Acute compartment syndrome: a rare but important complication of transradial cardiac catheterization

The transradial approach has become the gold-standard for coronary angiography. It is better tolerated by patients, associated with less bleeding, earlier post-procedure mobilization, and reduced mortality in patients with myocardial infarction. Given the hand's dual arterial supply and extensive collateral circulation, the risk of serious functional injury after radial catheterization is essentially reduced to zero. However, even a small amount of bleeding in the volar compartment can lead to compartment syndrome (CS) and permanent neurovascular injury. The purpose of this paper is to describe our experience with an unusual case of late-onset acute CS following transradial coronary angiography, and to summarize the available literature on this topic

Anti-troponin antibodies following myocardial infarction

Recent improvements in medical and surgical coronary revascularization techniques have significantly improved outcomes for patients with acute myocardial infarction (MI). However, large infarctions are often followed by a poorly understood process of pathological ventricular remodelling, which fails to return the heart to its premorbid state. Although it remains incompletely understood, there is increasing interest in the role of the immune system in this process. One hypothesis is that released cardiac proteins become the focus of an immune response that results in the formation of functionally significant autoantibodies. This review summarizes the current literature, both human and animal, relating to the formation and clinical relevance of anti-troponin antibodies (ATAs) in patients with MI

The role of anti-myosin antibodies in perpetuating cardiac damage following myocardial infarction

Recent improvements in the medical and surgical management of myocardial infarction mean that many patients are now surviving with greater impairment of cardiac function. Despite appropriate management, some of these patients subsequently develop pathological ventricular remodelling, which compounds their contractile dysfunction and can lead to congestive cardiac failure (CCF). The pathophysiological mechanism underpinning this process remains incompletely understood. One hypothesis suggests that a post-infarction autoimmune response, directed against constituents of cardiac myocytes, including cardiac myosin, may make an important contribution. Our review summarises the current literature related to the formation and clinical relevance of anti myosin antibodies (AMAs) in patients with myocardial infarction. This discussion is supplemented with reference to a number of important animal studies, which provide evidence of the potential mechanisms underlying AMA formation and autoantibody mediated cardiac dysfunction

The role of anti-myosin antibodies in perpetuating cardiac damage following myocardial infarction

Recent improvements in the medical and surgical management of myocardial infarction mean that many patients are now surviving with greater impairment of cardiac function. Despite appropriate management, some of these patients subsequently develop pathological ventricular remodelling, which compounds their contractile dysfunction and can lead to congestive cardiac failure (CCF). The pathophysiological mechanism underpinning this process remains incompletely understood. One hypothesis suggests that a post-infarction autoimmune response, directed against constituents of cardiac myocytes, including cardiac myosin, may make an important contribution. Our review summarises the current literature related to the formation and clinical relevance of anti-myosin antibodies (AMAs) in patients with myocardial infarction. This discussion is supplemented with reference to a number of important animal studies, which provide evidence of the potential mechanisms underlying AMA formation and autoantibody mediated cardiac dysfunction

Significance of anti-myosin antibody formation in patients with myocardial infarction: a prospective observational study

Background: Anti-myosin antibodies (AMAs) are often formed in response to myocardial infarction (MI) and have been implicated in maladaptive cardiac remodelling. We aimed to: (1) compare AMA formation in patients with Non-ST-Elevation MI (NSTEMI) and ST-Elevation MI (STEMI); (2) evaluate factors predicting autoantibody formation; and, (3) explore their functional significance. Methods: Immunoglobulin M (IgM) and Immunoglobulin G (IgG) AMA titres were determined in serum samples collected at admission, 3 and 6 months post MI. The relationship between demographic and clinical data, and antibody formation, was investigated to determine factors predicting antibody formation and functional significance. Results: Forty-three patients were consecutively recruited; 74.4% were positive for IgM at admission, compared with 23.3% for IgG. Mean IgG levels increased by 1.24% (±0.28) at 3 months, and 13.55% (±0.13) at 6 months post MI. Mean antibody levels were significantly higher in the NSTEMI cohort at both follow-up time points for IgG (p < 0.001, p < 0.0001), but not IgM (p = 0.910, p = 0.066). A moderately positive correlation between infarct size and increase in mean IgM concentration was observed at 3 months (r(98) = 0.455; p = 0.015). Anti-myosin antibody formation was not associated with an unfavourable outcome at follow-up. Conclusions: Anti-myosin antibodies are formed in a significant proportion of patients following MI, particularly among those with NSTEMI. While IgM levels fall after infarction, IgG levels increase and persist beyond 6 months of follow-up. This raises the possibility that they may contribute to long-term myocardial damage and dysfunction. Future research should focus on the specific epitopes that are targeted by these antibodies, and their functional significance. This may result in the emergence of novel therapies to attenuate cardiac dysfunction in MI patients