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Anthracycline-associated cardiotoxicity in childhood cancer survivors may relate to global or segmental left ventricular abnormalities from associated thromboembolic events and myocardial microinfarcts. We characterized left ventricular segmental changes by two-dimensional speckle-tracking echocardiography in anthracycline-treated asymptomatic childhood cancer survivors.
Methods and Results:
Childhood cancer survivors’ echocardiograms with normal left ventricular fractional shortening >1 year after anthracycline chemotherapy were studied. Cancer-free control children had normal echocardiograms. Apical two-, three-, and four-chamber peak systolic left ventricular longitudinal and global longitudinal strain, and peak systolic left ventricular radial and circumferential strain at papillary muscle levels were analyzed. The mean (standard deviation) age was 12.7 (3.8) years in 41 childhood cancer survivors. The median (interquartile range) follow-up after anthracycline chemotherapy was 4.73 (2.15–8) years. The median (range) cumulative anthracycline dose was 160.2 (60–396.9) mg/m2. In childhood cancer survivors, the mean (standard deviation) left ventricular longitudinal strain was lower in two- (−18.6 [3.2] versus −21.3 [2.5], p < 0.001), three- (−16.3 [6.0] versus −21.7 [3.0], p < 0.001), and four- (−17.6 [2.7] versus −20.8 [2.0], p < 0.001) chamber views compared to controls. The left ventricular global longitudinal strain (−17.6 [2.7] versus −21.3 [2.0]) and circumferential strain (−20.8 [4.3] versus −23.5 [2.6], p < 0.001) were lower in childhood cancer survivors. Among childhood cancer survivors, 12 out of 16 left ventricular segments had significantly lower longitudinal strain than controls.
Asymptomatic anthracycline-treated childhood cancer survivors with normal left ventricular fractional shortening had lower global longitudinal and circumferential strain. The left ventricular longitudinal strain was lower in majority of the segments, suggesting that anthracycline cardiotoxicity is more global than regional.
Cardiomyopathy is a rare disorder of the heart muscle, affecting 1.13 cases per 100,000 children, from birth to 18 years of age. Cardiomyopathy is the leading cause of heart transplantation in children over the age of 1. The Pediatric Cardiomyopathy Registry funded in 1994 by the National Heart, Lung, and Blood Institute was established to examine the epidemiology of the disease in children below 18 years of age. More than 3500 children across the United States and Canada have been enrolled in the Pediatric Cardiomyopathy Registry, which has followed-up these patients until death, heart transplantation, or loss to follow-up. The Pediatric Cardiomyopathy Registry has provided the most in-depth illustration of this disease regarding its aetiology, clinical course, associated risk factors, and patient outcomes. Data from the registry have helped in guiding the clinical management of cardiomyopathy in children under 18 years of age; however, questions still remain regarding the most clinically effective diagnostic and treatment approaches for these patients. Future directions of the registry include the use of next-generation whole-exome sequencing and cardiac biomarkers to identify aetiology-specific treatments and improve diagnostic strategies. This article provides a brief synopsis of the work carried out by the Pediatric Cardiomyopathy Registry since its inception, including the current knowledge on the aetiologies, outcomes, and treatments of cardiomyopathy in children.
Cardiovascular complications are among the leading causes of morbidity and mortality among survivors of childhood cancer, after cancer relapse and secondary malignancies. Although advances in cancer treatment have improved the 5-year survival rates, the same treatments, such as anthracyclines, that cure cancer also increase the risk for adverse cardiovascular effects. Anthracycline-related cardiotoxicity in survivors of childhood cancer is progressive and can take years to develop, initially presenting as sub-clinical cardiac abnormalities that, if left undetected or untreated, can lead to heart failure, myocardial infarction, or other clinical cardiac dysfunction. A higher cumulative dose of anthracycline is associated with cardiotoxicity in children; however, sub-clinical cardiac abnormalities are evident at lower doses with longer follow-up, suggesting that there is no “safe” dose of anthracycline. Other risk factors include female sex, younger age at diagnosis, black race, trisomy 21, longer time since treatment, and the presence of pre-existing cardiovascular disease and co-morbidities. Cardioprotective strategies during treatment are limited in children. Enalapril provides only temporary cardioprotection, whereas continuous anthracycline infusion extends none. On the other hand, dexrazoxane successfully prevents or reduces anthracycline-related cardiotoxicity in children with cancer, without increased risks for recurrence of primary or second malignancies or reductions in anti-tumour efficacy. With more childhood cancer survivors now reaching adulthood, it is vital to understand the adverse effects of cancer treatment on the cardiovascular system and their long-term consequences to identify and establish optimal prevention and management strategies that balance oncologic efficacy with long-term safety.
