A risk prediction index for amiodarone-induced thyrotoxicosis in adults with congenital heart disease.
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ABSTRACT:
SUBMITTER: Stan MN
PROVIDER: S-EPMC3306911 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:There is a lack of information about a mixed type of amiodarone-induced thyrotoxicosis (AIT) after heart transplantation (HTx) with no amiodarone treatment in almost 1 year. Frequent ventricular extrasystoles (VES) associated with a mixed type of AIT can often be treated using thiamazole and prednisolone, without the need for specific antiarrhythmic treatment. We present a clinical case of a 65-year-old heart transplanted male patient with frequent VES associated with mixed type of AIT. Recipient had managed with amiodarone prior to HTx but there were no indications for it after the surgery. One year after antiarrhythmic treatment was discontinued, monomorphic VES (total amount: 27 472/day) were diagnosed. In addition, our investigation revealed that thyrotoxicosis developed. Prednisolone and thiamazole were added to the treatment with positive outcomes. The antithyroid treatment had been discontinued after 9 months and results of the 24-h Holter electrocardiogram monitoring showed only two VES/24 h. The case highlights the association of amiodarone, thyroid disorders, and VES. In mixed type AIT or if diagnosis is uncertain, it is reasonable to use mixed therapy. Next is to decide whether you need special treatment for VES. There was no evidence of ventricular tachycardia. Thyroid function tests remained normal off antithyroid medications and the total amount of VES significantly decreased. There were no indications for any antiarrhythmic treatment or ablation.
| S-EPMC6601152 | biostudies-literature
Project description:Possible triggers and genetic markers involved in pathogenesis of amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH) are currently unknown. This study aimed to analyze the association between polymorphisms in the genes involved in thyroid hormones biosynthesis and metabolism. Thirty-nine consecutive patients with confirmed type 2 amiodarone-induced thyrotoxicosis were enrolled; 39 patients on the same therapy for at least 6 months without thyroid pathology were included as a control group. A comparative study was carried out to determine the distribution and genotypes of polymorphic markers of the (Na)-iodide symporter (NIS) genes (rs7250346, C/G substitution), thyroid stimulating hormone receptor (TSHR) (rs1991517, C/G substitution), thyroid peroxidase (TPO) (rs 732609, A/C substitution), DUOX 1-1 (C/T substitution), DUOX 1-2 (G/T substitution), DUOX 1-3 (C/T substitution), glutathione peroxidase 3 (GPX3) (C/T substitution), glutathione peroxidase 4 (GPX4) (C/T substitution). Statistical analysis was performed using Prism (Version 9.0.0 (86)). This study showed that the risk of AIT2 is 3.18 times higher in the G/T of the DUOX1 gene carriers. This study is the first report of genetic markers associated with amiodarone-related adverse events conducted in humans. The obtained results indicate the necessity for a personalized approach to amiodarone administration.
| S-EPMC9964217 | biostudies-literature
Project description:The adult with congenital heart disease (CHD) is at risk of developing atherosclerotic cardiovascular disease (ASCVD). We performed a cross-sectional study to describe established ASCVD risk factors and estimate 10-year and lifetime risk of ASCVD in adults over age 18 with CHD of moderate or great complexity using 3 validated risk assessment tools-the Framingham Study Cardiovascular Disease Risk Assessment, the Reynolds Risk Score, and the ASCVD Risk Estimator. We obtained extensive clinical and survey data on 178 enrolled patients, with average age 37.1 ± 12.6 years, 51% men. At least 1 modifiable ASCVD risk factor was present in 70%; the 2 most common were overweight/obesity (53%) and systemic hypertension (24%). Laboratory data were available in 103 of the 178 patients. Abnormal levels of glycated hemoglobin, high-sensitivity C-reactive protein, and high-density lipoprotein were each found in around 30% of patients. The 10-year ASCVD predicted risk using all 3 tools was relatively low (i.e., at least 90% of patients <10% risk), yet the median estimated lifetime risk was 36%. In conclusion, ASCVD risk factors are prevalent in adults with CHD. The risk estimation tools suggest that this population is particularly vulnerable to ASCVD with aging and should undergo guideline-based screening and management of modifiable risk factors.
