Graham Jackson, Suite 301, London Bridge Hospital, Tooley St, London, SE1 2PR, UK.


erectile dysfunction


coronary artery disease.


It is now well recognized that erectile dysfunction (ED) and vascular disease, especially coronary artery disease (CAD), frequently coexist [1]. The penile and coronary arteries share the same endothelium, and endothelial dysfunction secondary to shared risk factors is the common denominator [2]. ED might be a marker for silent CAD, with an average lead-time of 2–5 years between ED presenting and a coronary event occurring [3]. The penile arteries are smaller than the coronary arteries (1–2 vs 3–4 mm) which might explain why a similar degree of endothelial dysfunction presents with ED but is subclinical in the larger coronary arteries. Coronary disease is usually symptomatic for angina when a stenosis exceeds 70%, but an acute event is usually secondary to rupture of a previously subclinical and silent lipid-rich plaque [4].

The Princeton Consensus Guidelines include the statement that a man with ED and no cardiac symptoms is a cardiac or vascular patient until proved otherwise, and exercise electrocardiography is advocated to identify increased risk and the need for risk-factor modification [1]. Whilst exercise testing will identify a flow-limiting coronary stenosis, it will not detect plaque disease that is not flow limiting and that might be vulnerable to rupture. ED can precede an acute coronary event, identifying the need to develop a means of detecting early unobstructive but vulnerable coronary lesions [5]. Multi-detector CT is a minimally invasive outpatient procedure that makes it possible to accurately identify coronary calcification and angiographic lesions which might be obstructive or unobstructive [6]. We therefore compared multi-detector CT with maximal exercise electrocardiography to determine if we could increase the detection of silent CAD. We evaluated 20 non-diabetic men with ED and no cardiac symptoms [7].

All the men exercised to >90% of their maximum heart rate for age, and none had chest pain. The exercise electrocardiogram was abnormal in two men who developed transient minor ischaemic changes. Fifteen men had abnormal calcium scores and five were normal, all of whom were considered to have ED of psychological origin before multi-detector CT. Therefore, maximal exercise electrocardiography failed to identify most men with evidence of early CAD. Two of the 15 men smoked, eight were hypertensive controlled on medication, three had evidence of glucose intolerance, all had hyperlipidaemia (untreated) and nine had abdominal obesity; in short, a cluster of cardiometabolic risk factors.

Coronary calcium scores predict cardiac events [6]; a negative score identifies a good prognosis and a healthy lifestyle is recommended. By contrast, the presence of calcium increases the risk of a cardiovascular event four-fold and the rate of myocardial infarction and cardiac death in the next 3–5 years (i.e. the same ED-to-CAD event interval) is 4.6% when the score is 400–999 and 7.1% when >1000. The increased relative risk for mild (1–100) and moderate (100–400) scores compared to zero is 1.9 and 4.3, respectively. Of special importance, the risk is greater in the cardiac asymptomatic (e.g. men with ED) because risk-reduction therapy has not been initiated.

Our study reinforces the view that organic ED should be treated as a ‘cardiovascular equivalent’ and an aggressive guideline-driven reduction in risk factors should be initiated in all cases [8]. We have a window of opportunity to prevent a cardiac event of 2–5 years, so it is important that men with ED are thoroughly assessed. A normal exercise electrocardiogram does not exclude silent CAD. Nine modifiable risk factors account for >90% of the risk of an acute myocardial infarction, i.e. smoking, hypertension, hyperlipidaemia, abdominal obesity, diabetes, reduced fruit and vegetable intake, excess alcohol, inactivity and psychosocial stresses; adding ED makes 10 [9].


None declared.