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Pubblicazioni recenti - cardio-oncology
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International Consensus Statement on the diagnosis, multidisciplinary management and lifelong care of individuals with achondroplasia.
Nat Rev Endocrinol2021 Nov;():. doi: 10.1038/s41574-021-00595-x.
Savarirayan Ravi, Ireland Penny, Irving Melita, Thompson Dominic, Alves Inês, Baratela Wagner A R, Betts James, Bober Michael B, Boero Silvio, Briddell Jenna, Campbell Jeffrey, Campeau Philippe M, Carl-Innig Patricia, Cheung Moira S, Cobourne Martyn, Cormier-Daire Valérie, Deladure-Molla Muriel, Del Pino Mariana, Elphick Heather, Fano Virginia, Fauroux Brigitte, Gibbins Jonathan, Groves Mari L, Hagenäs Lars, Hannon Therese, Hoover-Fong Julie, Kaisermann Morrys, Leiva-Gea Antonio, Llerena Juan, Mackenzie William, Martin Kenneth, Mazzoleni Fabio, McDonnell Sharon, Meazzini Maria Costanza, Milerad Josef, Mohnike Klaus, Mortier Geert R, Offiah Amaka, Ozono Keiichi, Phillips John A, Powell Steven, Prasad Yosha, Raggio Cathleen, Rosselli Pablo, Rossiter Judith, Selicorni Angelo, Sessa Marco, Theroux Mary, Thomas Matthew, Trespedi Laura, Tunkel David, Wallis Colin, Wright Michael, Yasui Natsuo, Fredwall Svein Otto,
Abstract
Achondroplasia, the most common skeletal dysplasia, is characterized by a variety of medical, functional and psychosocial challenges across the lifespan. The condition is caused by a common, recurring, gain-of-function mutation in FGFR3, the gene that encodes fibroblast growth factor receptor 3. This mutation leads to impaired endochondral ossification of the human skeleton. The clinical and radiographic hallmarks of achondroplasia make accurate diagnosis possible in most patients. However, marked variability exists in the clinical care pathways and protocols practised by clinicians who manage children and adults with this condition. A group of 55 international experts from 16 countries and 5 continents have developed consensus statements and recommendations that aim to capture the key challenges and optimal management of achondroplasia across each major life stage and sub-specialty area, using a modified Delphi process. The primary purpose of this first International Consensus Statement is to facilitate the improvement and standardization of care for children and adults with achondroplasia worldwide in order to optimize their clinical outcomes and quality of life.
© 2021. Springer Nature Limited.
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Impact of -Related Metabolic Syndrome Parameters on Arterial Hypertension.
Microorganisms2021 Nov;9(11):. doi: 2351.
Kountouras Jannis, Papaefthymiou Apostolis, Polyzos Stergios A, Deretzi Georgia, Vardaka Elisabeth, Soteriades Elpidoforos S, Tzitiridou-Chatzopoulou Maria, Gkolfakis Paraskevas, Karafyllidou Kyriaki, Doulberis Michael,
Abstract
Arterial hypertension is a risk factor for several pathologies, mainly including cardio-cerebrovascular diseases, which rank as leading causes of morbidity and mortality worldwide. Arterial hypertension also constitutes a fundamental component of the metabolic syndrome. infection is one of the most common types of chronic infection globally and displays a plethora of both gastric and extragastric effects. Among other entities, has been implicated in the pathogenesis of the metabolic syndrome. Within this review, we illustrate the current state-of-the-art evidence, which may link several components of the -related metabolic syndrome, including non-alcoholic fatty liver disease and arterial hypertension. In particular, current knowledge of how exerts its virulence through dietary, inflammatory and metabolic pathways will be discussed. Although there is still no causative link between these entities, the emerging evidence from both basic and clinical research supports the proposal that several components of the infection-related metabolic syndrome present an important risk factor in the development of arterial hypertension. The triad of infection, the metabolic syndrome, and hypertension represents a crucial worldwide health problem on a pandemic scale with high morbidity and mortality, like COVID-19, thereby requiring awareness and appropriate management on a global scale.
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Immune Checkpoint Inhibitor Therapy Induces Inflammatory Activity in the Large Arteries of Lymphoma Patients under 50 Years of Age.
Biology (Basel)2021 Nov;10(11):. doi: 1206.
