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CARDIOLOGY ASPRESENTEDINTHEROUNDSOF Rounds THEDIVISIONOFCARDIOLOGY, ST. MICHAEL’S HOSPITAL, UNIVERSITY OF TORONTO Endothelial dysfunction/Erectile dysfunction: Common mechanisms, common management Division of Cardiology Endothelial dysfunction, considered by many to be at the root of atherosclerotic vascular disease, shares many common risk factors with erectile dysfunction. In addition, they fre- quently occur in the same patients. A common mechanism that may explain the coexistence of these two seemingly disparate conditions is a decrease in the bioavailability of nitric oxide (NO), a small unstable molecule that mediates many of the normal functions of the endothe- lium. NO is also responsible for neurally-induced vasomotor changes at the level of the corpora cavernosa that underlie penile erection. A state of increased oxidative stress not only renders NO inactive, but also, through the reaction of oxygen-free radicals with NO, may lead to the formation of potentially toxic products. Therefore, addressing common risk fac- tors is important because it may reduce cardiovascular events and improve erectile function. In addition, control of risk factors may increase the possibility of safely resuming sexual activ- ity in the patient with coronary artery disease (CAD), although this has yet to be proven in properly designed randomized trials. Most cardiac patients, when appropriately risk-stratified and managed, can resume sexual activity safely, while many who also exhibit erectile dysfunction are eligible for first-line therapeutic modalities, including phosphodiesterase-5 inhibitors such as sildenafil. This issue of Cardiology Rounds examines the research linking endothelial with erectile dysfunction and discusses patient management.
In October 1998, some of the major national and international media outlets announced
that the Nobel Prize for Physiology and Medicine had been awarded to three American
St. Michael’s Hospital
researchers for “the discovery of the Viagra principle.” By the following day, some local and sec-
ondary media organizations had transformed this news to “Viagra discoveries win Nobel Prize
Room 9-004, Queen WingToronto, Ont. M5B 1W8
for Medicine.” It should have come as no surprise that the link between the Nobel Prize-
winning discoveries of Furchgott, Ignarro, and Murad and sildenafil, the novel therapy for erectiledysfunction, was so quickly established by the media, given the great interest of the media and
The opinions expressed are only those of the Divisional members. This publication is
the public following the release of sildenafil. However, the Nobel-winning discoveries – start-
made possible through unrestricted grants.
ing with the description by Furchgott of an endothelium-derived relaxing factor (EDRF) – wereactually related to a simple molecule called nitric oxide (NO). NO, besides being the biologicprinciple responsible for EDRF activity, is also, among many other functions, the physiologicalmediator of penile erection.1-5
The search for catchy headlines notwithstanding, the media, perhaps inadvertently, were
right in establishing a link between endothelial dysfunction and erectile dysfunction. Furchgottdiscovered the former condition when he observed that arteries denuded of endothelium con-
Leading with InnovationServing with Compassion
tracted in response to acetylcholine, while normal arteries dilated. Endothelial dysfunction iscaused by a decrease in the bioavailability of endothelial NO and erectile dysfunction is very
often also caused by a decrease in NO of endothelial or neural origin. Therefore, both conditions
A teaching hospital affiliated with the University of Toronto
share the same mechanisms and in many cases, the same risk factors. It is reasonable to postulatethat addressing common mechanisms and modifying common risk factors may be indicated inthe management of patients with erectile dysfunction. Nitric oxide: a key biologic mediator
disease, or stroke. The patients were evaluated with a fast-
Nitric oxide is a volatile gas formed during the con-
ing lipid profile and penile Doppler ultrasound to assess
version of L-arginine to L-citrulline by an enzyme called
blood flow. Patients were divided into two groups: normal
nitric oxide synthase. Three isoforms of NO synthase are
cholesterol (total cholesterol <5.2 mmol/L) comprising
40% of patients, or abnormal cholesterol (60% of
• Endothelial NO synthase (eNOS) is expressed main-
patients). In the abnormal cholesterol group, 91% had
ly, but not exclusively, in endothelial cells and this expres-
Doppler evidence of penile arterial disease, a finding that
sion is a hallmark of endothelial health.
