analogue (SSA) therapy and more recently suggested for use in SAA-naïve higher risk grade 2 and grade 3 NETs. However, Lu-177 DOTATATE therapy has been found to have potentially serious adverse effects both locally and systemically. Overall, the clinical significance of cardiac metastasis of NET, as well as the safety and efficacy of Lu-177 DOTATATE in this cohort, has not been thoroughly evaluated.

Purpose
This study assessed the outcomes and clinical consequences of cardiac metastatic involvement in patients with NET. Furthermore, this study investigated the safety of Lu-177 DOTATATE therapy in patients with cardiac metastases from NET.

Methods
All patients who underwent 68Ga-DOTATATE positron emission tomography for evaluation of NET across three tertiary centers between 2016 and 2022 were retrospectively evaluated. Patients with evidence of cardiac metastasis were further evaluated. Baseline characteristics, treatment modality, and clinical outcomes including mortality, arrhythmia or conduction disease, carcinoid heart disease, and heart failure admissions were recorded. Patients with cardiac metastases were grouped and compared based on therapeutic modality (conservative therapy with surveillance or SSA, Lu-177 DOTATATE therapy, or surgical resection of metastases).

Results
From 3253 patients with NET, 51 patients were identified to have cardiac metastases (mean age 66.7 ± 12.2 years, 54% male). Three patients underwent surgical resection of cardiac metastases, and in two of whom this was concomitant while undergoing valve surgery for carcinoid heart disease. Patients with cardiac metastasis had significantly higher mortality than patients without cardiac metastasis (HR 2.12, 95%CI 1.00 – 4.52, p = 0.049, Figure 1A). Median follow-up from diagnosis of cardiac metastasis was 3.64 years [IQR 1.59 – 5.64]. There was no significant difference in clinical outcomes between patients that received Lu-177 DOTATATE therapy (n = 27) and conservative therapy (n = 21). Specifically, there was no significant difference in mortality risk at five years post the diagnosis of cardiac metastasis between these groups (p = 0.47, Figure 1B).

Conclusion
Patients with cardiac metastasis from NETs have worse clinical outcomes than NET patients without cardiac metastatic involvement. Lu-177 DOTATATE therapy appears to be safe in patients with cardiac metastasis from NET.Figure 1AFigure 1B
A study to assess the ability of the HFA-ICOS risk stratification tool to predict cancer therapy-related cardiac dysfunction for patients receiving anthracycline chemotherapy
Authors: Bannister C , Tam To B , Byrne A , Simela C , Cannata A , Bromage D , Ghosh A K , Mcdonagh T 
Published: October 2024

Abstract

Introduction
The use of anthracycline chemotherapy is complicated by the risk of developing cancer therapy-related cardiac dysfunction (CTRCD). The Heart Failure Association (HFA) and International Cardio-Oncology Society (ICOS) have jointly published a novel cardiovascular risk stratification tool for patients receiving anthracycline chemotherapy which categorises patients according to their risk of CTRCD (1). The risk tool has not yet been validated for use in the United Kingdom.

Purpose
In this study, we test the ability of the HFA-ICOS risk stratification tool to predict CTRCD for patients receiving anthracycline chemotherapy.

Methods
A retrospective study of patients ≥18 years who received anthracycline chemotherapy between January 2019 to January 2023 at two cardio-oncology centres in the United Kingdom. Patients were eligible if they had ≥1 follow up echocardiogram after the end of anthracycline treatment. Patients receiving HER-2 targeted therapies were excluded. Patients were classified into low/medium/high/very-high risk categories using the HFA/ICOS tool. The prevalence of CTRCD was assessed during the follow up period; a minimum of 6 months after the end of chemotherapy.

Results
288 patients met eligibility criteria for the study. 59 patients (20%) were treated for leukaemia, 104 (36%) lymphoma, 63 (22%) sarcoma and 49 (17%) breast cancer. The mean age was 49±18yrs, with 56% females. The mean cumulative dose of doxorubicin (or equivalent) was 235±104mg/m2. Using the HFA/ICOS tool, 50% of patients were deemed low risk, 31% medium risk, 16% high risk and 3% very high risk at baseline.
Using guideline recommended CTRCD definitions, there was an overall incidence of 9% of symptomatic CTRCD and 22% of asymptomatic CTRCD (Table 1). The incidence of symptomatic CTRCD significantly increased as the baseline risk of CTRCD increased. 20% of patients deemed high or very-high risk at baseline subsequently developed symptomatic CTRCD (Fig 1). Furthermore, patients at high or very-high risk were 4.4 times more likely to develop symptomatic CTRCD than patients who were low risk (OR 4.4, 95% CI 1.7-11.6, p=0.003).
There was no association with baseline risk and the development of asymptomatic CTRCD. The incidence of mild asymptomatic CTRCD may be underestimated due to the lack of routine surveillance with cardiac biomarkers and left ventricular global longitudinal strain (LV GLS) imaging for asymptomatic disease during the study period.

