Sexual Activity and
Cardiovascular Disease
Melvin D. Cheitlin,
Cardiovascular disease and erectile dysfunction (ED) are
frequently comorbid. Therefore, it is important to con-
sider the risk of renewed sexual activity after successful
treatment of ED in men with cardiovascular disease. This
article reviews the limited existing knowledge of the
metabolic and cardiovascular demands of sexual activ-
ity. Evidence suggests that there is a small increase in
cardiovascular risk related to sexual activity. Overall,
however, the metabolic and cardiovascular demands
Itheyntextbooks,
1969, after reviewing almost 3 dozen cardiology
1
Hellerstein and Friedman reported that
had found ⬍1,000 words on the sexual aspects of
heart disease. In the same decade, Masters and John-
son2 were the first to study scientifically the physio-
logic response to sexual activity and to record heart
rate and blood pressure responses to intercourse.
However, clinical trial data on both the effect of
sexual activity on myocardial oxygen demand (MV̇O2)
and the magnitude of increased risk that sexual activ-
ity poses to patients with cardiovascular disease are
still sparse.
The paucity of such studies is all the more striking
because so many patients with erectile dysfunction (ED)
have coincident cardiovascular disease, and vice versa.3
This is not surprising; endothelial dysfunction, which is
common in patients with ED, is important in the patho-
physiology of hypertension and coronary artery disease
(CAD). Moreover, drugs used in the treatment of hyper-
tension can cause ED as a side effect.4 Patients with
life-threatening congestive heart failure or a history of
acute myocardial infarction (MI) also have a high inci-
dence of some degree of ED, the etiology of which may
be organic or associated with depression and anxiety.5
The known concurrence of ED and cardiovascular
disease should alert physicians to the importance,
when discovering one condition, of looking carefully
for the other. Unfortunately, cardiologists, as well as
internists and family practitioners, rarely inquire about
the sexual function of their patients with cardiovascu-
lar disease. However, ED markedly diminishes the
quality of life of some patients, and its detection and
treatment can make an important contribution to pa-
tient care.
From the Department of Medicine, University of California, San Fran-
cisco, San Francisco, California, USA.
Melvin D. Cheitlin, MD, is a speaker for Lilly ICOS and Pfizer.
Address for reprints: Melvin D. Cheitlin, MD, Department of Med-
icine, Box 0846, SFGH 5G1, University of California, San Francisco,
San Francisco, California 94143. E-mail: mdc@itsa.ucsf.edu.
©2003 by Excerpta Medica, Inc.
All rights reserved.
MD
of sexual activity are modest, and regular physical
activity can almost eliminate the increase in risk
occurring during sex. In addition, it is unlikely that any
direct effect of a phosphodiesterase 5 inhibitor increases
cardiovascular risk in patients with cardiovascular dis-
ease, absent the coadministration of organic
nitrates. 䊚2003 by Excerpta Medica, Inc.
Am J Cardiol 2003;92(suppl):3M– 8M
HEMODYNAMIC EFFECTS OF SEXUAL
ACTIVITY
Data that characterize the effect of sexual activity
on metabolic demand, especially MV̇O2, are limited.
In 1984, Bohlen et al6 studied 10 healthy men, aged 25
to 43 years, during 4 specified sexual activities (car-
ried to orgasm) with their wives: (1) self-stimulation,
(2) partner stimulation, (3) coitus with the woman on
top, and (4) coitus with the man on top. The men were
monitored for heart rate, blood pressure, and oxygen
consumption (V̇O2). A subsequent symptom-limited
exercise test (using the Bruce protocol) determined
maximal heart rate and total body V̇O2.
