Clinically Suspected Exercise-Induced Myocarditis in a Patient With Vascular Ehlers-Danlos Syndrome.

Ehlers-Danlos syndrome (EDS) is an inherited condition that affects connective tissue structures throughout the body. EDS type IV is a specific subset of EDS that targets vascular structures. Patients with EDS type IV can have a wide range of vascular disorders such as myocarditis and are advised to refrain from participating in contact sports and high-intensity physical exercises to avoid life-threatening cardiovascular conditions such as arterial dissection or rupture. In this report, we present the case of an EDS type IV patient with myocarditis secondary to exercise. The patient received supportive treatment including beta-blockers, bed rest, and refraining from intense physical exertion.

Post-COVID-19 Syndrome: A Novel Diagnosis.

Patients with post-COVID-19 syndrome have reported a wide array of symptoms that include autonomic dysfunction. It is hypothesized that this may be secondary to interruption of baroreflex pathways in the carotid arteries or nucleus tractus solitarius, however, confirming studies have yet to be performed. A limited number of studies have highlighted the presence of an exaggerated baroreflex response in patients with a post-COVID-19 syndrome that mirror other chronic autonomic dysfunction-related conditions.

Incidence of Atrioventricular Block After Valve Replacement in Carcinoid Heart Disease.

BACKGROUND: Carcinoid heart disease (CaHD) is a rare condition that has a high impact on the morbidity and mortality of its patients. Once heart failure symptoms develop in the patient with CaHD, cardiac valve surgery is often the only effective treatment. Although atrioventricular block (AVB) is a known postoperative complication of the valve surgery, the incidence of AVB in this population has not been well described. METHODS: Comprehensive records were collected retrospectively on consecutive patients with CaHD who underwent a valve surgery at a tertiary medical center from January 2001 to December 2015. We excluded patients with pre-existing permanent pacemaker (PPM). RESULTS: Nineteen consecutive patients were included in this study and 18 of them underwent at least dual valve (tricuspid and pulmonary valve) replacement surgery. Our 30-day post-surgical mortality was 0%. During the 6-month observation period following the surgery, 31.5% (n = 6) required PPM implantation due to complete AVB. There was no statistical difference in baseline characteristics and electrocardiographic and echocardiographic parameters between the patients who did or did not require PPM placement. CONCLUSIONS: Our study revealed that almost one-third of CaHD patients who underwent a valve replacement surgery developed AVB requiring PPM implantation. Due to high incidence of PPM requirement, we believe that prophylactic placement of an epicardial lead during the valve surgery can be helpful in these patients to reduce serious complication from placement of pacemaker lead on a later date through a prosthetic valve.

What is causing extremely elevated amino terminal brain natriuretic peptide in cancer patients?

High levels of B-type natriuretic peptide in cancer patients are poorly studied. Previously published data suggest that they are not related to fluid overload and are encountered mostly in solid cancers. The authors investigated the distribution of amino terminal pro-brain natriuretic peptide (NT-proBNP) between hematologic and solid organ malignancies and the relationship of NT-proBNP with volume status in oncologic patients. A total of 145 consecutive patients with at least one occurrence of NT-proBNP exceeding the upper normal range 10-fold were identified. The authors retrospectively reviewed their records including clinical, laboratory, and radiological data and echocardiograms. More than 70% of patients had hematologic malignancies. Patients with NT-proBNP >50,000 pg/mL had only hematologic malignancies, primarily multiple myeloma. There was no association between M-spike proteins and NT-proBNP. About 80% of patients had signs of fluid overload. The magnitude of NT-proBNP elevation was similar between those with and without heart failure or volume overload, as well as with solid cancers vs hematologic malignancies. Contrary to prior reports, it was found that very high NT-proBNP in cancer patients is usually encountered in the context of fluid overload and most often in hematologic malignancies.

Role of the carboxy-terminal transactivation domain and active transcription in the ligand-induced and ligand-independent degradation of the mouse Ahb-1 receptor.

To assess the importance of transactivation domains (TAD), DNA binding and transcription on the degradation of the AH receptor (AHR), Hepa-1 cells were pre-treated with actinomycin D (AD) or cycloheximide (CHX) and exposed to 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). AD or CHX did not affect nuclear localization or DNA binding of the AHR but inhibited ligand-induced degradation. In contrast, AD or CHX did not inhibit geldanamycin (GA) induced degradation of the AHR. To assess the role of the COOH-terminal TAD in AHR degradation, stop codons were placed at nucleotide 1501 and 1921 of the Ah(b-1) AHR coding region to generate AHR(500) and AHR(640). Stable cell lines were generated and exposed to TCDD. Cells expressing AHR(500) did not induce CYP1A1 protein, but exhibited significant degradation of AHR(500). Cells expressing AHR(640) induced CYP1A1 protein to 50% of the level of cells expressing wild type AHR and exhibited significant degradation of AHR(640). Importantly, AD and CHX did not inhibit the TCDD-induced degradation of either AHR(500) and AHR(640) and these receptors showed a more rapid profile of ligand-induced degradation compared to cells expressing wild type AHR. TCDD exposure to Hepa-1 cells with reduced aryl hydrocarbon receptor nuclear translocator (ARNT), showed ligand-induced degradation of the AHR that was not blocked by AD. However, AD inhibited TCDD-induced degradation when ARNT expression was restored. These results show that multiple mechanisms exist for the ligand and GA-induced degradation of the AHR and suggest that ligand-induced degradation can switch between two mechanisms depending on the presence of a functional TAD and the binding to DNA.