Background Primary prevention needs to be improved because up to 70% of cardiovascular (CV) events occur outwith those classified as high risk by CV risk scores currently used in clinical practice (eg, Framingham). One possible way to improve primary prevention of CV disease is to identify those patients who may already harbour silent pancardiac target organ damage in the form of left ventricular hypertrophy (LVH), systolic dysfunction (LVSD), diastolic dysfunction (LVDD), left atrial enlargement (LAE) or silent myocardial ischaemia. This could be achieved by reapplying traditional CV risk scores to primary prevention patients after they have been treated or by screening with a simple biomarker like B-type natriuretic peptide (BNP).

Methods We prospectively recruited 300 asymptomatic individuals without known cardiovascular disease already on primary prevention therapy. Patients with valvular heart disease, atrial fibrillation and renal impairment were excluded. We measured BNP and calculated 10-year global CV risk scores (based on Framingham, QRISK and ASSIGN) in each participant. Transthoracic echocardiography was used to assess LV mass, LV systolic and diastolic function, and left atrial volume while the presence of inducible ischaemia was assessed by dobutamine stress echocardiography or dipyridamole myocardial perfusion imaging. Patients were divided into low, intermediate and high risk groups based on 10-year global CV risk. The prevalence of various cardiac TOD in each group was compared and ROC curves were constructed for BNP and for 10-year global CV risk scores to assess their ability to detect presence of silent cardiac TOD.

Results One hundred and two (34%) patients (Mean age 64±6.0 years, 58% males) had evidence of silent cardiac TOD (29.7% LVH, 18% LAE, 17.3% LVDD, 7.3% LVSD and 6.3% Ischaemia). The prevalence of cardiac TOD ranged from 19 to 28% in the low risk, 26%–33% in the intermediate risk and 36%–41% in the high risk groups based on three commonly used CV risk equations. BNP levels were significantly higher (median (IQR); 21.6 (13.6–40.0) vs 11.4 (6.3–20.0) pg/ml, p<0.0001) in those with cardiac TOD compared to those without. The AUC for BNP to identify any form of cardiac TOD was 0.77 (p<0.0001) overall and 0.83 (p<0.0001) in males. However, discrimination power of CV risk scores was poor with area under curve of only 0.58 (p=0.02) for QRISK, 0.62 (p=0.001) for Framingham and 0.62 (p=0.001) for ASSIGN to detect presence of any form of TOD.

Conclusion Silent cardiac TOD is highly prevalent (34%) in already treated primary prevention population but current CV risk estimation alone performs poorly in the detection of these silent cardiac abnormalities. However, a raised BNP is able to identify existing silent cardiac TOD of various subtypes particularly in males. Using BNP to identify silent cardiac TOD could, in the future, become a new way to improve the primary prevention of CV events.