Background/Objectives: Pulmonary embolism (PE) is a major cause of cardiovascular mortality, particularly in high-risk cases complicated by hemodynamic instability. Systemic thrombolysis is the recommended treatment in such settings; however, the coexistence of thrombocytopenia represents a major therapeutic challenge due to concerns regarding bleeding risk. Evidence guiding thrombolytic therapy in thrombocytopenic patients with PE is limited. This study aimed to present a representative case and review the available literature addressing thrombolysis in PE complicated by thrombocytopenia. Methods: A qualitative review of published case reports was conducted using the PubMed and Scopus databases, and articles describing adult patients with objectively confirmed PE, documented thrombocytopenia, and treatment with thrombolytic therapy were included. Eight case reports met the inclusion criteria, and the clinical characteristics, severity markers, platelet dynamics, treatment strategies and outcomes were analyzed and compared with the reported case. Results: Most of the reported patients presented with high-risk pulmonary embolism, defined by hemodynamic instability, including shock or cardiac arrest. Thrombolysis was frequently administered despite platelet counts below conventional thresholds. Platelet levels at the time of thrombolysis varied widely, including cases of severe thrombocytopenia. Clinical and hemodynamic improvement was observed in most of the cases, while major bleeding complications were infrequent. The reported case demonstrated successful systemic thrombolysis with rt-PA in a postpartum patient with suspected heparin-induced thrombocytopenia and high-risk PE, without hemorrhagic events. Conclusions: Available evidence suggests that thrombolytic therapy may be a viable life-saving option in carefully selected thrombocytopenic patients with high-risk pulmonary embolism. Therapeutic decisions should prioritize clinical severity and hemodynamic status over platelet count alone, emphasizing individualized, multidisciplinary risk–benefit assessment.

Mechanical complications after acute myocardial infarction (MI)—ventricular septal rupture (VSR), free-wall rupture (FWR), and papillary muscle rupture (PMR)—have become uncommon in the primary percutaneous coronary intervention (PCI) era, yet remain among the most lethal cardiovascular emergencies, with contemporary mortality largely driven by cardiogenic shock and delays to definitive treatment. Although major society documents agree on urgent imaging, early mechanical circulatory support when shock is present, and multidisciplinary decision-making, important transatlantic differences persist, particularly regarding timing of intervention in ventricular septal rupture. This review synthesises current surgical and transcatheter evidence and proposes a unified, physiology-centred framework integrating shock staging, anatomical feasibility, and response to mechanical support. We also introduce STABLE, a structured bedside checklist designed to support consistent daily triage across all three lesions and to align timing decisions with haemodynamic stabilisation rather than centre-specific habit.

Background: The clinical significance of inflammatory phenotypes and their temporal relationship with natriuretic peptide dynamics in acute heart failure (AHF) remain poorly defined. We investigated admission inflammatory phenotypes, in-hospital C-reactive protein (CRP) trajectories, and their relationship with N-terminal pro-B-type natriuretic peptide (NT-proBNP) dynamics. Methods: In this retrospective single-center cohort of 306 patients hospitalized for AHF, patients were stratified according to admission CRP (≤10 vs. >10 mg/L). Among patients with dual biomarker measurements (n = 147), a CRP–procalcitonin (PCT) concordance phenotype was evaluated. Serial CRP measurements were available in 65 patients, and NT-proBNP response (≥30% reduction) was assessed in 42 patients; because these repeat measurements were obtained at the treating physician’s discretion, the corresponding subgroups were older and more severely ill than the full cohort and are treated as exploratory. Results: Elevated admission CRP (>10 mg/L) was associated with higher NT-proBNP levels (3621 vs. 1251 pg/mL, p < 0.001), more severe symptoms (New York Heart Association [NYHA] III–IV: 45.9% vs. 29.8%, p = 0.006), and greater PCT positivity (21.8% vs. 8.7%, p = 0.029), independent of left-ventricular ejection fraction; the association persisted after adjustment for age, sex, and ejection fraction (adjusted odds ratio 2.40, 95% CI 1.27–4.55). The biomarker-defined CRP+/PCT+ phenotype showed the greatest concurrent NT-proBNP burden and the highest prevalence of heart failure with preserved ejection fraction (HFpEF, 70.6%). Despite declining NT-proBNP, CRP increased during hospitalization in 69.2% of patients (median ΔCRP +5.9 mg/L, p < 0.001), and the two changes were uncorrelated, indicating divergent biomarker trajectories. Conclusions: Admission CRP identifies patients with a more severe concurrent inflammatory and hemodynamic profile, while combined CRP–PCT phenotyping further characterizes this profile. Divergent CRP and NT-proBNP trajectories suggest that inflammatory and hemodynamic changes follow distinct time courses during AHF hospitalization. Because no post-discharge outcomes were available, these findings describe concurrent associations rather than prognosis.

Perioperative bleeding after frozen elephant trunk (FET) surgery is reported using heterogeneous endpoints. This structured narrative review examines bleeding sources, measurement and haemostatic management, prioritising recent literature while retaining established landmark definitions. Twelve primary FET clinical publications are tabulated, with technical reports and wider cardiac-surgery evidence providing context. Re-exploration, postoperative drainage, estimated blood loss, transfusion and fabric oozing describe related but distinct phenomena. Established classifications, particularly the Universal Definition of Perioperative Bleeding (UDPB), provide a severity-reporting reference and should not be displaced by a new FET scale. We propose six parallel reporting domains: procedural context; bleeding measurement; haemostatic status; verified source; treatment exposure; and outcomes.. The study-level mapping shows that published FET reports often permit extraction of drainage, re-exploration or treatment exposure, whereas haemostatic status and a directly verified bleeding source are rarely recoverable from published reports. The dataset therefore makes these information gaps explicit and supports prospective evaluation; it does not infer an anatomical source from laboratory findings, drainage or treatment. The proposed reporting dataset is not a validated severity scale or treatment algorithm.