Cardiovascular Risk and Sildenafil
Robert A. Kloner, MD, PhD
Sildenafil citrate is the first oral agent approved for the
treatment of erectile dysfunction (ED); other oral agents are
in the process of development. Because the mechanism of
action of many of these agents involves vasodilation, there
is a potential for interaction with the cardiovascular sys-
tem. Sildenafil inhibits phosphodiesterase-5 (PDE-5) which
is found in the corpus cavernosum and in the systemic
vasculature. Sildenafil causes a mild decrease in systemic
arterial pressure (⬃ⴚ8/ⴚ5.5 mm Hg); it causes a syner-
gistic and often major decrease in systemic arterial pres-
sure in the presence of organic nitrates (nitric oxide do-
nors). Sildenafil is therefore contraindicated in patients
taking organic nitrates. A review was made of clinical trials
in populations of men with (1) erectile dysfunction; (2)
chronic stable ischemic heart disease and erectile dysfunc-
tion; and (3) hypertension and erectile dysfunction. This
review showed that sildenafil was effective and not asso-
ciated with an increase in serious cardiovascular adverse
events, myocardial infarction (MI), or death compared with
placebo. Although there have been spontaneous reports of
R isk factors for erectile dysfunction (ED) include
many of the same risk factors for cardiovascular
disease: hypertension; lipid abnormalities, including
low high-density lipoprotein cholesterol; smoking;
and diabetes.1–3 Therefore, some patients with ED will
have coronary artery disease. With the advent of new
therapies for ED that have broad appeal—such as the
oral agents sildenafil, phentolamine (in development),
and apomorphine (in development), there will be more
men seeking treatment for ED and more men with
coronary artery disease resuming sexual activity after
a period of quiescence. Because oral agents used to
treat ED may have vasodilatory properties and will
enable men who have been sexually (and perhaps
physically) inactive to resume sexual activity, there
has been a recent increase in interest in sexual activity
as a trigger for cardiac events and the potential for
these new oral agents to interact with the cardiovas-
cular system.
As described elsewhere in this supplement by Muller
and DeBusk, there is a physiologic cost to sexual activity
that has been likened to moderate physical activity.4,5
When a man who has been inactive resumes sexual
activity, he will increase myocardial oxygen demand by
increasing heart rate and blood pressure. In addition, the
excitement and/or anxiety of resuming sexual activity
From the The Heart Institute, Good Samaritan Hospital, Section of
Cardiology, University of Southern California, Los Angeles, California,
USA.
Dr. Kloner is a speaker, consultant and researcher for Pfizer Inc.
Address for reprints: Robert A. Kloner, MD, PhD, Heart Institute,
Good Samaritan Hospital, 1225 Wilshire Boulevard, Los Angeles,
California 90017.
©2000 by Excerpta Medica, Inc.
All rights reserved.
death among men using sildenafil, there are limitations to
spontaneous-event reporting. In addition. the numbers of
such reports are well below the expected numbers of
deaths when considering the number of men who have
received prescriptions for sildenafil and their age and car-
diovascular risk factor profile. Because there is a small but
finite risk of having a cardiac event with sexual activity,
physicians should discuss with their cardiac patients the
risks of sexual activity before prescribing any treatment for
ED. In addition, they should evaluate their patients’ cardiac
status when considering the safety of administering any ED
treatment that may have systemic vasodilatory properties
and can potentially lower blood pressure. In some cases,
exercise treadmill testing may be warranted to determine
whether ED patients with coronary artery disease can
achieve the physiologic workload (4 – 6 metabolic equiva-
lents) associated with sexual intercourse. 䊚2000 by Ex-
cerpta Medica, Inc.
Am J Cardiol 2000;86(suppl):57F– 61F
have the potential to stimulate the sympathetic nervous
system with additional stress on the heart. Therefore, it is
not surprising that there is a definite, albeit small, risk of
having a cardiac event with sexual activity. There is no
reason to suspect that the same phenomena will not
occur in women as well.
There has been concern that an agent that is given
systemically for the treatment of ED might interact
with the cardiovascular system in a negative fashion
and trigger an event. This concern is the focus of the
following discussion. Because sidenafil is the only
oral agent on the market (at the time of this writing),
it will serve as the focus for this discussion.