Conclusion
The novel HFA/ICOS risk stratification tool is useful in predicting patients who will develop symptomatic CTRCD in a contemporary UK setting.
A matter of inflammation: CAR T-cell therapy and atrial fibrillation
Authors: Chen S , Gonzalez H , Ghorbanzadeh A , Korleski J , Donisan T , Lewis B , Lin Y , Herrmann J 
Published: October 2024

Abstract

Background
Chimeric antigen receptor (CAR) T-cell therapy has been revolutionary in the treatment of blood cancers, but has been associated with arrhythmias such as atrial fibrillation (AF). Whether the incidence of AF has changed over time and if contributing risk factors are present remains to be defined.

Methods
Leveraging the Mayo Electronic Medical Record, we extracted a cohort of patients who underwent CAR T-cell therapy between 2016 and 2022. From this cohort, we identified those who had a diagnosis of AF at any point. We then defined the endpoint of interest as the first episode of new or recurrent AF during or after CAR T-cell infusion. Fine and Gray subdistribution hazard modeling was used to calculate the association of patient characteristics to the endpoint of interest. Variables with P&lt;0.20 in univariate modeling were chosen for the multivariate model. Significance was defined as P&lt;0.05.

Results
There were 328 patients who underwent CAR T-cell therapy between 2016 and 2022. Of this cohort, 27 (8.2%) patients had a pre-existing diagnosis of AF, of which 6 had recurrence of AF after CAR T (22.2%), while 21 (77.8%) did not. Of the 301 patients without a prior history of AF, 8 (2.7%) patients developed new-onset AF after CAR T. The majority of the 14 new or recurrent AF events (4.3% overall incidence) occurred within 30 days of receiving CAR T (N=10, 71.4%), the remainder after 180 days (Figure 1). No trend in declining incidence over time was noted. Prior AF, neurotoxicity, and inflammation (cytokine release syndrome and macrophage activating syndrome-like (MAS-L)) were strongly associated with the risk of developing new or recurrent AF (Table 1). Only presence of MAS-L remained an independent predictor in the multivariate model (HR 15.4, 95% CI 3.9-61.2, P&lt;0.001).

Conclusion
AF is mainly seen early following CAR T-cell therapy, and mainly in association with severe inflammatory responses. Early and aggressive treatment of CRS and MAS-L may be recommendable for patients undergoing CAR-T therapy, especially for those with a prior history of AF.
Angiotensin II as a linking factor in cardiovascular disease enhanced cancer growth
Authors: Van Berlo B , Civati C , Esposito P , De Keulenaer G W , Guns P J D F , Segers V F M 
Published: October 2024

Abstract

Introduction
Several publications have demonstrated that cardiovascular diseases (CVD) promote tumor growth in mouse models of breast, lung, and colon cancer, suggesting a causal relationship between both diseases. Cancer and CVD share several risk factors and pathophysiological mechanisms, including inflammation, oxidative stress, neurohormonal activation, and immune system dysfunction that combined could explain why patients with CVD are prone to develop cancer.
Recent reports also suggest a link between hypertension and lung cancer, and between cardiac hypertrophy and breast cancer. Angiotensin II (ANGII) is a hormone involved in blood pressure regulation, vascular hemostasis and hypertrophy development. Moreover, ANGII is cancerogenic by increasing proliferation of several cancer cell types. Hence, ANGII could be a link in CVD-induced enhancement of cancer growth. Here, we investigated whether ANGII treatment, and subsequent hypertension and cardiac hypertrophy, could promote cancer growth and metastasis.

Methods
ANGII (2000ng.kg-1.min-1, 4w) was administered to 10w old C57B6/J mice using subcutaneous osmotic minipumps. After 3w, 5*10^5 Lewis lung carcinoma (LLC) cells or 2*10^5 MC38 colon cancer cells were injected onto the right flank of the mice. Tumor growth was monitored over 21d using a digital caliper. Tumor volume was calculated using the following formula:
Length × width² × 0.5
On day 22, mice were sacrificed for further post-mortem analysis. Cardiac echography was performed after 3w of ANGII treatment and before sacrifice to assess cardiac function (data not shown). To assess the formation of cardiac fibrosis trichrome staining’s were performed. In addition, the effect of ANGII on LLC metastasis was investigated. Mice were treated with ANGII as described above. LLC cells, 2*10^6, were injected intravenously (i.v.). Mice were sacrificed 21d after cell injection. Metastatic growth was visualized and quantified by organ weighing and H&E staining.