Calabretta Raffaella, Staber Philipp B, Kornauth Christoph, Lu Xia, Binder Patrick, Pichler Verena, Mitterhauser Markus, Haug Alexander, Li Xiang, Hacker Marcus,
Abstract
Immune checkpoint inhibitors (ICI) have transformed the management of various cancers. Serious and potentially fatal cardiovascular toxicity, as well as a progression of atherosclerosis, have been described, mainly in elderly and comorbid patients. We investigated 117 arterial segments of 12 young (under 50 years of age), otherwise healthy lymphoma patients pre/post-ICI treatment using 2-[18F]fluorodeoxyglucose (FDG) positron emission tomography (PET). Maximum FDG standardized uptake values (SUV) and target-to-background ratios (TBRs) were calculated along arterial segments. Additionally, metabolic activities (SUV) of the bone marrow, spleen, and liver were analyzed. The levels of high-sensitivity C-reactive protein (hsCRP) were assessed. ICI therapy induced arterial inflammatory activity, detected by increased TBR in arterial segments without pre-existing inflammation (TBRneg_pre = 1.20 ± 0.22 vs. TBRneg_post = 1.71 ± 0.45,
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Endothelial cell biomarkers in critically ill COVID-19-patients with encephalitis.
J Neurochem2021 Nov;():. doi: 10.1111/jnc.15545.
Altmayer Victor, Ziveri Jason, Frère Corinne, Salem Joe-Elie, Weiss Nicolas, Cao Albert, Marois Clémence, Rohaut Benjamin, Demeret Sophie, Bourdoulous Sandrine, Le Guennec Loic,
Abstract
COVID-19 is associated with encephalitis in critically ill patients and endothelial dysfunction seems to contribute to this life-threatening complication. Our objective was to determine the hallmark of endothelial activation in COVID-19 related encephalitis. In an observational study in intensive care unit (ICU), we compared vascular biomarkers of critically ill COVID-19 patients with or without encephalitis. To be classified in the Encephalitis group, patients had to have new onset of central neurologic symptom, and pathological findings on either brain magnetic resonance imaging (MRI) and/or electroencephalogram (EEG). Among the 32 critically ill COVID-19 consecutive patients, 21 were categorized in the Control group and 11 in the Encephalitis group. Encephalitis patients had a longer ICU-stay than Control patients (median length [25 -75 percentile] of 52[16-79] versus 20.5[11-44] days respectively, p=0.04). Nine-months overall follow-up mortality reached 21% (7/32 patients), with mortality rates in the Encephalitis-group and the Control group of 27% and 19% respectively. Encephalitis was associated with significant higher release of soluble endothelial activation markers (sE-selectin, Tumor-Necrosis-Factor-? (TNF-?), Interleukin-6, Placental Growth Factor and Thrombomodulin), but these increases were correlated with TNF-? plasmatic levels. The hypoxia-inducible protein Angiopoietin-like-4 (ANGPTL4) was at significantly higher levels in Encephalitis patients compared to Control patients (p=0.0099), and in contrary to the other increased factors, was not correlated with TNF-? levels (r=0.2832, p=0.1163). Our findings suggest that COVID-19 related encephalitis is a cytokine-associated acute brain dysfunction. ANGPTL4 was the only elevated marker found in Encephalitis patients, which was not correlated with systemic inflammation, suggesting that ANGPTL4 might be a relevant factor to predict encephalitis in critically ill COVID-19 patients.
This article is protected by copyright. All rights reserved.
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Coronary vasomotor dysfunction portends worse outcomes in patients with breast cancer.
J Nucl Cardiol2021 Nov;():. doi: 10.1007/s12350-021-02825-1.
Divakaran Sanjay, Caron Jesse P, Zhou Wunan, Hainer Jon, Bibbo Courtney F, Skali Hicham, Taqueti Viviany R, Dorbala Sharmila, Blankstein Ron, Groarke John D, Nohria Anju, Di Carli Marcelo F,
Abstract
BACKGROUND:
Impaired MFR in the absence of flow-limiting CAD is associated with adverse events. Cardiovascular disease is an important cause of morbidity and mortality in patients with breast cancer. We sought to test the utility of MFR to predict outcomes in a cohort of patients with breast cancer.
METHODS:
We retrospectively studied consecutive patients with breast cancer or breast cancer survivors who underwent cardiac stress PET imaging from 2006 to 2017 at Brigham and Women's Hospital. Patients with a history of clinically overt CAD, LVEF
RESULTS:
The final cohort included 87 patients (median age 69.0 years, 98.9% female, mean MFR 2.05). Over a median follow-up of 7.6 years after PET, the lowest MFR tertile was associated with higher cumulative incidence of MACE (adjusted subdistribution hazard ratio 4.91; 95% CI 1.68-14.38; p = 0.004) when compared with the highest MFR tertile.
