We report a case of pulmonary nocardiosis and pulmonary tuberculosis following steroid pulse therapy for presumed myelitis. A 74-year-old man with transthyretin amyloid cardiomyopathy, chronic heart failure, and type 2 diabetes mellitus received two courses of steroid pulse therapy for suspected inflammatory myelitis. One month later, he developed progressive dyspnea and was admitted to our hospital. Chest computed tomography revealed multifocal right-sided infiltrates and pleural effusion. Although empirical piperacillin/tazobactam was initiated for presumed bacterial pneumonia, sputum Gram and Kinyoun stains revealed thin, branching, partially acid-fast bacilli, and sequencing of the secA1 gene identified Nocardia exalbida. Polymerase chain reaction (PCR) analysis was positive for Mycobacterium tuberculosis. Pleural fluid culture yielded Nocardia species. The patient's condition improved following combined antituberculous and anti-nocardial therapy, along with optimized heart failure management. Coinfection with nocardiosis and tuberculosis should be considered in immunosuppressed patients following corticosteroid therapy.

Carcinoid heart disease (CHD) is a serious cardiac manifestation of carcinoid syndrome (CS), characterized by progressive fibrotic degeneration of cardiac valves and right-sided heart failure. We report the case of a 72-year-old man with a history of metastatic small-intestinal neuroendocrine tumor and CS diagnosed four years earlier, who presented with worsening dyspnea and peripheral edema. Transthoracic echocardiography revealed characteristic findings of advanced CHD, including severely thickened, retracted, and immobile tricuspid and pulmonary valve leaflets, resulting in severe tricuspid and pulmonary regurgitation. Additional findings included right ventricular dilatation, severe biatrial enlargement, moderate mitral regurgitation, a small pericardial effusion, and a 7-cm ascending aortic aneurysm. The diagnosis was established based on the characteristic echocardiographic appearance and elevated N-terminal pro-B-type natriuretic peptide levels. Notably, no routine cardiological surveillance had been performed following the diagnosis of CS. The patient was managed conservatively with intravenous diuretic therapy and optimization of heart failure treatment. Following multidisciplinary evaluation, surgical intervention was not pursued because of the patient's advanced disease stage, clinical instability, and concomitant ascending aortic aneurysm, which collectively rendered him a prohibitive surgical candidate. His clinical course was subsequently complicated by acute kidney injury with progressive renal dysfunction and anuria, and he ultimately died during hospitalization. This case highlights the importance of regular cardiovascular follow-up in patients with CS, as delayed recognition of cardiac involvement may lead to advanced and potentially irreversible valvular disease. Early detection remains crucial for timely intervention and may improve clinical outcomes.

RVAD thrombosis is a well-described complication that requires a high index of suspicion, as it can precipitate irreversible hemodynamic collapse. Here, we present a case of a 51-year-old man with end-stage heart failure who was placed on biventricular support using 2 HeartMate 3 devices. The patient's postoperative course was complicated by sudden RVAD flow cessation suspicious for inflow obstruction due to pump thrombosis or transient anatomic inflow occlusion. As the patient remained hemodynamically stable, the decision was made to proceed to the catheterization laboratory for fluoroscopic evaluation using a novel catheter-based approach. In addition to providing diagnostic information, this technique offered the potential for immediate thrombectomy if thrombotic obstruction of the RVAD was confirmed.

Hepatic vein catheterization (HVC) in man was first performed 80 years ago in the wake of right-sided heart catheterization. Several new methods, recognitions and concepts followed, especially the indirect Fick-method for determination of splanchnic blood flow. Five years passed before pressure measurements were performed and routine HVCs were done in liver patients. Later came splanchnic kinetics of test substances, dyes, metabolites, hormones and bioactive material and counter current wedged and balloon occlusion pressure. HVC has been a prerequisite for our understanding of the pathogenesis of portal hypertension and variceal bleeding leading to serial measurements, stratification, quantification and treatment of portal hypertension, and transvenous liver biopsy and portosystemic stent insertion (TIPS) followed. Measurements and pathophysiology of formation and amelioration of ascites advanced with HVC, likewise pathophysiology of known and new diseases in other organs, secondary to liver disease (kidney, heart, lung, systemic circulation). The hepatic venous pressure gradient (HVPG, i.e., wedged-to-free hepatic venous pressure) is today considered the gold standard for portal pressure measurement in intrasinusoidal and postsinusoidal portal hypertension. In spite of substantial developments in route, catheter type, pressure measurements and -registration, fluoroscopy, transvascular technique, etc. the basic concepts are the same today. New advanced technology, materials, imaging techniques and IT-power have together with the inborn dynamics of the catheterization given a progressive development, and there are potentials of further refinement and applications in science, clinical physiology, gastroenterology and hepatology.

