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.

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.

Tolvaptan sodium phosphate (Samtas®; Otsuka Pharmaceutical, Tokyo, Japan) is a newly available intravenous aquaretic diuretic (commercially available from May 2022), which acts as an arginine vasopressin V2 receptor antagonist. Thus far, optimal patient selection as well as safety and efficacy in real-world practice remain unknown. We experienced two patients with congestive heart failure treated with tolvaptan sodium phosphate. In one patient with right-sided heart failure, oral tolvaptan was converted to intravenous tolvaptan sodium phosphate, and another one with right and left-sided heart failure and impaired swallowing function received intravenous tolvaptan sodium phosphate on a de novo basis. Following the initiation of tolvaptan sodium phosphate, their congestive symptoms ameliorated immediately without any complications. Tolvaptan sodium phosphate may be safe and effective in real-world practice, although further studies are warranted to establish optimal patient selection and clinical management.
UNASSIGNED: We report here an initial experience of newly-introduced intravenous tolvaptan sodium phosphate in real-world practice. The novel medication might be particularly suitable for those with severe thirst, congestive gut edema, or requiring rapid amelioration of systemic/pulmonary congestion, although further accumulating experiences are warranted to establish optimal therapeutic strategy.

Early right-sided heart failure (RHF) was seen in 22% of recipients of a left ventricular assist device (LVAD) in the European Registry for Patients with Mechanical Circulatory Support (EUROMACS). However, the optimal treatment of post-LVAD RHF is not well known. Levosimendan has proven to be effective in patients with cardiogenic shock and in those with end-stage heart failure. We sought to evaluate the efficacy of levosimendan on post-LVAD RHF and 30-day and 1-year mortality.
The EUROMACS Registry was used to identify adults with mainstream continuous-flow LVAD implants who were treated with preoperative levosimendan compared to a propensity matched control cohort.
In total, 3661 patients received mainstream LVAD, of which 399 (11%) were treated with levosimendan pre-LVAD. Patients given levosimendan had a higher EUROMACS RHF score [4 (2- 5.5) vs 2 (2- 4); P < 0.001], received more right ventricular assist devices (RVAD) [32 (8%) vs 178 (5.5%); P = 0.038] and stayed longer in the intensive care unit post-LVAD implant [19 (8-35) vs 11(5-25); P < 0.001]. Yet, there was no significant difference in the rate of RHF, 30-day, or 1-year mortality. Also, in the matched cohort (357 patients taking levosimendan compared to an average of 622 controls across 20 imputations), we found no evidence for a difference in postoperative severe RHF, RVAD implant rate, length of stay in the intensive care unit or 30-day and 1-year mortality.
In this analysis of the EUROMACS registry, we found no evidence for an association between levosimendan and early RHF or death, albeit patients taking levosimendan had much higher risk profiles. For a definitive conclusion, a multicentre, randomized study is warranted.