CONCLUSIONS:
In patients with breast cancer, coronary vasomotor dysfunction was associated with incident cardiovascular events. MFR may have potential as a risk stratification biomarker among patients with/survivors of breast cancer.
© 2021. American Society of Nuclear Cardiology.
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High Sensitivity Troponin T and NT-proBNP in Patients Receiving Chimeric Antigen Receptor (CAR) T-Cell Therapy.
Clin Hematol Int2021 Sep;3(3):96-102. doi: 10.2991/chi.k.210718.001.
Hu Jiun-Ruey, Patel Ameet, Huang Shi, Su Yan Ru, Dahlman Kimberly B, Tomasek Kelsey, Zhang Yueli, O'Neil Richard T, O'Neal Jamye F, Turker Isik, Johnson Douglas B, Salem Joe-Elie, Moslehi Javid J, Oluwole Olalekan,
Abstract
Retrospective studies suggest that chimeric antigen receptor T-cell (CAR T) therapy may lead to cardiac injury, but this has not been assessed systematically or prospectively. In this prospective study of 40 patients who received CAR T, we systematically measured high-sensitivity troponin T (hsTropT) and N-terminal pro-B natriuretic peptide (NTproBNP) at baseline and on day 1, days 7, and 21 after CAR T. Biomarker elevations with respect to timepoint and cytokine release syndrome (CRS) status were examined using repeated measure analysis of variance. hsTropT did not differ with time or with the presence of grade 2 CRS. Median hsTropT was 12.1 ng/L [interquartile range (IQR): 9.2, 20.1] at baseline, 13.1 ng/L (IQR: 9.6, 24.2) at day 1, 11.9 ng/L (IQR: 9.6, 18.0) at day 7, and 15.3 ng/L (10.8, 20.2) at day 21. In contrast, NTproBNP rose on day 1 ( = 0.0002) and day 7 ( = 2.7 × 10), and the degree of elevation differed by the presence of grade 2 CRS ( = 0.002). Median NTproBNP was 179 pg/mL (IQR: 116, 325) at baseline, 357 pg/mL (IQR: 98, 813) at day 1, 420 pg/mL (IQR: 239, 1242) at day 7, and 177 pg/mL (IQR: 80, 278) at day 21. In conclusion, hsTropT l did not differ across timepoints after CAR T therapy, but NTproBNP rose at day 7, the prognostic implications of which should be the target of future research, as the indications for this therapy expand.
© 2021 International Academy for Clinical Hematology. Publishing services by Atlantis Press International B.V.
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Editorial: Recent Advances in Cardiotoxicity Testing.
Front Pharmacol2021 ;12():798189. doi: 10.3389/fphar.2021.798189.
Mohamed Tamer M A, Moslehi Javid, Satin Jonathan,
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Differentiation syndrome-induced Myopericarditis in the induction therapy of acute Promyelocytic leukemia: a case report.
Cardiooncology2021 Nov;7(1):39. doi: 10.1186/s40959-021-00124-9.
Shenoy Shabari Mangalore, Di Vitantonio Thomas, Plitt Anna, Perez-Johnston Rocio, Gutierrez Jillian, Knorr David A, Stein Eytan M, Liu Jennifer E, Feldman Stephanie,
Abstract
BACKGROUND:
All trans retinoic acid (ATRA) has revolutionized the treatment and outcomes of patients with Acute Promyelocytic Leukemia (APL). Induction therapy with ATRA is associated with the rare but potentially fatal complication of differentiation syndrome. While the presentation of this syndrome is varied, myopericarditis as a manifestation of differentiation syndrome is often fatal and rarely reported in literature. We present a case of myopericarditis as the sole manifestation of differentiation syndrome in a patient on induction therapy with ATRA and arsenic trioxide for APL.
CLINICAL PRESENTATION:
A 62?year old woman with remote history of breast and uterine cancer presented to the hospital for expedited work up of easy bruising and expanding hematomas. She was diagnosed with APL with peripheral blood and bone marrow cytogenetics revealing t (15;17) translocation and initiated on induction therapy with ATRA and ATO as well as steroids for differentiation syndrome prophylaxis. Eighteen days into induction therapy, patient developed pleuritic chest pain, elevated cardiac biomarkers, ECG changes suggestive of pericarditis. Cardiac magnetic resonance imaging showed patchy multifocal sub-epicardial late gadolinium enhancement and elevated T2 signal consistent with acute myopericarditis. Given the timing of symptom onset and lack of other identifiable cause, patient was diagnosed with differentiation syndrome- induced myopericarditis and promptly initiated on high dose steroids with rapid improvement in symptoms, ECG, and cardiac biomarkers. Patient successfully resumed dose-reduced ATRA and arsenic trioxide without complication.
