Late Versus Early Myocardial Remodeling After Acute Myocardial Infarction: A Comparative Review on Mechanistic Insights and Clinical Implications

Abstract

In the setting of acute myocardial infarction (AMI), adverse myocardial remodeling (AMR) has been universally regarded as an early-onset phenomenon generally arising within the first few weeks (usually within days in the infarct zone) following myocardial injury. On the other hand, onset of cardiac morphological changes in this setting may potentially extend far beyond this time frame (usually beyond several months after the index AMI), suggesting a prolonged latent period in certain cases. In clinical practice, this delayed form of post-AMI remodeling, namely late AMR, has emerged as an interesting and underrecognized phenomenon with poorly understood mechanisms. Notably, systemic inflammation and associated growth factors seem to play a pivotal role in this setting. Accordingly, the present article primarily aims to discuss potential mechanisms and clinical implications of late AMR (in a comparative manner with its classical early counterpart) among AMI survivors along with a particular emphasis on potential benefits of certain anti-inflammatory strategies in this setting.

ARNI versus ACEI/ARB in Reducing Cardiovascular Outcomes after Myocardial Infarction

“… 6 It is well established that the mechanisms of ventricular remodelling after AMI involve activation of neuroendocrine system including renin‐angiotensin‐aldosterone system (RAAS), sympathetic nervous system (SNS), and natriuretic peptide system. 7 SNS augments RAAS activity, while natriuretic peptides‐atrial natriuretic peptide and brain natriuretic peptide antagonize the RAAS and SNS by natriuresis and vasodilation. Conventionally, RAAS inhibition has focused on clinical utilization of ACEI and ARB, and recently, ARNI brings the latest addition to this armamentarium.…”

Value of acoustic cardiography in the clinical diagnosis of coronary heart disease

“…Some experts suggest that patients with asymptomatic LVSD after myocardial infarction with an LVEF less than 50% can be diagnosed with ventricular remodeling. [1][2][3][4] Because patients with asymptomatic LVSD often lack typical clinical features, they can easily be overlooked by doctors, resulting in aggravation of the disease. Although B-type brain natriuretic peptide (BNP) and echocardiography can be utilized in the diagnosis of LVSD, they carry several disadvantages including increased cost, the need for professional and technical personnel, and difficulty to achieve dynamic monitoring.…”

Late Coronary Aneurysm Formation after Kawasaki Disease: a Review of Mechanistic and Clinical Aspects

“…Reactive inflammation and subsequent fibrotic response are well known to serve as fundamental repair mechanisms usually in a well-balanced manner following tissue injury. 14) In the setting of KD, ‘mild coronary arteritis’ is usually characterized by a mild and transient segmental dilatation presenting with a diameter of ≤1.5 times that of the neighboring reference segment or an echocardiographic Z score of 2 to <2.5. 1) This form of coronary arteritis is well known to be an early and fully reversible phenomenon encountered in a significant portion of KD cases (up to 50% of cases), and usually resolves within 4 to 8 weeks after disease onset without any acute complications potentially suggesting little or no long-term prognostic relevance.…”

“…9) 11) 23) On the other hand, tissue over-healing following injury was previously suggested to harbor a substantial genetic basis, and hence; individual variation largely attributable to various gene polymorphisms associated with proinflammatory mediators and/or growth factors. 14) In particular, certain fibrogenic mediators including TGF-β (and associated SMAD3 signaling accounting for myofibroblast activation, fibrogenesis) and vascular endothelial growth factor were previously suggested to be significantly associated with classical early CAA formation in patients with KD. 1) 16) Pathogenetic roles of these mediators in genetically susceptible KD patients might be even more susbstantial in the genesis of ‘late CAAs’ due to the purely fibroproliferative nature of these aneurysms.…”