Early inflammatory cytokine response: a direct comparison between spontaneous coronary plaque destabilization vs angioplasty induced.

AIM: To compare inflammatory response accompanying acute coronary syndrome (ACS) with that following coronary plaque rupture caused by coronary angioplasty (PCI). METHODS: Twenty-seven consecutive subjects with either ACS or treated with PCI in the subacute phase of ACS underwent serial evaluation of circulating interleukin (IL)-2, IL-8, IL-10, interferon (IFN)-γ and tumor-necrosis-factor (TNF)-α levels. Blood samples were drawn immediately before angioplasty (T0) in the PCI group or at admission in the ACS group, 12 h (T1) and 24 h later (T2). RESULTS: Differences between cytokine levels were substantially not statistically significant when comparing PCI, non-ST-elevation-ACS, and ST-elevation-ACS groups, especially 24 h after plaque rupture (T2, Type-II error 85-94%). CONCLUSIONS: Inflammatory activation during the first 24 h of ACS or after PCI is comparable, regardless of myocardial damage in terms of troponin levels. Coronary plaque rupture may be presumed as being the main responsible for increased circulating cytokine levels in this early phase.

Characterization of the immune inflammatory profile in obese asthmatic children.

Asthma and obesity are two common disorders often associated in children and characterized by an inflammatory status. Growing evidences support a connection between obesity and asthma since weight reduction can improve asthmatic symptoms. In this study, we have enrolled eighty children: 17 non asthmatics and non obese, 19 obese, 28 asthmatics-obese and, 16 asthmatics non-obese, respectively. In all participants, respiratory functional tests and body mass index (BMI) were calculated. Moreover, systemic inflammation of biomarkers such as T helper (h)1-type, Th2-type and T regulatory-type serum cytokines along with major adipokines was determined. Data will show that the association between asthma and obesity leads to a predominant Th1-type response with an increase in pro-inflammatory cytokines. This inflammatory profile in asthmatics-obese children is sustained by elevated serum levels of leptin and visfatin, while adiponectin concentration is rather diminished. Finally, levels of systemic inflammatory biomarkers positively correlate with the increase in BMI values in all population subgroups.

Inflammatory cytokines imbalance in the very early phase of acute coronary syndrome: correlations with angiographic findings and in-hospital events.

The aim of this study is to investigate the release of some inflammatory cytokines (Cks) during the very early phase (first 24 h) of acute coronary syndrome (ACS). Twenty-six consecutive subjects admitted to coronary care unit with ACS underwent serial blood sampling in order to evaluate concentrations of interleukin (IL)-2, IL-10, IL-18, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ. Blood samples were taken within 6 h after onset of chest pain (T0), at 12 h (T1), and at 24 h (T2). Patients were thus divided into four groups comparing pro-inflammatory Ck release (IL-2, TNF-α, and IFN-γ) and anti-inflammatory activity (IL-10). Clinical features, risk factors, incidence of adverse events, and coronary angiography findings were compared with Ck activation. Ck levels were significantly increased if compared with baseline. Subjects with marked inflammatory response showed a higher incidence of left anterior descending coronary disease (IL-2, p < 0.001; TNF-α and IFN-γ, p < 0.05) and more often incurred early complications (IL-2, p < 0.05; IFN-γ, p < 0.001). A correlation was detectable between IL-18 levels and myocardial enzyme release (creatine kinase, r = 0.47; lactate dehydrogenase, r = 0.54; troponin I, r = 0.58; p < 0.05). TNF-α levels were associated with a worse prognosis at follow-up (Log rank, p < 0.05). A Ck activation characterizes the early phase of ACS. Early inflammatory reaction seems to correlate with coronary disease and adverse events.

Th2-dependent cytokine release in patients treated with coronary angioplasty.