Depending on the activity, the stimulation stage
averaged 3 to almost 6 minutes, orgasm averaged 10
to 16 seconds, and the resolution phase averaged ⬍40
seconds for noncoital activity and 1 to 2 minutes for
coital activity. Relatively small increases in heart rate
occurred during foreplay and stimulation (Figure 1).7
The highest heart rate, a mean maximum of 127 beats
per minute (67% of maximum heart rate), occurred
with man-on-top intercourse. Similarly, total body
V̇O2, which at baseline averaged ⬍10% of maximum
V̇O2, increased to 22% of maximum V̇O2 (equivalent
to 3.3 metabolic equivalents [METs]) during stimula-
tion and orgasm with man-on-top coitus (Figure 2).7
Vigorous sexual activity may increase the energy cost
to 5 to 6 METs.6 (Note: 1 MET ⫽ ⬇3.5 mL O2/kg per
minute [the amount of oxygen consumed while sitting
quietly in a chair].8)
Blood pressure and heart rate responses were in-
creased only briefly for 1 to 2 minutes during sexual
intercourse (Figure 3).9 Compared with the METs of
ordinary daily activities (Table 1), the total body ox-
ygen demand and increase in MV̇O2 during sexual
activity are modest, and the duration of the increase is
brief.6,8
SEXUAL ACTIVITY AND THE RISK OF
MYOCARDIAL INFARCTION
In the Myocardial Infarction Onset Study, Muller
et al10 assessed the risk of MI onset during and im-
mediately after sexual activity. They studied 1,774
0002-9149/03/$ – see front matter 3M
doi:10.1016/S0002-9149(03)03367-2
FIGURE 1. Heart rate in men during 4 types of sexual activity carried to orgasm: partner stimulation, self-stimulation, coitus with the
woman on top, and coitus with the man on top. Bars show baseline heart rates and heart rates during foreplay, stimulation, and or-
gasm. Numbers above bars are percentages of maximum heart rates, as determined by treadmill exercise testing. bpm ⴝ beats per
minute. (Adapted from Arch Intern Med6 and Am J Cardiol.7)

FIGURE 2. Average oxygen uptake (V̇O2) by men during 4 types of sexual activity carried to orgasm: partner stimulation, self-stimula-
tion, coitus with the woman on top, and coitus with the man on top. Values were converted to metabolic equivalents of the task
(METs) using the conversion 1 MET ⬇ 3.5 mL O2/kg per minute (V̇O2). Bars show baseline values and values during foreplay and
stimulation/orgasm. Numbers above bars are percentages of maximum V̇O2, as determined by treadmill exercise testing. (Adapted
from Arch Intern Med6 and Am J Cardiol.7)

hospitalized patients who had been admitted with an
acute MI. Patients were interviewed within a week of
admission to determine what they had been doing at
the onset of symptoms. They were also questioned
about their frequency of sexual intercourse during the
previous year, and the interval between sexual activity
and the onset of MI symptoms.
Of 1,633 patients who answered the question about
sexual activity, 858 patients (52%) reported sexual
activity in the year before the MI; the sexually active
patients were the basis for risk analyses. Of these, 27
(3%) reported sexual activity in the 2-hour period
before the onset of the infarction.10
Using a case-crossover study design, the investi-
gators defined the 2-hour period immediately preced-
ing MI onset as the hazard period.10,11 Odds ratios as
a measure of relative risk were calculated from the
observed frequency of sexual activity in the hazard
period compared with the expected frequency, based
on the control data. The relative risk of an MI trig-
gered by sexual activity was compared with the risk in
the absence of sexual activity, correcting for chance
occurrence.10
The relative risk of triggering the onset of an MI in
patients with a history of angina was 2.1 (95% confi-
dence interval [CI], 0.8 to 5.8), and the relative risk in

4M THE AMERICAN JOURNAL OF CARDIOLOGY姞 VOL. 92 (9A) NOVEMBER 6, 2003

FIGURE 3. Systolic and diastolic blood pressure (BP) and heart rate during rest (R), intromission (I), and orgasm (O) in 2 coital posi-
tions. bpm ⴝ beats per minute. (Reprinted with permission from Dr. Donald H. Schmidt, editor, Heart Disease and Rehabilitation.9)
TABLE 1 MET of Selected Daily Activities6,8
Activity
Sex with long-standing
partner (average)
Partner stimulation
Self-stimulation
Partner on top
Man on top
Recreational activities
Walking (5 km/hr)
Golf (carrying clubs)
Tennis
Household chores
Ironing
Washing floors
Gardening (digging)
Carpentry
MET ⫽ metabolic equivalents.
