Erectile Dysfunction As a Generalized Vascular Dysfunction

Erectile Dysfunction As a Generalized
Vascular Dysfunction
Nevzat Uslu, MD, Sevket Gorgulu, MD, Ahmet Taha Alper, MD, Mehmet Eren, MD,
Zekeriya Nurkalem, MD, Aydın Yildirim, MD, and Orhan Ozer, MD, Istanbul, Turkey
Objective: We hypothesize that generalized vascular
dysfunction may be the underlying cause in patients
with erectile dysfunction (ED) without atherosclerosis
and its major risk factors.
Methods: In all, 30 outpatients with ED and 25
healthy volunteers as a control group were enrolled
for this study. Aortic stiffness was calculated from
data obtained by echocardiographic examination,
which was performed using commercially available
equipment with a 2.5- to 3.5-MHz transducer. Endothelium-
dependent flow-mediated dilation (FMD) of
the brachial artery was assessed using a high-resolution
ultrasound system with a 10-MHz linear-array
vascular transducer. Shear stress and nitroglycerin
was used as a stimulus for assessing endotheliumdependent
FMD and nonendothelium-dependent dilation
of the brachial artery.
Results: FMD was significantly decreased in the ED
group compared with control group (4.1 3.1% vs
9.7 3.5%, P < .001). Nonendothelium-dependent
dilation was statistically insignificant in patients
with ED compared with control subjects (13 3.9%
vs 15.4 3.8%, P .55). The relationship between
ED and FMD was significant (r 0.66, P < .001),
whereas no relationship was found between ED and
nonendothelium-dependent dilation (r 0.23,
P > .05). Aortic strain (3.7 2.7% vs 9.5 3.2%, P <
.001) and distensibility (1.5 1.0 vs 4.7 2.9
cm2.dyne 1.10 3, P < .001) were found significantly
lower in the ED group than in the control group.
The relationship between ED and aortic stiffness
was also significant (for aortic strain; r 0.62, P <
.001 and for aortic distensibility; r 0.60, P <
.001).
Conclusion: Aortic and brachial artery functions are
impaired in men with ED without cardiovascular
disease or its major risk factors, indicating a more
generalized vascular disease. (J Am Soc Echocardiogr
2006;19:341-346.)
Erectile dysfunction (ED) is defined as the inability
to achieve and maintain an erection sufficient to
permit satisfactory sexual intercourse.1 Sexual function
is an important component of patient’s quality
of life and subjective well-being. ED is present in up
to 30 million men in the United States and approximately
100 million men worldwide,1 and affects up
to 52% of men between the ages of 40 and 70
years.2,3 It is now recognized that vascular disease of
the penile arteries is the most common cause of ED,
accounting for up to 80% of cases.4-6
The nitric oxide (NO)-cyclic guanosine-3=5=-monophosphate
system is important in the pathophysiology
of ED.7-9 This system has also a crucial role in maintaining
the function of vascular endothelium.10 ED and
endothelial dysfunction shares the same risk factors
such as atherosclerosis and its risk factors.3-9,11
However, it is not clear what causes ED in patients
without atherosclerosis and its major risk factors.
We hypothesize that endothelial dysfunction may be
the underlying cause of patients without atherosclerosis
and its major risk factors. If this is the case,
there should be a generalized vascular disease affecting
both elastic and muscular arteries. To test our
hypothesis, we investigated aortic and brachial artery
functions in patients with ED without atherosclerosis
or its major risk factors.
METHODS
Participants
In all, 30 outpatients with ED (age 53.9 9.3 years)
(consistent inability to achieve or sustain a sufficiently
rigid erection for sexual intercourse) for more than 1 year
and 25 healthy volunteers (age 52.2 6.8 years) as a
control group from the hospital staff were enrolled for this
study. Patients with neurogenic and psychiatric causes of
ED were excluded based on their history, physical examination,
and psychosocial questionnaire that assessed performance
anxiety, stress, depression, and relationship issues.
The diagnosis of ED was based on International Index of
From the Siyami Ersek Thoracic and Cardiovascular Surgery Center,
Cardiology Department.
Reprint requests: Nevzat Uslu, MD, Cumhuriyet Mah Uygarkent
Sit. 10 Blok D: 6, 34696, Uskudar-Istanbul, Turkey (E-mail:
drnuslu@yahoo.com).
0894-7317/$32.00
Copyright 2006 by the American Society of Echocardiography.
doi:10.1016/j.echo.2005.09.017
341