Rapid progression of heart failure secondary to radioactive iodine treatment of hyperthyroidism: A case report.

BACKGROUND: The deterioration of thyroid health is involved in the progression of heart failure (HF). This is usually a lengthy process, so there are almost no reports on its rapid development. Here we report a case of a young male who rapidly developed hypothyroid cardiomyopathy secondary to radioactive iodine treatment, suggesting that severe HF might occur even after a short period of hypothyroidism. CASE SUMMARY: A 26-year-old man was referred to our hospital for HF presenting with dyspnea on exertion and chest discomfort lasting for 1 mo. He received radioactive iodine treatment for hyperthyroidism 1 year ago and had an almost normal echocardiogram 6 mo ago. Admission echocardiogram and cardiac magnetic resonance (CMR) revealed left ventricle (LV) global hypokinesia and severely depressed systolic function. In addition, late gadolinium enhancement indicated no obvious changes in the myocardium. Thyroid function tests showed decreased serum levels of thyroid hormone (TH) and elevated thyroid-stimulating hormone. Based on an exclusionary examination, the patient was diagnosed with hypothyroid cardiomyopathy and was started on replacement therapy. His HF symptoms were completely relieved during the six-month follow-up, and echocardiogram and CMR revealed recovered LV size and ejection fraction. CONCLUSION: This report demonstrates that severe fluctuations in TH levels may lead to acute HF, which can completely recover with timely thyroid hormone replacement. In addition, our findings highlight the importance of routinely detecting cardiac function in patients treated with radioactive iodine.

Mortalité, congé et arythmie chez les patients ayant la COVID-19 et une atteinte cardiaque.

CONTEXTE: Les atteintes cardiaques sont fréquentes dans les cas graves de maladie à coronavirus 2019 (COVID-19) et sont associées à un mauvais pronostic. Notre étude portait sur les facteurs prédictifs de mortalité intrahospitalière, les caractéristiques de l'arythmie et les effets des traitements qui allongent l'intervalle QT chez les patients ayant une atteinte cardiaque. MÉTHODES: Nous avons fait une étude de cohorte rétrospective des cas graves de COVID-19 admis à l'hôpital Tongji, à Wuhan, en Chine, entre le 29 janvier et le 8 mars 2020. En examinant ceux qui avaient une atteinte cardiaque, définie ici comme un taux élevé de troponine I cardiaque (TnIc), nous avons déterminé les caractéristiques biologiques et cliniques associées à la mortalité et au besoin de ventilation invasive. RÉSULTATS: Parmi les 1284 cas graves de COVID-19, 1159 avaient au dossier un taux de TnIc mesuré à l'admission, qui pour 170 (14,7 %) participants indiquait une atteinte cardiaque. Les patients ayant une atteinte cardiaque avaient un taux de mortalité nettement plus élevé que les autres patients (71,2 % c. 6,6 %; p < 0,001). Nous avons constaté que le taux de TnIc initial (pour chaque augmentation d'un facteur 10, rapport de risque [HR] 1,32, intervalle de confiance [IC] à 95 % 1,06­1,66) et le taux de TnIc maximal atteint au cours de la maladie (pour chaque augmentation d'un facteur 10, HR 1,70, IC à 95 % 1,38­2,10) étaient associés à de minces chances de survie. Le taux de TnIc maximal était aussi associé au besoin de ventilation invasive (rapport de cotes 3,02, IC à 95 % 1,92­4,98). Sur les 170 patients ayant une atteinte cardiaque, 44 (25,9 %) présentaient une arythmie. Les 6 qui souffraient de tachycardie ou de fibrillation ventriculaires sont morts. Nous avons remarqué que les patients qui recevaient des médicaments allongeant l'intervalle QT avaient un intervalle QTc plus long que ceux qui n'en recevaient pas (différence entre les médianes 45 ms; p = 0,01), mais que ce traitement n'était pas directement lié à la mortalité (HR 1,04, IC à 95 % 0,69­1,57). INTERPRÉTATION: Chez les patients ayant la COVID-19 et une atteinte cardiaque, les taux initial et maximal de TnIc sont associés à de minces chances de survie, et le taux maximal est un facteur prédictif du besoin de ventilation invasive. Les malades de la COVID-19 doivent subir un dépistage des atteintes cardiaques et être surveillés, surtout si on leur fait suivre un traitement qui peut prolonger la repolarisation. Enregistrement de l'essai : Registre des essais cliniques chinois, n° ChiCTR2000031301.

