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Gastroschisis most commonly occurs in isolation buy discount extra super avana on-line erectile dysfunction pills online, and is rarely associated with genetic or cardiac disease (296 generic extra super avana 260mg with mastercard erectile dysfunction treatment scams,297,298). It may include liver, and is commonly associated with syndromic, chromosomal, and/or cardiac disease (296,297,298). While the concurrent diagnoses of omphalocele and cardiac structural disease typically carries a poor prognosis, coincident genetic disease and pulmonary hypertension may also play a significant role. Fetal Arrhythmia Abnormalities of fetal cardiac rhythm are an important aspect of fetal cardiology, accounting for 12% to 20% of referrals for fetal echocardiography (299). Ectopy is estimated to occur in at least 1% to 3% of pregnancies; however, only about 10% of those evaluated fetal arrhythmias have the potential to be life threatening (300,301). The fetal cardiologist must communicate and work closely with the obstetrician and maternal fetal medicine specialist to provide optimal, safe, and efficacious fetal therapy. The chronology and temporal relationship of atrial and ventricular contractions demonstrated by fetal echocardiography allows one to infer the electrical activation of the heart and thus the mechanism of the arrhythmia. M-mode allows recording of the sequence and time relationship of atrial and ventricular systolic wall movements. The M-mode cursor should traverse the most mobile region of the atria and ventricles to optimally display muscle contraction. Tissue Doppler: Allows examination of simultaneous atrial and ventricular segmental wall motion. They have been associated with the presence of a floppy, aneurysmal septum primum (306). Fetuses with infrequent ectopy persisting >1 to 2 weeks as well as those with frequent ectopy, defined as bigeminy, trigeminy, or >every 3 to 5 beats, should be referred for an echocardiogram (29). The initial study should confirm the mechanism of the arrhythmia, observe for tachycardia, and assess for any abnormalities of cardiac structure or function. If the fetal cardiologist does not detect any tachycardia, or evidence to raise the suspicion for tachycardia outside of the scan time (such as tricuspid regurgitation, pericardial effusion, ventricular dysfunction, abnormal fetal vessel flow), then serial fetal echocardiograms may not be necessary. Sinus Bradycardia Persistent fetal sinus bradycardia may be autoimmune mediated or infectious. Fetal distress or abnormalities of the nervous system may also result in sinus bradycardia. With heterotaxy syndrome, ectopic or low atrial foci generate fetal bradycardia typically in the range of 77 to 130 bpm, but can become lower as pregnancy progresses (29,309). These fetuses can be at risk for the development of hydrops, cardiac dysfunction, and fetal death (309). The subsequent early premature beat will demonstrate no corresponding ventricular contraction. Blocked atrial bigeminy typically results in ventricular rates between 75 and 90 bpm (312). Fetuses with normal hearts are usually asymptomatic, thus blocked atrial bigeminy does not require antiarrhythmic therapy. Management in either situation includes close serial assessment of the fetal heart rate and observation for the development of heart failure. In one study from two tertiary referral centers, only 9 of 16 such pregnancies intended to carry to term resulted in live births, and only 3 were still alive at 1 year of age (314). The presence of maternal hypothyroidism or vitamin D deficiency further increases the risk (318). Concern for myocardial involvement may justify additional fetal echocardiographic assessment in the third trimester even if the rhythm has remained sinus throughout gestation (29). Untreated, fetal mortality ranges from 9% to 34%, with risk of death increased in those diagnosed before 20 weeks, or with a ventricular rate <50 bpm, fetal hydrops, or impaired left ventricular function at diagnosis (322,323,324). Treatment may also be considered in fetuses manifesting with complete block to prevent dilated cardiomyopathy (29,322,324). Tachycardia Fetuses with any tachyarrhythmia of >180 bpm should undergo a complete fetal echocardiographic evaluation and consultation (29,307). Delivery may be considered in fetuses close to term with sustained tachycardia or evidence of compromise, weighing the risk of prematurity versus risks of maternal therapy. Fetuses with sustained tachycardia (>50% of time monitored) who are not near-term, or fetuses with intermittent tachycardia but evidence of ventricular dysfunction or hydrops should be treated pharmacologically transplacentally (29). Rather, treatment is aimed at sufficient arrhythmia control such that ventricular dysfunction or other evidence of significant compromise improves and resolves. Hydropic fetuses incur a greater mortality and medical management is more difficult with reduced efficacy of transplacental