CONCLUSION:
Myopericarditis can be the sole manifestation of differentiation syndrome and the presentation may be atypical owing to the use of prophylactic steroids as illustrated in our patient's case. A high index of suspicion for differentiation syndrome, multimodality imaging, and prompt input from multidisciplinary providers is crucial for making the timely diagnosis and initiating life-saving treatment.
© 2021. The Author(s).
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Chemotherapy-associated cardiomyopathy: Mechanisms of toxicity and cardioprotective strategies.
Pharmacotherapy2021 Nov;():. doi: 10.1002/phar.2638.
Veeder Justin A, Hothem Lauren N, Cipriani Amber E, Jensen Brian C, Rodgers Jo E,
Abstract
OBJECTIVE:
To describe the proposed mechanisms of chemotherapy-associated cardiomyopathy (CAC) and potential cardioprotective therapies for CAC including a comprehensive review of existing systematic analyses, guideline recommendations, and ongoing clinical trials.
DATA SOURCES:
A literature search of MEDLINE was performed (from 1990 to June 2020) using the following search terms: anthracycline, trastuzumab, cardiomyopathy, cardiotoxicity, primary prevention, angiotensin-converting enzyme inhibitor (ACEI), angiotensin receptor blocker (ARB), beta blocker, dexrazoxane (DEX) as well as using individual names from select therapeutic categories.
STUDY SELECTION AND DATA EXTRACTION:
Existing English language systematic analyses and guidelines were considered.
DATA SYNTHESIS:
The mechanisms of CAC are multifaceted, but various cardioprotective therapies target many of these pathways. To date, anthracyclines and HER-2 targeted therapies have been the focus of cardioprotective trials to date as they are the most commonly implicated therapies in CAC. While traditional neurohormonal antagonists (ACEIs, ARBs, and beta blockers) and DEX performed favorably in many small clinical trials, the quality of available evidence remains limited. Hence, major guidelines lack consensus on an approach to primary prevention of CAC. Given the uncertain role of preventive therapy, monitoring for a symptomatic or asymptomatic decline in LV function is imperative with prompt evaluation should this occur. Numerous ongoing randomized controlled trials seek to either confirm the findings of these previous studies or identify new therapeutic agents to prevent CAC. Clinical implications are derived from the available literature as well as current guideline recommendations for CAC cardioprotection.
CONCLUSION:
At this time, no single therapy has a clear cardioprotective benefit in preventing CAC nor is any therapy strongly recommended by current guidelines. Additional studies are needed to determine the optimal preventative regimens.
© 2021 Pharmacotherapy Publications, Inc.
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Corrigendum: Imaging Protocol, Feasibility, and Reproducibility of Cardiovascular Phenotyping in a Large Tri-Ethnic Population-Based Study of Older People: The Southall and Brent Revisited (SABRE) Study.
Front Cardiovasc Med2021 ;8():769050. doi: 10.3389/fcvm.2021.769050.
Al Saikhan Lamia, Alobaida Muath, Bhuva Anish, Chaturvedi Nish, Heasman John, Hughes Alun D, Jones Siana, Eastwood Sophie, Manisty Charlotte, March Katherine, Ghosh Arjun K, Mayet Jamil, Oguntade Ayodipupo, Tillin Therese, Williams Suzanne, Wright Andrew, Park Chloe,
Abstract
[This corrects the article DOI: 10.3389/fcvm.2020.591946.].
Copyright © 2021 Al Saikhan, Alobaida, Bhuva, Chaturvedi, Heasman, Hughes, Jones, Eastwood, Manisty, March, Ghosh, Mayet, Oguntade, Tillin, Williams, Wright and Park.
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Pre-existing cardiovascular disease increases risk of atrial arrhythmia and mortality in cancer patients treated with Ibrutinib.
Cardiooncology2021 Nov;7(1):38. doi: 10.1186/s40959-021-00125-8.
Avalon Juan Carlo, Fuqua Jacob, Miller Tyler, Deskins Seth, Wakefield Chelby, King Austin, Inderbitzin-Brooks Sonya, Bianco Christopher, Veltri Lauren, Fang Wei, Craig Michael, Kanate Abraham, Ross Kelly, Malla Midhun, Patel Brijesh,
Abstract
BACKGROUND:
Ibrutinib is a Bruton's tyrosine kinase inhibitor used in the treatment of hematological malignancies. The most common cardiotoxicity associated with ibrutinib is atrial arrhythmia (atrial fibrillation and flutter). It is known that patients with cardiovascular disease (CVD) are at an increased risk for developing atrial arrhythmia. However, the rate of atrial arrhythmia in patients with pre-existing CVD treated with ibrutinib is unknown.