Adapted from Arch Intern Med6 and Clin Cardiol.8
patients with a previous MI was 2.9 (95% CI, 1.3 to 6.5).
Neither value was statistically higher than the risk of 2.5
(95% CI, 1.7 to 3.7) in patients without prior cardiac
disease. After correcting for chance occurrence, 0.9% of
cases could be attributed to sexual activity within the
2-hour risk period before MI onset.10 However, a limi-
tation of this study was that only patients who survived
an acute MI and reached a hospital were evaluated.
Based on Framingham data, the risk of an MI occur-
ring in a healthy 50-year-old man is estimated at 1% per
year, or about 1 chance in a million per hour.12,13 Sexual
activity multiplies the relative risk of an MI by 2 to 3,
increasing the hourly risk to 2 to 3 chances in a million,
and only for a 2-hour period. Weekly sexual activity in a
healthy 50-year-old man without known CAD would
increase his annual risk of an MI from 1.0% to 1.01%.10
For a man with a previous MI, the annual risk of rein-
A SYMPOSIUM: ERECTILE DYSFUNCTION AND CARDIOVASCULAR RISK FACTORS
MET Score Rating
1.7
1.8
2.5
3.3
3.2
5.1
6.8
2.0
3.3
4.4
5–7
farction or death is estimated to be 10%, or as low as 3%
if he has good exercise tolerance.14 Sexual activity in
patients with a 10% annual risk transiently increases the
risk from 10 chances in a million per hour to 20 to 30
chances in a million per hour.10
Effect of exercise on risk of MI with sexual activity:
Another important finding of the Myocardial Infarction
Onset Study is that increased weekly frequency of reg-
ular exercise at ⱖ6 METs per episode lessens the relative
risk of MI associated with sexual activity. The relative
risk of men exercising ⱕ1 time per week was 3.0 (95%
CI, 2.0 to 4.5); twice a week, 1.9 (95% CI, 0.2 to 17.1);
and ⱖ3 times per week, 1.2 (95% CI, 0.4 to 3.7).10
Regular exercise, therefore, can almost eliminate the
increased risk of an MI triggered by sexual activity.
In 1977, Stein15 studied the effect of exercise train-
ing on heart rate response during coitus in 22 patients
5M
 TABLE 2 Studies of Ambulatory Monitoring During Sexual Activity in People with Cardiac Disease
Study Patients and Methods
Hellerstein and Friedman 14 men, post-MI;
(197019) Mean age, 48 yr
24–48 hr ECG
Johnston and Fletcher 24 men (9 post-MI, 15 post-MR);
(197920) Age range, 37–66 yr
24-hr ECG
Jackson (198117) 30 men and 5 women with angina;
Age range, 36–70 yr
24-hr ECG
Drory et al (199618) 88 men (73 post-MI, 15 with SAS);
Age range, 36–66 yr; mean, 52 yr
24-hr ECG
ECG ⫽ electrocardiogram; MI ⫽ myocardial infarction; MR ⫽ myocardial revascularization; PVC ⫽ premature ventricular contraction; SAS ⫽ stable anginal
syndrome; SVT ⫽ supraventricular tachycardia.
after MI. He demonstrated a smaller increase in peak
coital heart rate and coital MV̇O2 in patients with
exercise training (n ⫽ 16) compared with a control
group who did not receive training (n ⫽ 6).15 This is
a likely explanation for the findings of Muller et al.10
SEXUAL ACTIVITY IN MEN WITH
KNOWN CORONARY ARTERY
DISEASE
Drory et al16 reported the results of 24-hour am-
bulatory electrocardiographic monitoring, including
during sexual intercourse, in 88 men aged 36 to 66
years with known CAD. The men also underwent a
near-maximal bicycle exercise test. The investigators
found that 31% of the group developed ST-segment
depression consistent with myocardial ischemia dur-
ing coitus, most without angina. All patients with
coitus-induced myocardial ischemia also had ischemia
during the exercise test. Patients without myocardial
ischemia during the exercise test did not have coitus-
induced ischemia. Thus, an exercise test in these pa-
tients with CAD identified all those who would de-
velop ischemia during intercourse. An earlier study by
Jackson17 reported similar findings.