HOW SILDENAFIL WORKS
Sildenafil is an oral phosphodiesterase inhibitor
that enhances erectile function through the same gen-
eral pathway used by nature.6 – 8 Sildenafil requires
sexual stimulation to occur in order for it to work.
Sexual stimulation results in the release of nitric oxide
from nerves and endothelial cells in the corpus cav-
ernosum of the penis. Nitric oxide stimulates guany-
late cyclase with the subsequent formation of cyclic
guanosine monophosphate. Cyclic guanosine mono-
phosphate is the substance that leads to smooth muscle
cell relaxation in the arteries, arterioles, and sinusoids
of the corpus cavernosum that allows this erectile
tissue to fill with blood and causing an erection. Men
with ED may be unable to produce adequate amounts
of cyclic guanosine monophosphate. Cyclic guanosine
monophosphate is normally broken down by phospho-
diesterase. There are numerous phosphodiesterases
throughout the body, but the type 5 isoform (PDE5) is
found in high levels in the genitalia. Sildenafil inhibits
0002-9149/00/$ – see front matter 57F
PII S0002-9149(00)00895-X
PDE5 allowing an increase in cyclic guanosine mono-
phosphate and vasodilation. PDE5 is found in other
tissues besides the genitalia, including vascular and
visceral smooth muscles, platelets, and skeletal mus-
cle. Sildenafil is highly specific for PDE5 compared
with other PDE isoforms.9
EFFICACY OF SILDENAFIL IN MEN
WITH CORONARY ARTERY DISEASE
Is sildenafil effective in men with ischemic heart
disease? Conti et al10 reported the results of a retro-
spective analysis of 357 men with stable chronic cor-
onary artery disease not taking oral nitrates who were
part of randomized, placebo-controlled trials testing
the efficacy of sildenafil. Their mean age was 60
(placebo) and 62 (sildenafil) years and the mean du-
ration of ED was about 5.5 years. Approximately half
of the patients were on antihypertensives and a third
were on antidiabetic agents. The duration of sildenafil
therapy was 4 –24 weeks. Twenty percent of men who
were on placebo versus 70% of men on sildenafil
reported improved erections (p ⬍0.0001). Therefore,
the drug is effective in men with ischemic heart dis-
ease.
Sildenafil also has been shown to be effective in
men with hypertension, diabetes, nonvascular organic
etiologies for ED, and psychogenic causes.6 Although
men with chronic stable ischemic heart disease re-
sponded to sildenafil, the drug has not been system-
atically tested in patients with severe or acute cardio-
vascular or cerebrovascular disease, such as in pa-
tients with unstable angina or recent (within 6 months)
MI, stroke, or life-threatening arrhythmia. The drug
also has not been studied in a systematic fashion in
men with congestive heart failure.
FREQUENCY OF CARDIOVASCULAR
EVENTS IN PLACEBO-CONTROLLED
SILDENAFIL TRIALS
The issue of whether sildenafil could have an ad-
verse effect on cardiovascular outcomes is best deter-
mined by placebo-controlled trials. Morales et al11
reported the incidence of serious cardiovascular
events and MI among men who took part in 18 pla-
cebo-controlled studies. Serious cardiovascular events
were listed as MI, angina, and coronary artery disease.
The studies included 1,552 patients on placebo and
2,722 men on sildenafil. The duration of sildenafil use
was up to 6 months. Serious cardiovascular events
occurred at a rate of 5.7 per 100 man-years of treat-
ment on placebo, and 4.1 per 100 man-years of treat-
ment on sildenafil in phase II/III placebo-controlled
trials. In phase II/III open-label extension trials, seri-
ous cardiovascular events occurred at a rate of 3.5 per
100 man-years with sildenafil. The rate of MI was low
as well at 1.7 per 100 man-years in sildenafil patients
in phase II/III placebo-controlled studies; 1.0 in sil-
denafil patients in phase II/III open-label extension
trials; and 1.4 in placebo patients in phase II/III pla-
cebo-controlled trials. Thus, relative to placebo, sil-
denafil did not cause an increase in the incidence of
58F THE AMERICAN JOURNAL OF CARDIOLOGY姞 VOL. 86 (2A)
serious cardiovascular events or MIs in this patient
population of men with ED.
Did sildenafil increase the rates of cardiac events in
men with ED plus known coronary artery disease?