Results
LLC tumor growth was significantly increased by ANGII treatment. In addition, post-mortem tumor weight was increased (0.62 ± 0.05 g control vs. 1.17 ± 0.24 g ANGII). Furthermore, we found lung weight increased in the ANGII-treated group injected i.v. with LLC cells, indicating an increase in metastatic growth (0.41 ± 0.08 g control vs. 0.57 ± 0.04 g ANGII). Interestingly, MC38 tumor growth decreased in the ANGII treated group as portrayed by the tumor weight (0.42 ± 0.06 g control vs. 0.19 ± 0.05 g ANGII). Figure 1 shows the tumor growth over time and tumor volume, weight post-mortem.

Conclusion
Our data suggest a role for ANGII in CVD-enhanced cancer growth, but also that this effect is not universal, illustrated by a differential effect of ANGII on distinct cancer types. Although further investigation is required to unravel the role of ANGII, screening cancer patients with CVD comorbidities for ANGII involvement might be warranted.
PVC induced QT prolongation for unmasking the LQTS
Authors: Jalabadze K , Ketevani Khetsuriani K K , Ia Avaliani I A , Mindia Butskhridze M B , Giorgi Papiashvili G P , Kakhaber Etsadashvili K E 
Published: October 2024

Abstract

Background
Long QT Syndrome (LQTS) is a congenital or acquired disorder of cardiac ion channels resulting in disturbances of myocardial repolarization, usually manifested by QT prolongation. Diagnostic criteria include the presence of the corrected QT interval (QTc) of at least 480ms (milliseconds) in repeated 12-lead ECGs or confirmed LQTS gene mutations. Patients with LQTS have an increased likelihood of developing life-threatening ventricular arrhythmias and sudden cardiac death. Hence, establishing an accurate diagnosis is crucial.

Purpose
About 50% of patients with LQTS presents with normal or borderline QTc interval. Such cases warrant additional work-up to confirm the diagnosis and can often get overlooked. Based on two separate patient cases we hypothesized that significant QTc interval prolongation occurring after premature ventricular contractions (PVCs) may be a valuable diagnostic clue for suspected LQTS or potentially life-threatening arrhythmia in cases with unclear diagnosis. Above mentioned patients displayed normal baseline QTc interval values that prolonged only after PVC. Later, one of them was diagnosed with congenital and another with drug-induced LQTS (see ECG 1).

Methods
We observed QT interval behavior after PVC in three prespecified groups:(I) Electrocardiographically affected LQTS subjects (QTc ≥480ms) – 10 patients, (II) Control group of unaffected, asymptomatic, otherwise healthy subjects (QTc&lt;460ms) – 72 patients, (III) Index Group of 2 patients with baseline QTc interval of 360-460ms, prolonged only after PVC. 24-hour-ECG records were analyzed. We calculated means of QTc interval before and after PVC in abovementioned three groups and compared them to each other using ANCOVA analysis.

Results
The QT interval after PVC increased 488+23ms in the first and 390+10ms in the second group. In contrast to the index group, the QT interval was prolonged by 380+160ms after PVC. Post-PVC QTc interval mean difference adjusted to covariate, baseline QTc interval values, were statistically insignificant between I and II groups (P=0.o66), but significant between both I -III(P=0.000055) and II-III groups (P&lt;.0001).

Conclusion
There are several studies indicating that PVCs affect QT interval, but the phenomena need more investigation. From the perspective of our study, we have also observed that QTc interval indeed increased after PVCs in both ECG-phenotype positive LQTS individuals and healthy subjects, but not in the extent of the index patients. Our study is limited by the small number of concealed LQTS cases. However, it gives us some basis to think, that this finding could be particularly useful to suspect and unmask concealed LQTS in the patients with non-diagnostic baseline ECG.ECG1
The prognostic significance of Weber and ventilatory CPET classifications in amyloidosis patients
Authors: Santos Patarroyo S , Ortega-Aviles L , Grogan M , Allison T 
Published: October 2024

Abstract

Background
Cardiopulmonary exercise testing (CPET) has emerged as an important tool for risk stratification and prognosis assessment in patients with cardiac diseases. The Weber and Ventilatory Functional Classification have been correlated with outcomes in patients with Heart Failure (HF). Weber classification is based on VO2: Weber class A, peak VO2 &gt;20 mL/kg per minute; class B, peak VO2 16–20 mL/kg per minute; class C, peak VO2 10–16 mL/kg per minute; and class D, peak VO2 ≤10 mL/kg per minute and Ventilatory classification on VE/VCO2 slope I-IV (Figure A). Although VO2 and VE/VCO2 variables have found altered in the amyloidosis population, the applicability of this classification in a cohort of amyloidosis patients and its correlation with all-cause mortality have not been explored.

