Background: In patients with ischaemic cardiomyopathy and viable myocardium, left ventricular ejection fraction (LVEF) does not always improve after revascularisation. Whether this may affect prognosis is unclear. Objective: To evaluate the prognosis of viable patients with and without improvement of LVEF after coronary revascularisation. Methods: Before revascularisation, radionuclide ventriculography (RNV) and dobutamine stress echocardiography were performed to assess LVEF and myocardial viability, respectively. Nine to 12 months after revascularisation, LVEF improvement was assessed by RNV. Patients were divided into three groups: group 1, viable patients with LVEF improvement (n = 27); group 2, viable patients without LVEF improvement (n = 15), group 3, non-viable patients (n = 48). Cardiac events were evaluated during a 4-year follow-up. Results: After revascularisation, the mean (SD) LVEF improved from 32 (9)% to 42 (10)% in group 1, but did not change significantly in group 2 and in group 3, p<0.001 by analysis of variance (ANOVA). Heart failure symptoms improved in both groups 1 (mean (SD) NYHA class from 3.1 (0.9) to 1.7 (0.7)) and 2 (from 3.2 (0.7) to 1.7 (0.9)), but not in group 3 (from 2.8 (1.0) to 2.7 (0.5)), p<0.001 by ANOVA. During follow-up, the cardiac event rate was low (4%) in group 1, intermediate (21%) in group 2 and high (33%) in group 3 (p = 0.01). Conclusion: The best prognosis after revascularisation may be expected in those viable patients whose LVEF improves. Conversely, viable patients without functional improvement have an intermediate prognosis.

Background— Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that favors the expansion of CD4 ⁺ CD28 ^null T cells, an aggressive and unusual proinflammatory lymphocyte subset frequently observed in patients with unstable angina (UA). The purpose of the present ex vivo study was to evaluate whether inflammation in patients with UA may be modulated by selective blockade of TNF-α. Methods and Results— Peripheral blood samples were collected from 17 patients with UA (Braunwald’s class IIIB). CD4 ⁺ CD28 ^null T cells were assessed by flow cytometry and expressed as a percentage of all CD4 ⁺ T cells after 24 hours of incubation of whole blood with and without increasing doses (0.1, 1, 10, and 100 μg/mL) of infliximab, an anti–TNF-α monoclonal antibody. In addition, CD28 expression was assessed and expressed as mean fluorescence intensity (geometric mean of the CD28 fluorescence value on all CD4 ⁺ T cells). CD4 ⁺ CD28 ^null T-cell percentage decreased from a median of 6.2% (range, 1.2% to 23.9%) to 4.9% (range, 1.1% to 21.9%), 4.5% (range, 1.1% to 21.6%), and 4.1% (range, 0.4% to 21.4%) after incubation with 1, 10, and 100 μg/mL of infliximab ( P for trend=0.043). Analysis of CD28 mean fluorescence intensity showed that the expression of CD28 on cell surface significantly increased after incubation with increasing doses of infliximab ( P for trend=0.03). Conclusions— The findings of this ex vivo study show that CD4 ⁺ CD28 ^null T-cell expansion in patients with UA may be reduced by selective TNF-α blockade. Further studies are warranted to evaluate the clinical benefit of CD4 ⁺ CD28 ^null T-cell modulation.

Objective Patients with unstable angina (UA) and high C-reactive protein (CRP) have increased cardiovascular risk. Whether genetic factors such as the synonymous 1059G/C polymorphism within the exon 2 of the human CRP gene determine CRP levels and outcome is unclear. Methods In 105 consecutive patients with UA, we assessed the CRP 1059G/C polymorphism, CRP plasma levels and interleukin-6 production after in-vitro stimulation of whole blood with lipopolysaccharide (1 ng/ml). Coronary events during a 24-month follow-up were recorded. Results CRP levels (median, range) were significantly lower among C-allele carriers (2.3 mg/l, 0.5–26.9) than among GG homozygotes (5.9 mg/l, 0.8–72.12, P=0.009). Interleukin-6 production was lower in C-allele carriers (1645 pg/ml, 832.0–9522) than in GG homozygotes (3929 pg/ml, 670.8–10 582), (P=0.085). At follow-up, 1059C-allele carriers experienced fewer coronary events than 1059GG homozygotes (13 vs. 47%, P=0.021). At multivariable analysis, a CRP level >3 mg/l, but not the 1059G/C polymorphism, was an independent predictor of coronary events (odds ratio 10.04, 95% confidence interval 2.84–35.44, P=0.0002). Conclusion This study shows that the CRP synonymous 1059G/C polymorphism affects CRP levels. No independent association was, however, observed between this polymorphism and clinical outcome in UA.

