Markers of DNA damage and repair are present in both atherosclerotic plaques and peripheral blood mononuclear cells of patients with coronary artery disease. A positive correlation has been observed between the level of DNA damage and the severity of atherosclerotic lesions, as well as atherogenic risk factors such as smoking, hypertension and hyperlipidaemia. A number of in-vitro studies have implicated defective DNA repair in the development and progression of atherosclerotic lesions. In mouse models of atherosclerosis, the DNA repair signalling cascade has been shown to be amenable to pharmacological intervention and overexpression of specific repair proteins attenuate the development of atherosclerotic plaques. However, data regarding the role of DNA repair in the pathogenesis of atherosclerosis in humans are lacking. We have preliminary data indicating reduced DNA repair activity in patients with stable angina. This study will determine the molecular basis and the biological consequences of this observation.

Inclusion Criteria:

• Age ≥18 years
• Ability to provide written informed consent

Exclusion Criteria:

• Age ≥ 80 years
• Inability to provide written informed consent
• Presentation with an acute coronary syndrome
• Severe valvular heart disease
• Hypertrophic cardiomyopathy
• Left ventricular ejection fraction ≤ 35%
• Prior coronary revascularisation (surgical or percutaneous)
• Diabetes Mellitus
• Clinical evidence of peripheral vascular disease
• Prior history of cerebrovascular disease
• Malignancy
• Active inflammatory disorders (e.g. rheumatoid arthritis/connective tissue disorder)
• Renal impairment eGFR <60ml/min/1.73m2
• Anaemia (Hb <100g/dL)

Patients undergoing an assessment of thier coronary anatomy either by computerised tomography coronary angiogram or invasive coroanry angiogram at a large university teaching hospital performed as part of thier routine care.