drug transfer (338,339). A summary of the medications most commonly used in the management of fetal arrhythmias are outlined in Table 5. It is estimated that 50% to two-thirds of neonates will require antiarrhythmia therapy (301,340). Genetic disorders are thought to be even more prevalent in the fetal population than in the newborn population, given the potential of fetal death. This can be performed by chorionic villus sampling or amniocentesis at appropriate gestational ages, or most recently maternal serum testing (341). However, while maternal serum testing has high sensitivity and specificity for Trisomy 21, sensitivity is poorer for Trisomy 13 and 18, and specificity is low for sex chromosome abnormalities (342). Fetal Cardiac Intervention Fetal cardiac intervention is attractive given the potential to halt the progression of cardiovascular disease while still in the protective maternal environment (202). Fetal cardiac interventions were described as early as 1975, when maternal propranolol administration was used to treat fetal tachycardia (343). Current fetal cardiac interventions can generally be divided into three categories: (1) pharmacologic, (2) ultrasound-based, and (3) invasive. Diagnosis and treatment of fetal cardiac disease: A scientific statement from the American Heart Association. Diagnosis and treatment of fetal cardiac disease: A scientific statement from the American Heart Association. Pharmacologic Transplacental pharmacologic therapy for fetal arrhythmia has been utilized for decades, and is discussed in more detail in the fetal arrhythmia of this chapter. This is typically administered by oral or intravenous routes to the mother, although direct amnioinfusion has been described. Less-described therapies that are still being investigated include administration of digoxin for fetal heart failure, indomethacin to achieve restriction or closure of the ductus arteriosus in the setting of Ebstein anomaly or dysplastic tricuspid valve, and administration of oxygen to mothers for fetuses with left heart hypoplasia (138,226,238,345,346). The tenet of maternal hyperoxygenation is that increased maternal oxygen delivery results in a fall in fetal pulmonary vascular resistance and in turn, pulmonary venous return flow to the fetal left heart (116,124). Chronic maternal hyperoxygenation has also been described as a therapy for fetal left heart hypoplasia (345). Invasive Procedures Apart from pharmacologic intervention, the most frequent fetal cardiac interventions currently performed are catheter-based. While “open” fetal cardiac surgery has been described in isolated reports, the utility and efficacy of this approach are not clear (202,344).
Symptoms Heart failure symptoms can become evident at any age cheap 260mg extra super avana with mastercard impotence treatments natural, from young children to the elderly (2) purchase generic extra super avana from india erectile dysfunction without drugs. It is relatively uncommon for children or adolescents to experience marked progressive functional disability P. The predominant complaint is exertional limitation due to dyspnea and/or fatigue, which may be associated with chest discomfort either typical or atypical of angina. Several clinical parameters have been suggested to aid this differential diagnosis (Fig. In the United States, customary screening practice dictates that a personal and family history be obtained and a physical examination performed. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. This is compounded by the fact that most children who die suddenly have been previously asymptomatic (or only mildly symptomatic), and such catastrophes are often the first clinical manifestation of the disease (2,3,4,5,95,114,115,116). Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006. Nevertheless, the onset of symptoms and heart failure in infancy or early childhood appears to be an unfavorable prognostic sign indicative of early disease aggression (90,91,95,106) with high mortality in the ensuing months or years despite surgical and/or medical therapy. Noonan is also frequently associated with other congenital heart malformations, the most common of which are dysplastic pulmonary valve stenosis and atrial septal defect. It is more likely that such infrequent associations represent only the sporadic association of two rare diseases rather than constituting an etiologic relationship. Mild hypertrophy conveys generally lower risk and extreme hypertrophy (wall thickness ≥30 mm) the highest risk. Magnitude of left ventricular hypertrophy predicts the risk of sudden death in hypertrophic cardiomyopathy. Management Medical Response of heart failure symptoms to medical treatment is highly variable, and therapy must often be empirically tailored to the individual requirements of patients (see Fig. Long-acting preparations of propranolol, atenolol, metoprolol, or nadolol are now most commonly used. There is no evidence that taking β-blockers and verapamil together is advantageous, although