Conti et al10 reported the frequency of adverse events
in a population of men with stable ischemic heart
disease receiving sildenafil. Three out of 120 men in
the placebo group had MI (2.5%); 8 out of 237 in the
sildenafil groups had MI (3%). Seventeen patients
(7%) in the sildenafil groups and 12 patients (10%) in
the placebo groups had serious cardiovascular adverse
events. In addition, the incidence of nonserious ad-
verse events associated with sildenafil (such as head-
ache, flushing, dyspepsia, and abnormal vision) did
not differ between patients with ischemic heart disease
versus patients without ischemic heart disease.
We recently reported the incidence of adverse
events among men who had used sildenafil and were
either taking or not taking concomitant antihyperten-
sive medication.12 Men on antihypertensive medicines
plus sildenafil had the same rate of adverse events as
men not on antihypertensive medicines. Rates of hy-
potension were in general low at 0 to ⱕ1%; flushing
occurred in 11–15%. Importantly, there was no inci-
dence of MI, angina, worsening heart disease, or
cerebrovascular accident.
Information on the most recent, updated database of
patients receiving placebo versus sildenafil in clinical
trials at the time of this writing is shown in Tables I and
II.13 This represents a significant increment compared
with data when sildenafil was first approved by the US
Food and Drug Administration (FDA) in the United
States. At that time there were 1,719 man-years of ex-
posure to sildenafil (1 man-year represents 1 man on the
drug for 1 year; or 2 men on the drug for 6 months; or 4
men on the drug for 3 months, etc). As of December 31,
1998, there were ⬎6000 sildenafil man-years and 474
placebo man-years of experience. Tables I and II list
exposure as man-years and incidence as events per 100
man-years, which is a standard way of reporting such
data. The incidence of all-cause mortality was low in
patients on sildenafil at 0.46 per 100 man-years com-
pared with placebo at 0.84 per 100 man-years. The
incidence of MI was also low at 0.84 per 100 man-years
in sildenafil patients and 1.05 per 100 man-years in the
placebo group.
Thus, the early study by Morales,11 the studies in
men with ischemic heart disease10 and hypertension,12
and the most recent database comparing sildenafil to
placebo13 do not show an increase in either MI or
other serious cardiovascular events with this agent.
SPONTANEOUS REPORTS OF DEATH
AND CARDIAC EVENTS TO THE FDA
In November of 1998, the FDA placed information
on its website on spontaneous reports of death and
serious cardiovascular/cerebrovascular events among
men who had used sildenafil.7,14 Cases of death among
men using sildenafil were seized upon by the media. It
is worthwhile reviewing the advantages and disadvan-
tages of this spontaneous reporting system and then
putting the reports into perspective in relation to
JULY 20, 2000

TABLE I Sildenafil: Incidence of All-Cause Mortality (Updated
Database, December 31, 1998)
Sildenafil Placebo
Exposure (man-yr) 6,053 474
Events (n) 28 4 ous reporting is voluntary. A high percentage of reports
Incidence* 0.46 0.84
(95% CI) (0.31–0.67) (0.23–2.16)
CI ⫽ confidence interval.
*Per 100 man-years
Adapted from data on file, Pfizer, Inc.13
TABLE II Sildenafil: Incidence of Myocardial Infarction
(Updated Database, December 31, 1998)
Sildenafil Placebo
Exposure (man-yr) 6,053 474
Events (n) 51 5 and incomplete information such as certainty of drug
Incidence* 0.84 1.05
(95% CI) (0.63–1.11) (0.34–2.46)
*Per 100 man-years.
Adapted from data on file, Pfizer Inc.13
known rates of death and MI in a large population of
men over a known duration of time. Many of these
issues are described in detail in an excellent article
entitled “Limitations and Strengths of Spontaneous
Reports Data” by Stephen A. Goldman, of the US
Food and Drug Administration.15
The FDA’s spontaneous adverse event reporting sys-
tem (MedWatch) was established to allow “adverse
event reports.” It is a voluntary reporting system and any
person, whether healthcare professional or consumer,
can report an adverse event. It is interesting to note that
the total number of adverse event reports is increasing
and the proportion of cases reported by consumers has
been steadily increasing over the past 5 years.