OBJECTIVE:
This study examined whether patients with pre-existing CVD are at a higher risk for developing atrial arrhythmias compared to those without prior CVD.
METHODS:
A single-institution retrospective chart review of patients with no prior history of atrial arrhythmia treated with ibrutinib from 2012 to 2020 was performed. Patients were grouped into two cohorts: those with CVD (known history of coronary artery disease, heart failure, pulmonary hypertension, at least moderate valvular heart disease, or device implantation) and those without CVD. The primary outcome was incidence of atrial arrhythmia, and the secondary outcomes were all-cause mortality, risk of bleeding, and discontinuation of ibrutinib. The predictors of atrial arrhythmia (namely atrial fibrillation) were assessed using logistic regression. A Cox-Proportional Hazard model was created for mortality.
RESULTS:
Patients were followed for a median of 1.1?years. Among 217 patients treated with ibrutinib, the rate of new-onset atrial arrhythmia was nearly threefold higher in the cohort with CVD compared to the cohort without CVD (17% vs 7%, p?=?0.02). Patients with CVD also demonstrated increased adjusted all-cause mortality (OR 1.9, 95% CI 1.06-3.41, p?=?0.01) and decreased survival probability (43% vs 54%, p?=?0.04) compared to those without CVD over the follow-up period. There were no differences in risk of bleeding or discontinuation between the two cohorts.
CONCLUSIONS:
Pre-existing cardiovascular disease was associated with significantly higher rates of atrial arrhythmia and mortality in patients with hematological malignancies managed with ibrutinib.
© 2021. The Author(s).
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An ongoing evolution of cardio-oncology with the rapid development of modern immunotherapy.
Int J Cardiol -
Missense mutation in selenocysteine synthase causes cardio-respiratory failure and perinatal death in mice which can be compensated by selenium-independent GPX4.
Redox Biol2021 Nov;48():102188. doi: S2213-2317(21)00348-7.
Fradejas-Villar Noelia, Zhao Wenchao, Reuter Uschi, Doengi Michael, Ingold Irina, Bohleber Simon, Conrad Marcus, Schweizer Ulrich,
Abstract
Selenoproteins are a small family of proteins containing the trace element selenium in form of the rare amino acid selenocysteine (Sec), which is decoded by the UGA codon. In humans, a number of pathogenic variants in genes encoding distinct selenoproteins or selenoprotein biosynthesis factors have been identified. Pathogenic variants in selenocysteine synthase (SEPSECS), which catalyzes the last step in Sec-tRNA biosynthesis, were reported in children suffering from progressive cerebello-cerebral atrophy. To understand the pathomechanism associated with SEPSECS deficiency, we generated a novel mouse model recapitulating the respective human pathogenic p.Y334C variant in the murine Sepsecs gene (Sepsecs). Unlike in patients, pups homozygous for the p.Y334C variant died perinatally with signs of cardio-respiratory failure. Perinatal death is reminiscent of the Sedaghatian spondylometaphyseal dysplasia disorder in humans, which is caused by pathogenic variants in the gene encoding the selenoprotein and key ferroptosis regulator glutathione peroxidase 4 (GPX4). Protein expression levels of distinct selenoproteins in Sepsecs mice were found to be generally reduced in brain and isolated cortical neurons, while transcriptomics analysis uncovered an upregulation of NRF2-regulated genes. Crossbreeding of Sepsecs mice with mice harboring a targeted mutation of the catalytically active Sec to Cys in GPX4 rescued perinatal death of Sepsecs mice, showing that the cardio-respiratory defects of Sepsecs mice were caused by the lack of GPX4. Like in Sepsecs mice, selenoprotein expression levels remained low and NRF2-regulated genes remained highly expressed in these compound mutant mice, indicating that selenium-independent GPX4, along with a sustained antioxidant response are sufficient to compensate for dysfunctional Sec-tRNA biosynthesis. Our findings imply that children with pathogenic variants in SEPSECS or GPX4 may even benefit from treatments that incompletely compensate for impaired GPX4 activity.
Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.
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Incidence, risk factors, and mortality of atrial fibrillation in breast cancer: a SEER-Medicare analysis.
Eur Heart J2021 Nov;():. doi: ehab745.
Guha Avirup, Fradley Michael G, Dent Susan F, Weintraub Neal L, Lustberg Maryam B, Alonso Alvaro, Addison Daniel,
Abstract
AIMS :
The national incidence, risk factors, and associated mortality of atrial fibrillation (AF) in breast cancer patients are unknown.
