In Kawasaki disease, although coronary dilatation is attributed to vasculitis, the effect of myocardial inflammation is underestimated. Coronary dilatations are determined by Z-scores, which do not take into account dominance. The aim of the present study was to describe the impact of coronary dominance on dilatation in Kawasaki disease.

We performed a retrospective analysis of coronary dilatations according to angiography categorisation of dominance.

Of 28 patients (2.6 [0.2–10.1] years), right dominance was present in 15 patients and left in 13. Early dilatation was present in all patients, of whom 11 were ipsilateral to the dominant segment and 17 contralateral. Ipsilateral dilatations were present at diagnosis (9/11 versus 6/17, p=0.02) compared with contralateral dilatations, which developed 2 weeks after diagnosis (9/11 versus 16/17, p=0.29). Coronary artery Z-scores of patients with contralateral dilatation increased at 2 weeks, before returning to baseline values (2.0±2.2 at diagnosis, 4.1±1.8 at 2 weeks, 1.8±1.2 at 3–6 months, p=0.001), compared with patients with ipsilateral dilatation in whom Z-scores were maximal at diagnosis and remained stable (3.0±0.9, 2.7±1.1 and 2.6±1.5, respectively, p=0.13). Dominant coronary artery Z-scores were higher compared with non-dominant segments at diagnosis (3.0±0.9 versus 1.0±0.8, p<0.001) and at late follow-up (2.6±1.5 versus 0.4±1.4, p=0.002) in patients with ipsilateral dilatation.

Progression of coronary dilatation after diagnosis may be a sign of dilatation secondary to vasculitis, as opposed to regression of Z-scores in ipsilateral dilatations, probably related to physiological vasodilatation in response to carditis. This needs to be validated in larger studies against vasculitic and myocardial inflammatory markers.

Dilatation of the ascending aorta is described in Turner’s syndrome with variable prevalence (6.8–32%). Reported series typically include patients with associated cardiac anomalies.

To characterise the prevalence, age of onset, and the progress of dilatation of the ascending aorta in Turner’s syndrome patients free of structural cardiac anomalies. Potential risk factors such as karyotype and growth hormone therapy were analysed for correlation with aortic dilatation.

We carried out a retrospective study with data collected from medical records and echocardiography studies. Patients with Tuner’s syndrome followed-up between 1992 and 2010 with at least two echocardiography studies were eligible. Patients with previous cardiac surgery or under anti-hypertensive medication were excluded. Ascending aorta diameter measurements were adjusted for body surface area, and dilatation was defined as Z-score>2.

The study population consisted of 44 patients, aged 11.9±7.4 years at the first echocardiogram and 17.9±7.3 years at the last follow-up, with a follow-up duration of 6.0±3.7 years. A total of 13 (29.5%) patients exhibited aortic dilatation during follow-up, suggesting an actuarial estimate of the freedom from aortic dilatation dropping from 86 to 70% and then to 37% at 10, 20, and 30 years of age, respectively. There was no statistically significant impact of karyotype or growth hormone therapy on aortic Z-score progression.

The prevalence of dilatation of the ascending aorta in Turner’s syndrome patients free of structural aortic anomalies is comparable with published data with associated lesions. Growth hormone therapy and karyotype had no significant impact; however, longitudinal follow-up is warranted.

Pattern analysis has emerged as a tool to depict the role of multiple nutrients/foods in relation to health outcomes. The present study aimed at extracting nutrient patterns with respect to breast cancer (BC) aetiology.

Nutrient patterns were derived with treelet transform (TT) and related to BC risk. TT was applied to twenty-three log-transformed nutrient densities from dietary questionnaires. Hazard ratios (HR) and 95 % confidence intervals computed using Cox proportional hazards models quantified the association between quintiles of nutrient pattern scores and risk of overall BC, and by hormonal receptor and menopausal status. Principal component analysis was applied for comparison.

The European Prospective Investigation into Cancer and Nutrition (EPIC).

Women (n 334 850) from the EPIC study.

The first TT component (TC1) highlighted a pattern rich in nutrients found in animal foods loading on cholesterol, protein, retinol, vitamins B12 and D, while the second TT component (TC2) reflected a diet rich in β-carotene, riboflavin, thiamin, vitamins C and B6, fibre, Fe, Ca, K, Mg, P and folate. While TC1 was not associated with BC risk, TC2 was inversely associated with BC risk overall (HRQ5 v. Q1=0·89, 95 % CI 0·83, 0·95, Ptrend<0·01) and showed a significantly lower risk in oestrogen receptor-positive (HRQ5 v. Q1=0·89, 95 % CI 0·81, 0·98, Ptrend=0·02) and progesterone receptor-positive tumours (HRQ5 v. Q1=0·87, 95 % CI 0·77, 0·98, Ptrend<0·01).

TT produces readily interpretable sparse components explaining similar amounts of variation as principal component analysis. Our results suggest that participants with a nutrient pattern high in micronutrients found in vegetables, fruits and cereals had a lower risk of BC.

We have lately documented the importance of N-terminal pro-brain natriuretic peptide in aiding the diagnosis of Kawasaki disease.

We sought to investigate the potential value of N-terminal pro-brain natriuretic peptide pertaining to the prediction of coronary artery dilatation (Z-score>2.5) and/or of resistance to intravenous immunoglobulin therapy. We hypothesised that increased serum N-terminal pro-brain natriuretic peptide level correlates with increased coronary artery dilatation and/or resistance to intravenous immunoglobulin.

We carried out a prospective study involving newly diagnosed patients treated with 2 g/kg intravenous immunoglobulin within 5–10 days of onset of fever. Echocardiography was performed in all patients at onset, then weekly for 3 weeks, then at month 2, and month 3. Coronary arteries were measured at each visit, and coronary artery Z-score was calculated. All the patients had N-terminal pro-brain natriuretic peptide serum level measured at onset, and the Z-score calculated.

There were 109 patients enrolled at 6.58±2.82 days of fever, age 3.79±2.92 years. High N-terminal pro-brain natriuretic peptide level was associated with coronary artery dilatation at onset in 22.2 versus 5.6% for normal N-terminal pro-brain natriuretic peptide levels (odds ratio 4.8 [95% confidence interval 1.05–22.4]; p=0.031). This was predictive of cumulative coronary artery dilatation for the first 3 months (p=0.04–0.02), but not during convalescence at 2–3 months (odds ratio 1.28 [95% confidence interval 0.23–7.3]; p=non-significant). Elevated N-terminal pro-brain natriuretic peptide levels did not predict intravenous immunoglobulin resistance, 15.3 versus 13.5% (p=1).

Elevated N-terminal pro-brain natriuretic peptide level correlates with acute coronary artery dilatation in treated Kawasaki disease, but not with intravenous immunoglobulin resistance.