Advantages of this postmarketing system are that
they provide surveillance that is large-scale as well as
cost effective. Spontaneous reports can lead to impor-
tant hypotheses and “generate signals of potential
problems that warrant further investigation.”15 Signals
are (1) rare events that occur so infrequently that they
may not show up during clinical trials (e.g., if an
adverse event occurs with an incidence rate of 1 per
100,000 patients and a clinical trial database contains
5,000 patients, it is unlikely for that event to have
occurred during those trials) or (2) events that did
show up during these trials but are now occurring with
a frequency that is significantly greater than expected,
given the known mechanism of action of the drug and
the background rate of the adverse event in the patient
population using it. Adverse events that rarely occur
and may not have been picked up during clinical trials
have a greater chance of emerging once the product
has been on the market and exposed to many more
patients. Finally, spontaneous reports can provide in-
formation on the chronology of exposure to the agent
and the development of the adverse events.
There are also numerous limitations and disadvan-
tages of the spontaneous reporting system that merit
review.15,16 These limitations can lead to reporting
bias that must be taken into account when trying to
interpret data based on spontaneous reports. Reports
to the FDA can come from all sources: consumers
themselves, media reports, lawyers, friends, relatives
of consumers, and healthcare professionals. Spontane-
come from manufacturers themselves.16 Larger pharma-
ceutical companies tend to have more comprehensive
postmarketing surveillance programs, and are therefore
more likely to report a greater number of events. Rec-
ognition of an adverse drug event usually is subjective,
imprecise, and not necessarily truly caused by the drug;
both under- and over-reporting can result. Some reports
made to the FDA are unsubstantiated or anecdotal.
Sometimes the FDA receives duplicate reports dealing
with the same case; and event reporting can be second-
hand. The reporters themselves have variable expertise
ingestion. Spontaneous reports are uncontrolled, and un-
like most clinical trials are not carefully reviewed by
outside monitors.
Biases in spontaneous reporting also include such
factors as the length of time a product has been on the
market. Typically, spontaneous reporting of adverse
events peaks at the end of the second marketing year,
and then decreases precipitously (independently of
subsequent sales and use of the drug). Reporting of
spontaneous events is highly dependent on the novelty
of the agent. A pharmaceutical that is first in its class
typically receives more attention and more reports.
Bias in reporting also will occur depending on the
amount of media attention and publicity that a drug
has received. The more publicity a pharmaceutical
receives, and the more the drug enters the public
consciousness, the greater the number of spontaneous
reports likely to be filed. The greater the volume of
sales, the more the reporting. The longer the amount
of time the sales force spends on detailing the drug,
the more likely spontaneous reports will be filed.
Because of these limitations and the great potential
for reporting bias, this reporting system cannot be
used to determine absolute incidence (unknown nu-
merator and denominator), cannot be used to assess
causality, and should not be used to compare events
across drugs. Nevertheless, some have used the FDA
spontaneous reporting system to try to make compar-
isons across drugs and devices.
In November 1998, the FDA website reported 130
deaths among men who used sildenafil.7,14,17 This com-
prised about 3 million men who filled sildenafil prescrip-
tions over 7.5 months of experience. Details of the FDA
report have been reviewed in previous articles by the
author and others.7,14 Since that time, information on
deaths among men using sildenafil can be obtained by
the Freedom of Information Act.18 As of February 1999,
the number of spontaneous reports of death to the FDA
among men who had received a prescription for silden-
afil was 401 (over 10 –11 months, among about 4.5
million men, and about 9 million prescriptions).18 A total
of 219 were cardiac (MI, arrhythmia, cardiac arrest,
collapse), 140 were sudden deaths, and 18 were cerebro-
vascular accidents. From the November 1998 FDA re-
A SYMPOSIUM: SEXUAL ACTIVITY AND CARDIAC RISK 59F
port, 44 of 77 cardiovascular deaths (where the timing of
deaths was known) occurred within 4 –5 hours of silden-
afil use and 27 deaths occurred during or just after sexual
intercourse.7,14 Do these numbers provide a signal that
sildenafil is causing an increase in cardiovascular events?