Purpose
To evaluate if the Weber and Ventilatory Classification of HF predicts mortality amyloidosis patients.

Methods
194 with diagnosis of amyloidosis who underwent CPET from February 2010 to February 2024 were included in this retrospective cohort study. Patients with at least one CPET complete data were included in the analysis. Data on the type of amyloidosis, comorbidities, and echocardiogram were retrieved from medical records. Cohort was divided into two groups according to the Weber Classification: Weber Class A/B and Weber Class C/D. Individuals with CPET studies after heart transplant were excluded from the analysis. Statistical analyses including Fisher’s exact test, chi-square, Tukey-Kramer (TK), Cox regression model analysis, proportional hazards model for time to event, and Kaplan–Meier curves were performed. A p-value &lt;0.05 was considered significant.

Results
Out of the 194 patients, 94 were classified as Weber A-B and 100 as Weber B-C. The age at stress test was similar between the groups: Weber A/B 62.9 ± 11.7 years and Weber C/D 62.3 ± 10.7 years (p=0.087). Ejection Fraction was similar between groups, 32% and 28.9% in A-B and C-D respectively (p =0.207). Higher levels of NT-proBNP were found in the Weber C/D group. The prevalence of comorbidities was balanced among the groups except chronic kidney disease, which was higher in Weber Class C/D (40%) vs (20.2%) in Weber Class A/B (Table 1). Cox analysis revealed a strong association between higher Weber class and the outcome HR 2.36 (1.18 – 4.71) p=0.014. For Higher Ventilatory Class (Group III-IV) similar results were found HR 2.95 (1.60 – 5.45) p=0.005(Table 2). Mortality was significantly higher during the follow-up in the Weber C/D group (25%) vs (10%) in the Weber A-B group p=0.007(Figure D).

Conclusion
Weber and ventilatory Classification based on CPET, besides predicting outcomes in patients with cardiac disease, are strong predictors of mortality in patients with amyloidosis. These findings suggest that this patient group benefits from earlier stratification to assess prognosis and the potential requirement for transplant independently from other factors.
Low clinical utility of global longitudinal strain in a real-world breast cancer population
Authors: Ruane L , Prasad S , Atherton J 
Published: October 2024

Abstract

Background
The 2022 European Society of Cardiology (ESC) Cardio-Oncology guidelines recommend the use of global longitudinal strain (GLS) to detect mild asymptomatic cancer therapy related cardiac dysfunction (ma-CTRCD). However, it remains unknown how to best manage these patients in order to prevent clinically significant CTRCD.

Purpose
To assess the course and outcomes of breast cancer patients meeting criteria for ma-CTRCD.

Methods
Echocardiograms and medical records were assessed for breast cancer patients receiving trastuzumab or an anthracycline, who underwent serial echocardiographic monitoring, including routine GLS. CTRCD was defined as an absolute decline in LVEF of &gt;10% to &lt;50%. ma-CTRCD was defined as a relative decline in average GLS of &gt;15%, in the absence of significant LVEF decline. Normal was defined as no significant change in LVEF or GLS during cancer therapy. Clinical and echocardiographic course post ma-CTRCD detection was assessed. Baseline risk factors were compared between the three groups.

Results
878 echocardiograms from 258 patients were analysed. GLS analysis was available in 76% of echocardiograms. CTRCD occurred in 23 (9%) and ma-CTRCD in 63 (24%). Only eight ma-CTRCD patients had management altered (cancer therapy withheld/ceased in three and heart failure medication commenced in six). Only two ma-CTRCD patients subsequently developed CTRCD, and GLS improved in 74%. Compared to the normal group (172, 67%), at baseline the ma-CTRCD group had higher average GLS (-21.8 vs -19.4, p&lt;0.0001) and less borderline/abnormal average GLS (4% vs 36%, p&lt;0.004).

Conclusion
Isolated declines in GLS are common and may have low clinical utility in preventing CTRCD. The findings support ESC guideline recommendations that cancer therapy should not be withheld in these patients. Those with higher baseline GLS may be more prone to clinically insignificant declines in GLS during cancer therapy.