METHODS AND RESULTS :
Using the Surveillance, Epidemiology, and End Results-Medicare-linked database, we identified females, ?66?years old, with a new primary diagnosis of breast cancer from 2007 through 2014. These patients were individually matched 1:1 to Medicare enrolees without cancer, and each pair was followed for 1 year to identify a primary outcome of AF. Cumulative incidence was calculated using competing risk survival statistics. Following this, identifying risk factors of AF among breast cancer patients was conducted using the adjusted Cox proportional hazards model. Finally, Kaplan-Meier methods and adjusted Cox proportional hazards modelling were performed to estimate mortality in breast cancer patients with incident and prevalent AF. This study included 85 423 breast cancer patients. Among these 9425 (11.0%) had AF diagnosis prior to the breast cancer diagnosis. New-onset AF was diagnosed in 2993 (3.9%) patients in a 1-year period after the breast cancer diagnosis [incidence 3.3%, 95% confidence interval (CI) 3.0-3.5%, at 1?year; higher rate in the first 60?days (0.6%/month)]. Comparatively, the incidence of new-onset AF in matched non-cancer controls was 1.8% (95% CI 1.6-2.0%). Apart from traditional demographic and cardiovascular risk factors, breast cancer stage was strongly associated with the development of AF [American Joint Committee on Cancer (AJCC) Stage II/III/IV vs. I: adjusted hazard ratio (aHR) 1.51/2.63/4.21, respectively]. New-onset AF after breast cancer diagnosis (aHR 3.00) is associated with increased 1-year cardiovascular mortality.
CONCLUSION :
AF incidence is significantly higher in women after a breast cancer diagnosis. Higher breast cancer stages at diagnos are significantly associated with a higher risk of AF. New-onset AF in the new breast cancer diagnosis setting increases 1-year cardiovascular mortality but not breast cancer-related mortality.
KEY QUESTION:
What are the incidence, prevalence, risk factors and mortality outcomes of atrial fibrillation (AF) in a multi-ethnic representative United States cohort of breast cancer patients?
KEY FINDING:
Annual incidence for AF is 3.9% with highest rate in the first 60 days after cancer diagnosis. Cancer stage and grade are the strongest risk factors for AF. New onset AF after breast cancer increases all-cause and cardiovascular mortality.
TAKE HOME MESSAGE:
AF incidence is higher in breast cancer patients and is associated with later stage and grade at diagnosis of breast cancer. Involving cardio-oncology in those who develop AF after cancer diagnosis should be encouraged to improve their cardiovascular and overall prognosis.
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.
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Multidisciplinary surgical approach for renal cell carcinoma with inferior vena cava tumor thrombus.
Surg Today2021 Nov;():. doi: 10.1007/s00595-021-02415-1.
Yano Daisuke, Yokoyama Yukihiro, Tokuda Yoshiyuki, Kato Masashi, Mashiko Yuji, Kuwabara Fumiaki, Ebata Tomoki, Usui Akihiko,
Abstract
PURPOSES:
The optimal surgical management of renal cell carcinoma with tumor thrombus within the inferior vena cava (IVC) remains to be clarified.
METHODS:
Sixteen consecutive cases were reviewed. Incision, the IVC clamping position, and the venous drainage procedure were modified according to the tumor thrombus extension level: level I or II (below the hepatic vein, n?=?8), level III (above the hepatic vein but below the right atrium, n?=?5), and level IV (extending into the right atrium, n?=?3).
RESULTS:
For level I or II, resection could be simply achieved by clamping the IVC below the hepatic vein, without hemodynamic collapse. For level III, clamping the IVC above the hepatic vein and the hepatoduodenal ligament was required. Venous drainage from the lower body (cannulation to distal IVC) and portal system (cannulation to ileocolic vein) were applied. When opening the IVC, the significant backflow was controlled using cardiopulmonary bypass with drop-in suckers. For level IV, median sternotomy, exposure of the right atrium, and cardiopulmonary bypass were mandatory. With the combination of these approaches, the perioperative mortality rate was 0% and the 5-year overall survival rate was 52%.
CONCLUSIONS:
A multidisciplinary surgical approach is essential, especially for level III and IV cases.
© 2021. The Author(s) under exclusive licence to Springer Nature Singapore Pte Ltd.
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Targeted treatments of AL and ATTR amyloidosis.
Heart Fail Rev2021 Nov;():. doi: 10.1007/s10741-021-10180-z.
