Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper airway obstruction during sleep, and it is closely linked to several cardiovascular issues due to intermittent hypoxia, nocturnal hypoxemia, and disrupted sleep patterns. Pulmonary hypertension (PH), identified by elevated pulmonary arterial pressure, shares a complex interplay with OSA, contributing to cardiovascular complications and morbidity. The prevalence of OSA is alarmingly high, with studies indicating rates of 20-30% in males and 10-15% in females, escalating significantly with age and obesity. OSA\'s impact on cardiovascular health is profound, particularly in exacerbating conditions like systemic hypertension and heart failure. The pivotal role of hypoxemia increases intrathoracic pressure, inflammation, and autonomic nervous system dysregulation in this interplay, which all contribute to PH\'s pathogenesis. The prevalence of PH among OSA patients varies widely, with studies reporting rates from 15% to 80%, highlighting the variability in diagnostic criteria and methodologies. Conversely, OSA prevalence among PH patients also remains high, often exceeding 25%, stressing the need for careful screening and diagnosis. Treatment strategies like continuous positive airway pressure (CPAP) therapy show promise in mitigating PH progression in OSA patients. However, this review underscores the need for further research into long-term outcomes and the efficacy of these treatments. This review provides comprehensive insights into the epidemiology, pathophysiology, and treatment of the intricate interplay between OSA and PH, calling for integrated, personalized approaches in diagnosis and management. The future landscape of OSA and PH management hinges on continued research, technological advancements, and a holistic approach to improving patient outcomes.

Congestive hepatopathy (CH), stemming from compromised hepatic venous flow or heightened intrahepatic pressure, represents a significant consequence of cardiovascular conditions like congestive heart failure (CHF). This review of literature encapsulates the core aspects of this condition, characterized by hepatic congestion, cellular injury, and impaired liver function. Diagnostic challenges arise due to symptoms mirroring primary liver diseases. Management revolves around addressing the underlying cause and mitigating fluid retention. This review of literature provides a snapshot of CH\'s complexity, emphasizing its clinical implications and the need for comprehensive understanding in clinical practice.

Oral treprostinil, approved for the treatment of pulmonary arterial hypertension, remains an attractive option in combination with other medications to delay disease progression and improve exercise capacity. However, patients are often challenged with the ability to overcome adverse effects as outpatients and reach effective doses in a timely manner. We describe a case of a 47-year-old female on oral treprostinil who presented to the clinic with worsening symptoms of disease, necessitating higher dosing. This patient was previously uptitrated outpatient with oral treprostinil, which had allowed her to remain stable for years. Once uptitrated with additional intravenous therapy, the oral treprostinil dose was gradually further increased to the new goal dosage, resulting in improvements in symptoms and right ventricular function. This case highlights the versatility of dose optimization of oral treprostinil with rapid bridging through intravenous therapy.

A previously healthy 31-year-old man presented with worsening shortness of breath and a petechial rash. Echocardiography showed severe right-sided heart failure with midsystolic notching of the antegrade right ventricular outflow Doppler envelope suggesting pulmonary hypertension. An extensive work-up revealed scurvy, with a dramatic resolution of symptoms shortly after vitamin C supplementation.

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Pulmonary tumor thrombotic microangiopathy (PTTM ) is a rare condition of uncertain incidence given its likely underdiagnosis. PTTM has been described most frequently in association with gastric adenocarcinoma, but other primary malignancies have been identified. The prognosis of PTTM is very poor, and patients often die within days or weeks of diagnosis. There are, however, several medications currently being used with unknown therapeutic benefits. The case presented below describes a patient with PTTM and esophageal adenocarcinoma, which may be the first report of its kind. One other case of esophageal cancer associated with PTTM was found in the literature review, but it is of squamous cell carcinoma histology. Herein, we report a case of a male with rapidly progressive pulmonary hypertension and right heart failure who, in the course of treatment/evaluation, was found to have esophageal adenocarcinoma. While early diagnosis may not alter the course of the disease, antemortem diagnosis may identify better therapeutic options and better inform patients of their prognosis, allowing them to maintain autonomy in their medical decisions.

Etiologies of tricuspid regurgitation are often explored in patients with symptoms of right-sided heart failure. Blunt chest trauma is the major cause of traumatic tricuspid valve regurgitation (TTVR), a secondary type of tricuspid regurgitation. It is a rare condition; however, it may lead to severe consequences if not treated in a timely manner. TTVR should be considered in a patient presenting with chest trauma. In this case, we report a case of a young male who presented after a motor vehicle accident with secondary tricuspid valve regurgitation due to blunt chest trauma as well as a patent foramen ovale.