| S-EPMC5334785 | biostudies-literature
Project description:BACKGROUND AND OBJECTIVES:The objective of this study was to analyze cardiovascular risk factors in adults with congenital heart disease (ACHD). SUBJECTS AND METHODS:The subjects for this study comprised 135 patients, aged 18 years and above, who visited the ACHD clinic at the Samsung Medical Center and 135 adults with a structurally normal heart who were randomly selected from the Center for Health Promotion during the same period. For the analysis, the ACHD group was further divided into an ACHD group that underwent correction by cardiac surgery and a cyanotic group. RESULTS:The mean (standard diviation) age (years) of patients in the surgically corrected group was 48.4 (10.9) years, while that of patients in the cyanotic group was 43.1 (9.0) years and that of patients in the control group was 47.1 (10.3) years (p=0.042). The adjusted odds ratios (ORs) for past smoking, hypertension, diabetes mellitus, hypercholesterolemia, obesity, and metabolic syndrome were significantly higher in the surgically corrected patients than in the controls. However, the ORs for all variables excluding past smoking were significantly lower in the cyanotic group compared with the control group. After adjustment for age, gender, smoking, alcohol use, and exercise, the ORs for metabolic syndrome were 0.46 (0.35-0.57, p<0.001) and 1.48 (1.14-1.92, p=0.003) in the cyanotic and surgically corrected groups, respectively. CONCLUSION:Cardiovascular risk factors need to be considered in surgically corrected ACHD patients as well as in adults with a structurally normal heart. A further study with a long-term follow-up is needed for developing guidelines for prevention.
| S-EPMC4580701 | biostudies-literature
Project description:Metabolic syndrome increases risk for atherosclerotic coronary artery disease, and its prevalence increases with increasing age and body mass index. Adults with congenital heart disease (ACHD) are now living longer and accruing coronary artery disease risk factors. However, the prevalence of metabolic syndrome in ACHD patients is unknown.We conducted a retrospective cohort study of ACHD patients at our center to quantify the prevalence of metabolic syndrome in an ACHD population. Using case-control matching, we constructed a comparable control group from a population-based sample of 150 104 adults. International Diabetes Federation criteria were used to define metabolic syndrome. We used logistic regression to compare the risk of metabolic syndrome across the resulting cohorts, which were composed of 448 ACHD patients and 448 controls matched by age and sex. Mean age of both groups was 32.4±11.3 years, and 51.3% were female. Obesity was present in 16.1% of the ACHD patients and 16.7% of the controls. Metabolic syndrome was more common in ACHD patients than in controls (15.0% versus 7.4%; odds ratio 1.82, 95% CI 1.25-2.65).Our data suggest that metabolic syndrome is more common among adults with congenital heart disease than in the general population. Thus, patients with congenital heart disease should be screened for metabolic syndrome and risk factors mitigated where possible to prevent atherosclerotic coronary artery disease. Preventive cardiology should be included during routine ACHD care.
| S-EPMC4802435 | biostudies-other
Project description:AimsAdequate risk prediction can optimize the clinical management in adult congenital heart disease (ACHD). We aimed to update and subsequently validate a previously developed ACHD risk prediction model.Methods and resultsA prediction model was developed in a prospective cohort study including 602 moderately or severely complex ACHD patients, enrolled as outpatients at a tertiary centre in the Netherlands (2011-2013). Multivariable Cox regression was used to develop a model for predicting the 1-year risks of death, heart failure (HF), or arrhythmia (primary endpoint). The Boston ACHD Biobank study, a prospectively enrolled cohort (n = 749) of outpatients who visited a referral centre in Boston (2012-2017), was used for external validation. The primary endpoint occurred in 153 (26%) and 191 (28%) patients in the derivation and validation cohorts over median follow-up of 5.6 and 2.3 years, respectively. The final model included 5 out of 14 pre-specified predictors with the following hazard ratios; New York Heart Association class ≥II: 1.92 [95% confidence interval (CI) 1.28-2.90], cardiac medication 2.52 (95% CI 1.72-3.69), ≥1 reintervention after initial repair: 1.56 (95% CI 1.09-2.22), body mass index: 1.04 (95% CI 1.01-1.07), log2 N-terminal pro B-type natriuretic peptide (pmol/L): 1.48 (95% CI 1.32-1.65). At external validation, the model showed good discrimination (C-statistic 0.79, 95% CI 0.74-0.83) and excellent calibration (calibration-in-the-large = -0.002; calibration slope = 0.99).ConclusionThese data support the validity and applicability of a parsimonious ACHD risk model based on five readily available clinical variables to accurately predict the 1-year risk of death, HF, or arrhythmia. This risk tool may help guide appropriate care for moderately or severely complex ACHD.
| S-EPMC8728026 | biostudies-literature
Project description:BackgroundMore children with congenital heart disease (CHD) are surviving to adulthood, and CHD is associated with risk factors for dementia. We compared the risk of dementia in CHD adults to that of the general population.MethodsIn this cohort study, we used medical registries and a medical record review covering all Danish hospitals to identify adults with CHD diagnosed between 1963 and 2012. These individuals with CHD were followed from January 1, 1981, 30 years of age, or date of first CHD registration (index date for matched members of the general population cohort) until hospital diagnosis of dementia, death, emigration, or end of study (December 31, 2012). For each individual with CHD, we identified 10 members of the general population utilizing the Danish Civil Registration System matched on sex and birth year. We computed cumulative incidences and hazard ratios (HRs) of dementia, adjusting for sex and birth year.ResultsThe cumulative incidence of dementia was 4% by 80 years of age in 10 632 adults with CHD (46% male). The overall HR comparing adults with CHD with the general population cohort was 1.6 (95% confidence interval [CI], 1.3-2.0). The HR among individuals with CHD without extracardiac defects was 1.4 (95% CI, 1.1-1.8). Adults with mild-to-moderate CHD had an HR of 1.5 (95% CI, 1.1-2.0), whereas the HR was 2.0 (95% CI, 1.2-3.3) for severe CHD, including univentricular hearts. The HR for early onset dementia (<65 years of age) was 2.6 (95% CI, 1.8-3.8), whereas the late-onset HR was 1.3 (95% CI, 1.0-1.8).ConclusionsCHD was associated with an increased risk of dementia compared with the general population, in particular for early onset dementia. Further understanding of dementia risk in the population with CHD is a potential target for future investigation.