Aortic stenosis (AS) is defined as severe in the presence of: mean gradient ≥40 mmHg, peak aortic velocity ≥4 m/s, and aortic valve area (AVA) ≤1 cm² (or an indexed AVA ≤0.6 cm²/m²). However, up to 40% of patients have a discrepancy between gradient and AVA, i.e. AVA ≤1 cm² (indicating severe AS) and a moderate gradient: >20 and <40 mmHg (typical of moderate stenosis). This condition is called ‘low-gradient AS’ and includes very heterogeneous clinical entities, with different pathophysiological mechanisms. The diagnostic tools needed to discriminate the different low-gradient AS phenotypes include colour-Doppler echocardiography, dobutamine stress echocardiography, computed tomography scan for the definition of the calcium score, and recently magnetic resonance imaging. The prognostic impact of low-gradient AS is heterogeneous. Classical low-flow low-gradient AS [reduced left ventricular ejection fraction (LVEF)] has the worst prognosis, followed by paradoxical low-flow low-gradient AS (preserved LVEF). Conversely, normal-flow low-gradient AS is associated with a better prognosis. The indications of the guidelines recommend surgical or percutaneous treatment, depending on the risk and comorbidities of the individual patient, both for patients with classic low-flow low-gradient AS and for those with paradoxical low-flow low-gradient AS.

Promoter of the CD14-receptor gene, an important mediator of the inflammatory response to lipopolysaccharide. Methods and results CD14 C(−260)T polymorphism was assessed in 100 patients with an acute presentation of CAD (group 1), 66 patients with stable presentation (group 2) and 88 healthy people (group 3); all patients were whites. In addition, baseline sCD14 plasma levels, and interleukin-6 production by circulating monocytes after in-vitro stimulation with lipopolysaccharide (1 ng/ml) were assessed. T/T homozygosis was more frequent in group 1 (36%, P < 0.001 versus others). Interleukin-6 production was higher in T/T homozygotes (median 4092.4; range 387–10 582 pg/ml) than in C/T heterozygotes (median 2442, range 40.5–9625 pg/ml, P < 0.001) and C/C homozygotes (median 3277.5; range 374.4–6250 pg/ml, P < 0.001). At multivariate analysis, T/T homozygosis and interleukin-6 production were independent predictors of acute presentation of CAD. Conclusion The present study shows that genetic factors that influence the reactivity of inflammatory cells may play a role in determining the first clinical presentation of CAD....

A 24-year-old woman was referred to our Cardiology Department because of cardiomegaly at a routine chest X-ray. She was asymptomatic except for some fatigability. Physical examination was unremarkable. Electrocardiogram showed only low QRS voltages. Echocardiography revealed large pericardial effusion with right atrial and ventricular collapse. Pericardiocentesis was performed and 1100 mL of milky fluid were removed, suggesting chylopericardium. The chylous nature of the fluid was confirmed by high content of triglycerides (1200 mg/dL) and by cholesterol/triglyceride ratio <1. Sudan III stain of the fluid revealed fat globules. Bacterial and tubercoulous cultures were negative. Cytology demonstrated abundance of lymphocytes, with no tumour cells. A subxiphoid exterior tube drainage was maintained and alipidic diet was started. After an initial success of this treatment, significant chylopericardium recurred. Thoracic computed tomography was negative. Thus, lymphangiogram was performed by slow injection of ethiodized oil into a cannulated lymphatic vessel of the right foot showing an open thoracic duct with lymphangiectasias at pericardial level (Figure). Left thoracotomy was indicated. The pleural cavity appeared normal; the pericardium appeared thickened with numerous lymphangiectasias. Ligation of the thoracic duct, closure between metallic clips of lymphangiectasias, and pericardial fenestration were performed. Pericardial biopsies showed a chronic inflammatory process with haemorrhagic infiltrate and a large number of lymphangiectasias. After 15 days, the patient was discharged and in 4 weeks she returned to normal diet, full-time work, and full activities. Echocardiography showed no recurrence of chylopericardium at late follow-up.