Sex has a profound impact on myocardial remodeling, which is defined as the molecular and cellular events after an injury to the myocardium (i.e., necrosis, pressure overload, volume overload, and aging) leading to a change in shape, dimension, and function of cardiac chambers. Indeed, experimental studies and post-mortem and observational clinical studies suggest the presence of important differences in myocardial remodeling between females and males in response to different types of injures including aging, pressure and volume overload, and myocardial infarction. Interestingly, the remodeling process appears to be more favorable in women versus men; women are more likely to present heart failure with preserved systolic function and are at greater risk for low output syndrome acutely. These differences between men and women are widely held to be related to sex hormones such as estrogen, although the molecular effects of estrogen on ventricular cardiomyocytes are incompletely understood. In this review, we summarize the evidence supporting these notions and discuss the underlying mechanisms and the clinical implications.

These results suggest that PDI promotes survival after ischemic damage and that zinc-superoxide dismutase is one of the PDI molecular targets. Pharmacological modulation of this pathway might prove useful for future prevention and treatment of HF.

Background-Heat shock proteins (HSPs) are a family of proteins with immunogenic and proinflammatory properties.Human and Chlamydia pneumoniae (Cp) HSP60 were found in patients with stable coronary disease. Methods and Results-We measured the levels of anti-Cp-HSP60 and anti-Cp immunoglobulin G (IgG) in 179 patients with unstable angina, 40 with acute myocardial infarction, and 40 with stable angina (SA), as well as 100 control subjects. Forty-one patients with acute coronary syndromes (ACS) were also studied at follow-up. We also measured plasma levels of high-sensitivity C-reactive protein (hs-CRP) and troponin T (TnT). Seropositivity to Cp-HSP60 was found in 99% of ACS patients but in only 20% of SA patients and none of the control subjects. Seropositivity to Cp was detected in 67% of ACS patients, 60% of SA patients, and 30% of the control subjects. No differences in Cp-HSP60 IgG and in Cp IgG were observed between patients with myocardial infarction and patients with unstable angina. No correlation was found between Cp-HSP60 IgG, TnT, and hs-CRP or between IgG against Cp and hs-CRP. In ACS patients at follow-up, Cp-HSP60 IgG decreased from 0.88Ϯ0.25 to 0.45Ϯ0.14 arbitrary units (PϽ0.0001), becoming negative in 12 patients. Conclusions-Seropositivity for Cp-HSP60 appears to be a very sensitive and specific marker of ACS, unrelated to Cp IgG antibody titers or hs-CRP and TnT levels. Its causal involvement in instability and its diagnostic role in ACS deserve further study.

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Our study demonstrates delayed PMN apoptosis in UA. This alteration might be involved in the persistence of inflammatory activation and affects recurrence of instability.