Anorexia nervosa affects most organ systems, with 80% suffering from cardiovascular complications.

To define echocardiographic abnormalities in anorexia nervosa through systematic review and meta-analysis.

Two reviewers independently assessed eligibility of publications from Medline, EMBASE and Cochrane Database of Systematic Reviews registries. Studies were included if anorexia nervosa was the primary eating disorder and the main clinical association in described cardiac abnormalities. Data was extracted in duplicate and quality-assessed with a modified Newcastle–Ottawa scale. For continuous outcomes we calculated mean and standardised mean difference (SMD), and corresponding 95% confidence interval. For dichotomous outcomes we calculated proportion and corresponding 95% confidence interval. For qualitative data we summarised the studies.

We identified 23 eligible studies totalling 960 patients, with a mean age of 17 years and mean body mass index of 15.2 kg/m2. Fourteen studies (469 participants) reported data suitable for meta-analysis. Cardiac abnormalities seen in anorexia nervosa compared with healthy controls were reduced left ventricular mass (SMD 1.82, 95% CI 1.32–2.31, P < 0.001), reduced cardiac output (SMD 1.92, 95% CI 1.38–2.45, P < 0.001), increased E/A ratio (SMD −1.10, 95% CI −1.67 to −0.54, P < 0.001), and increased incidence of pericardial effusions (25% of patients, P < 0.01, 95% CI 17–34%, I2 = 80%). Trends toward improvement were seen with weight restoration.

Patients with anorexia nervosa have structural and functional cardiac changes, identifiable with echocardiography. Further work should determine whether echocardiography can help stratify severity and guide safe patient location, management and effectiveness of nutritional rehabilitation.

Depression is associated with increased risk of several general medical conditions, including diabetes and cardiovascular disease. The nature of the association is complex and may involve bidirectional causation or a common pathophysiology.

To determine whether young people without depression but at increased familial risk have altered metabolic and blood pressure markers relative to matched controls.

We studied young people (n = 85), who had a parent with depression but no personal history of depressive illness (FH+) and healthy controls (n = 69). Cardiovascular risk profile was assessed by a fasting blood sample to measure insulin, glucose, lipids and high-sensitivity C-reactive protein (CRP) and blood pressure was measured centrally and peripherally. Arterial stiffness and waking cortisol concentration were also measured.

Compared with controls, the FH+ group demonstrated increased peripheral and central systolic blood pressure, increased arterial stiffness and diminished insulin sensitivity but they did not differ from controls in measures of lipids, CRP or waking cortisol.

Our data suggest that young people at increased familial risk of depression show evidence of altered cardiovascular risk profile in young adulthood even in the absence of depressive symptoms. It is possible therefore that vulnerability to conditions such as hypertension and diabetes may precede the onset of major depression and may share common risk factors.