was also present in 83% of the patients in the normal cho-
• Brain or neuronal NO synthase (bNOS) is expressed
lesterol group. However, nearly 90% of the patients with
in central and peripheral nervous tissues, including cav-
abnormal Doppler studies and normal total cholesterol val-
ues had LDL cholesterol levels that were above the rec-
• Inducible NO synthase (iNOS); expression can be
ommended target of 2.5 mmol/L for patients with CAD.8
induced in macrophages and other cell types in response to
Another study evaluated the relationship between the
severity of CAD and impairment of erectile function in 40
NO is a rather unstable and short-lived molecule that
men, aged 40-73, who were undergoing coronary angiog-
acts locally, near the cells that produce it. After its secre-
raphy to evaluate symptoms of ischemic heart disease. The
tion, it can follow one of three directions. First, it can act
patients completed a standardized questionnaire on sexual
on guanylyl cyclase located in a target cell to generate
function and their cardiovascular risk factors were docu-
cGMP, and if the target cell is a vascular smooth muscle
mented. Men with 2- or 3-vessel CAD had significantly
cell, this leads to vasodilatation. Second, it can be exposed
fewer erections during a 30-day period and also scored
to hemoglobin and be inactivated. Third, it can react with
lower on an index of erection firmness than men with sin-
oxygen-free radicals such as superoxide, leading not only
gle-vessel disease. This study also confirmed that diabetic
to its inactivation, but also to the formation of potentially
patients scored significantly worse on both parameters
The levels of cardiovascular risk factors present in men
Oxidative stress – A common element of endothelial
seeking treatment for erectile dysfunction were the subject
dysfunction and some forms of erectile dysfunction
of another study. The investigator evaluated the results of
An enhanced state of oxidative stress is present in all
cardiovascular stress testing, risk profile analysis, and coro-
common cardiovascular risk factors associated with
nary angiography (not performed in all subjects) in 50
endothelial dysfunction, such as diabetes mellitus, hyper-
asymptomatic men with erectile dysfunction of presumed
lipidemia, hypertension, or smoking. Indeed, the produc-
vascular origin. Multiple risk factors were present in 80%
tion of superoxide is increased in these conditions and
of the subjects, including smoking in 80% and a total cho-
leads to inactivation of NO and the production of peroxy-
lesterol level >5.2 mmol/L in 70%. Graded exercise testing
nitrite. Experimental studies have demonstrated that
was positive in 28/50 patients and following this test, coro-
cardiovascular risk factors enhance the production of
nary angiography was performed in 20 of them, revealing
superoxide in the same endothelial cells where NO is
severe left main or 3-vessel disease in 6, 2-vessel disease in
being produced, leading to an immediate decrease in NO
7, and single-vessel disease in 7. This study demonstrates
bioavailability, even if normal amounts are produced.6,7
the high prevalence of cardiac risk factors and significant
Therefore, the amount of biologically-active NO is a func-
CAD in men presenting with no symptoms other than
tion of the state of oxidative stress in the endothelium, as
erectile dysfunction.10 This finding is likely explained by
much as of the total amount of NO synthesized by eNOS
the common mechanism underlying both endothelial dys-
and, in the case of penile erection, also by bNOS.
function and erectile dysfunction of vascular origin, name-ly the decreased availability of NO. The two EDs (endothelial and erectile dysfunction): Common presentations Mechanism of penile erection
Erectile dysfunction is occasionally the presenting
Neural impulses resulting from sexual stimulation lead
symptom in patients who have a variety of diseases char-
to the release of NO by bNOS located in nonadrenergic,
acterized by endothelial dysfunction, (eg, diabetes melli-
noncholinergic cavernous nerves. Similarly, cholinergic
tus, CAD, arterial hypertension, and hyperlipidemia). As
nerves release acetylcholine that acts on the surface recep-
an example of this association, a recent study assessed the
tors of the endothelial cells, leading to activation of eNOS
incidence of lipid abnormalities and penile arterial insuffi-
and, in the healthy endothelium, a release of significant
ciency in men presenting with erectile dysfunction and no
levels of bioactive NO.11 In the presence of an increased
other known vascular abnormalities. This study included
state of oxidative stress, much of the NO would be inacti-
57 men presenting to a clinic over a 3-month period with
vated; otherwise, it diffuses to the trabecular smooth
erectile dysfunction and no history of heart disease,
muscle cells surrounding the sinusoidal spaces and acts on
diabetes, hypertension, hyperlipidemia, peripheral vascular
guanylyl cyclase. The cGMP thus generated mediates
Figure 1: Mechanism of action of sildenafil12 Figure 2: Sildenafil – Improvement in erections NO-cGMP mechanism of penile erection and the Efficacy in sub-populations NO-enhancing effect of the PDE5 inhibitor sildenafil Sildenafil
