5,557

Cracking the Culprit Calcium in Coronaries

Azeem S Sheikh1, B Sc MBBS FCPS MRCP PG Cert; Nadeem S Sheikh2, MBBS DCP M Phil FCPS; Samira Yahya3, MBBS MMedEd

1 Consultant Interventional Cardiologist, Sandwell & West Birmingham Hospitals NHS Trust, Birmingham, UK;
2 Chairman and Dean Department of Pathology, Bolan University of Medical and Health Sciences, Quetta, Balochistan, Pakistan;
3 Senior Education Fellow, East Lancashire Hospitals NHS Trust, Blackburn, UK.

Conflict-of-interest statement: The author(s) declare(s) that there is no conflict of interest regarding the publication of this paper.

Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http: //creativecommons.org/licenses/by-nc/4.0/

Correspondence to: Azeem S Sheikh, Consultant Interventional Cardiologist, Sandwell & West Birmingham Hospitals NHS Trust, Dudley Road, Birmingham, B18 7QH, United Kingdom.
Email: drazeemsheikh@hotmail.com

Received: May 16, 2021
Revised: May 22, 2021
Accepted: May 25 2021
Published online: June 3, 2021

ABSTRACT

Coronary artery calcium score, which is calculated by computed tomography (CT), is an independent predictor of adverse cardiac events in both symptomatic as well as asymptomatic patients. CT coronary angiography is growingly employed not only to evaluate the vessel stenosis, but also to characterise and quantify the extent and amount of coronary atherosclerosis. The four features of high-risk plaques on CT coronary angiography include napkin-ring sign, low CT attenuation, spotty calcification, and the remarkable positive remodelling. Spotty calcium is closely associated with unstable plaques and acute coronary syndrome. Managing patients with calcified coronaries is a dilemma for the interventional cardiologists. Intravascular imaging, either an IVUS or OCT, is recommended in order to have a meticulous analysis of the severity and characterization of the plaque morphology as coronary angiography alone underestimates calcium and does not easily allow its quantification. Performing percutaneous coronary intervention on a heavily calcified coronary lesion poses several technical challenges. IVL is an up-and-coming new treatment modality for tackling coronary artery calcification. In the foreseeable future, this calcium-modification technique is likely to become the established strategy for dealing with challenging complex, calcified lesions.

Key words: Coronary calcification; Calcified coronaries; Calcium-modification; Rotablation; Atherectomy; Intravascular lithotripsy; IVL

© 2021 The Author(s). Published by ACT Publishing Group Ltd. All rights reserved.

Sheikh AS, Sheikh NS, Yahya S. Cracking the Culprit Calcium in Coronaries. Journal of Cardiology and Therapy 2021; 8(1): 963-965 Available from: URL: http://www.ghrnet.org/index.php/jct/article/view/3161

EDITORIAL

Coronary artery calcification (CAC) is considered to be a distinctive feature of atherosclerosis, a variant of an ectopic bone formation[1]. Coronary artery calcium score, which is calculated by computed tomography (CT), is an independent predictor of adverse cardiac events in both symptomatic as well as asymptomatic patients, as described by Budoff et al. in the Multi - Ethnic Study of Atherosclerosis (MESA) study[2].

There are two recognised types of coronary calcification; intimal and medial. Atherosclerotic calcification is seen to occur in the intima[3]. It is thought that inflammatory mediators and elevated levels of lipid within the atherosclerotic lesions provoke osteogenic differentiation of vascular smooth muscle cells[4]. On the other hand, medial calcification, also known as Monckeberg’s sclerosis, is less prevalent in coronary arteries and is more often linked to advanced age, diabetes mellitus and chronic kidney disease[5].

Computed tomographic coronary angiography (CTCA) and intracoronary imaging quantify plaque volume and macro-calcifications (calcium deposits > 200 mm), however, these modalities fail to detect micro-calcifications (calcium deposits < 50 mm). CTCA is not able to distinguish between intimal and medial calcification. Macro-calcifications are recognized as spotty and sheet calcifications; spotty calcification is considered to be a high-risk plaque. Micro-calcifications have been described in the fibrous cap of atherosclerotic plaques, where they may be linked to biomechanical instability[6].