either drug can be administered first. When patients fail to experience symptom control from β-blockers and verapamil, empiric trials with disopyramide have been reported to reduce outflow gradient and symptoms (125), although there is little experience with this drug in children. In symptomatic patients, diuretic agents may be administered judiciously, either alone or in conjunction with either β-blockers or verapamil, to reduce pulmonary congestion and improve symptoms. The usual circumstance occurs in children or adults who experience exertional dyspnea associated with preserved or hyperdynamic systolic function. The therapeutic approach to these patients has been similar to that of congestive heart failure in other cardiac diseases, including administration of β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and diuretics, as well as selectively digoxin, spironolactone, and warfarin. Vegetations most commonly involve the anterior mitral leaflet or septal endocardium at the site of mitral valve–septal contact and less commonly involve the aortic valve. Surgical Septal Myectomy Based on substantial data assembled over >40 years, surgical septal myectomy is the primary treatment option for most patients with severe drug-refractory symptoms resulting in functional P. The traditional operative procedure has been the transaortic septal myectomy (Morrow procedure) in which a portion of muscle is resected from the basal septum (usually about 2 to 5 g). More recently, some surgeons have practiced a more extensive myectomy extended much more distally in the septum, often associated with realignment of the papillary muscles and resection of aberrant muscular structures contributing to obstruction. Occasionally, it is necessary to surgically remove both right and left ventricular outflow tract obstruction in the same patient. Stored intracardiac ventricular electrogram from an asymptomatic 16-year-old male patient who underwent implantation for primary prevention of sudden death (age 15 years). Intracardiac electrogram obtained at 1:20 am with patient asleep, 5 years after implant. A virtually identical sequence occurred 9 years later, also during sleep; patient is now 53 years old and asymptomatic. Efficacy of implantable cardioverter- defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. No differences in intervention rates are evident relative to the number of risk factors (i. Results achieved with septal myectomy at several institutions over the past 45 years have been excellent (2,3,4,5,9,133,134,135,136,137,138,139). Long-term follow-up studies from surgical centers have demonstrated that basal outflow obstruction does not recur and heart failure is largely reversed by surgical septal myectomy, with symptoms relieved long term in about 90% of patients (138). Of particular note, in addition to improved quality of life, recent data from the Mayo Clinic myectomy cohort show that operated patients achieve the same longevity as the general population and demonstrate significantly better survival than nonoperated patients with outflow obstruction (see Fig. For example, congenital anomalous papillary muscle insertion directly into anterior mitral leaflet (without interposition of chordae tendineae) produces muscular midventricular obstruction (135,139,140), and requires extended myectomy to relieve obstruction (140,141). Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy. A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines Committee to Develop an Expert Consensus Document on Hypertrophic Cardiomyopathy. Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006. Hypertrophic cardiomyopathy: present and future, with translation into contemporary cardiovascular medicine. Phenotypic spectrum and patterns of left ventricular hypertrophy in hypertrophic cardiomyopathy: morphologic observations and significance as assessed by two-dimensional echocardiography in 600 patients. Hypertrophic cardiomyopathy phenotype revisited after 50 years with cardiovascular magnetic resonance. Developed in collaboration with the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Epidemiology and cause-specific outcome of hypertrophic cardiomyopathy in children: findings from the Pediatric Cardiomyopathy Registry. Risk stratification at diagnosis for children with hypertrophic cardiomyopathy: an analysis of data from the Pediatric Cardiomyopathy Registry. Clinicopathological profiles of progressive heart failure in hypertrophic cardiomyopathy. Apical hypertrophic cardiomyopathy: clinical and two-dimensional echocardiographic assessment. Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy. Narrative review: harnessing molecular genetics for the diagnosis and management of hypertrophic cardiomyopathy. Proposal for contemporary screening strategies in families with hypertrophic cardiomyopathy. Dilemmas in nomenclature characterizing hypertrophic cardiomyopathy and left ventricular hypertrophy.
