Dysfunction In Myocardial Infarction Patients Research Articles

Effect of Metabolic Syndrome on Left Atrial and Left Ventricular Deformation and Atrioventricular Interactions in Patients With Myocardial Infarction.

Metabolic syndrome (MetS) is associated with worse prognosis in patients with myocardial infarction (MI). However, it is unclear how MetS in MI patients is associated with left atrial (LA) and left ventricular (LV) deformation. To determine the effect of MetS on LA and LV deformation and atrioventricular interactions in MI patients. Retrospective. One hundred eighty-one MI patients (73 MetS+ and 108 MetS-), 107 age- and sex-matched controls (49 MetS+ and 58 MetS-). 3.0 T/balanced steady-state free precession (SSFP)/segmented phase-sensitive inversion recovery SSFP sequence. LA strain and strain rates (reservoir, conduit, and active), left atrioventricular coupling index (LACI), and LV geometry and radial, circumferential and longitudinal global peak strains (PS) were compared among groups. Two-way analysis of variance, Spearman and Pearson's correlation coefficients, and multivariable linear regression analysis. P value <0.05 indicated statistical significance. Compared with controls, the MI patients with or without MetS showed impaired LA function (reservoir, conduit, and active) and LV deformation (radial, circumferential, and longitudinal PS) and higher LACI. The MetS+ group had lower LA reservoir and conduit function and LV deformationthan MetS- group. The MetS-MI interaction was not statistically significant. Furthermore, multivariable linear regression showed that MetS was independently associated with LA and LV deformation (β = -0.181 to -0.209) in MI patients; LA function was independently associated with LV circumferential PS (β = 0.230 to 0.394) and longitudinal PS (β = 0.189 to 0.420), and LA passive strain and strain rate were negatively associated with LV mass (β = -0.178 and -0.298). MetS may be associated with the LA and LV dysfunction in MI patients. Impaired LV deformation and LV hypertrophy are independently associated with LA dysfunction in MI patients, and the MI patients have higher LACI than controls, suggesting atrioventricular interaction alterations. 4 TECHNICAL EFFICACY: 3.

Inhibition of peptidyl arginine deiminase-4 protects against myocardial infarction induced cardiac dysfunction

Peptidyl arginine deiminase-4 (PAD4), a PAD enzyme family member, catalyzes the posttranslational conversion of arginine residues to citrulline in target proteins. Although PAD4 is believed to play a crucial role in various pathological conditions such as infectious diseases, autoimmune diseases, and ischemic conditions, the effect of PAD4 in myocardial infarction (MI)-induced cardiac injury remains to be examined. Here, we hypothesize that PAD4 contributes to cardiac ischemic injury by exacerbating the inflammatory response and promoting neutrophil extracellular trap (NET) formation after MI.Permanent left coronary artery ligation, a condition that mimics MI, was performed on male C57BL/6 mice. [(3S,4R)-3-amino-4-hydroxy-1-piperidinyl] [2-[1-(cyclopropylmethyl)-1H-indol-2-yl]-7-methoxy-1-methyl-1H-benzimidazol-5-yl]-methanone (GSK484), an inhibitor of PAD4, was delivered via intraperitoneal injection to inhibit PAD4 activity. Cardiac PAD4 expression, tissue injury scoring, neutrophil infiltration, cit-H3 expression, NET formation, inflammatory cytokine secretion, apoptosis, and cardiac function were analyzed.In the current study, we discovered the protective effect of PAD4 inhibition using the PAD4-specific inhibitor GSK484 in cardiomyocytes challenged by MI. GSK484-mediated PAD4 inhibition can moderately preserve ventricle histological structure and myocardium integrity after MI, thereby reducing the infarct size and decreasing myocardial enzyme levels in serum. PAD4 inhibition also effectively protects cardiomyocytes from MI-induced NET formation and inflammatory cytokine secretion, in turn alleviating cardiac ischemia-induced apoptosis of cardiomyocytes.Collectively, these findings demonstrate the efficacy of specific PAD4 inhibition in reducing MI-induced neutrophil infiltration, NET formation, inflammatory reaction, and cardiomyocyte apoptosis, thereby increasing overall cardiac function improvement. These results provide novel insights for the development of new strategies to treat cardiovascular dysfunction in MI patients.

Impact of myocardial infarction on intraventricular vortex and flow energetics assessed using computational simulations.

Flow energetics have been proposed as early indicators of progressive left ventricular (LV) functional impairment in patients with myocardial infarction (MI), but its correlation with individual MI parameters has not been fully explored. Using electro-fluid-structure interaction LV models, this study investigated the correlation between four MI parameters: infarct size, infarct multiplicity, regional enhancement of contractility at the viable myocardium area (RECVM), and LV mechanical dyssynchrony (LVMD) with intraventricular vortex and flow energetics. In LV with small infarcts, our results showed that infarct appearance amplified the energy dissipation index (DI), where substantial viscous energy loss was observed in areas with high flow velocity and near the infarct-vortex interface. The LV with small multiple infarcts and RECVM showed remarkable DI increment during systole and diastole. In correlation analysis, the systolic kinetic energy fluctuation index (E') was positively related to ejection fraction (EF) (R2 =0.982) but negatively correlated with diastolic E' (R2 =0.970). Diastolic E' was inversely correlated with vortex kinetic energy (R2 =0.960) and vortex depth (R2 =0.876). We showed an excessive systolic DI could differentiate infarcted LV with normal EF from healthy LV. Strong flow acceleration, LVMD, and vortex-infarct interactions were predominant factors that induced excessive DI in infarcted LVs. Instead of causing undesired flow turbulence, high systolic E' suggested the existence of energetic flow acceleration, while high diastolic E' implied an inefficient diastolic filling. Thus, systolic E' is not a suitable early indicator for progressive LV dysfunction in MI patients, while diastolic E' may be a useful index to indicate diastolic impairment in these patients.

Significance of Anti-Myosin Antibody Formation in Patients With Myocardial Infarction: A Prospective Observational Study

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. 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. Forty-three (43) 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. 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.