Hostname: page-component-78c5997874-t5tsf Total loading time: 0 Render date: 2024-11-17T18:22:35.203Z Has data issue: false hasContentIssue false
  • English
  • Français

Recombinant tissue plasminogen activator as a novel treatment option for infective endocarditis: a retrospective clinical study in 32 children

Published online by Cambridge University Press:  16 February 2015

Aviva Levitas ,
Hanna Krymko ,
Justin Richardson ,
Eli Zalzstein  and
Viktoriya Ioffe
Aviva Levitas*
Affiliation:
Pediatric Cardiology Unit, Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of Negev, Beer-Sheva, Israel
Hanna Krymko
Affiliation:
Pediatric Cardiology Unit, Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of Negev, Beer-Sheva, Israel
Justin Richardson
Affiliation:
Department of Neonatology Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of Negev, Beer-Sheva, Israel
Eli Zalzstein
Affiliation:
Pediatric Cardiology Unit, Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of Negev, Beer-Sheva, Israel
Viktoriya Ioffe
Affiliation:
Pediatric Cardiology Unit, Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of Negev, Beer-Sheva, Israel
*
Correspondence to: Dr A. Levitas, Pediatric Cardiology Unit, Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, 84105, Israel. Tel: +9 728 640 0111; Fax: 972 863 65499; E-mail: [email protected]
Get access Rights & Permissions [Opens in a new window]

Abstract

Infective endocarditis is a life-threatening infectious syndrome, with high morbidity and mortality. Current treatments for infective endocarditis include intravenous antibiotics, surgery, and involve a lengthy hospital stay. We hypothesised that adjunctive recombinant tissue plasminogen activator treatment for infective endocarditis may facilitate faster resolution of vegetations and clearance of positive blood cultures, and therefore decrease morbidity and mortality. This retrospective study included follow-up of patients, from 1997 through 2014, including clinical presentation, causative organism, length of treatment, morbidity, and mortality. We identified 32 patients, all of whom were diagnosed with endocarditis and were treated by recombinant tissue plasminogen activator. Among all, 27 patients (93%) had positive blood cultures, with the most frequent organisms being Staphylococcus epidermis (nine patients), Staphylococcus aureus (six patients), and Candida (nine patients). Upon treatment, in 31 patients (97%), resolution of vegetations and clearance of blood cultures occurred within hours to few days. Out of 32 patients, one patient (3%) died and three patients (9%) suffered embolic or haemorrhagic events, possibly related to the recombinant tissue plasminogen activator. None of the patients required surgical intervention to assist vegetation resolution. In conclusion, it appears that recombinant tissue plasminogen activator may become an adjunctive treatment for infective endocarditis and may decrease morbidity as compared with current guidelines. Prospective multi-centre studies are required to validate our findings.

Keywords

Infective endocarditisrecombinant tissue plasminogen activator (rt-PA)retrospective studyvegetation
Type
Original Articles
Information
Cardiology in the Young , Volume 26 , Issue 1 , January 2016 , pp. 110 - 115
Check for updates
Copyright
© Cambridge University Press 2015 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Day, MD, Gauvreau, K, Shulman, S, Newburger, JW. Characteristics of children hospitalized with infective endocarditis. Circulation 2009; 119: 865–870.Google Scholar
2. Kliegman, RM, Stanton, BMD, St. Geme, J, Schor, N, Behrman, RE. Nelson Pediatrics, 19th edn. Saunders Elsevier, Philadelphia, PA, 2011.Google Scholar
3. Rimensberger, PC, Humbert, JR, Beghetti, M. Management of preterm infants with intracardiac thrombi: use of thrombolytic agents. Paediatr Drugs 2001; 3: 883–898.Google Scholar
4. Levitas, A, Zucker, N, Zalzstein, E, Sofer, S, Kapelushnik, J, Marks, KA. Successful treatment of infective endocarditis with recombinant tissue plasminogen activator. J Pediatr 2003; 143: 649–652.Google Scholar
5. Marks, KA, Zucker, N, Kapelushnik, J, Karplus, M, Levitas, A. Infective endocarditis successfully treated in extremely low birth weight infants with recombinant tissue plasminogen activator. Pediatrics 2002; 109: 153–158.CrossRefGoogle ScholarPubMed
6. Anderson, B, Urs, P, Tudehope, D, Ward, C. The use of recombinant tissue plasminogen activator in the management of infective intracardiac thrombi in pre-term infants with thrombocytopaenia. J Paediatr Child Health 2009; 45: 598–601.Google Scholar
7. Aydemir, C, Erdeve, O, Oguz, SS, Altug, N, Dilmen, U. Successful treatment of Candida albicans endocarditis vegetations with recombinant tissue plasminogen activator in an extremely low birth weight preterm infant. Mycoses 2011; 54: e590–e592.Google Scholar
8. Tardin, FA, Avanza, AC Jr, Andião, MR, et al. Combined rtPA and aspirin therapy for intracardiac thrombosis in neonates. Arq Bras Cardiol 2007; 88: e121–e123.Google Scholar
9. Johnson, JA, Boyce, TG, Cetta, F, Steckelberg, JM, Johnson, JN. Infective endocarditis in the pediatric patient: a 60-year single-institution review. Mayo Clin Proc 2012; 87: 629–635.Google Scholar
10. Marom, D, Levy, I, Gutwein, O, Birk, E, Ashkenazi, S. Healthcare-associated versus community-associated infective endocarditis in children. Pediatr Infect Dis J 2011; 30: 585–588.CrossRefGoogle ScholarPubMed
11. Tan, M, Armstrong, D, Birken, C, et al. Bacterial endocarditis in a child presenting with acute arterial ischemic stroke: should thrombolytic therapy be absolutely contraindicated? Dev Med Child Neurol 2009; 51: 151–154.Google Scholar
12. Andrew, M, Paes, B, Milner, R, et al. Development of the human coagulation system in the healthy premature infant. Blood 1988; 72: 1651–1657.Google Scholar