In the United States alone, ∼14,000 children are hospitalised annually with acute heart failure. The science and art of caring for these patients continues to evolve. The International Pediatric Heart Failure Summit of Johns Hopkins All Children’s Heart Institute was held on February 4 and 5, 2015. The 2015 International Pediatric Heart Failure Summit of Johns Hopkins All Children’s Heart Institute was funded through the Andrews/Daicoff Cardiovascular Program Endowment, a philanthropic collaboration between All Children’s Hospital and the Morsani College of Medicine at the University of South Florida (USF). Sponsored by All Children’s Hospital Andrews/Daicoff Cardiovascular Program, the International Pediatric Heart Failure Summit assembled leaders in clinical and scientific disciplines related to paediatric heart failure and created a multi-disciplinary “think-tank”. The purpose of this manuscript is to summarise the lessons from the 2015 International Pediatric Heart Failure Summit of Johns Hopkins All Children’s Heart Institute, to describe the “state of the art” of the treatment of paediatric cardiac failure, and to discuss future directions for research in the domain of paediatric cardiac failure.
Gul H. Dadlani, Congenital Heart Institute of Florida, All Children's Hospital and University of South Florida, St. Petersburg, FL, USA,
Steven E. Lipshultz, Sylvester Comprehensive Cancer Center University of Miami and Miller School of Medicine, Holtz Children's Hospital, University of Miami-Jackson Memorial Medical Center, FL, USA
As the survival of HIV-infected patients improves, the cardiovascular complications of HIV infection are becoming an increasingly common cause of morbidity and mortality. The prevalence of cardiovascular disease is estimated to be more than 90% in pediatric HIV patients [1–3]. The spectrum of cardiovascular disorders includes abnormalities in left ventricular performance, wall thickness, contractility, dilated cardiomyopathy, myocarditis, pericarditis, and rhythm disturbances. Cardiac complications have surpassed pulmonary disease as the leading cause of death in HIV-infected patients . The recognition of cardiovascular complications can be very difficult because many patients are asymptomatic until late in the disease course. In addition, the cardiac symptoms can be inadvertently attributed to other causes such as pulmonary or infectious etiologies. Early detection of these symptoms is only possible if clinicians have a fundamental understanding of the wide array of cardiovascular complications associated with HIV infection. The initiation of routine screening and monitoring will allow clinicians the ability to intervene and hopefully prevent or delay the onset of these complications in the future.
Several risk factors for cardiovascular disease among HIV-infected children have been described. The triad of encephalopathy, wasting, and low CD4 counts in children with HIV have been shown to be associated with an increased the risk of cardiovascular complications and decreased survival . Encephalopathy can lead to an autonomic neuropathy, which may precipitate arrhythmias or even sudden death .
Clinical manifestations of HIV infection in children
Gul H. Dadlani, Divison of Pediatric Cardiology, Golisano Children's Hospital at Strong and University of Rochester Medical Center, Rochester, NY,
Steven E. Lipshultz, Divison of Pediatric Cardiology, Golisano Children's Hospital at Strong and University of Rochester Medical Center, Rochester, NY
The cardiovascular complications of HIV infection are increasingly contributing to the overall morbidity and mortality of this pediatric population. The prevalence of cardiovascular disease is estimated to be more than 90% in both symptomatic and asymptomatic HIV-infected children . The spectrum of cardiovascular disorders includes abnormalities in left ventricular (LV) performance, wall thickness, and contractility; dilated cardiomyopathy; myocarditis; pericarditis; and rhythm disturbances. These children may have a wide spectrum of presenting symptoms for their cardiovascular complications, but most are initially asymptomatic. The cardiovascular symptoms may be inadvertently attributed to other causes, such as pulmonary or infectious processes, which may delay treatment. Early detection of and intervention for subclinical cardiovascular abnormalities through routine screening and monitoring will allow the clinician to initiate therapy with the goal of preventing or delaying the onset of clinical cardiovascular complications. Today the survival of pediatric HIV patients has improved and cardiac complications are increasing as the underlying cause of death (Figure 30.1) [2, 3]. Therefore, clinicians need a fundamental understanding of the cardiovascular complications that can arise from HIV infection in pediatric patients.
Several risk factors for cardiovascular disease among HIV-infected children have been described. The triad of encephalopathy, wasting, and low CD4+ counts in children with HIV has been shown to be associated with an increased risk of cardiovascular complications and a decreased survival . Encephalopathy can lead to an autonomic neuropathy, which may precipitate arrhythmias or even sudden death .
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