1. Hulting C et al. Int J Impot Res 1998;10(3):532.
NO= nitric oxide. cGMP = cyclic guanosine monophosphate. PDE5 = phosphodiesterase
2. Price D. Int J Impot Res 1998;10(3):534.
4. Conti CR et al. Am J Cardiol 1999;83:3C-12C.
type 5. GTP = guanosine triphosphate. NANC = nonadrenergic-noncholinergic neurons.
and in those requiring frequent doses of sublingual nitrates
relaxation of the smooth muscle, allowing an inflow of
for symptomatic relief of angina pectoris.14
blood into the sinusoidal spaces and engorgement of the
Sildenafil has been shown to improve erections signif-
penis. Release of norepinephrine from the adrenergic
icantly in patients with ischemic heart disease and in those
nerves, coupled with the endothelial release of endothelin
with risk factors like hypertension and diabetes. It is also
(a potent vasoconstrictor whose synthesis is increased in
helpful in the management of erectile dysfunction due to
endothelial dysfunction), induce smooth muscle cell con-
nonvascular causes such as depression, spinal cord injury,
traction and hinder penile erection. These mechanisms
or following radical prostatectomy (Figure 2). Due to the
provide the common link between the two EDs, erectile
potentially disastrous interactions with nitrates and the
additive effects with antihypertensive agents, reasonableconcerns have been raised regarding the use of sildenafil in
Development of phosphodiesterase inhibitors and
the cardiovascular patient. However, in 53 clinical trials
treatment of erectile dysfunction
with sildenafil that included over 6000 patients, no excess
Phosphodiesterases are enzymes that catabolize cyclic
incidence of myocardial infarction (MI) or death was
nucleotides such as cGMP. Because of the vasodilatory
observed.15 Similarly, in a prescription event-monitoring
effects of cGMP, phosphodiesterase inhibitors were felt to
study of more than 5000 men conducted in the United
be a good target for development of inhibitors that, by
Kingdom, there was no increased incidence of MI,
enhancing cGMP levels, would be of potential benefit for the
ischemic heart disease, death or total mortality, compared
treatment of hypertension and angina pectoris. Sildenafil,
the first phosphodiesterase inhibitor approved for the treat-
Sexual activity in patients with CAD
ment of erectile dysfunction, exhibits high affinity for thephosphodiesterase-5 (PDE-5) isoform that is abundant in
Sexual activity can be associated with a transient
the corpus cavernosum, but is also present in platelets, skele-
increase of 50-60 bpm in heart rate and 50-60 mm Hg in
tal muscle, and visceral and vascular smooth muscle cells.
systolic blood pressure. The risk of non-fatal MI transiently
Sildenafil was originally developed as a cardiovascular
doubles following sexual activity, but the absolute risk is
drug of potential antianginal and antihypertensive efficacy.
quite small. In individuals free of cardiac disease, weekly sex-
However, the observation of interesting “side-effects” led to
ual activity would only increase the annual risk of MI from
its study in the management of erectile dysfunction where
1% to 1.01%. In subjects with a prior MI history, sexual activ-
it was proven to be highly effective (Figure 1).12,13 Sildenafil
ity transiently doubles the risk from 10 in a million per hour
is a modest vasodilator, similar to a weak nitrate, and it has
to 20 in a million per hour. Nevertheless, the absolute risk
no direct cardiac effects given the absence of PDE-5 in the
remains low since, in the clinically high-risk patient, weekly
myocardium. By itself, sildenafil results in a modest 10/5
sexual activity increases the risk of MI from 10% to 10.2%.17
mm Hg reduction in blood pressure that is not dose-relat-
In order to assess whether a cardiac patient is fit to
ed within and beyond the recommended dose range. There
resume sexual activity, it is crucial to obtain a history of the
are additive blood-pressure lowering effects when com-
activities that the patient is able to perform and correlate
bined with other antihypertensive drugs and special caution
them with the workload required for sexual intercourse.