Triple valve surgery is performed in only a small minority of valvular procedures and carries substantial perioperative risk and a demanding postoperative course. Pericardial complications after cardiac surgery are well recognized, but progression to constrictive physiology following a minimally invasive triple valve operation is exceptionally uncommon and poorly characterized. We describe an elderly woman with longstanding hypertension, dyslipidemia, and paroxysmal atrial fibrillation who underwent minimally invasive replacement of the aortic, mitral, and tricuspid valves for combined multivalvular disease. Her recovery was complicated by recurrent pleural and pericardial effusions that evolved into constrictive pericarditis, with clinical and imaging features supporting the diagnosis, although distinguishing it from a restrictive process remained challenging despite complementary multimodality imaging and invasive hemodynamic assessment. Although pericardiectomy was undertaken, she deteriorated into refractory cardiogenic shock and died shortly afterwards. This report illustrates the difficulty of distinguishing constriction from restriction in the postoperative setting and underscores the value of close multidisciplinary follow-up after extensive valve surgery in older patients.

A woman in her early 20s at 30 weeks of gestation presented with elevated blood pressure, transaminitis, progressive dyspnoea, orthopnoea, exertional chest pain and peripheral oedema, raising concern for preeclampsia-associated cardiopulmonary disease or peripartum cardiomyopathy. Transthoracic echocardiography showed preserved left ventricular systolic function, normal left-sided filling pressures, right ventricular dilatation and an estimated right atrial pressure of 15 mmHg; N-terminal pro-brain natriuretic peptide was 57 pg/mL. Cross-sectional imaging revealed a large multi-cystic anterior mediastinal mass occupying the left hemithorax, displacing the heart and abutting/compressing major cardiopulmonary structures. Labour was induced at 34 weeks after clinical stabilisation. Three months postpartum, the patient re-presented with worsening dyspnoea and haemoptysis and underwent complete surgical resection. Pathology confirmed mature cystic teratoma and cardiopulmonary symptoms resolved after resection.

We report a serum BNP cut-off of 800 pg/mL above which all patients with LVAD HeartMate-3 had elevated biventricular filling pressures, suggesting it may be used to prompt invasive ramp study during routine post-LVAD clinic visit. We found stepwise increase in BNP levels across hemodynamic groups, with the lowest levels in patients with normal filling pressures, intermediate in those with elevated right or left-sided filling pressure and highest in those with elevated biventricular filling pressures. Furthermore, most patients with BNP above median value (335 pg/mL) required speed changes for either elevated right sided or left sided filling pressures. Conversely, patients with BNP below 335 pg/mL rarely required speed change. In conclusion, elevated serum BNP in patients with durable LVAD HeartMate-3 may have clinical value in prompting invasive hemodynamic assessment.

A 4-year-old boy with a diagnosis of right-sided heterotaxy syndrome was transferred to our hospital under the extracorporeal membrane oxygenation (ECMO). He had undergone an extracardiac total cavopulmonary connection (TCPC) with a fenestration. Approximately 6 months after the TCPC procedure, common atrioventricular valve regurgitation worsened and persisted despite multiple valve repair procedures. ECMO support was initiated 318 days after the TCPC procedure for progressive heart failure and multiple organ dysfunction. Although ECMO was initially discontinued after transient improvement, recurrent circulatory failure necessitated reinitiation, and the patient remained ECMO-dependent thereafter. We implanted a Berlin Heart EXCOR® Pediatric ventricular assist device. In the operation, the fenestration of the TCPC conduit was closed. An expanded polytetrafluoroethylene conduit for the arterial cannula was anastomosed to the ascending aorta in an end-to-side fashion. The apex of the left-sided ventricle was incised, followed by the meticulous resection of residual ventricular septal tissue to obtain effective venting from both ventricles. An inflow cannula was anastomosed to the coring site. Ventricular assist support was initiated without complications. On the postoperative day 433, intracerebral hemorrhage was abruptly developed, necessitating management in the intensive care unit. Two hematoma evacuation procedures of decompressing surgery for intracerebral hemorrhage were required. Despite these interventions, the patient ultimately died on postoperative day 488. The autopsy confirmed that the residual ventricular septum-like tissue had been almost completely resected and that the inflow cannula tip was positioned away from any muscular structures, suggesting that the resection enabled effective ventricular drainage without obstruction or suction.

Malignant pleural effusions (MPEs) are almost always exudative, with only an estimated 3-4% meeting biochemical criteria for a transudate. Light's criteria remain the standard method for classifying pleural effusions, and transudative effusions typically do not undergo cytologic evaluation. This may delay the diagnosis of malignancy in rare cases where malignant cells are present in a biochemically transudative effusion. We present a 41-year-old homeless man with no established primary care who presented with progressive muscle cramping and was found to have severe electrolyte abnormalities, leukocytosis, and a right-sided pleural effusion with new bilateral pulmonary nodules on computed tomography. Pleural fluid analysis met clear transudative criteria by Light's criteria (protein ratio 0.24, LDH ratio 0.44). However, cytology revealed clusters of atypical cells consistent with pulmonary adenocarcinoma, confirmed by thyroid transcription factor-1 (TTF-1) positivity. The patient had no identifiable cause of transudative effusion, including heart failure, cirrhosis, nephrotic syndrome, or significant hypoalbuminemia. This case illustrates a rare presentation of malignant pleural effusion masquerading as a transudate in the absence of confounding systemic conditions. The mechanism likely involves early pleural metastatic involvement before the development of significant vascular permeability changes or lymphatic obstruction. This report underscores the importance of maintaining clinical suspicion for malignancy despite transudative biochemistry, particularly when features such as unilateral effusion, atypical imaging findings, or absence of an alternative systemic cause are present.