RESUMO
Previous studies have shown that both sympathetic hyperactivity and enhanced inflammatory responses are associated with poor outcomes in patients with acute coronary syndrome (ACS). Whether there is a correlation between these two characteristics remains unclear. Thirty-four patients with uncomplicated ACS were evaluated; their mean age was 51.7±7.0 years, 79.4% were male, and 94.1% had myocardial infarction (MI). On the fourth day of hospitalization, they underwent muscle sympathetic nerve activity (MSNA) analysis (microneurography), as well as ultrasensitive C-reactive protein (usCRP), interleukin-6 (IL-6), and lipoprotein-associated phospholipase A2 (Lp-PLA2) activity measurements. These evaluations were repeated at 1, 3, and 6 months after hospitalization. Both MSNA and inflammatory biomarkers were elevated during the acute phase of ACS and then decreased over time. At hospitalization, the median usCRP level was 17.75 (IQR 8.57; 40.15) mg/l, the median IL-6 level was 6.65 (IQR 4.45; 8.20), the mean Lp-PLA2 activity level was 185.8 ±52.2 nmol/min per ml, and mean MSNA was 64.2±19.3 bursts/100 heart beats. All of these variables decreased significantly over 6 months compared with the in-hospital levels. MSNA was independently associated with the peak level of creatine kinase isoenzyme MB (CKMB) in the acute phase (P=0.027) and with left ventricular ejection fraction (LVEF) at 6 months (P=0.026). Despite the increased levels of inflammatory biomarkers and sympathetic hyperactivity in the initial phase of ACS, no significant correlations between them were observed in any of the analyzed phases. Our data suggest that although both sympathetic hyperactivity and inflammation are concomitantly present during the early phase of ACS, these characteristics manifest via distinct pathological pathways.
Assuntos
Síndrome Coronariana Aguda/fisiopatologia , Biomarcadores/sangue , Mediadores da Inflamação/sangue , Inflamação/fisiopatologia , Sistema Nervoso Simpático/fisiopatologia , 1-Alquil-2-acetilglicerofosfocolina Esterase/sangue , Síndrome Coronariana Aguda/sangue , Adulto , Proteína C-Reativa/metabolismo , Creatina Quinase Forma MB/sangue , Feminino , Humanos , Inflamação/sangue , Interleucina-6/sangue , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/sangue , Infarto do Miocárdio/fisiopatologiaRESUMO
Autonomic dysfunction, including baroreceptor attenuation and sympathetic activation, has been reported in patients with myocardial infarction (MI) and has been associated with increased mortality. We tested the hypotheses that exercise training (ET) in post-MI patients would normalize arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA), and long-term ET would maintain the benefits in BRS and MSNA. Twenty-eight patients after 1 month of uncomplicated MI were randomly assigned to 2 groups, ET (MI-ET) and untrained. A normal control group was also studied. ET consisted of three 60-minute exercise sessions per week for 6 months. We evaluated MSNA (microneurography), blood pressure (automatic oscillometric method), heart rate (ECG), and spectral analysis of RR interval, systolic arterial pressure (SAP), and MSNA. Baroreflex gain of SAP-RR interval and SAP-MSNA were calculated using the α-index. At 3 to 5 days and 1 month after MI, MSNA and low-frequency SAP were significantly higher and BRS significantly lower in MI patients when compared with the normal control group. ET significantly decreased MSNA (bursts per 100 heartbeats) and the low-frequency component of SAP and significantly increased the low-frequency component of MSNA and BRS of the RR interval and MSNA. These changes were so marked that the differences between patients with MI and the normal control group were no longer observed after ET. MSNA and BRS in the MI-untrained group did not change from baseline over the same time period. ET normalizes BRS, low-frequency SAP, and MSNA in patients with MI. These improvements in autonomic control are maintained by long-term ET. These findings highlight the clinical importance of this nonpharmacological therapy based on ET in the long-term treatment of patients with MI.