AIM: The aim of this study is to investigate the T helper (Th)2-dependent release of interleukin(IL)-4 and IL-13 in patients with unstable angina treated with coronary angioplasty (PCI). METHODS: This study involved 48 consecutive patients with unstable angina who underwent PCI. Blood samples were taken before and 48 h after PCI to evaluate serum IL-4 and IL-13 levels. Coronary atherosclerosis was assessed in terms of the severity of the treated lesions and the presence of multivessel disease, and compared with IL release. RESULTS: Before and after PCI, serum IL-4 levels were, respectively, 53.1+/-110.7 and 35.1+/-16.9 pg/ml (P not significant), and serum IL-13 levels 6.7+/-3.7 and 6.0+/-2.9 pg/ml (P<0.05). A correlation was present between the severity of the treated coronary lesions and serum IL-13 levels (r 0.36; P<0.05). The patients with multivessel coronary artery disease had a higher periprocedure ratio of IL-4 than those with single-vessel coronary artery disease (1.46+/-0.76 vs. 0.89+/-0.34, P<0.001). CONCLUSION: A significant decrease was observed in Th2-dependent IL concentrations after PCI; increased Th2-dependent IL levels before PCI seem to correlate with the severity of coronary atherosclerosis.

Inflammatory cytokine imbalance after coronary angioplasty: links with coronary atherosclerosis.

AIM: To investigate release of some inflammatory cytokines (Cys) after coronary angioplasty and its links with coronary atherosclerosis. METHODS: Twenty-seven consecutive subjects with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) were enrolled in the study: serial blood samples were taken in order to evaluate plasma concentrations of Interleukin (IL)-2, IL-10, IL-18, TNFalpha, and IFNgamma just before PCI at 12 and 24 hours. Patients were then divided, considering balance between each inflammatory Cy and IL-10, an antiinflammatory Cy, into four groups, ranging from a prevalent antiinflammatory response (stable inflammatory Cy-increasing IL-10 values) to a marked inflammatory imbalance (increasing inflammatory Cy-stable IL-10 values). RESULTS: All Cys showed significant increases in plasma concentrations if compared with baseline values. Release curves were not significantly different when comparing subjects with ST-elevation myocardial infarction (STEMI) versus unstable angina-non-STEMI (UA-NSTEMI), diabetics versus controls. Subjects with marked inflammatory response showed a higher incidence of stenosis on left anterior descending (LAD) coronary artery (IL-2 chi(2) and IFNgamma P < 0.05); Cy release was higher in patients with multivessel coronary disease (IL-2 and IFNgamma, ANOVA P < 0.01). Correlations were also referable between Cys and myocardial enzyme release. Subjects treated with sirolimus-eluting stents (SES) showed significantly lower Cy periprocedure ratio if compared with those treated with bare metal stents. CONCLUSIONS: A significant Cy release is detectable after PCI: inflammatory response seems to correlate with both PCI due to plaque instabilization and coronary atherosclerosis. A blunted inflammatory response is detectable in subjects treated with SES.

ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure.

RATIONALE: In patients with acute respiratory distress syndrome (ARDS), a focal distribution of loss of aeration in lung computed tomography predicts low potential for alveolar recruitment and susceptibility to alveolar hyperinflation with high levels of positive end-expiratory pressure (PEEP). OBJECTIVES: We tested the hypothesis that, in this cohort of patients, the table-based PEEP setting criteria of the National Heart, Lung, and Blood Institute's ARDS Network (ARDSnet) low tidal volume ventilatory protocol could induce tidal alveolar hyperinflation. METHODS: In 15 patients, physiologic parameters and plasma inflammatory mediators were measured during two ventilatory strategies, applied randomly: the ARDSnet and the stress index strategy. The latter used the same ARDSnet ventilatory pattern except for the PEEP level, which was adjusted based on the stress index, a monitoring tool intended to quantify tidal alveolar hyperinflation and/or recruiting/derecruiting that occurs during constant-flow ventilation, on a breath-by-breath basis. MEASUREMENTS AND MAIN RESULTS: In all patients, the stress index revealed alveolar hyperinflation during application of the ARDSnet strategy, and consequently, PEEP was significantly decreased (P < 0.01) to normalize the stress index value. Static lung elastance (P = 0.01), plasma concentrations of interleukin-6 (P < 0.01), interleukin-8 (P = 0.031), and soluble tumor necrosis factor receptor I (P = 0.013) were significantly lower during the stress index as compared with the ARDSnet strategy-guided ventilation. CONCLUSIONS: Alveolar hyperinflation in patients with focal ARDS ventilated with the ARDSnet protocol is attenuated by a physiologic approach to PEEP setting based on the stress index measurement.