A 49-year-old gentleman who was a company director attended my outpatient clinic with his wife. He was a type II diabetic with treated hypertension and a non-smoker. He was treated for hyperlipidaemia with atorvastatin 40 mg daily.

He had suffered from ED for 1 year. I began to advise the patient about the treatment of ED when his wife interrupted the conversation and said she did not want her husband to be treated for ED, she just wanted his heart checked up. She had read in a newspaper that ED may be a marker of silent CAD. She was quite adamant that was the priority, and that was the reason for the consultation with a cardiologist.

Further evaluation followed direct questioning to make sure he was asymptomatic, which he was, and the lack of symptoms had also been documented by the family doctor who referred him.

A 12 lead ECG was normal and an echocardiogram showed good left ventricular function but did demonstrate left ventricular hypertrophy and some impaired left ventricular relaxation. There was no evidence of valvar heart disease.

Because of the risk factor of ED which we knew added to conventional risk factors, he underwent CT angiography. He had a calcium score of 1,598 (normal score 0, >1,000 extensive plaque) and evidence of widespread and significant CAD, and invasive angiography was recommended.

Invasive angiogram (Fig. 8.1) showed that the left anterior descending coronary artery was totally occluded but filled retrogradely from the right system. There was atheromatous disease to about 90 % in the circumflex coronary artery and a 90 % lesion in the right coronary artery which was particularly important as the right coronary artery was filling the left anterior descending retrogradely.

He had severe three-vessel coronary artery disease therefore, and was at risk because he was type II diabetic. The evidence base would support coronary artery bypass grafting rather than attempted angioplasty. Quadruple coronary bypass grafting was therefore performed with three arterial grafts and one vein graft: the left internal mammary was grafted to an occluded heavily diseased left anterior descending and after a long arteriotomy a radial sequential graft was applied to obtuse marginal 1 and 2; a vein graft was applied to the right coronary artery.

The post operative course was uneventful and he was discharged home on the seventh post operative day fully well. He has been seen in the outpatient clinic, and on the statin therapy his cholesterol is 3.6 mmol/L with LDL 1.5. He has been advised about treatment for his ED.

Several studies suggest that there is a strong temporal relationship between ED and CAD, with ED preceding a cardiovascular event by at least 2–5 years [11]. This temporal relationship was investigated in a questionnaire-based study that included 207 patients with CVD attending cardiovascular rehabilitation programmes and 165 age-matched controls from general practice in the UK. Patients completed up to four questionnaires including the IIEF. Of the individuals with CVD, 56 % were experiencing symptoms of ED at the time of the study and had done so for a mean of 5 ± 5.3 years. In contrast, 37 % of individuals in the control group had ED symptoms for a mean of 6.6 ± 6.8 years. This interesting finding in the controls reflects the importance of asking about ED routinely.

In the AssoCiation Between eRectile dysfunction and coronary Artery disease (COBRA) trial, 93 % of patients with a chronic coronary syndrome reported ED symptoms before the onset of angina pectoris, with a mean interval of 24 (range 12–36) months [12]. This finding further reinforces the concept of a lead time of at least 2–5 years between the development of ED and symptomatic CAD. The time intervals (range) for patients with one-, two- and three-vessel disease were 12 (9.5–24), 24 (16.5–36) and 33 (21–47) months, respectively. There was a significant relationship between the length of time from ED to CAD onset and the number of vessels involved (p = 0.016). Importantly, given that men with ED may be at cardiovascular risk, this long lead time provides an early opportunity for cardiovascular risk reduction.

Two recent meta-analyses and one systematic review have greatly helped our assessment of the link between ED and the prediction of CVD including mortality [7, 13–15]. Prior to these analyses studies had evaluated the effect of age on the ED link to increased cardiovascular risk, identifying the importance of ED as an especially powerful predictor of CVD events in young- and middle-aged men (ages 30–60 years) where CVD preventative resources should be maximised.

A study of 1,400 men aged 40–75 years with no known CAD was prospectively followed for 10 years [15]. As can be seen from Table 8.2, men in their 40s with ED have a 50-fold increase in CAD events per 1,000 patient years compared with men with normal erectile function, and fivefold in men in their 50s (is there a more powerful risk factor?). In a retrospective study from Western Australia over 10–15 years, men in their 20s and 30s were more than seven times more likely to have a CVD event if they had ED [16], and Riedner and colleagues found in a coronary angiographic study that CAD was 2.3 times higher in men <60 years of age with ED [17]. In all three studies the ED/CAD link became less marked with age over 70 years.