For (ventricular) septal defects order extra super avana 260mg on line erectile dysfunction depression, one case-control study did not show evidence of risk reduction (281) generic extra super avana 260mg fast delivery erectile dysfunction 16, whereas two others did (108,280). Why the studies are not entirely consistent is unclear, but methodologic differences as well as varying degrees of bias and confounding could have played a role. In summary, at this time the preponderance of clinical and epidemiologic data, including findings from a randomized clinical trial, seems to indicate a moderate risk reduction for congenital heart defects in the aggregate with periconceptional use of a multivitamin supplement containing folic acid. Ideally a new, well-designed clinical trial or a large, carefully implemented prospective case-control study, preferably with biologic markers, could provide conclusive data on this important issue. Rates after Fortification Several countries in North and South America and Middle East, as well as Australia (but no countries in Europe yet) have introduced folic acid fortification, that is, have added variable amounts of folic acid to the food supply, typically in cereal grain products that make their way into common staples such as breads and pasta. The main goal was to reduce the occurrence of neural tube defects by increasing folic acid consumption in the population as a whole. Fortification has also allowed the opportunity to examine changes in the rates of major congenital heart defects in response to overall changes in folic acid consumption. In the United States, a study using birth defect surveillance data from 23 state programs compared rates of selected congenital heart defects in 1999 to 2000 versus 1994 to 1996 (283). For heart defects, the study reported a modest (12%) but significant decline in d-transposition of the great arteries (12% reduction, rate ratio 0. In Canada, studies from two provinces also reported a modest decline in some heart defects after fortification. In Alberta, researchers using data from a well-established population-based birth defect registry reported a 20% decline in secundum atrial septal defects (rate ratio 0. In Quebec, researchers using linked administrative databases evaluated trends of a group of severe heart defects, including conotruncal defects (60% of the case group), single ventricle, and atrioventricular septal defects (285). They reported a significant decline of these defects, 6% for every year after fortification (yearly rate ratio 0. Limited additional information is available from Latin America, where several countries, including Chile, Argentina, and Brazil introduced fortification at different times and levels. For heart defects, they reported a statistically significant reduction of septal defects. In a similar pattern, a moderate nonsignificant decline in an aggregate group of severe heart defects (conotruncal defects, single ventricle, atrioventricular septal defects) was observed in Argentina (rate ratio, 0. By contrast, the decline for neural tube defects was marked and consistent across the three countries (286). Prevalence rate ratios over 1 indicate increased rates after fortification, prevalence rate ratios below 1 indicate decreased rates. Changes in the birth prevalence of selected birth defects after grain fortification with folic acid in the United States: findings from a multi-state population-based study. Changes in frequencies of select congenital anomalies since the onset of folic acid fortification in a Canadian birth defect registry. Prevalence of severe congenital heart disease after folic acid fortification of grain products: time trend analysis in Quebec, Canada. Some statistically significant reductions have been observed but so far these have not been consistent across phenotypes and geographic areas, even within the same country. Contributing factors could include variations in the effectiveness of fortification (as documented by blood folate levels) and in study methodology (inclusion criteria and classification scheme). In addition, without a concurrent control group, it is difficult to assess the influence of structural changes in reporting and ascertainment, including the influence of elective terminations of pregnancy. Maternal fever, multivitamin use, and selected birth defects: evidence of interaction? However, this seems to be true even for neural tube defects, for which the protective effect of folic acid is well established: with fortification, the reduction in occurrence is less and take longer compared to what is seen in observational studies and clinical trials. But the different findings for heart defects and neural tube defects can have other explanations. For example, folic acid may not be effective for heart defects at all; it may be effective only in larger amounts than those typically consumed through fortification or standard folic acid pills (0. In fact, the reported studies all looked at multivitamin supplement use rather than folic acid alone. Ancillary Data from Genetic and Environmental Studies Potentially