SEXUAL ACTIVITY AND SUDDEN
DEATH
As mentioned above, a limitation of the Myocar-
dial Infarction Onset Study was that only patients who
survived an acute MI and reached a hospital were
evaluated.10 This does not rule out the possibility of an
increased risk of sudden death related to sexual activ-
ity, presumably caused by the development of a sud-
den arrhythmia, such as ventricular tachycardia or
ventricular fibrillation.
There is no evidence that sexual activity in healthy
men is associated with serious arrhythmias, however,
and few studies of ambulatory electrocardiographic
monitoring during sexual activity in men with known
CAD have been reported (Table 2).17–20 In the study
6M THE AMERICAN JOURNAL OF CARDIOLOGY姞 VOL. 92 (9A)
ECG Findings During Sexual Activity
Angina in 4; ectopic beats in 3; ventricular beats in 2;
atrial and ventricular beats in 1
Findings were comparable in frequency and severity
during sex and during usual work activities
12 (50%) had cardiac abnormalities during sex
Of these, 5 had the abnormalities only, or more
frequently, during sex
14 underwent 24-hour ECG, 4 of whom had complained
of palpitations during intercourse
2 of the patients with palpitations had SVT during sex and
2 of the other patients had sinus tachycardia
Complex PVCs were seen in 13% during sex and in 9%
during exercise
Simple PVCs were seen in no patients during sex and in
30% during exercise
by Drory et al18 of 88 men with CAD (most patients
post-MI), complex premature ventricular contractions
were seen with sexual activity in 13%. However, these
events (including complex premature ventricular con-
tractions) are seen frequently in patients after MI with
24-hour ambulatory electrocardiographic monitoring.
Unfortunately, there are no adequate studies of the
incidence of sudden death associated with sexual ac-
tivity. A universally cited study by Ueno21 was re-
ported in the Japanese Journal of Legal Medicine in
1963. This was an autopsy study of 5,559 instances of
sudden death, of which 34 had occurred during inter-
course (0.6%). Of these 34 sudden deaths, 27 occurred
during extramarital intercourse.
This study was severely biased, however. In a
society in which privacy is highly valued, such as that
found in Japan, it is conceivable, even likely, that the
proximity of sudden death to intercourse would not be
mentioned. Conversely, sudden death might be more
likely to be reported when it occurs under unusual
circumstances, such as intercourse with a partner other
than the spouse. Consequently, it is possible that the
incidence of sudden death occurring during inter-
course was underestimated, and the effect of extra-
marital sex in precipitating an MI was overestimated.
The only other mention in the literature of sudden
death during intercourse is in a 1970 study by Heller-
stein and Friedman,19 in which a pathologist estimated
the incidence to be ⬍1%. No data were given, how-
ever, and this percentage was based on opinion.
The probability that the incidence of sudden death
precipitated by sexual activity is low has statistical
support, however. In the United States, the risk of
sudden cardiac death is much lower than that of non-
fatal MI; approximately 1.2 million nonfatal MIs oc-
cur per year, 4 times the annual incidence of 300,000
sudden cardiac deaths.22 Mittleman et al23 showed
that, although exertion does confer some increased
risk, the exertion-related risk of sudden death is sim-
ilar to the risk of an exertion-related nonfatal MI. The
NOVEMBER 6, 2003
 TABLE 3 Frequency of Orgasm and Odds Ratios for Mortality Adjusted for Age and Risk
Factors: The Caerphilly Cohort Study
Frequency of
Orgasm
All-cause mortality
Low
Medium
High
p Value for trend
CAD
Low
Medium
High
p Value for trend
Other causes
Low
Medium
High
p Value for trend
CAD ⫽ coronary artery disease; CI ⫽ confidence interval.
*Age, social class, systolic blood pressure, smoking, and CAD at baseline. Odds ratios for mortality from CAD
were also adjusted for cholesterol at baseline.
