Coronary flow velocity reserve reduction is comparable in patients with erectile dysfunction and in patients with impaired fasting glucose or well-regulated diabetes mellitus.
BACKGROUND
There is growing evidence that erectile dysfunction is a sentinel for future coronary artery disease. Recently published studies have shown signs of impaired coronary endothelial function in patients with erectile dysfunction, without clinical cardiovascular disease and diabetes. We evaluated the magnitude of coronary vasodilatory dysfunction in men with erectile dysfunction, as compared with men with impaired glucose metabolism (impaired fasting glucose or diabetes) and healthy controls.


METHODS
We investigated men aged 68-73 years with erectile dysfunction (n=12), age-matched men with impaired glucose metabolism, who all proved to have erectile dysfunction (n=15), and age-matched male controls (n=12). Erectile dysfunction was evaluated using the International Index of Erectile Function (IIEF)-5 questionnaire. Coronary flow velocity reserve in the left anterior descending artery was examined using Doppler ultrasound and intravenous adenosine provocation.


RESULTS
Coronary flow velocities at rest did not differ between the three groups, but maximum coronary flow velocity was significantly lower in the erectile dysfunction group (P=0.004) and in the impaired glucose metabolism group (P=0.019), as compared with controls. There was no difference between the erectile dysfunction and impaired glucose metabolism groups. Coronary flow velocity reserve was reduced in the erectile dysfunction group (P=0.026) compared to controls, but was similar compared to the impaired glucose metabolism group. In multivariate analysis including all groups, erectile dysfunction score was the only independent predictor of reduced coronary flow velocity reserve (P=0.020).


CONCLUSIONS
The magnitude of early coronary endothelial and smooth muscle cell dysfunction in otherwise healthy men with erectile dysfunction was comparable to that of patients with impaired glucose metabolism: a well known risk factor for coronary artery disease.
Borgquist
Rasmus
R
Department of Cardiology, Faculty of Medicine, Lund University, Malmoe University Hospital, Malmö, Sweden. rasmus.borgquist@med.lu.se
Nilsson
Peter M
PM
Gudmundsson
Petri
P
Winter
Reidar
R
Léosdottír
Margret
M
Willenheimer
Ronnie
R
D000241:Adenosine; D000368:Aged; D000704:Analysis of Variance; D001783:Blood Flow Velocity; D001786:Blood Glucose / Q000378:metabolism*; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003326:Coronary Circulation; D003920:Diabetes Mellitus / Q000097:blood / Q000503:physiopathology*; D018618:Echocardiography, Doppler, Color; D007172:Erectile Dysfunction / Q000503:physiopathology*; D005215:Fasting / Q000097:blood*; D006801:Humans; D007262:Infusions, Intravenous; D016014:Linear Models; D008297:Male; D009200:Myocardial Contraction; D011237:Predictive Value of Tests; D012107:Research Design; D011795:Surveys and Questionnaires; D013548:Sweden / Q000453:epidemiology; D014664:Vasodilation; D014665:Vasodilator Agents
D001786:Blood Glucose; D014665:Vasodilator Agents; D000241:Adenosine