Chandrashekar Pranav, Desai Anish K, Trachtenberg Barry H,
Abstract
The therapeutic landscape for cardiac amyloidosis is rapidly evolving. In the last decade, our focus has shifted from dealing with the inevitable complications of continued extracellular infiltration of amyloid fibrils to earlier identification of these patients with prompt initiation of targeted therapy to prevent further deposition. Although much of the focus on novel targeted therapies is within the realm of transthyretin amyloidosis, light chain amyloidosis has benefited due to an overlap particularly in the final common pathway of fibrillogenesis and extraction of amyloid fibrils from the heart. Here, we review the targeted therapeutics for transthyretin and light chain amyloidosis. For transthyretin amyloidosis, the list of current and future therapeutics continues to evolve; and therefore, it is crucial to become familiar with the underlying mechanistic pathways of the disease. Although targeted therapeutic choices in AL amyloidosis are largely driven by the hematology team, the cardiac adverse effect profiles of these therapies, particularly in those with advanced amyloidosis, provide an opportunity for early recognition to prevent decompensation and can help inform recommendations regarding therapy changes when required.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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Evaluation of Vascular Health of E-Beta Thalassemia Patients: Effect of Iron Overload.
J Assoc Physicians India2021 Nov;69(11):11-12.
De Dibyendu, Nath Uttam Kumar, Chakrabarti Prantar,
Abstract
Hb E-? thalassemia is the most common form of hemoglobinopathy in Southeast Asia and eastern India. Iron overload resulting from blood transfusion and increased intestinal iron absorption promotes the formation of reactive oxygen species (ROS), leading to oxidative stress, organ dysfunction, and tissue damage. Of these, cardiovascular complications are the leading cause of mortality. Impaired endothelial function is a biomarker of vascular health in patients with cardiovascular risks. Therefore, assessment of endothelial function is a useful prognostic tool. In the present study, 60 E- ? thalassemia patients and 60 healthy, age, sex matched control subjects were taken. The mean hemoglobin and ferritin of thalassemic patients were 7.43gm/dl and 1032 mcg/dl respectively. The vascular health was compared by measuring flow-mediated vasodialation (FMD), arterial elastic parameters, and carotid intima-medial thickness (CIMT). There was lower FMD (7.49%) and higher CIMT (0.46mm) in thalassemic group than control (10.52 % and 0.36mm respectively) (p value< 0.05). Also arterial stiffness is elevated and arterial distensibility is lower in thalassemic patients than control. Among the thalassemic patients FMD or CIMT did not correlate with serum ferritin value. So, the E- ? thalassemia patients had poor vascular health and are at a higher risk of developing atherosclerosis and cardio-vascular complication than normal population. The vascular dysfunction does not correlate with serum ferritin value, so regular monitoring with Doppler study is required for early diagnosis of subclinical atherosclerosis in this group of patients. However the effects of chelation therapy, Hydroxyurea, or other targeted therapies needs to be validated by further study.
© Journal of the Association of Physicians of India 2011.
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Distribution of subcutaneous and intermuscular fatty tissue of the mid-thigh measured by MRI-A putative indicator of serum adiponectin level and individual factors of cardio-metabolic risk.
PLoS One2021 ;16(11):e0259952. doi: 10.1371/journal.pone.0259952.
Hassler Eva Maria, Deutschmann Hannes, Almer Gunter, Renner Wilfried, Mangge Harald, Herrmann Markus, Leber Stefan, Michenthaler Manuela, Staszewski Alexander, Gunzer Felix, Partl Richard, Reishofer Gernot,
Abstract
Obesity and metabolic syndrome (MetS) are associated with hypoadiponectinemia. On the contrary, studies revealed correlations between the amount of subcutaneous adipose tissue (SAT) and higher serum adiponectin levels. Furthermore, independent association of intermuscular adipose tissue (IMAT) deposit in the thigh with cardiometabolic risk factors (including total blood cholesterol, low-density lipoprotein (LDL), and triglycerides), and decreased insulin sensitivity, as MetS components, are sufficiently described. The combined relationship of thigh IMAT and SAT with serum adiponectin, leptin levels, and cardiometabolic risk factors have not been investigated till date. Since both SAT and IMAT play a role in fat metabolism, we hypothesized that the distribution pattern of SAT and IMAT in the mid-thigh might be related to adiponectin, leptin levels, and serum lipid parameters. We performed adipose tissue quantification using magnetic resonance imaging (MRI) of the mid-thigh in 156 healthy volunteers (78 male/78 female). Laboratory measurements of lipid panel, serum adiponectin, and leptin levels were conducted. Total serum adiponectin level showed a significant correlation with the percentage of SAT of the total thigh adipose tissue (SAT/ (IMAT+SAT)) for the whole study population and in sex-specific analysis. Additionally, SAT/(IMAT+SAT) was negatively correlated with known cardiometabolic risk factors such as elevated total blood cholesterol, LDL, and triglycerides; but positively correlated with serum high-density lipoprotein. In multiple linear regression analysis, (SAT/(IMAT+SAT)) was the most strongly associated variable with adiponectin. Interestingly, leptin levels did not show a significant correlation with this ratio. Adipose tissue distribution in the mid-thigh is not only associated to serum adiponectin levels, independent of sex. This proposed quantitative parameter for adipose tissue distribution could be an indicator for individual factors of a person`s cardiometabolic risk and serve as additional non-invasive imaging marker to ensure the success of lifestyle interventions.
