Trends in Cardiovascular Medicine最新文献

Arrhythmogenic cardiomyopathy (ACM) is a genetically determined myocardial disease characterized by myocyte loss, fibro-fatty replacement, and electrical instability. In a subset of patients, episodes of chest pain with troponin release and electrocardiographic abnormalities occur in the absence of ischemic causes. These events, commonly referred to as "hot phases" (HP), often mimic acute myocarditis and raise important diagnostic and prognostic considerations. Among ACM-related genes, desmoplakin (DSP) variants are most frequently associated with HP, although episodes have also been observed in carriers of genes not classically associated with this presentation. Evidence suggests that HP presentation may vary across genotypes and ACM phenotypes, with DSP carriers more often exhibiting left sided or biventricular involvement. Growing data indicate that inflammation, autoimmunity, and innate immune activation play a central role in HP expression and ACM pathobiology, supported by findings of myocardial inflammatory infiltrates, circulating anti-desmosomal and anti-intercalated disc autoantibodies, and activation of NLRP3-inflammasome pathways. These mechanisms may contribute to disease progression and arrhythmic vulnerability. Therapeutic strategies remain empirical, but recent observations suggest that immunosuppressive therapy may modulate arrhythmic and heart-failure outcomes in DSP carriers. This review summarizes current knowledge on the clinical, genetic and immunologic features of HP in ACM, and discusses how these findings may refine the diagnostic approach and clinical interpretation of myocarditis-like presentations.

Cardiogenic shock (CS) is a life-threatening condition characterized by severe systemic hypoperfusion that may progress into multi-organ failure. Immediate optimization of organ perfusion is therefore considered a critical priority. However, first-line therapy with inotropes and vasopressors carries significant risks, adding stress to an already severely failing heart, and may eventually contribute to further clinical deterioration. Subsequent temporary mechanical circulatory support (tMCS) has been traditionally viewed upon as a means to restore systemic circulation. Recent approaches have, however, suggested that the hemodynamic buffer provided by tMCS may create a therapeutic window for the initiation of evidence-based heart failure therapies. Nevertheless, interfering in a jeopardized hemodynamic and failing homeostasis is extremely challenging and the devices carry a significant risk of serious adverse events. In this review, we discuss the potential use of heart failure therapies in patients with CS who are supported with tMCS. We highlight the feasibility and potential efficacy of this combined therapeutic approach from the perspective of a novel, aviation-inspired safety framework referred to as the 'hemodynamic envelope'. This concept may inspire future study designs and support clinicians in initiating established heart failure therapies during tMCS.

Cellular senescence is a stress responsive program that critically affects chronological and biological aging, ischemia reperfusion injury (IRI), and age related cardiovascular diseases. Of relevance, cardiac senescent cells exhibit altered characteristics that promote inflammation, remodeling, and fibrosis, ultimately contributing to the functional decline following myocardial infarction (MI). At the same time, emerging evidence suggests that senescence may also exert protective effects post-MI, limiting fibrosis. Thus, understanding the mechanisms and pathways of cardiac senescence appears critical for delineating the consequences of IRI, including identification of novel therapeutic targets for improving post-MI recovery.