When looking at the FDA data, it is important to not
only recall the limitations of the spontaneous reporting
system, but also to ask the question: What is the expected
death rate of 4.5 million men over a period of 10 –11
months? Because men with ED often share the same risk
factors for cardiovascular disease, cases of death due to
heart disease obviously would be expected. According to
the American Heart Association (AHA), the number of
men who die from heart disease is approximately 185 for
white to 275 for African American males per million per
month.19 According to the data from the National Center
for Health Statistics20 mortality rates from MI or stroke
for men in the age range common for ED is even high-
er.21 Thus, the number of spontaneous reports of death
among sildenafil users as of February 1999 (401 deaths/
10 –11 months/4 –5 million men who filled a prescription
or about 8.5 deaths/million men/month) does not suggest
a signal for an increased rate of death. One possibility is
that the number of events is under-reported, an acknowl-
edged limitation of spontaneous reporting. But even if
only 1 in 10 deaths had been reported and we corrected
for this, then the numbers would still be well within (or
perhaps even below) the expected rates.
One might argue that because some of the deaths
occurred temporally close to the use of sildenafil (4 –5
hours), sildenafil was causative. However, it is likely
that a certain number of these deaths would have
occurred during this time, irrespective of the use of the
drug or sexual activity. When Muller et al4 assessed
the potential of sexual activity to trigger an MI, about
3% of myocardial infarcts were associated with sexual
activity. However, when a case– crossover technique
was used that takes into account background noise,
only 0.9% of infarcts could be directly attributed to
sexual activity. Thus only a certain percentage of the
27 cases of death reported to occur during or imme-
diately after sexual intercourse in sildenafil users (No-
vember 1998 report) likely were related to this activity
or to the drug.
POTENTIAL CAUSES OF DEATH IN
MEN ON SILDENAFIL
How does one explain the observation that some
deaths were temporally coupled to the use of sildenafil?
One explanation is that some of these deaths were
merely coincidental. A second is that they are the result
of “reporting bias” (i.e., a person who takes a drug and
experiences an adverse event soon afterward is more
likely to associate the event with the drug. Therefore, he
is more likely to report it than if he had taken the drug
many hours or days before the event; neither situation
either proves or disproves a cause-and-effect relation).
Also, having a cardiac event after sexual activity is a
dramatic event that is more likely to be reported. A third
explanation is that sildenafil is an “enabler.” It enables
men with coronary artery disease who may have been
sexually and physically inactive to engage in sexual
60F THE AMERICAN JOURNAL OF CARDIOLOGY姞 VOL. 86 (2A)
activity (likened to moderate exercise) with subsequent
increases in oxygen demand.5 As reviewed elsewhere in
this supplement, heart rate and systolic and diastolic
blood pressure are elevated during sexual intercourse and
approximately 4 – 6 METS (metabolic equivalents) are
expended. A fourth explanation also relates to another
aspect of sildenafil as an “enabler.” It enables men with
coronary artery disease or other heart disease to experi-
ence the “excitement” and “anticipation” of reengaging
in sexual activity with an increase in catecholamines and
subsequent arrhythmias. These latter 2 potential causes
clearly support the recommendations of the American
College of Cardiology (ACC) and AHA,22 as well as the
sildenafil package insert, that the risk of engaging in
sexual activity be assessed and discussed with the car-
diac patient who requests any treatment for ED, includ-
ing sildenafil. Certainly in some patients, an exercise
stress test might be considered. If a patient can achieve
heart rates of 120 –130 beats/min, systolic blood pres-
sures of 150 –180 mm Hg, and can expend 5– 6 METS
without angina or ischemia, he probably will be at low
risk for developing ischemia during sexual activity.7
A fifth potential concern among physicians pre-
scribing sildenafil to cardiac patients is that it will
cause a precipitous drop in blood pressure. However,
studies have shown that sildenafil causes only mild-
to-moderate decreases in systolic and diastolic blood
pressure of about ⫺8/⫺5.5 mm Hg.7,14,23 Further-
more, when sildenafil was given to patients on anti-
hypertensives (calcium antagonists, ␤ blockers, di-
uretics, angiotensin-converting enzyme inhibitors, or
␣ blockers), there was only a small additive decrease
in blood pressure and no increase in adverse events
compared with patients not on antihypertensives.24 –26
As already discussed, sildenafil patients on multiple
antihypertensive drugs had no increase in adverse
events compared with sildenafil patients on one or no
antihypertensive drugs.12 Thus, it is unlikely that sud-
den large decreases in pressure are precipitating death.