The impact of CAC on prognosis following percutaneous coronary intervention have been established in 16 randomized, controlled trials including a total of 23,481 patients with a mean follow-up of 18 months[7]. The data demonstrated that severe coronary calcification resulted in sub-optimal revascularization (48% vs. 55.6%, p < 0.001), and was associated with significantly higher mortality (10.8% vs. 4.4%, p < 0.001), higher rate of death and myocardial infarction (23.2% vs. 10.9%, p < 0.001) and higher incidence of coronary revascularization (31.8% vs. 22.4%, p < 0.001)[7].

CTCA is growingly used not only to assess the lesion stenosis but also to characterize and quantify the extent of coronary atherosclerosis. Measuring the CAC and coronary plaque burden on CTCA helps in predicting the atherosclerotic cardiovascular disease risk in the long-term. CTCA may play a role in visualizing coronary calcification, particularly for the detection of type I (ratio of calcified plaque volume to vessel circumference (RVTC ≤ 25%) and type II ( RVTC 26-50%) calcified plaques, in contrast to type III (RVTC 51-75%) and type IV (RVTC 76-100%)[8].

The four features of high-risk plaques on CTCA include napkin-ring sign, low CT attenuation, spotty calcification, and the remarkable positive remodelling. Spotty calcium is closely associated with unstable plaques and acute coronary syndrome. CTCA is considered to be an imperative tool for the procedural success during coronary intervention as it helps in recognizing and localizing the calcium in the coronary arteries[9-12].

Intravascular imaging, either an IVUS or OCT, is recommended in order to have a meticulous analysis of the severity and characterization of the plaque morphology as coronary angiography alone underestimates calcium and does not easily allow its quantification.

IVUS is the most effective diagnostic tool to detect endo-luminal and deep calcium, but one of the major issues is that the leading edge of the endo-luminal calcium conceals in its shadow the actual mass of calcium in the vessel wall. On the other hand, optical coherence tomography (OCT) has a restricted depth penetration but can image superficial calcium and determine the back side of the calcified plaque, making the measurement of the total calcified mass possible[13]. Delineating calcification in the vessel by using intracoronary imaging guides the interventionists in using the appropriate techniques for calcium-modification and lesion preparation prior to stent implantation.

Currently there is no proven medical therapy that can reverse coronary calcification. In St. Francis Heart Study[14], 1005 asymptomatic, healthy men and women, age 50 to 70 years, with CAC score > 80th percentile for age and gender were randomized to atorvastatin 20 mg daily or placebo. Atorvastatin resulted in reduction of total cholesterol, low-density lipoprotein cholesterol and triglycerides but had no effect on the progression of coronary calcium score. The treatment also failed to show any significant decline in atherosclerotic cardiovascular disease events[14].

Other treatments like calcium-channel blockers[15], phosphate-binders[16,17] and hormone therapy[18] have all been shown to reduce CAC progression in small randomized trials, however, these findings need to be confirmed in large-scale randomized trials.

The cornerstone of treatment is lifestyle modification, like smoking cessation, alcohol abstinence, weight loss, optimal control of blood pressure, blood sugar and lipid levels that may help to slow the progression of coronary calcification. In symptomatic patients with heavily calcified coronary arteries, complex coronary intervention or coronary artery bypass grafting may need to be considered[19].

Managing patients with calcified coronaries is a dilemma for the interventionists. The severity of a calcified lesion is usually underestimated because the density of the calcium makes it incredibly difficult to assess the severity of the lesion meticulously. Performing percutaneous coronary intervention on a heavily calcified coronary lesion poses several challenges such as difficulty in passing the wire down the lesion, tracking the balloons and devices and dilating the lesion and are, furthermore, associated with significant risks and complications and unfavourable clinical outcomes.