| S-EPMC5930034 | biostudies-literature
Project description:Amiodarone has a profound adverse toxicity profile. Large population-based analyses quantifying the risk of thyroid dysfunction (TD) in adults with and without congenital heart disease (ACHD) are lacking. All adults registered with a major German health insurer (≈9.2 million members) with amiodarone prescriptions were analyzed. Occurrence of amiodarone-associated TD was assessed. Overall, 48,891 non-ACHD (37% female; median 73 years) and 886 ACHD (34% female; median 66 years) received amiodarone. Over 184,787 patient-years, 10,875 cases of TD occurred. The 10-year risk for TD was 38% in non-ACHD (35% ACHD). Within ACHD, compared to amiodarone-naïve patients, the hazard ratio (HR) for TD was 3.9 at 4 years after any amiodarone exposure. TD was associated with female gender (HR 1.42, p < 0.001) and younger age (HR 0.97 per 10 years, p = 0.009). Patients with congenital heart disease were not at increased risk (HR 0.98, p = 0.80). Diagnosis of complex congenital heart disease, however, was a predictor for TD (HR 1.56, p = 0.02). Amiodarone was continued in 47% of non-ACHD (38% ACHD), and 2.3% of non-ACHD (3.5% ACHD) underwent thyroid surgery/radiotherapy. Amiodarone-associated TD is common and comparable in non-ACHD and ACHD. While female gender and younger age are predictors for TD, congenital heart disease is not necessarily associated with an elevated risk.
| S-EPMC8999848 | biostudies-literature
Project description:Metabolomic analysis may provide an integrated assessment in genetically and pathologically heterogeneous populations. We used metabolomic analysis to gain mechanistic insight into the small and diverse population of adults with congenital heart disease (ACHD). Consecutive ACHD patients seen at a single institution were enrolled. Clinical variables and whole blood were collected at regular clinical visits. Stored plasma samples were analyzed for the concentrations of 674 metabolites and metabolic markers using mass spectrometry with internal standards. These samples were compared to 28 simultaneously assessed healthy non-ACHD controls. Principal component analysis and multivariable regression modeling were used to identify metabolites associated with clinical outcomes in ACHD. Plasma from ACHD and healthy control patients differed in the concentrations of multiple metabolites. Differences between control and ACHD were greater in number and in degree than those between ACHD anatomic groups. A metabolite cluster containing amino acids and metabolites of amino acids correlated with negative clinical outcomes across all anatomic groups. Metabolites in the arginine metabolic pathway, betaine, dehydroepiandrosterone, cystine, 1-methylhistidine, serotonin and bile acids were associated with specific clinical outcomes. Metabolic markers of disease may both be useful as biomarkers for disease activity and suggest etiologically related pathways as possible targets for disease-modifying intervention.
| S-EPMC8398700 | biostudies-literature
Project description:The adult congenital heart diseases (ACHD) population is exceeding the pediatric congenital heart diseases (CHD) population and is progressively expanding each year, representing more than 90% of patients with CHD. Of these, about 75% have undergone surgical and/or percutaneous intervention for palliation or correction. Autopsy can be a very challenging procedure in ACHD patients. The approach and protocol to be used may vary depending on whether the pathologists are facing native disease without surgical or percutaneous interventions, but with various degrees of cardiac remodeling, or previously palliated or corrected CHD. Moreover, interventions for the same condition have evolved over the last decades, as has perioperative myocardial preservations and postoperative care, with different long-term sequelae depending on the era in which patients were operated on. Careful clinicopathological correlation is, thus, required to assist the pathologist in performing the autopsy and reaching a diagnosis regarding the cause of death. Due to the heterogeneity of the structural abnormalities, and the wide variety of surgical and interventional procedures, there are no standard methods for dissecting the heart at autopsy. In this paper, we describe the most common types of CHDs that a pathologist could encounter at autopsy, including the various types of surgical and percutaneous procedures and major pathological manifestations. We also propose a practical systematic approach to the autopsy of ACHD patients.
| S-EPMC7272495 | biostudies-literature