Drożdż, Jarosław

Kaczmarek, Daria

Krekora, Jan

Matuszewska-Brycht, Oliwia

Piestrzeniewicz, Katarzyna

Rudziński, Tomasz

Via Medica Journals

 This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.   Patent ductus arteriosus: Generally an anomaly of childhood, but is it always? Clinical implications in an adult patient  Authors: Daria Kaczmarek, Oliwia Matuszewska-Brycht, Katarzyna Piestrzeniewicz, Tomasz Rudziński, Jan Krekora, Jarosław Drożdż Article type: Clinical vignette Received: March 20, 2023 Accepted: May 13, 2023 Early publication date: June 11, 2023                    Patent ductus arteriosus: Generally an anomaly of childhood, but is it always? Clinical implications in an adult patient   Short communication: Clinical implications of patent ductus arteriosus in an adult patient  Daria Kaczmarek, Oliwia Matuszewska-Brycht, Katarzyna Piestrzeniewicz, Tomasz Rudziński, Jan Krekora, Jarosław Drożdż  2nd Department of Cardiology, Medical University of Lodz, Łódź, Poland   Correspondence to: Daria Kaczmarek, MD, 2nd Department of Cardiology, Medical University of Lodz,  Pomorska 251, 92–213 Łódź, Poland,  phone: +48 42 2014316,  e-mail: dariaa.jedrzejewska@gmail.com   Patent ductus arteriosus (PDA) is a remnant from fetal life that connects the aorta to the pulmonary artery. PDA closes physiologically after birth, however, when it does not happen, pharmacological treatment or interventional closure is implemented. When the shunt volume is small it does not cause symptoms at an early age, so the patent vessel may be diagnosed not until the adult age [1]. We present the case of a 39-year-old male patient, previously without comorbidities, with history of drug use, who was referred to the hospital because of heart failure symptoms such as significant deterioration of exercise tolerance, resting dyspnea and lower limb oedema that occurred de novo. The patient had been treated for an upper respiratory tract infection with antibiotic therapy (doxycycline) without clinical improvement. Laboratory tests revealed elevated concentrations of: C-reactive protein (CRP, 76.2 mg/l), leukocytes, N-terminal prohormone of brain natriuretic peptide (NT-proBNP 16656.0 pg/ml), D-dimer (5.43 mg/l) and a slightly elevated troponin T concentration. Chest X-ray showed an enlarged cardiac silhouette, right pleural fluid and inflammatory lesions of the right lung. Electrocardiogram (ECG) recorded sinus tachycardia with heart rate 120/min, negative T-wave in leads V5–V6 and QTc of 481 ms. Due to the high level of D-dimer, Computed Tomography (CT) pulmonary angiogram was performed excluding pulmonary embolism, but raising the suspicion of PDA. Prior to further diagnostics, the patient experienced sudden cardiac arrest in the monitor-recorded torsade de pointes mechanism (TdP), which was terminated by an effective defibrillation. QTc prolongation to 600 ms was observed in subsequent ECG (Figure 1A–C). Transthoracic echocardiography (TTE) revealed: global left ventricular hypokinesis with reduced left ventricular ejection fraction (LVEF) of 29%, left ventricular end-diastolic diameter enlarged to 77 mm, a severe mitral regurgitation, a dilated pulmonary trunk and a blood flow from the aorta to the pulmonary trunk visible in color Doppler. Systolic pulmonary arterial pressure (SPAP) was 31 mm Hg, without features of pulmonary hypertension (PH) in TTE. Transesophageal echocardiography confirmed the PDA with permanent left-to-right shunt (Qp/Qs ratio 1.7). The patient did not have an audible Gibson murmur typical of PDA [2]. Coronary CT Angiography did not show any narrowing in coronary arteries but highlighted the exact anatomy of the PDA (Supplementary material, Figure S1A–D). After stabilization of the clinical status the patient was qualified for the percutaneous closure of the PDA. The procedure was performed with a good result with an implanted device Amplatzer Duct Occluder 10 mm (Supplementary material, Figure S2A–B).  During the follow up performed 2 months after the surgery, the patient feels well, QTc length is normal, and TTE shows: a good long-term outcome of the procedure, normokinesis of the inferolateral wall with LVEF of 30%, mild mitral regurgitation.  We cannot exclude the involvement of drug use in the aetiology of heart failure in this case, but PDA seems to be the key cause of this condition. On the basis of this case, it is important to assess the heart echocardiographically for various congenital defects even in old age. Due to the increased frequency of premature infants in recent years, detection of congenital heart defects has raised, including PDA in adult patients [3]. PDA should be suspected in adults with an audible characteristic machine murmur. Also, when no other cause of heart failure, right ventricle overload or PH is found, congenital defects such as PDA should be actively searched for. Transcatheter closure of PDA remains an internationally recognized method in both children and adults with symptoms of heart failure. The procedure is safe when up-to-date devices are used [4].   Supplementary material Supplementary material is available at https://journals.viamedica.pl/kardiologia_polska.  Article information Conflict of interest: None declared. Funding: None. Open access: This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, which allows downloading and sharing articles with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially. For commercial use, please contact the journal office at kardiologiapolska@ptkardio.pl.  REFERENCES 1. Anilkumar M. Patent ductus arteriosus. Cardiol Clin. 2013; 31(3): 417–430, doi: 10.1016/j.ccl.2013.05.006, indexed in Pubmed: 23931103. 2. Marquis RM. The continuous murmur of persistence of the ductus arteriosus-an historical review. Eur Heart J. 1980; 1(6): 465–478, doi: 10.1093/oxfordjournals.eurheartj.a061149, indexed in Pubmed: 7023946. 3. Mullins CE. Patent ductus arteriosus. In: Garson A, Bricker JT, McNamara DG (ed.). The Science and Practice of Pediatric Cardiology. Lea & Febiger, Philadelphia 1990: 1055. 4. Baruteau AE, Hascoët S, Baruteau J, et al. Transcatheter closure of patent ductus arteriosus: past, present and future. Arch Cardiovasc Dis. 2014; 107(2): 122–132, doi: 10.1016/j.acvd.2014.01.008, indexed in Pubmed: 24560920.   Figure 1. Electrocardiography. A. On admission. B. After effective defibrillation. C. Two months after the patent ductus arteriosus closure procedure      

Patent ductus arteriosus: Generally an anomaly of childhood, but is it always? Clinical implications in an adult patient

https://journals.viamedica.pl/kardiologia_polska/article/download/95576/71928

Patent ductus arteriosus – generally an anomaly of childhood, but is it always? Clinical implications in an adult patient

Abstract

Similar works

Full text

Available Versions

Via Medica Journals