Adapted with permission from BMJ.26
absolute risk remains small. Most convincingly, in
both open-label and double-blind placebo-controlled
sildenafil trials, no increase was observed in cardio-
vascular or total deaths in sildenafil patients versus
placebo controls.24,25
Finally, evidence suggests that increased sexual
activity actually decreases mortality. The Caerphilly
cohort study observed 918 men from South Wales
aged 45 to 59 years (at the time of recruitment) for a
mean period of 10 years.26 Both 10-year all-cause and
CAD mortality decreased as the frequency of orgasm
increased (Table 3). The age-adjusted odds ratio for
total mortality associated with an increase of 100
orgasms per year was 0.64 (95% CI, 0.44 to 0.95). The
10-year mortality was 50% lower in men with rela-
tively high orgasmic frequency compared with those
having low orgasmic frequency. The conclusion is
that, over a 10-year period, increased sexual frequency
was associated with a lower risk of death, especially
from CAD.
PHOSPHODIESTERASE 5 INHIBITORS
AND CARDIOVASCULAR RISK
The development of phosphodiesterase 5 (PDE5)
inhibitors, which offer effective oral therapy for ED,
has raised concern about whether these agents in-
crease cardiovascular risk. Potential direct effects
might include plaque vulnerability, platelet aggrega-
tion, thrombogenicity, arrhythmogenicity, myocardial
contractility, vasoconstriction, and decrease in perfu-
sion pressure. Potential indirect effects might include
increased MV̇O2, effects on sympathetic tone, and
arrhythmogenicity. These effects might contribute to
the development of MI or ischemia, arrhythmia, and
sudden death. In particular, if MV̇O2 does increase, it
is important to know the magnitude of the increased
risk in patients with CAD.
A SYMPOSIUM: ERECTILE DYSFUNCTION AND CARDIOVASCULAR RISK FACTORS
Odds Ratios for Mortality (95% CI)
Age-Adjusted Fully Adjusted*
2.0 (1.1–3.5) 1.9 (1.0–3.4)
1.6 (1.0–2.6) 1.6 (1.0–2.8)
1.0 1.0
0.02 0.04
2.2 (1.0–5.2) 2.1 (0.9–5.1)
1.7 (0.8–3.6) 1.8 (0.8–4.0)
1.0 1.0
0.06 0.10
1.7 (0.8–3.5) 1.6 (0.7–3.3)
1.5 (0.8–2.8) 1.5 (0.8–3.0)
1.0 1.0
0.19 0.27
PDE5 inhibitors prolong smooth muscle and arte-
rial, arteriolar, and venous relaxation and cause a
decrease in peripheral vascular resistance. The PDE5
inhibitor sildenafil alone will cause a decrease in sys-
tolic blood pressure of about 8 to 10 mm Hg and a
decrease in diastolic blood pressure of 5 to 6 mm Hg.
The major cardiovascular danger recognized with use
of sildenafil, the first PDE5 inhibitor approved for
clinical use, is the marked decrease in arterial blood
pressure that can result from its interaction with or-
ganic nitrates.27 In patients with severely obstructed
vessels, myocardial blood flow is dependent on per-
fusion pressure, and a steep decrease in blood pressure
could produce severe ischemia and infarction.
Data were analyzed from extensive double-blind,
placebo-controlled studies and open-label follow-up
studies with sildenafil equivalent to ⬎6,884 patient-
years of exposure and 543 placebo patient-years. The
incidence of nonfatal acute MI, cardiovascular death,
and all-cause mortality across these studies was not
increased in sildenafil-treated patients compared with
patients receiving placebo.24 Therefore, it is unlikely
that any direct effect of a PDE5 inhibitor increases
cardiovascular risk in patients with cardiovascular dis-
ease, absent coadministration of organic nitrates.
CONCLUSION
In general, the absolute risk of MI with sexual
activity is extremely low, even in patients with known
CAD. There is no evidence that PDE5 inhibitors
increase the risk of MI, although sufficient evidence
suggests that there is a small increase in risk related to
sexual activity. Overall, however, the metabolic and
myocardial work costs of sexual activity are modest,
and regular physical activity can almost eliminate the
small increase in risk occurring during sex. In addi-
tion, it is unlikely that any direct effect of a PDE5
7M
inhibitor increases cardiovascular risk in patients with
cardiovascular disease, unless it is coadministered
with organic nitrates.
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