scholarly journals Is it possible to operate four heart valves in a patient with heart failure, congenital heart disease and pulmonary hypertension?

Cor et Vasa ◽  
2012 ◽  
Vol 54 (9-10) ◽  
pp. e295-e299 ◽  
Author(s):  
Marie Zvěřinová ◽  
Jana Popelová ◽  
Petr Pavel ◽  
Roman Gebauer ◽  
Pavel Jehlička ◽  
...  
2021 ◽  
Vol 61 (3) ◽  
pp. 119-24
Author(s):  
Weny Inrianto ◽  
Indah Kartika Murni ◽  
Ida Safitri

Background Left-to-right shunting in acyanotic congenital heart disease (CHD) is the most common type of defect in childhood heart disease. Limited access to specialist health services causes delays in CHD management. In limited resource settings, identification of factors that influence the occurrence of pulmonary hypertension is important in order to decide which patients should be prioritized for defect closure to prevent further complications. Objective To determine predictive factors of pulmonary hypertension after a left-to-right shunt CHD diagnosis. Methods This retrospective cohort study included children aged 1 month to 17 years with isolated atrial septal defect, or ventricular septal defect, or patent ductus arteriosus. Potential predictors studied were iron deficiency anemia, mitral regurgitation, pneumonia, and heart failure. Bivariate analysis was done with Chi-square test and multivariate analysis was done with Cox regression to determine the hazard ratio. Results Pulmonary hypertension occurred in 68 of 176 subjects. Iron deficiency anemia, mitral regurgitation, and pneumonia were not predictives of pulmonary hypertension. However, heart failure was a significant predictive factor for pulmonary hypertension, with a hazard ratio of 4.1 (95%CI 2.2 to 7.5; P=0.001). Conclusions Heart failure is a predictive factor of pulmonary hypertension in children with left-to-right shunting in acyanotic CHD.


Heart ◽  
2020 ◽  
Vol 106 (17) ◽  
pp. 1302-1309 ◽  
Author(s):  
Robert M Radke ◽  
Tim Frenzel ◽  
Helmut Baumgartner ◽  
Gerhard-Paul Diller

Adults with congenital heart disease (ACHD) may be at high risk in the case of COVID-19. Due to the heterogeneity of ACHD and secondary complications, risk profiles are, however, not uniform. This document aims to give an overview of relevant data and outline our pragmatic approach to disease prevention and management. Based on anatomy and additional physiological factors including symptoms, exercise capacity, heart failure, pulmonary hypertension and cyanosis, we propose a pragmatic approach to categorising patients into low-risk, intermediate-risk and high-risk groups. We regard especially patients with complex cyanotic conditions, those with palliated univentricular hearts, heart failure, severe valvular disease or pulmonary hypertension as high-risk patients. To avoid infection, we recommend self-isolation and exemption from work for these cohorts. Infected ACHD patients with low or moderate risk and without signs of deterioration may be remotely followed and cared for at home while in self isolation. High-risk patients or those with signs of respiratory or cardiovascular impairment require admission ideally at a tertiary ACHD centre. Especially patients with complex, cyanotic disease, heart failure and arrhythmias require particular attention. Treatment in patients with cyanotic heart disease should be guided by the relative degree of desaturation compared with baseline and lactate levels rather than absolute oxygen saturation levels. Patients with right heart dilatation or dysfunction are potentially at increased risk of right heart failure as mechanical ventilation and acute respiratory distress syndrome can lead to increase in pulmonary arterial pressures.


Heart ◽  
2018 ◽  
Vol 105 (6) ◽  
pp. 465-469 ◽  
Author(s):  
Despoina Ntiloudi ◽  
Sotiria Apostolopoulou ◽  
Konstantinos Vasiliadis ◽  
Alexandra Frogoudaki ◽  
Aphrodite Tzifa ◽  
...  

ObjectiveDespite the progress in the management of patients with adult congenital heart disease (ACHD), a significant proportion of patients still develop pulmonary hypertension (PH). We aimed to highlight the rate of the complications in PH-ACHD and the predicting factors of cumulative mortality risk in this population.MethodsData were obtained from the cohort of the national registry of ACHD in Greece from February 2012 until January 2018.ResultsOverall, 65 patients receiving PH-specific therapy were included (mean age 46.1±14.4 years, 64.6% females). Heavily symptomatic (New York Heart Association (NYHA) class III/IV) were 53.8% of patients. The majority received monotherapy, while combination therapy was administered in 41.5% of patients. Cardiac arrhythmia was reported in 30.8%, endocarditis in 1.5%, stroke in 4.6%, pulmonary arterial thrombosis in 6.2%, haemoptysis in 3.1% and hospitalisation due to heart failure (HF) in 23.1%. Over a median follow-up of 3 years (range 1–6), 12 (18.5%) patients died. On univariate Cox regression analysis history of HF hospitalisation emerged as a strong predictor of mortality (HR 8.91, 95% CI 2.64 to 30.02, p<0.001), which remained significant after adjustment for age and for NYHA functional class.ConclusionsLong-term complications are common among patients with PH-ACHD. Hospitalisations for HF predict mortality and should be considered in the risk stratification of this population.


2013 ◽  
Vol 11 (4) ◽  
pp. 189-195 ◽  
Author(s):  
Jamil A. Aboulhosn

This manuscript is intended to provide a brief overview of the indications for and outcomes of surgical and transcatheter interventions for congenital heart disease and pulmonary hypertension (PH). Pulmonary hypertension is frequently encountered in children and adults with congenital heart disease and is most commonly related to large “central” shunts, ie, those occurring at the ventricular or great arterial level (Figure 1). If uncorrected early in infancy or childhood, large central shunts result in increased pulmonary blood flow, left heart volume overload, PH, and heart failure. If the child survives this initial period of volume overload and heart failure, they will very likely develop effacement of the normal pulmonary arterial architecture and severe elevations in pulmonary arterial resistance, eventually resulting in cyanosis and Eisenmenger syndrome.1


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