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Study results consistently show that tadalafil treatment has little effect
on systemic arterial pressure. This is supported by data reported on more
than 5700 subjects treated with tadalafil in more than 22 clinical trials. One study, conducted in 80 healthy subjects, showed that single
doses of 10 or 20 mg of tadalafil have only modest effects on systolic blood
pressure (SBP) or diastolic blood pressure (DBP). Continued dosing once a day for 10 d revealed no clinically significant
changes in standing or supine SBP or DBP or in heart rate. Additionally,
20 mg of tadalafil, administered to healthy male subjects produced no
significant difference compared with placebo in supine SBP and DBP
(difference in the mean maximal decrease of 1.6 and 0.8 mmHg, respectively)
and in standing SBP and DBP (difference in the mean maximal
decrease of 0.2 and 4.6 mmHg, respectively). In addition, there was no
significant effect on heart rate.
The modest hemodynamic effects of tadalafil in healthy subjects are
reflected in the analyses of five placebo-controlled studies in a general
population of men with ED and of one in men with comorbid diabetes.
Men with significant CVD (for example, history of myocardial infarction,
unstable angina, uncontrolled hypertension) were excluded from
these studies. Blood pressure and heart rate were measured at baseline
and at monthly intervals until the end of the 12-wk treatment period. No
clinically or statistically significant effects on SBP or DBP or heart rate
were observed over a range of doses of tadalafil (2.5–20 mg) compared
with placebo.

Patients receiving tadalafil would appear to be at no greater risk for
cardiovascular-related side effects, including flushing, dizziness, hypertension, and syncope, than are patients taking placebo because the incidence
of these adverse events is low (0.1–3.7%) and not statistically significantly
different among the two patient populations. Importantly,
the rate of myocardial infarction among patients taking tadalafil (0.43 per
100 patient-years) was no greater than that among a group of age-standardized
men.
Despite these assurances from the clinical trial database, the potential
cardiac risk of sexual activity in patients with pre-existing CVD should be
considered.

Because ED and CAD may often coexist, a study was conducted in men
with stable CAD who demonstrated ischemia during a screening exercise
test to examine the effects of tadalafil on physical exercise at a workload
similar to that experienced during sexual activity. The study was a
randomized, double-blind, two-way crossover design in which patients
(aged 53–75 yr) received 10 mg of both placebo and tadalafil on separate
occasions approx 2 to 2.5 h before exercise. As assessed by the primary end
point of time to limiting ischemia, tadalafil did not affect the exercise time
or time to ischemia in these men. The mean difference in total exercise time
was 3 s (10 mg of tadalafil minus placebo), which represented no clinically
meaningful difference.

The effect of a single 100-mg dose of tadalafil on QT interval, which
represents ventricular depolarization and repolarization, was evaluated at
the time of peak tadalafil concentration in a randomized, double-blind,
placebo- and active (intravenous ibutilide)-controlled crossover study in
90 healthy males 18 to 53 yr of age. The mean change in QTc (Fridericia
QT correction) for tadalafil, relative to placebo, was 3.5 ms (two-sided
90%, confidence interval = 1.9, 5.1). The mean change in QTc (individual
QT correction) for tadalafil, relative to placebo, was 2.8 ms (two-sided
90%, confidence interval = 1.2, 4.4). A 100-mg dose of tadalafil (five times
the recommended dose) was chosen because this dose yields exposures
covering those observed on coadministration of tadalafil with potent
CYP3A4 inhibitors. In this study, the mean increase in heart rate associated
with a 100-mg dose of tadalafil compared with placebo was 3.1 beats
per min. These changes are not likely to be clinically relevant.

ED is a frequent complication of radical prostatectomy. Despite improvements
in surgical techniques used in prostatectomy, trauma to neurovascular
bundles leaves many patients with ED. In fact, more than 50% of patients
who undergo prostatectomy procedures will have ED. In one study, the
effects of tadalafil were examined in men who had developed ED after
bilateral nerve-sparing radical retropubic prostatectomy (BNRRP). After a
4-wk no-treatment baseline period, patients received 20 mg of tadalafil or
placebo as needed for the next 12 wk. Patients who received tadalafil had
significantly improved EF, with a five-point increase in scores for the
EF domain of the IIEF (compared with a one-point increase for placebo
[p < 0.001]). (An increase of just five points in the IIEF EF domain is consistent
with an improvement, such as moving from severe to moderate ED
or from moderate to mild ED). By the end of the 12-wk treatment period, the
group of all randomized patients receiving 20 mg of tadalafil after BNRRP
had significantly better rates of successful intercourse attempts (41%) than
those receiving placebo (19%) (p < 0.001) (Fig. 7). All randomized patients responded positively to the GAQ (62% with
20 mg of tadalafil vs 23% with placebo; p < 0.001). Additionally, encouraging
results for patients with this type of ED were observed in a subgroup
of men who exhibited at least some erection or tumescence at baseline and
experienced an even better response to tadalafil than subjects in a separate
study. Another study showed that after nerve-sparing surgery, the highest
dose of a PDE5 inhibitor, such as tadalafil, is usually the most efficacious
dose, and that best results are seen 12 mo after surgery.