relevant data have been generated by studies looking at interactions between multivitamin supplement use and risk factors such as certain medications (224), febrile illnesses (107,163), and pregestational diabetes (133). The odds ratio estimated the relative risk for the different types of heart defects among women reporting a first- trimester febrile illness. Although these risk estimates have wide confidence intervals, there appears to be a fairly consistent P. This would suggest that taking the supplement could mitigate the risk for congenital heart defects associated with fever (107). The contribution of chromosomal abnormalities to congenital heart defects: a population-based study. Current tobacco use and secondhand smoke exposure among women of childbearing age—14 countries, 2008–2010. Congenital Heart Disease: Molecular Genetics, Principles of Diagnosis and Treatment: S. For folate-related genes, most studies do not show an association with conotruncal or other heart defects (291,292,293,294,295,296), although some positive associations have been reported (297,298,299,300). In summary, folic acid and multivitamin supplementation could have a role in reducing the risk for some congenital heart defects, but evidence, while suggestive, is not conclusive. If confirmed, the impact would be considerable, because the fraction of preventable heart defects may be large. Also, vitamins, including folic acid, are inexpensive and easily transportable, making prevention through vitamin supplementation a viable strategy also in developing countries. Because of the potential implications, a large randomized trial of vitamin supplementation (vs. The resources needed for such study would be considerable, but will likely be minimal compared to the high societal and personal costs of heart defects. Because of the established protective effect against neural tube defects, daily periconceptional use of folic acid is recommended for all women of childbearing age. By simply promoting periconceptional use of a multivitamin supplement containing folic acid (400 μg), pediatric cardiologists would (and should) provide all women with the benefits of a reduced risk for a neural tube defect–affected pregnancy. The protection against heart defects, to the extent that is present, will be an added benefit, at no additional cost or risk. Strategies: Epidemiology of Prevention Prevention is motivated by incentives and driven by evidence. The next step, implementation, requires strategies to maximize the impact of interventions, and tools to make prevention practical, coherent with the goals, and consistent across practitioners. Integrating Interventions The scientific evidence characterizing modifiable risk factors is a crucial, but not the only component of effective prevention. Translating such evidence into maximal prevention requires strategic thinking, an integrated approach across disciplines, and a combination of personal and population interventions throughout the lifespan (2,303). For example, integrating interventions will have benefits beyond a more efficient prevention of congenital heart defects. For these reasons, when developing recommendations for the primary prevention of heart defects it is reasonable to incorporate information not only on the risk for congenital heart defects, but also the overall benefits to fetal, infant, and maternal health. The heart develops early in pregnancy: The primordial cardiac tube starts beating rhythmically at around 21 days postfertilization and continues to develop through complex processes of looping, septation, valve formation, and cell migration (neural crest cells, secondary heart field), all contributing to the final anatomy and function (304).
Endomyocardial biopsy in pediatric heart transplant recipients: a useful exercise? Is biopsy-proven cellular rejection an important clinical consideration in heart transplantation? Identifying cardiac transplant rejection in children: diagnostic utility of echocardiography cheap 260mg extra super avana overnight delivery impotence male, right heart catheterization and endomyocardial biopsy data cheap extra super avana 260 mg with visa impotence treatment options. An improved echocardiographic rejection-surveillance strategy following pediatric heart transplantation. Value of plasma B- type natriuretic peptide as a marker for rejection in pediatric heart transplant recipients. B-type natriuretic peptide is a sensitive screening test for acute rejection in pediatric heart transplant patients. The International Society for Heart and Lung Transplantation grading system for heart transplant biopsy specimens: clarification and commentary. Association of viral genome with graft loss in children after cardiac transplantation. Viral endomyocardial infection is an independent predictor and potentially treatable risk factor for graft loss and coronary vasculopathy in pediatric cardiac transplant recipients. The 2013 International Society for Heart and Lung Transplantation Working Formulation for the