Death, discharge and arrhythmias among patients with COVID-19 and cardiac injury.

BACKGROUND: Cardiac injury is common in severe coronavirus disease 2019 (COVID-19) and is associated with poor outcomes. We aimed to study predictors of in-hospital death, characteristics of arrhythmias and the effects of QT-prolonging therapy in patients with cardiac injury. METHODS: We conducted a retrospective cohort study involving patients with severe COVID-19 who were admitted to Tongji Hospital in Wuhan, China, between Jan. 29 and Mar. 8, 2020. Among patients who had cardiac injury, which we defined as an elevated level of cardiac troponin I (cTnI), we identified demographic and clinical characteristics associated with mortality and need for invasive ventilation. RESULTS: Among 1284 patients with severe COVID-19, 1159 had a cTnI level measured on admission to hospital, of whom 170 (14.7%) had results that showed cardiac injury. We found that mortality was markedly higher in patients with cardiac injury (71.2% v. 6.6%, p < 0.001). We determined that initial cTnI (per 10-fold increase, hazard ratio [HR] 1.32, 95% confidence interval [CI] 1.06-1.66) and peak cTnI level during illness (per 10-fold increase, HR 1.70, 95% CI 1.38-2.10) were associated with poor survival. Peak cTnI was also associated with the need for invasive ventilation (odds ratio 3.02, 95% CI 1.92-4.98). We found arrhythmias in 44 of the 170 patients with cardiac injury (25.9%), including 6 patients with ventricular tachycardia or fibrillation, all of whom died. We determined that patients who received QT-prolonging drugs had longer QTc intervals than those who did not receive them (difference in medians, 45 ms, p = 0.01), but such treatment was not independently associated with mortality (HR 1.04, 95% CI 0.69-1.57). INTERPRETATION: We found that in patients with COVID-19 and cardiac injury, initial and peak cTnI levels were associated with poor survival, and peak cTnI was a predictor of need for invasive ventilation. Patients with COVID-19 warrant assessment for cardiac injury and monitoring, especially if therapy that can prolong repolarization is started. TRIAL REGISTRATION: Chinese Clinical Trial Registry, No. ChiCTR2000031301.

A new method for the assessment of endothelial function with peripheral arterial volume.

BACKGROUND: Currently, many methodological approaches have been developed to assess peripheral endothelial function. However, a development of the noninvasive and automated technique for routinely assessing endothelial function is still required. We evaluated the potential value of a new method to measure peripheral endothelial function with reactive hyperemia peripheral arterial volume (RH-PAV) in patients with chest pain. METHODS: We used a novel oximeter-like probe to detect the peripheral arterial volume (PAV) of the finger and compared it with brachial flow-mediated dilation (FMD) performed in 93 consecutive patients with chest pain. The RH-PAV index was defined as the ratio of the digital pulse volume during reactive hyperemia relative to the baseline. RESULTS: Ninety-three patients (53 men, 58 ± 5 years) completed the study, and 53 patients demonstrated coronary artery disease (CAD) following scheduled coronary angiography. There was a moderate linear relationship between PAV and FMD (r = 0.69, p < 0.01). Similar to FMD, PAV was more impaired in patients who have more cardiovascular risk factors (CRFs). The subjects with CAD had lower PAV and FMD, compared with those without CAD (1.05 ± 0.23 VS. 1.41 ± 0.37, p < 0.01; 6.7% ± 2.9% VS. 10.4% ± 2.9%, p < 0.01, respectively), and the relationships between FMD and PAV were also significant in both CAD (r = 0.54, p < 0.01) and non-CAD (r = 0.62, p < 0.01) patients. CONCLUSIONS: Endothelial function of digital artery assessed with the novel PAV method demonstrated a profile similar to that of brachial artery measured with FMD. The hyperemia PAV was decreased by factors which were considered to impair endothelial function, suggesting that PAV has the potential to be a novel method to study endothelial function.

Realization of fully automated quantification of left ventricular volumes and systolic function using transthoracic 3D echocardiography.

