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Page 4 of 12 Sciahbasi et al. Vessel Plus 2023;7:19 https://dx.doi.org/10.20517/2574-1209.2023.22

[21]
At the end, the balloon must be deflated carefully to allow the exit of small air bubbles [Figure 1].

HOW SHOCK WAVE CREATE CALCIUM FRACTURE
Different mechanisms, generally inter-related, are involved in the fragmentation of the calcific plaques by
acoustic shockwaves: squeezing, cavitation, fatigue, and spallation . Squeezing depends on the different
[18]
speeds of sonic wave propagation between calcific deposits and soft tissue: shock waves move faster across
calcium, causing a circumferential force on the calcified tissue and shear stress evolving in an axial splitting
[22]
failure . Cavitation refers to the generation of bubbles in the fluid, produced by the negative pressure of
the acoustic wave. The collapse of these bubbles generates a micro-jet of fluid that strikes the calcium
surface with a velocity upward of 100 m/s and a secondary shock wave, with an amplitude comparable with
[23]
the original one . Differently, fatigue is a process of progressive development of cracks located in
correspondence of little imperfections of the solid calcific deposit. With multiple shock waves, the micro-
fractures evolve into macro-fractures, creating cracks large enough to induce failure. This is why repeated
shock waves are necessary to progressively fragment solid calcific deposits and the technique uses multiple
stress cycles . Finally, spallation is an effect of the reflection of the shock wave from the rear of the calcific
[24]
[22]
deposit, generating a large negative tensile stress . All these effects impact superficial and deep
calcifications, allowing better stent expansion and luminal gaining, representing a significant advantage over
atherectomy devices that target only superficial calcium. Other advantages of the shock wave are: the
possibility of protecting side branch with second wire, no requirement for a specialized wire, and reduced
risk of distal embolization since calcium remains within the vessel after shock disruption.

The method also has some limitations, the main of which is that if the IVL device cannot pass through a
severely calcified lesion, extensive vessel preparation may be required: pre-dilatation is performed in
50%-60% of cases and sometimes other techniques such as rotational or orbital atherectomy may be
combined to get a better result. If there is any angiographic narrowing left in the lesion, high-pressure NC
balloon should be used post IVL. Furthermore, limited data are available on long-term follow-up when IVL
is used in particular settings such as intra-stent restenosis, stent under-expansion, acute coronary
syndromes, chronic total occlusions, or left main stenosis.

CLINICAL STUDIES
Feasibility and safety of the IVL system have been demonstrated in the four DISRUPT-CAD trials that led
to the European approval of the device for the treatment of heavy calcified coronary lesions [13,25-27] . Globally,
these trials were multicenter prospective single-arm studies that enrolled patients with de-novo calcified
lesions (lesion length < 40 mm with vessel diameter between 2.5 and 4.0 mm) [Table 1]. An important
inclusion criterion was the circumferential distribution of calcium fluoroscopically detected on both sides of
the arterial wall or by the presence of ≥ 270 degrees of calcium on intravascular imaging. In general, the
procedural success was very high, ranging from 92% to 95%, with a low rate of complications. On average,
1.3 ± 0.6 catheters were used with a mean number of pulses of 75 ± 43. Intravascular imaging studies
confirmed the effectiveness of the device showing intraplaque calcium fracture, in particular in the most
[26]
heavily calcified lesions Figure 2. An interesting observation was that the fracture was detected by
intravascular imaging in less than 70% of lesions but without differences in final angiographic result or
clinical outcome compared to patients in whom there was not a macroscopic modification of the calcified
lesions . This suggests that the absence of imaging fracture detection is not a sign of ineffective therapy
[13]
because the sonic waves may produce microfractures that are beyond the resolution power of imaging
devices.