Upfront combination therapy including intravenous prostaglandin I2 (PGI2-IV) is recognized as the most appropriate treatment for patients with severe pulmonary arterial hypertension (PAH). This retrospective study aimed to determine reasons why this therapy is not used for some patients with severe PAH and describe the hemodynamic and clinical prognoses of patients receiving initial combination treatment with (PGI2-IV+) or without (PGI2-IV-) PGI2-IV.Data for patients with severe PAH (World Health Organization Functional Class III/IV and mean pulmonary arterial pressure [mPAP] ≥ 40 mmHg) were extracted from the Japan Pulmonary Hypertension Registry. Overall, 73 patients were included (PGI2-IV + n = 17; PGI2-IV- n = 56). The PGI2-IV+ cohort was younger than the PGI2-IV- cohort (33.8 ± 10.6 versus 52.6 ± 18.2 years) and had higher mPAP (58.1 ± 12.9 versus 51.8 ± 9.0 mmHg), greater prevalence of idiopathic PAH (88% versus 32%), and less prevalence of connective tissue disease-associated PAH (0% versus 29%). Hemodynamic measures, including mPAP, showed improvement in both cohorts (post-treatment median [interquartile range] 38.5 [17.0-40.0] for the PGI2-IV + cohort and 33.0 [25.0-43.0] mmHg for the PGI2-IV - cohort). Deaths (8/56) and lung transplantation (1/56) occurred only in the PGI2-IV - cohort.These Japanese registry data indicate that older age, lower mPAP, and non-idiopathic PAH may influence clinicians against using upfront combination therapy including PGI2-IV for patients with severe PAH. Early combination therapy including PGI2-IV was associated with improved hemodynamics from baseline, but interpretation is limited by the small sample size.

A 58-year-old male with an unknown medical history presented with acute encephalopathy, receptive aphasia, and hypertensive emergency. The patient did not have any family members from whom a collateral history could be obtained. He underwent X-rays of the abdomen and bilateral humeri/femurs to check for foreign bodies. He was found to have right femoral open reduction and internal fixation with retained screw fragments. He was diagnosed with ischemic stroke on MRI. Transthoracic echocardiogram (TTE) revealed right-sided heart failure and a tricuspid valve mass as well as right to left shunting. This raised concern for large atrial septal defect (ASD) with paradoxical embolization from tricuspid valve mass. Transesophageal echocardiogram (TEE) redemonstrated large ASD. Concern was raised for the ASD closure device as the cause of this \"tricuspid mass.\" Due to history of orthopedic procedure, it was hypothesized that the patient had an IVC filter placed in the setting of pulmonary embolism (PE) prior to an orthopedic procedure. The tricuspid valve was visualized under fluoroscopy and was confirmed to be a migrated IVC filter. He was taken to the operating room (OR) for cardiac surgery for the removal of the IVC filter and repair of ASD. Surprisingly, no ASD was found.

BACKGROUND: Right-side heart failure could accelerate mortality in patients of pulmonary hypertension, Jiedu Quyu Decoction (JDQYF) was used to manage pulmonary hypertension, but its right-sided heart protective effect associated with pulmonary artery hypertension is still unclear.
OBJECTIVE: Here, we evaluated the therapeutic effect of JDQYF on monocrotaline-induced right-sided heart failure associated with pulmonary arterial hypertension in Sprague-Dawley (SD) rats and investigated the potential mechanism of action.
METHODS: The main chemical components of JDQYF were detected and analyzed using ultra-high-performance liquid chromatography quadrupole time-of-flight mass spectrometry. The effects of JDQYF were investigated using a rat model of monocrotaline-induced right-sided heart failure associated with pulmonary arterial hypertension. We assessed the morphology of cardiac tissue using histopathology and the structure and function of the right heart using echocardiography. The biomarkers of heart failure, atrial natriuretic peptide and B-type natriuretic peptide, as well as serum pro-inflammatory markers, interleukin (IL)-1β, and IL-18, were measured by enzyme-linked immunosorbent assay (ELISA). Furthermore, the mRNA and protein expression levels of NLRP3 (NOD-, LRR-, and pyrin domain-containing 3), capase-1, IL-1β, and IL-18 in the right heart tissue were examined by real-time quantitative reverse transcription PCR and western blotting.
RESULTS: JDQYF improved ventricular function, alleviated pathological lesions in the right cardiac tissue, reduced the expression levels of biomarkers of heart failure and serum pro-inflammatory factors (IL-1β and IL-18), and downregulated the mRNA and protein expression levels of NLRP3, caspase-1, IL-1β, and IL-18 in the right cardiac tissue.
CONCLUSIONS: JDQYF possesses cardioprotective effect against right heart failure induced by pulmonary arterial hypertension, possibly owing to reduction of cardiac inflammation through the inhibition of NLRP3 inflammasome activation.