However, one situation where precipitous decreases in
blood pressure may have caused or contributed to
death was when sildenafil was inappropriately admin-
istered to patients on organic nitrates. Use of organic
nitrates (including nitroglycerin, isosorbide mononi-
trate, isosorbide dinitrate, other organic nitrate phar-
maceuticals, and amyl nitrite or amyl nitrate, also
called “poppers”) are absolute contraindications to
sildenafil use. These agents are nitric oxide donors
that can result in large synergistic decreases in blood
pressure when sildenafil is on board.24
In one study, volunteers were given sildenafil and
then an hour later sublingual nitroglycerin. Systolic
blood pressure decreased by 26 –51 mm Hg systolic
and volunteers became symptomatic.24 Among the
130 deaths reported by the FDA in November 1998,
16 patients had taken an organic nitrate and 3 addi-
tional patients had nitrates in their possession. The
ACC/AHA consensus statement22 reiterates the im-
portance of avoiding nitrates in patients taking silden-
afil and suggests that nitrates not be given within 24
hours of the use of sildenafil. Thus, a sixth potential
and likely very real cause for some of the deaths were
JULY 20, 2000
not heeding the contraindication of using sildenafil in
patients on organic nitrates.
A seventh potential concern is that sildenafil as a
vasodilator could be causing a “coronary steal phe-
nomenon”—that is, robbing blood from an ischemic
zone and shunting it to a nonischemic zone. Although
this concept is a theoretical concern, experimental
studies to date have not supported it. Traverse et al27
recently reported data from a preliminary study in
which chronically instrumented dogs were subjected
to a partial coronary artery occlusion during treadmill
exercise, before and after sildenafil (50 mg, by
mouth). Coronary blood flow tended to improve with
sildenafil and there was a favorable but small increase
in subendocardial regional myocardial blood flow. A
recent preliminary study from our laboratory (K. Pr-
zyklenk, R.A. Kloner, unpublished observations) also
did not observe a coronary steal phenomenon with
sildenafil. Thus, it is unlikely that sildenafil is causing
deaths through a coronary steal mechanism.
An eighth theoretical concern is that sildenafil
might have a milrinone-like effect on the heart that
induces cardiac arrhythmia.22 Theoretically, if cardiac
myocytes contained both PDE5 and PDE3 (PDE3 is
known to be present in heart) then inhibition of PDE5
by sildenafil would result in a buildup of cyclic
guanosine monophosphate, which is a known inhibitor
of PDE3. Inhibition of PDE3 causes an accumulation
of cyclic adenosine monophosphate, which can in-
crease contractility and exacerbate arrhythmia, which
was thought to have occurred in some studies involv-
ing milrinone. These concepts were mentioned in the
ACC/AHA consensus paper.22 However, a published
study by Wallis et al9 did not observe PDE5 in the
heart using anti-PDE5 antibodies. Furthermore, silden-
afil, even at high doses, had no effect on contractility
of canine ventricular trabeculae, which is consistent
with a lack of expression of PDE5 in cardiac muscle.9
Although the concept of “cross-talk” between PDE5
and PDE3 remains a theoretical concern, additional
research in this field would be useful. Until more data
on this issue are available, the ACC/AHA22 recom-
mendation that caution be used in prescribing silden-
afil with active ischemic heart disease and heart failure
with borderline low blood volume and blood pressure
seems reasonable.
CONCLUSION
Sildenafil is an effective oral medicine for ED. It
improves erectile function in patients with ischemic
heart disease and hypertension. In placebo-controlled
trials including patients with ischemic heart disease
and hypertension, the incidence of adverse cardiovas-
cular events among patients on sildenafil was low and
did not differ from placebo. Data from spontaneous
reports of death among men using sildenafil have not
demonstrated a signal that suggests an increased num-
ber of deaths above what would be expected for men
with ED. Sildenafil did not cause major decreases in
blood pressure when given to patients taking antihy-
pertensive medicines. It was associated with small
additive decreases rather than large synergistic de-
creases (as occurs when it is taken with organic ni-
trates). Sildenafil is absolutely contraindicated in pa-
tients taking organic nitrates. Experimental studies to
date do not suggest that sildenafil causes a coronary
artery steal phenomenon.
Patients with ED who come to the office requesting
treatment for ED including sildenafil should be queried
about their cardiac status. The physician should try to
determine whether the patient would be at increased
cardiac risk resuming sexual activity or receiving a va-
sodilator. In some patients, an exercise stress test or
pharmacologic stress test may be considered.
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A SYMPOSIUM: SEXUAL ACTIVITY AND CARDIAC RISK 61F