standardization of nomenclature in the pathologic diagnosis of antibody-mediated rejection in heart transplantation. Controversies in defining cardiac antibody-mediated rejection: need for updated criteria. A clinical correlation study of severity of antibody-mediated rejection and cardiovascular mortality in heart transplantation. National conference to assess antibody-mediated rejection in solid organ transplantation. The role of proteasome inhibition with bortezomib in the treatment of antibody-mediated rejection after kidney-only or kidney-combined organ transplantation. Rapid reduction in donor-specific anti-human leukocyte antigen antibodies and reversal of antibody-mediated rejection with bortezomib in pediatric heart transplant patients. The pharmacokinetics of a microemulsion formulation of cyclosporine in primary renal allograft recipients. Randomized clinical trial of tacrolimus- vs cyclosporine-based immunosuppression in pediatric heart transplantation: preliminary results at 15-month follow-up. Sirolimus in de novo heart transplant recipients reduces acute rejection and prevents coronary artery disease at 2 years: a randomized clinical trial. Sirolimus immunosuppression in pediatric heart transplant recipients: a single-center experience. Sirolimus as primary immunosuppression attenuates allograft vasculopathy with improved late survival and decreased cardiac events after cardiac transplantation. Everolimus initiation and early calcineurin inhibitor withdrawal in heart transplant recipients: a randomized trial. Indications, tolerance and complications of a sirolimus and calcineurin inhibitor immunosuppression regimen: intermediate experience in pediatric heart transplantation recipients. Sirolimus as primary immunosuppressant reduces left ventricular mass and improves diastolic function of the cardiac allograft. Recommendations for the use of everolimus (Certican) in heart transplantation: results from the second German-Austrian Certican Consensus Conference. Prospective study of everolimus with calcineurin inhibitor-free immunosuppression in maintenance heart transplant patients: results at 2 years. A randomized active-controlled trial of mycophenolate mofetil in heart transplant recipients. Three-year results of a randomized, double-blind, controlled trial of mycophenolate mofetil versus azathioprine in cardiac transplant recipients. Methotrexate or total lymphoid radiation for treatment of persistent or recurrent allograft cellular rejection: a comparative study. Methotrexate therapy in pediatric heart transplantation as treatment of recurrent mild to moderate acute cellular rejection. Safety and early outcomes using a corticosteroid-avoidance immunosuppression protocol in pediatric heart transplant recipients. Long-term survivors of pediatric heart transplantation: a multicenter report of sixty-eight children who have survived longer than five years. Rejection is reduced in thoracic organ recipients when transplanted in the first year of life. Nonadherence is associated with late rejection in pediatric heart transplant recipients. Impact of medication non- adherence on survival after pediatric heart transplantation in the U. An update on immunizations before and after transplantation in the pediatric solid organ transplant recipient. Children are not small adults: some differences between pediatric and adult cardiac transplantation. The longitudinal impact of psychological functioning, medical severity, and family functioning in pediatric heart transplantation. Should physical activity and/or competitive sports be curtailed in pediatric heart transplant recipients? Atrial tachyarrhythmias and permanent pacing after pediatric heart transplantation. Cardiac pacemakers in pediatric heart transplant recipients: incidence, indications, and associated factors. Longitudinal changes in heart rate recovery after maximal exercise in pediatric heart transplant recipients: evidence of autonomic re-innervation? Serial assessment of sympathetic reinnervation after orthotopic heart transplantation. Sympathetic reinnervation of the sinus node and exercise hemodynamics after cardiac transplantation. Iodine-123 metaiodobenzylguanidine scintigraphic assessment of the transplanted human heart: evidence for late reinnervation. Reversal of severe late left ventricular failure after pediatric heart transplantation and possible role of plasmapheresis. Total lymphoid irradiation for refractory rejection in pediatric heart transplantation. Has late rejection decreased in pediatric heart transplantation in the current era? Lymphoproliferative disorders after paediatric heart transplantation: a multi-institutional study. Post-transplantation lymphoproliferative disorders: diagnosis, prognosis, and current approaches to therapy. Diagnosis and treatment of post-transplantation lymphoproliferative disorder in pediatric heart transplant patients. Monitoring of Epstein-Barr viral load in pediatric heart and lung transplant recipients by real-time polymerase chain reaction.