Atrial fibrillation (AF) is the most common arrhythmia in humans. After successful cardioversion, there is a recurrence of 60% due to atrial remodeling, and it has been shown that the global peak atrial longitudinal strain (GPALS) is decreased in these subjects. The aim of this study was to evaluate the predictive value of GPALS for AF recurrence. A prospective cohort of patients with persistent (PnVAF) and long standing persistent non-valvular AF (LSPnVAF) which underwent electrical cardioversion was evaluated with standard echocardiographic variables and GPALS quantification. The primary endpoint was AF recurrence at 6 months. We included PnVAF (n = 50, aged 68.4 ± 10.2 years, female 46%, lasted AF 6 months) and LSPnVAF (n = 81, aged 66.5 ± 13.1 years, female 36%, lasted AF 18 months). At 6 months there were a 68% of recurrence of AF in PnVAF and 53% in LSPnVAF group. GPALS was lower in recurrence 7.8 ± 2.0% versus 21.2 ± 8.9% (p < 0.001) for PnVAF and 7.3 ± 2.7% versus 20.7 ± 7.6% (p < 0.001) in LSPnVAF. GPALS ≤ 10.75% discriminates recurrence at 6 months with a sensitivity of 85%, specificity 99%, PPV 85%, NPV 90%, LR + 8.5 and LR- 0.17. The independent predictors of recurrence in PnVAF were GPALS ≤ 10.75% HR 8.89 [(2.2–35.7), p < 0.01] meanwhile in LSPnVAF were age HR 1.039 [(1.007-1.071), p = 0.01], and GPALS ≤ 10.75% HR 28.1 [(7.2–109.1), p < 0.001]. In subjects with PnVAF and LSPnVAF with successful electrical cardioversion, GPALS ≤ 10.75% predicts arrhythmia recurrence at 6-month follow-up.

Interleukin- (IL-) 17 is increased in acute myocardial infarction (AMI) and plays a key role in inflammatory diseases through its involvement in the activation of leukocytes. Here, we describe for the first time the effect of IL-17 in the migration and activation of monocyte subsets in patients during ST-segment elevation myocardial infarction (STEMI) and post-STEMI. We analyzed the circulating levels of IL-17 in patient plasma. A gradual increase in IL-17 was found in STEMI and post-STEMI patients. Additionally, IL-17 had a powerful effect on the recruitment of CD14⁺⁺CD16⁺/CD14⁺CD16⁺⁺monocytes derived from patients post-STEMI compared with the monocytes from patients with STEMI, suggesting that IL-17 recruits monocytes with inflammatory activity post-STEMI. Furthermore, IL-17 increased the expression of TLR4 on CD14⁺CD16^-and CD14⁺⁺CD16⁺/CD14⁺CD16⁺⁺monocytes post-STEMI and might enhance the response to danger-associated molecular patterns post-STEMI. Moreover, IL-17 induced secretion of IL-6 from CD14⁺⁺CD16⁻and CD14⁺⁺CD16⁺/CD14⁺CD16⁺⁺monocytes both in STEMI and in post-STEMI, which indicates that IL-17 has an effect on the secretion of proinflammatory cytokines from monocytes during STEMI and post-STEMI. Overall, we demonstrate that in STEMI and post-STEMI, IL-17 is increased and induces the migration and activation of monocyte subsets, possibly contributing to the inflammatory response through TLR4 and IL-6 secretion.

Acute ST-elevation myocardial infarction (STEMI) leads to myocardial injury or necrosis, and M1 macrophages play an important role in the inflammatory response. Bone marrow mesenchymal stem/stromal cells (BM-MSCs) are capable of modulating macrophage plasticity, principally due to their immunoregulatory capacity. In the present study, we analyzed the capacity of MSCs to modulate macrophages derived from monocytes from patients with STEMI. We analyzed the circulating levels of cytokines associated with M1 and M2 macrophages in patients with STEMI, and the levels of cytokines associated with M1 macrophages were significantly higher in patients with STEMI than in controls. BM-MSCs facilitate the generation of M1 and M2 macrophages. M1 macrophages cocultured with MSCs did not have decreased M1 marker expression, but these macrophages had an increased expression of markers of the M2 macrophage phenotype (CD14, CD163 and CD206) and IL-10 and IL-1Ra signaling-induced regulatory T cells (Tregs). M2 macrophages from patients with STEMI had an increased expression of M2 phenotypic markers in coculture with BM-MSCs, as well as an increased secretion of anti-inflammatory cytokines and an increased generation of Tregs. The findings in this study indicate that BM-MSCs have the ability to modulate the M1 macrophage response, which could improve cardiac tissue damage in patients with STEMI.

The oxidative stress state is characterized by an increase in oxygen reactive species that overwhelms the antioxidant defense; we do not know if these pathological changes are correlated with alterations in left ventricular mechanics. The aim was correlating the oxidative stress state with the left ventricular global longitudinal strain (GLS) and the left ventricular end diastolic pressure (LVEDP). Twenty-five patients with essential hypertension and 25 controls paired by age and gender were studied. All of the participants were subjected to echocardiography and biochemical determination of oxidative stress markers. The hypertensive patients, compared with control subjects, had significantly (p<0.05) higher levels of oxidized proteins (5.03±1.05versus4.06±0.63 nmol/mg), lower levels of extracellular superoxide dismutase (EC-SOD) activity (0.045±0.02versus0.082±0.02 U/mg), higher LVEDP (16.2±4.5versus11.3±1.6 mm Hg), and lower GLS (−12% versus −16%). Both groups had preserved ejection fraction and the results showed a positive correlation of oxidized proteins with GLS (r=0.386,p=0.006) and LVEDP (r=0.389,p=0.005); we also found a negative correlation of EC-SOD activity with GLS (r=-0.404,p=0.004) and LVEDP (r=-0.347,p=0.014).

Recent studies demonstrated that the expression of coxsackievirus and adenovirus receptor (CAR) is implicated in the pathophysiology of myocarditis. The aim of the present study was to assess the association between active and borderline myocarditis and CAR expression in endomyocardial tissues, and analyze the association between CAR expression and treatment response. An analytic, cross‑sectional, retrospective study was performed in 26 patients with myocarditis and 10 control subjects without heart disease. Myocardial biopsies were obtained and CAR transcription was measured by reverse transcription‑quantitative polymerase chain reaction analysis. The association between CAR mRNA levels and the response to immunosuppressive or conventional therapy (treatment responders, n=17; non‑responders, n=9) or with the type of histological myocarditis (active myocarditis, n=16; borderline myocarditis, n=10) was analyzed. CAR transcription levels were significantly lower (P=0.012) in patients with myocarditis compared with controls, and a significant decrease was observed (P=0.023) in CAR mRNA levels among patients with borderline myocarditis compared with the no myocarditis group. Patients responding to therapy exhibited higher CAR mRNA levels (P=0.036) compared with patients not responding to treatment, as evaluated based on clinical and echocardiographic criteria (immunosuppressive therapy, n=8; conventional therapy, n=1). Myocarditis in non‑responders was associated with fewer clinical manifestations and lower CAR mRNA levels. A significant difference was only found regarding the use of oral steroids in patients with active myocarditis who responded to treatment (P=0.02), with no difference in borderline myocarditis. In conclusion, the transcriptional level of CAR is low in the endomyocardial tissue of patients with myocarditis, and it is lower in borderline myocarditis and in non‑responder patients. These findings may enable early identification of patients who may benefit from treatment and timely determination of prognosis.