Lower urinary tract symptoms/benign prostatic hyperplasia and erectile dysfunction: from physiology to clinical aspects

Figures & data

Figure 1. Penile anatomy.

Figure 2. Endothelial and nitrergic dysfunction in microcirculation.

Table 1. Etiology of erectile dysfunction.

Etiology of erectile dysfunction
Psychogenic (stress, depression, anxiety)
Organic   Nonendocrine     Vasculogenic       Arterial inflow disorders (atherosclerosis, ischemic heart disease, peripheral vascular disease, cavernosal disorders)       Venous outflow disorders (venous incompetence, injuries of tunica albuginea, Peyronie’s disease, often associated with arterial, neurogenic or psychogenic etiology)     Neurogenic       Upper motor neuron lesions (above spinal nerve T10)       Sacral lesions (S2–S4)       Lesions of pudendal nerves     Iatrogenic       Pelvic surgery (non-nerve sparing)       Medications (thiazide diuretics, β-blockers, spironolactone, digoxin, 5α-reductase inhibitors, anti-androgens, luteinizing hormone-releasing agonists and antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, benzodiazepines, antipsychotics and phenytoin, H2 blockers, opiates)     Dysgenesis issues (i.e. phymosis, frenulum breve)   Endocrine     Hypogonadism     Hyperprolactinemia     Hyper- or hypothyroidism     Cushing’s syndrome     Addison’s disease

Figure 3. Normal and pathological hypothalamic–pituitary–testicular axis. (A) Normally functioning hypothalamic–pituitary–testicular axis. Gonadotropin-releasing hormone (GnRH) stimulates the release of luteinizing hormone (LH). This triggers the testes to respond by secreting testosterone, which, in turn, exerts a negative feedback on the hypothalamus and pituitary gland. Both circulating LH and testosterone are within the normal range. (B) Central hypogonadism. The pituitary release of LH is impaired, the testes are no longer stimulated and testosterone production drops; both circulating LH and testosterone are decreased. (C) Subclinical or compensated hypogonadism. The testicular responsiveness to LH is impaired, testosterone production is maintained owing to overstimulation by LH; circulating testosterone is normal or borderline, whereas LH is increased. In this case, the system is driven to its maximal capacity and no further adjustment can be achieved. (D) Primary hypogonadism. In testicular failure, increases in LH serum levels can no longer sustain testosterone release by Leydig cells; circulating testosterone is low and LH is high.

Table 2. Differences in symptoms of erectile dysfunction by etiology.

Symptoms of erectile dysfunction
Rapid and sudden onset	Gradual onset
Situational, variable	Often constant response
Defect in maintaining erection	Defect in achieving and/or maintaining erection
Good nocturnal erection	Lack or absence of nocturnal erection
Excellent response to PDEI-5	Erection better in standing position than lying down (in the presence of venous leak)

Table 3. Princeton III consensus recommendations for risk stratification and cardiovascular evaluation for sexual activity.

Profile	Description	Sexual activity and PDE5 inhibitor use
Low	Fewer than three risk factors for coronary artery disease^a (excluding sex) Controlled hypertension Class I or II stable angina^b Successful coronary revascularization History of uncomplicated myocardial infarction Mild valvular disease, congestive heart failure without left ventricular dysfunction and/or New York Heart Association class I heart failure	Cleared to resume sexual activity Cleared to take PDE5 inhibitors
Intermediate	At least three risk factors for coronary artery disease^a (excluding sex) Class I or II stable angina^b Recent myocardial infarction (within 2–6 weeks) Left ventricular dysfunction and/or New York Heart Association class II congestive heart failure Noncardiac sequela from atherosclerotic disease (stroke and/or peripheral vascular disease)	Cardiac evaluation necessary prior to resuming sexual activity No contraindication to PDE5 inhibitor use
High	Unstable or refractory angina Uncontrolled hypertension New York Heart Association class III–IV congestive heart failure Recent myocardial infarction (within two weeks) High-risk arrhythmias Severe cardiomyopathy Moderate to severe vascular disease	Sexual activity delayed until cardiac condition stabilized

^aMajor cardiovascular risk factors include age, male gender, hypertension, type 1 and type 2 diabetes mellitus, smoking, dyslipidemia, a sedentary lifestyle and a family history of premature cardiovascular disease.

^bDefined by the Canadian Cardiovascular Society (Reference: Campeau, L. (1976) Grading of angina pectoria. Circulation 54, 522–523.

Figure 4. Schematic representation of the main phases of cavernosal artery waveform during a penile Doppler ultrasound examination. (A) In basic conditions, the waveform appears hardly detectable in a velocity/time curve. (B) A few minutes after injection of alprostadil, the cavernosal artery inflow becomes well detectable. (C) The waveform continues to modify with increasing peak systolic velocity (PSV, cutoff >35 cm/s) and decreasing end-diastolic velocity (EDV, cutoff <5 cm/s), until the systolic velocity peaks, indicating the grade of arterial inflow. Acceleration time (AT, cutoff <100) narrows, and can be measured from the bottom to the top of the peak. (D) Later, diastolic flow reversal is shown, indicating an intact venous occlusion mechanism. (E) Intracavernosal pressure exceeds systolic pressure at maximal tumescence, causing reduction in the systolic velocity and narrowing of the systolic peak.