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Clinical Profile and Prognosis of a Real-World Cohort of Patients With Moderate or Severe Cancer Therapy-Induced Cardiac Dysfunction.
Front Cardiovasc Med2021 ;8():721080. doi: 10.3389/fcvm.2021.721080.
Esteban-Fernández Alberto, Carvajal Estupiñan Juan Fernando, Gavira-Gómez Juan José, Pernas Sonia, Moliner Pedro, Garay Alberto, Sánchez-González Álvaro, Fernández-Rozas Inmaculada, González-Costello José,
Abstract
Cancer therapy-related cardiac dysfunction (CTRCD) is a common cause of cancer treatment withdrawal, related to the poor outcomes. The cardiac-specific treatment could recover the left ventricular ejection fraction (LVEF). We analyzed the clinical profile and prognosis of patients with CTRCD in a real-world scenario. A retrospective study that include all the cancer patients diagnosed with CTRCD, defined as LVEF
Copyright © 2021 Esteban-Fernández, Carvajal Estupiñan, Gavira-Gómez, Pernas, Moliner, Garay, Sánchez-González, Fernández-Rozas and González-Costello.
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Radiotherapy and High-Dose Interleukin-2: Clinical and Immunological Results of a Proof of Principle Study in Metastatic Melanoma and Renal Cell Carcinoma.
Front Immunol2021 ;12():778459. doi: 10.3389/fimmu.2021.778459.
Bulgarelli Jenny, Piccinini Claudia, Petracci Elisabetta, Pancisi Elena, Granato Anna Maria, de Rosa Francesco, Guidoboni Massimo, Petrini Massimiliano, Ancarani Valentina, Foschi Giovanni, Romeo Antonino, Tontini Luca, De Giorgi Ugo, Lolli Cristian, Gentili Giorgia, Valmorri Linda, Rossi Alice, Ferroni Fabio, Casadei Carla, Cortesi Pietro, Crudi Laura, Ridolfi Laura,
Abstract
High-dose interleukin-2 (HD IL-2) has curative potential in metastatic melanoma (MM) and renal cell carcinoma (RCC). Radiotherapy (RT) kills cancer cells and induces immunomodulatory effects. Prospective trials exploring clinical and immunological properties of combined RT/HD IL-2 are still needed. We designed a phase II, single-arm clinical trial for patients with MM and RCC. The treatment schedule consisted of 3 daily doses of 6-12 Gy of RT to 1-5 non-index metastatic fields, before IL-2 at the first and third treatment cycle. HD IL-2 was administered by continuous infusion for 72 hours and repeated every 3 weeks for up to 4 cycles, thereafter every 4 weeks for a maximum of 2 cycles. The primary endpoint was the immunological efficacy of the combined RT/HD IL-2 treatment (assessed by IFN-? ELISPOT). Nineteen out of 22 patients were evaluable for immunological and clinical response. Partial response occurred in 3 (15.7%) patients and stable disease was observed in 7 (36.8%). The disease control rate was 52.6% after a median follow up of 39.2 months. According to Common Terminology Criteria for Adverse Events 4.0 (CTCAE 4.0), the majority of toxicities were grade 1-2. Immunological responses were frequent and detected in 16 (84.2%) patients. Increased levels of IL-8 and IL-10 in melanoma, circulating effector memory CD4+ and intratumoral CD8+ T cells in both tumor types were detected after therapy. Overall the treatment was well tolerated and immunologically active. Immunomonitoring and correlative data on tumor and peripheral blood cell subsets suggest that this combination treatment could be a promising strategy for patients progressing after standard treatments.
Copyright © 2021 Bulgarelli, Piccinini, Petracci, Pancisi, Granato, de Rosa, Guidoboni, Petrini, Ancarani, Foschi, Romeo, Tontini, De Giorgi, Lolli, Gentili, Valmorri, Rossi, Ferroni, Casadei, Cortesi, Crudi and Ridolfi.
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