Citations

Problem Statement: The prognostic value of troponin elevation in septic ICU patients without known history of cardiac disease remains unclear, particularly after accounting for overall illness severity. Background: Minor troponin rises are frequent during sepsis, yet clinicians still lack a clear cut-point that signals danger once cardiac disease is ruled out. We asked whether a modest increase in troponin-T predicts in-hospital death beyond global illness severity. Methods: We studied 1 221 adult first ICU stays labelled “sepsis” in the eICU Collaborative Research Database and removed any case with a cardiac admission diagnosis. Implausible or missing laboratory values were imputed by multiple imputation. Hospital mortality was modelled with logistic regression that included troponin (a continuous and a binary model with threshold > 0.04 ng/mL) together with age, sex, lactate, albumin, BUN, creatinine, intubation status, vasopressor use, dialysis requirement and APACHE-IV predicted mortality. A natural-spline model explored non-linear behavior. Findings were checked in a 1:1 propensity-matched cohort. Results: Overall mortality was 11.7%. Troponin exceeded 0.04 ng/mL in 38% of patients. After adjustment for APACHE-IV probability and other covariates, a troponin level > 0.04 ng/mL was associated with almost twice the odds of death (OR ≈ 1.9), whereas the continuous model suggested only a modest trend (OR ≈ 1.1 per ng/mL). The spline curve rose steeply between 0 and 0.10 ng/mL and flattened thereafter, pinpointing an inflection near 0.05 ng/mL. Matching on all measured confounders confirmed that high-troponin patients had about three-fold greater mortality (OR ≈ 2.8, 1.55-5.05; p<0.001), highlighting that even modest troponin elevation is an independent risk marker for death in septic ICU patients. A bedside heat-map combining troponin, albumin and need for intubation illustrated a simple gradient: risk climbs from 2 % in low-troponin, well-albuminised, non-intubated patients to nearly 7 % when troponin exceeds 0.10 ng/mL in intubated, hypo-albuminemic patients. Conclusions: Even modest troponin elevations (> 0.04 ng/mL) independently predict mortality in sepsis after rigorous adjustment and matching on APACHE-IV physiology, lactate, and organ-support variables. This biologic threshold supports incorporating troponin into bedside triage and future septic cardiomyopathy trials.

Acquired angioedema due to C1-inhibitor deficiency (AAE-C1INH) is a rare condition characterized by the localized swelling of the deeper skin layers and mucous membranes, especially the face, lips, tongue, throat, and gastrointestinal tract. AAE-C1INH is strongly associated with lymphoproliferative disorders, although it can also be linked to autoimmune conditions, solid tumors, infections, or even occur without an identifiable cause. We present the case of a 45-year-old female patient with complaints of recurrent abdominal pain, bloating, and joint swelling. Laboratory testing showed decreased C1q and C4 complement levels, and C1 esterase inhibitor levels, indicative of AAE-C1INH. Further work up confirmed a diagnosis of extranodal marginal zone lymphoma with involvement of the bone marrow and spleen. Treatment with rituximab led to resolution of angioedema symptoms and almost complete remission of underlying lymphoma. This case underscores the importance of evaluating an underlying lymphoproliferative disorder in AAE-C1INH. Therefore, the early participation of a multidisciplinary team including specialists in immunology, hematology, and oncology is necessary for appropriate management.

This case report describes a woman in her early 60s who went into cardiac arrest immediately after administration of an echocardiogram contrast agent.

The growing adoption of advanced imaging modalities, such as transesophageal echocardiography (TEE), has led to more frequent detection of cardiac structural abnormalities. While intracardiac cardiac tumors and shunts are infrequent and typically asymptomatic, their existence can precipitate severe outcomes, including stroke, myocardial infarction and sudden death. Case Description: A 69-year-old female presented with left sided facial droop, slurred speech and left arm weakness. A computed tomography angiography revealed focal occlusion of the distal right middle cerebral artery. She was initiated on thrombolytic therapy and experienced resolution of symptoms. Transthoracic echocardiogram revealed right to left shunting consistent with a patent foramen ovale (PFO). Further workup with TEE confirmed the presence of a PFO but also detected a mobile echogenic mass on the aortic valve leaflet, indicative of papillary fibroelastoma (PFE). Cerebral infarction was attributed to an embolic event, with the PFO and PFE being likely culprits. Discussion: Current guidelines give a conditional recommendation, low certainty of evidence, for PFO closure in adults older than 60 years, although some observational studies have shown some risk reduction in older patients. The key trials showing clinical benefit of PFO closure were in adults younger than the age of 60. For left sided cardiac tumors, such as PFE, guidelines give a 2A recommendation for resection. Addressing the risk for recurrent stroke in this 69-year-old patient was an essential part of stroke care, as such, a multi-disciplinary team of experts including cardiology, neurology, and cardiothoracic surgery was conveyed. The decision was to proceed with surgical intervention in addition to antiplatelet therapy to achieve optimal risk reduction. The patient subsequently underwent successful surgical removal of the PFE with native valve preservation and PFO closure. Conclusion: Cardiac PFEs and PFOs can be associated with increased stroke risk. Employing appropriate imaging techniques and timely interventions are of utmost importance in stroke management.

Introduction: Fontan pathway obstruction is a serious complication characterized by an anatomical or functional narrowing anywhere in the cavo-pulmonary pathways. Here we report the first case where an innovative Fontan conduit rehabilitation procedure with intravascular lithotripsy was used achieving a significant increase in the pathway size. Case: A 28-year-old male with tricuspid atresia status-post Fontan palliation (age 23 months) with bare metal stent implant to treat obstruction at age 15, presented with syncope, ascites and varicose veins. Imaging studies revealed a cirrhotic liver morphology and Fontan pathway obstruction with minimal diameter of 12 mm. Cardiac catheterization confirmed severe Fontan conduit obstruction in addition to LPA stenosis. Serial covered Cheatham-Platinum stents were implanted for conduit coverage followed by Palmaz stents. Non-compliant Atlas balloon dilation to 20 atm was performed without expansion of the Fontan pathway beyond 12 mm due to severe calcification. A 7.0 x 60 mm shock-wave lithotripsy balloon was added alongside the Atlas balloon to modulate the heavily calcified wall with subsequent expansion of the conduit to 21 mm after inflating the Atlas balloon to 14 atm. Discussion: Several studies demonstrated that transcatheter stenting of stenotic Fontan conduits can be safely performed. Intravascular lithotripsy has emerged as a novel therapy for the treatment of coronary vascular calcification. We report the first case of an innovative percutaneous Fontan conduit rehabilitation procedure using a lithotripsy shock wave balloon in an adult with severely calcified Fontan pathway obstruction and prior stents, achieving a 75% increase in the pathway size without significant complications. Further studies are needed to evaluate the long-term safety and efficacy of this novel approach, but this case presents an exciting option for future directions in the percutaneous treatment of Fontan pathway obstruction.