must be exercised in patients taking multiple agents. A
The workload can be expressed in metabolic equivalents or
particularly striking synergistic effect is observed when
METs. One MET is the amount of oxygen consumed at
sildenafil is co-administered with nitrates, explained by the
rest, which is 3.5 ml/kg/minute. Other activities can then
induction of cGMP synthesis that is the mechanism of
be measured against this standard. For instance, walking at
action of these agents. Thus, sildenafil is absolutely con-
2 mph requires 2-3 METS, gardening or digging requires
traindicated in patients on regular oral or topical nitrates
5-6 METS, swimming 9-10 METS, whereas sexual activity
Table 1: Energy requirements of selected Figure 3: Algorithm for sexual activity and physical activities (in METs) cardiac risk
Pashkow and Dafoe, Eds. Clinical Cardiac Rehabilitation, Appendix A. 1999.
with the usual partner requires only 3-5 METS. Sexualintercourse with an extramarital or much younger
eral arterial disease or stroke. These patients must be
partner is associated with significantly greater energy
reclassified to the low- or high-risk categories based
requirements and a higher risk of MI (Table 1). If nec-
on cardiac testing, including a graded exercise test
essary, an exercise test can be obtained to determine
and an echocardiogram. In some cases, a cardiology
objectively the patient’s exercise tolerance and work-
load achieved in METS. A patient who is able to
• Patients in the high-risk category are those who
achieve 6 METS on a treadmill (for instance, follow-
have a cardiac condition sufficiently severe or unsta-
ing the Bruce protocol) without any symptoms, ECG
ble that sexual activity may constitute significant risk.
changes, arrhythmias, or hemodynamic instability,
This category includes patients with unstable or
can resume sexual activity safely, provided that there
refractory angina, uncontrolled hypertension, NYHA
are no other absolute contraindications.
class III or IV heart failure, recent MI (within 2weeks), high-risk arrhythmias, hypertrophic obstruc-
The management of erectile dysfunction in
tive or other cardiomyopathies, and moderate to
patients with cardiovascular disease
severe valvular heart disease. These patients should
Establishing whether a patient is eligible to
have high priority for referral to a cardiovascular
receive therapy with sildenafil requires a determina-
specialist and the initiation of sexual activity should
tion of the patient’s risk. The Princeton Consensus
be deferred until the cardiac condition is stabilized or
Panel in the United States suggests stratifying the
managed appropriately and a specialist determines
patients in low-risk, intermediate- or indeterminate-
that it can be safely resumed (Figure 3).
• The low-risk category includes subjects with no
Sildenafil in the cardiovascular patient: Position
significant cardiac risk associated with sexual activity
of the Heart and Stroke Foundation of Canada
(ie, asymptomatic individuals or those with <3 cardiac
and the Canadian Cardiovascular Society
risk factors). Also in the low-risk group are patients
These two organizations have jointly stated that
with controlled hypertension, mild stable angina, prior
the majority of cardiovascular patients can be treated
successful coronary revascularization, uncomplicated
with sildenafil except those already taking any form of
prior MI, mild valvular disease, and NYHA class I
nitrates. Patients for whom nitrate therapy is essential
heart failure patients. Patients in the low-risk cate-
must be considered for other forms of therapy for
gory require no special cardiac testing or evaluation
erectile dysfunction. Patients who are receiving
prior to resuming sexual activity or initiating therapy
multiple, concomitant, antihypertensive therapy must
for erectile dysfunction. All the first-line treatment
be assessed carefully to ensure that there is no
modalities, including sildenafil, can be considered in
symptomatic hypotension. Of great interest is the
recommendation that etiological and risk factors
• Individuals at intermediate- or indeterminate-
contributing to both cardiovascular disease and erec-
risk include those with ≥3 cardiac risk factors, moder-
tile dysfunction be diagnosed and treated.19 This may
ate stable angina, recent MI (>2, but <6 weeks),
prove to be remarkable foresight by the authors of the
NYHA class II heart failure, or significant manifesta-
recommendations. Although the hypothesis that treat-
tions of noncoronary vascular disease such as periph-
ing endothelial dysfunction also improves erectile
CARDIOLOGY Rounds Figure 4: Decision tree for treating patients with cardiovascular disease and ED with sildenafil19 Diagnose and treat etiological and risk factors contributing to both diseases Should patient be considered for sildenafil treatment?
