19 The clinical evidence base The rst sham-controlled randomised trial showed that focused Li-ESWT produced a measurable physiological improvement in erectile function, establishing proof of [2] concept . A series of meta-analyses has since broadly conrmed a statistically signicant, if modest, treatment effect in men with vasculogenic ED: • A meta-analysis of seven randomised controlled trials (602 men) found a mean improvement in the Erectile Function domain of the International Index of Erectile Function (IIEF-EF) of 6.40 points with active treatment versus 1.65 with [3] sham . • A larger synthesis of 14 studies (833 men) in European Urology reported a pooled IIEF improvement of about 2 points and a signicant Erection Hardness Score (EHS) response, with benet most evident in mild-to-moderate disease and sustained [4] for at least three months . • A meta-analysis of nine studies (637 men) found an IIEF improvement of around 2.5 points and suggested that lower energy ux density combined with a higher pulse count (in the region of 3,000 pulses per session) was associated with better [5] outcomes . • A meta-analysis of 16 RCTs (1,064 men) reported IIEF improvements of roughly 3 points sustained to six months and found that men with a baseline EHS of 2 or below were about ve times more likely to improve to a functionally meaningful EHS of 3 or above with Li-ESWT than with sham (odds ratio 5.07; 95% CI 1.78 to 14.44). The same analysis suggested an energy density near 0.09 mJ/mm² with 1,500 to 2,000 pulses, and a more pronounced [6] effect in moderate ED . • A systematic review and meta-analysis of randomised trials similarly concluded that the therapy produces a clinically relevant improvement in appropriately selected men [7], and the most recent update (12 RCTs, 882 men) continues to report signicant gains in IIEF-EF and EHS versus [8] sham . These consistent positive signals must, however, be weighed against the most rigorous recent appraisal. The 2025 Cochrane review judged the overall certainty of evidence to be low, cautioned that the true effect size may fall below the minimal clinically important difference, and emphasised that the literature is limited by substantial heterogeneity in devices and protocols and [9] by industry involvement in several trials . A fair reading is therefore not that Li-ESWT is proven, but that it probably produces a real, modest and possibly time-limited improvement in mildto-moderate vasculogenic ED. That is strong enough to justify clinical use in selected men, but not strong enough to displace established rst-line therapy. Patient selection: who is most likely to benet The evidence points consistently to one prole: men with mild-to-moderate vasculogenic ED. Benet is least convincing in severe disease and in ED of predominantly neurogenic or psychogenic origin. A second, clinically valuable group is PDE5i poor responders. One of the most frequently cited rationales for the therapy is its potential to "convert non-responders to responders": to improve cavernosal haemodynamics enough that a previously ineffective oral agent begins to work. Real-world cohorts of PDE5i-refractory men support a meaningful response in a proportion of patients. The signal that combination therapy outperforms monotherapy is among the more practically useful recent ndings. A severitystratied protocol has been proposed: for example, a shorter Li-ESWT course plus daily low-dose tadalal for mild disease, and a longer course with daily tadalal in partial responders with more severe disease. This rests on evidence that pairing shockwave with a daily PDE5i yields better outcomes than either [10] alone . Special populations Diabetic and vasculogenic-comorbid ED. Men with diabetes and cardiovascular disease represent the most therapeutically resistant vasculogenic subgroups. Emerging randomised data suggest Li-ESWT retains efcacy and safety even when ED is attributable to these conditions, which is
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