Dipeptidyl peptidase 3 (DPP3) is a zinc-dependent aminopeptidase that is found in several places and is thought to be a cytosolic enzyme that helps break down peptides. Recent studies, however, have revealed its extensive therapeutic relevance upon release into circulation, functioning not only as a biomarker for cellular injury but also as an active modulator of cardiovascular homeostasis and critical disease. High levels of circulating DPP3 (cDPP3) have been linked to the causes of cardiogenic shock, septic shock, acute coronary syndromes, heart failure, and serious viral diseases like COVID-19. Its enzymatic breakdown of angiotensin II disrupts vascular tone and myocardial contractility, leading to hemodynamic instability and multi-organ failure. In numerous cohorts, cDPP3 levels reliably correspond with disease severity, acute renal damage, and death, but dynamic trajectories yield superior predictive information relative to single assessments. In addition to risk stratification, translational studies utilizing rodent and porcine models illustrate that antibody-mediated inhibition of cDPP3 with the humanized monoclonal antibody Procizumab reinstates cardiac function, stabilizes renal perfusion, diminishes oxidative stress and inflammation, and enhances survival. First-in-human experiences in patients with refractory septic cardiomyopathy have further emphasized its therapeutic promise. DPP3 is a good example of a biomarker and a mediator in cardiovascular and critical care. Its growing clinical and translational profile makes cDPP3 a strong predictor of bad outcomes and a prospective target for treatment. Ongoing clinical trials using Procizumab will determine if neutralizing cDPP3 can lead to enhanced outcomes in individuals with cardiogenic and septic shock. This review outlines the physiological mechanisms, clinical implications, and emerging therapeutic potential of DPP3 in cardiovascular and critical care. Ongoing trials with Procizumab will clarify whether neutralizing cDPP3 can improve outcomes in patients with cardiogenic and septic shock.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD), the hepatic manifestation of cardiometabolic dysfunction, is closely linked to atherosclerosis, heart failure, and adverse cardiovascular outcomes. This review summarizes current evidence on the biological basis of the MASLD–heart axis, with particular emphasis on vascular injury and adverse cardiac remodeling. Methods: A narrative review of contemporary literature was conducted, including experimental studies, observational cohorts, meta-analyses, randomized clinical trials, and current guideline recommendations addressing the cardiohepatic axis. Results: The interaction between the liver and the heart involves interconnected mechanisms, including insulin resistance, lipotoxicity, oxidative stress, chronic inflammation, endothelial dysfunction, and neurohormonal activation. Experimental and translational evidence supports biologically plausible links between MASLD-related metabolic and inflammatory pathways and vascular or myocardial injury, while clinical studies consistently associate MASLD with arterial stiffness, microvascular dysfunction, atherosclerotic disease, adverse cardiac remodeling, heart failure, atrial fibrillation, and cardiovascular events. Several of these associations persist after adjustment for conventional cardiometabolic risk factors, although residual confounding and shared risk determinants limit causal inference. Non-invasive tools, including the Fibrosis-4 (FIB-4) score and transient elastography, may help identify patients at higher risk of advanced fibrosis and cardiometabolic complications. Lifestyle interventions remain the cornerstone of management, while glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, and fibroblast growth factor-21 analogs may provide combined hepatic and cardiovascular benefits. Conclusions: The cardiohepatic axis is an important component of cardiometabolic disease, linking hepatic dysfunction with vascular and myocardial injury through shared biological pathways. Incorporating hepatic assessment into cardiovascular risk evaluation may support earlier identification of high-risk patients.

Background and Clinical Significance: Mechanical complications and intracavitary thrombus are both recognized causes of clinical deterioration following acute myocardial infarction, yet they require fundamentally different therapeutic approaches. Distinguishing between these entities is critical, as misdiagnosis may lead to unnecessary surgical intervention or delayed anticoagulation with serious consequences. Left ventricular (LV) thrombus typically appears as a well-defined mass; however, atypical and highly mobile morphologies may closely mimic catastrophic post-infarction mechanical complications, creating significant diagnostic uncertainty. This case highlights the pivotal role of contrast-enhanced echocardiography in resolving such ambiguity and guiding appropriate management in a high-stakes clinical setting. Case Presentation: A 60-year-old man presented with acute dyspnea and pulmonary edema ten days after an anterior myocardial infarction treated with percutaneous coronary intervention, complicated by ischemic stroke. Transthoracic echocardiography demonstrated severe LV systolic dysfunction with moderate-to-severe mitral regurgitation and an unexpected, highly mobile, irregular mass protruding into the LV apex. The mass exhibited a shredded, tissue-like appearance, raising urgent concern for post-infarction mechanical complications, including papillary muscle rupture or apical myocardial disruption, and prompting immediate consideration of surgical intervention. Contrast-enhanced echocardiography was performed and revealed a mobile LV apical thrombus. Surgical management was avoided, and systemic anticoagulation was initiated, followed by transition to rivaroxaban in combination with ongoing dual antiplatelet therapy. The patient demonstrated rapid clinical improvement with optimized heart failure treatment and was discharged after four days, with planned follow-up imaging to assess thrombus resolution. Conclusions: Left ventricular thrombus may present with atypical, misleading morphologies that closely resemble life-threatening mechanical complications after myocardial infarction.

Shock is traditionally classified according to its primary etiology—septic, hypovolemic, obstructive, or cardiogenic—yet these syndromes frequently converge on a common feature: disturbances of cardiac performance, ventricular loading, and tissue perfusion. Despite distinct initiating mechanisms, altered preload and afterload, ventricular interdependence, vascular dysfunction, maladaptive neurohormonal responses, and, in selected states, impaired myocardial contractility may ultimately reduce effective forward flow and tissue perfusion. Echocardiography provides a rapid, noninvasive bedside tool for characterizing these evolving cardiovascular effects. It enables assessment of left and right ventricular function, cardiac filling, preload responsiveness, pulmonary and systemic venous congestion, fluid tolerance, and broader hemodynamic profiles while facilitating recognition of reversible causes such as cardiac tamponade, acute pulmonary embolism, or severe hypovolemia. This allows clinicians to move beyond static etiologic classifications toward a physiology-based assessment of shock. Beyond diagnosis, echocardiography can inform fluid resuscitation and vasoactive or inotropic therapy. Serial assessment also permits evaluation of therapeutic response and evolving hemodynamic phenotypes. This review synthesizes the mechanisms of cardiac involvement across shock syndromes and highlights echocardiography as a unifying tool for their evaluation and management. By integrating pathophysiology, bedside imaging, and hemodynamic treatment, we propose a physiology-based framework that complements traditional shock classification and may improve diagnostic precision and individualized management in critically ill patients.