Phosphodiesterase type 5 (
PDE5) inhibitors such as
tadalafil, can improve cardiac output by increasing left ventricular preload; however, there are concerns that this can increase the risk of
heart failure due to pulmonary congestion in patients with elevated left ventricular end-diastolic pressure. We encountered a case in which low dose
tadalafil improved the hemodynamics of a 66-year-old male patient with
dilated cardiomyopathy (DCM) with congestion and
low cardiac output due to biventricular dysfunction. The patient received a
cardiac resynchronization therapy defibrillator (CRT-D) and appropriate medical
therapy for
heart failure. During a hemodynamic evaluation after
heart failure symptoms were alleviated, we attempted to increase the dose of renin-angiotensin-aldosterone system (RAAS) inhibitors, which contribute to
low cardiac output,
hypotension, and worsening of renal function. However, the administration of a low dose of
tadalafil for the patient's
benign prostatic hyperplasia allowed for the increase in the dose of RAAS inhibitors and markedly improved his subjective symptoms and hemodynamics. Because of the biventricular dysfunction in severe cases, we often experience further promotion of
low cardiac output by standard treatments such as RAAS inhibitors, in which low doses of
PDE5 inhibitors may be effective in maintaining biventricular linkage.
PDE5 inhibitors may be effective in patients, who are not able to increase the dose of RAAS inhibitors due to
low cardiac output.