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All Journal Journal of the Medical Sciences (Berkala Ilmu Kedokteran)
Anggoro Budi Hartopo
Department of Cardiology and Vascular Medicine, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta
Immunology & microbiology Neuroscience

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Pulmonary arterial hypertension after atrial septal defect closure: a case report Lucia Kris Dinarti; Dyah Wulan Anggrahini; Muhammad Reyhan Hadwiono; Abdul Majid Halim Wiradhika; Vera Dewanto; Anggoro Budi Hartopo
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 53, No 4 (2021)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19106/JMedSci005304202111

Abstract

Most patients with congenital heart disease (CHD) who underwent successful shunts defect repair can be remained asymptomatic for years. It leads to a high number of losses to follow-up after patients discharge. After closure, pulmonary hypertension (PH) prevalence seems to be high and associated with increased morbidity and mortality. We reported a 55 y.o. female diagnosed with pulmonary arterial hypertension (PAH) and atrial fibrillation (AF) 31 years after atrial septal defect (ASD) closure by surgery, who never had routine follow-up evaluation because she remained asymptomatic for years. Physical examination revealed heart enlargement with irregular rhythm and pan systolic murmur in the fourth left sternal border. Electrocardiogram showed AF normal ventricular response, right axis deviation and suggestive for right ventricular hypertrophy. Laboratory testing found the NT pro-BNP level was 2,476 pg/mL. The chest X-ray showed enlargement of the heart and was representative of PH. From echocardiography study, transthoracic and transoesophageal echocardiography, we found no sign of residual shunt. There were right atrial and right ventricular dilatation, severe tricuspid regurgitation (TR) and a high probability of PH with TR velocity of 4.46 m/s. Right heart catheterization concluded mean pulmonary arterial pressure 46 mmHg, flow ratio 1.1, and pulmonary artery resistance index 15.5 Woods unit.m-2. We highlight this case because of the high incidence of PH long after defect closure. The high number of lost to follow-up patients can lead to morbidity and mortality.
Pulmonary vascular resistance/systemic vascular resistance (PVR/SVR) ratio changes after sildenafil therapy in uncorrected congenital heart disease-associated pulmonary arterial hypertension Evita Devi Noor Rahmawati; Putrika Prastuti Ratna Gharini; Anggoro Budi Hartopo; Lucia Kris Dinarti; Dyah Wulan Anggrahini
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 55, No 1 (2023)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19106/JMedSci005501202305

Abstract

Pulmonary vascular resistance (PVR) to systemic vascular resistance (SVR) ratio is a prognostic predictor in congenital heart disease (CHD)-associated pulmonary arterial hypertension (PAH) after defect correction. Sildenafil, widely used as a PAH drug, can decrease PVR with minimal or without changes in SVR, resulting in decreased PVR/SVR ratio after treatment. However, there is limited evidence that PVR/SVR ratio reduced after sildenafil therapy in uncorrected CHD-associated PAH patients. This study aimed to investigate the decreasing of the PVR/SVR ratio after ≥ 1-year oral sildenafil therapy in adult uncorrected CHD-associated PAH. A total of 30 uncorrectable CHD-associated PAH subjects derived from the COHARD-PH registry were included in this study. Right heart catheterization (RHC) was performed during the first visit and further evaluations were conducted after ≥1-year oral sildenafil therapy. The PVR/SVR ratio at the baseline and after the evaluation was collected. The primary outcome of this study was the changes in PVR/SVR ratio from baseline to evaluated RHC. Characteristic analysis of subjects with decreased PVR or PVR/SVR ratio was perforemd as the secondary outcome. The mean PVR and SVR were not different from baseline and evaluated RHC (15.98± 10.67 vs. 18.38±13.93 WU, p=0.206 and 36.65±13.99 vs. 39.34±15.46 WU, p=0.262). There was no significant difference in the baseline PVR/SVR ratio and the evaluated PVR/SVR ratio after ≥1-year sildenafil therapy (0.48 ±0.32 vs. 0.49±0.36; p=0.882). As much as 15 subjects (50%) experienced decreased PVR/SVR ratio. However, there was no significant difference in the characteristics, including age, Eisenmenger syndrome, type of shunts, baseline PVR, PAH-specific treatment, and baseline NT-proBNP level (p>0.05). In conclusion, sildenafil therapy does not change PVR/SVR ratio in adults with uncorrected CHD-associated PAH.
Co-Authors Abdul Majid Halim Wiradhika Dyah Wulan Anggrahini Evita Devi Noor Rahmawati Gharini, Putrika Prastuti Ratna Krisdinarti, Lucia Muhammad Reyhan Hadwiono Vera Dewanto