BACKGROUND: Study on automated three-dimensional (3D) quantification of left heart parameters by using Heartmodel software is still in the early stage and fully automatic analysis was not clearly achieved. The aim of our study was to evaluate the performance of this new technology in measuring left ventricular (LV) volume and ejection fraction (EF) in patients with a variety of heart diseases on the basis of rationally determining the default endocardial border values. METHODS: Subjects with a variety of heart diseases were included prospectively. High quality Heartmodel images were selected to determine the end-diastolic and end-systolic default values of endocardial border. The accuracy and reproducibility of automated three-dimensional echocardiography (3DE) for measuring LV end-diastolic volume (EDV), end-systolic volume (ESV) and EF were evaluated with the traditional manual 3DE as the relative standard. RESULTS: Ninety seven subjects were enrolled in the study. The default endocardial border values were determined as 66% and 40% for end-diastole (ED) and end-systole (ES), respectively. Most of the subjects (84/97) were automatically analyzed by Heartmodel software without manual adjustment, revealing a close correlation of automated 3DE with manual 3DE in measuring EDV, ESV and EF (r-values: EDV: 0.96, ESV: 0.97, EF: 0.96). The EDV and ESV values obtained by automated 3DE were higher than those measured by manual 3DE (biases: EDV: 16 ± 18 ml, ESV: 11 ± 12 ml). The intra- and inter-observer reproducibility of automated 3DE was better than that of manual 3DE. Automated 3DE with manual adjustment showed good consistency with manual 3DE in assessing the impairment degree of systolic function in patients with wall motion abnormalities (n = 58), (Kappa = 0.74, P = 0.00). CONCLUSION: Fully automated 3DE quantification of LV volume and EF could be achieved in most patients. Since automated 3DE was accurate and more reproducible, it could replace the existing manual 3DE technology and be routinely used in clinical practice.

The effects of amlodipine and S(-)-amlodipine on vascular endothelial function in patients with hypertension.

BACKGROUND: Amlodipine has been shown to improve vascular endothelial function in hypertensive patients, but whether S(-)-amlodipine has a similar effect remains controversial. This study compared the effects of amlodipine and S(-)-amlodipine on vascular endothelial function in hypertensive patients and investigated relevant mechanisms of action in cell culture. METHODS: Twenty-four patients with essential hypertension received amlodipine and S(-)-amlodipine for 6 weeks in a randomized, crossover study. Associated flow-mediated dilation (FMD), nitric oxide (NO), and endothelial nitric oxide synthase (eNOS) levels were determined. NO levels were measured after exposure of human umbilical vein endothelial cells (HUVECs) to amlodipine, S(-)-amlodipine, the eNOS inhibitor N w-nitro-L-arginine (L-NA), and the Protein Kinase C (PKC) inhibitor Ro 31-8220. Phosphorylation levels of Ser(1177) and Thr(495) in eNOS were determined after exposure to amlodipine, S(-)-amlodipine, and Ro 31-8220. RESULTS: FMD, NO, and eNOS levels significantly improved after treatment with amlodipine and S(-)-amlodipine. The levels were all higher with amlodipine, although the between-treatment difference was not statistically significant. Amlodipine and S(-)-amlodipine significantly increased NO levels in cultured HUVECs, but increases in NO levels were more marked with amlodipine. Western blot assay showed that both amlodipine and Ro31-8220 induced Ser(1177) phosphorylation and weakened Thr(495) phosphorylation in eNOS. S(-)-amlodipine had no similar effects. Amlodipine, but not S(-)-amlodipine, decreased the PKC phosphorylation in a time-dependent manner. CONCLUSIONS: Amlodipine and S(-)-amlodipine can both improve endothelial function in hypertensive patients. Amlodipine has greater potential for vascular endothelial protection than S(-)-amlodipine. It affects eNOS phosphorylation at Ser(1177) and Thr(495) by the PKC pathway, further enhancing eNOS activation.

Primary pulmonary artery rhabdomyosarcoma.

A 69-year-old woman presented with a 4-month history of dyspnoea and radiating upper-right quadrant pain and oedema in her lower extremities for more than 20 days. The ultrasonographic study of the heart revealed the adherence of a substantive hypoechoic mass (73 x 34 mm) to the antelateral wall of the pulmonary artery and resultant pulmonary stenosis. Computed tomographic imaging of the pulmonary artery revealed an irregularly shaped filling defect (approximately 41 x 39 x 59 mm) in the main pulmonary artery. The boundary of the defect was irregular, but demarcation with healthy tissue was clear. After surgical treatment, the histologic and immunohistochemical assays revealed a primary pulmonary artery rhabdomyosarcoma. Pulmonary artery rhabdomyosarcomas are usually misdiagnosed as other pulmonary artery obstructive diseases. There should be a greater focus of clinical attention and resection is the appropriate surgical treatment for such malignant tumours.