Patients in whom nitrate therapymay be needed:A) Acute coronary syndromesB) Ischemia provoked within 3
function has yet to be studied in randomized con-
with sildenafil, but it is important to emphasize that
trolled trials, the biological plausibility is strong. As
close monitoring of these patients must be continued
discussed above, treating the risk factors or etiologies
or intensified after initiation of therapy (Figure 4).
of endothelial dysfunction would lead to a reductionin oxidative stress and an increase in the bioavailabil-
Conclusion
ity of NO leading, theoretically, to an increase in the
In summary, NO bioavailability is at the center of
efficacy of an agent like sildenafil. At the very least,
both erectile and endothelial function and this could
treatment of risk factors for endothelial dysfunction
explain why erectile dysfunction and cardiovascular
with agents such as statins or ACE inhibitors, would
disease share so many common risk factors. Patients,
reduce the risk of coronary events and possibly make
whose presenting complaint is erectile dysfunction,
the initiation of therapy for erectile dysfunction and
may have previously unrecognized risk factors for
the resumption of sexual activity safer.
atherosclerotic vascular disease such as hyperlipi-
In the Canadian recommendations, patients who
demia, hypertension, or diabetes. Treatment of the
should not be considered for sildenafil treatment are
underlying conditions common to both disorders
those for whom nitrate therapy is prescribed and
should be instituted in the appropriate patients in
used. As well, sildenafil should be avoided in patients
order to improve endothelial function and NO
for whom nitrate therapy may be needed, such as
bioavailability. Sexual activity usually implies a mild
patients with acute coronary syndromes, ischemia
to moderate level of energy expenditure that could be
provoked within 3 minutes of exercise on the Bruce
safely achieved by many cardiac patients. It is impor-
protocol, and patients who develop angina during
tant to stratify patients by risk and address correctable
intercourse. A potential exception, and one that has to
causes of structural heart disease or optimize medical
be considered with great caution, are patients taking
therapy before the resumption of sexual activity. Most
nitrates only very sporadically. A rule-of-thumb in
cardiac patients thus stratified and treated may be eli-
these patients is that sildenafil should not be used
gible for treatment of erectile dysfunction with a PDE
within 24 hours of any nitrate therapy and, converse-
inhibitor such as sildenafil or other first-line therapies.
ly, nitrates should be avoided completely within a
In patients who require therapy with nitrates or
24-hour period of any dose of sildenafil. Patients with
multiple antihypertensive agents, other therapeutic
symptomatic hypotension of any etiology are not
Patients, who may be considered for treatment
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Email: [email protected]: www.cardiocongress.org
Abstract of Interest
13-20 November, 2002 American Heart Association Scientific Sessions 2002 Oral sildenafil is an effective and specific pulmonary vasodilator in patients with pulmonary arterial hypertension
MICHELAKIS ED, TYMCHAK W, LIEN D, DASILVA L,
HASHIMOTO K, ARCHER SL. EDMONTON, ALBERTA
Background: The prognosis of patients with severe pulmonary hyper- tension (PHT) is poor. To determine prognosis and guide chronic therapy, an acute trial of a selective pulmonary vasodilator, usually inhaled nitric oxide (INO), is performed during cardiac catheteriza- tion. We hypothesized that oral sildenafil, a phosphodiesterase V
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inhibitor, is a safe and effective alternative to INO.
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Methods: We studied 12 consecutive patients (mean±SEM, 43±2
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years, 8 female) referred during one year, for consideration of heart-
lung transplantation or as a guide to medical therapy. All but one were
This publication is made possible by an educational grant from
Novartis Pharmaceuticals Canada Inc.
2002 Division of Cardiology, St. Michael’s Hospital, University of Toronto, which is solely responsible for the contents. The opinions expressed in this publication do not necessarily reflect those
of the publisher or sponsor, but rather are those of the authoring institution based on the available scientific literature. Publisher: SNELL Medical Communication Inc. in cooperation with the
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