The various calcium-modification interventional techniques currently available can be broadly divided into two groups: 1) techniques without using balloon or atherectomy; 2) techniques using balloon-based plaque rupture.

Among the techniques without using balloon include rotational atherectomy (RA), orbital atherectomy (OA) and Excimer laser coronary atherectomy (ELCA)[20,21]. The procedures with devices based on techniques using balloon constitute super high-pressure non-compliant balloon, cutting/scoring balloon and intravascular lithotripsy (IVL).

RA fractures the calcified plaque efficiently by high-speed rotation of an elliptical diamond-tipped burr, which works judiciously on the calcium in the vessels and culminates in debulking of the plaque. RA has been in use for over three decades and was primarily developed to aid atherosclerotic plaque debulking but has eventually faded in view of the significant procedure - related complications and restenosis[22]. After the inception of drug-eluting stents, interventionists started using RA again not for plaque debulking but for lesion preparation in order to facilitate balloon expansion and optimal stent apposition in cases of severe coronary calcification. Significant vessel dissection abutting acute closure, slow/no re-flow, peri-procedural myocardial infarction, athero-embolism and transient profound hypotension are the most commonly encountered risks associated with RA.

OA is an adjunctive technique which intends to prepare the heavily calcified lesion prior to stenting. Genereux and his colleagues[23], in ORBIT II trial, recruited 443 patient with significant coronary calcification who underwent OA. They reported an impressive device success rate of 98.6% with residual stenosis of < 50%. A 2 - year follow-up demonstrated major adverse cardiovascular events (MACE) of 19.4% with target lesion revascularization (TLR) rate of 6.2%[23]. The most notable complications associated with this technique include coronary dissection, slow-flow/no-reflow and coronary perforation.

IVL is an up-and-coming new treatment modality for tackling coronary artery calcification. The recent clinical trials[24-26] support the efficacy of IVL in triggering circumferential fracture in heavily calcified plaques, resulting in significant luminal gain and paving the way for optimal stent expansion.

The IVL system is a single-use, disposable low-pressure balloon-based system that has two emitters, 6 mm apart, which transforms electrical energy into acoustic circumferential pulses emitting sonic waves safely breaking both superficial as well as deep calcium deposits within the arteries[27,28].

IVL is unique in the way that it does not depend on mechanical tissue injury by physical interaction, seen in other techniques like atherectomy or cutting/ scoring balloon, but instead by a diffuse acoustic pulse through a balloon inflated at low pressure of 4 to 6 atm. By conveying shockwave energy locally, the effect of IVL is more marked with incremental severity of calcification. IVL causes circumferential plaque modification which leads to optimal stent apposition and expansion[29].

The Disrupt CAD[24], a prospective, multi-centre, single-arm, non-randomized study, enrolled 60 patients and used Shockwave IVL to pre-dilate significantly calcified coronary lesions. By using OCT, the authors displayed enhanced circumferential calcium fracture and luminal gain, with 98.3% device success (defined as precise device delivery and application of IVL to the target lesion) and 100% stent delivery. The study reported 95% freedom from MACE at 30-day and 92% at 6 months.

The Disrupt CAD II[25], was a prospective, multicentre, single-arm study which aimed to assess the safety and effectiveness of intracoronary lithotripsy[25]. The study recruited 120 patients over a period of 10 months. Severe calcification was reported in 94.2% of lesions (defined as calcification within the lesion on both sides of the vessel assessed by angiography)[25]. IVL catheter was effectively delivered to all target lesions, and IVL was performed in all of the cases. Using OCT, calcium fracture was identified in 78.7% of lesions. The primary end point of in-hospital MACE [including cardiac death, MI, or target vessel revascularisation], occurred in 5.8% of patients, consisted of seven non-Q-wave myocardial infarctions. IVL was safely accomplished in 92.4% of the cases.

The Disrupt CAD III[26] a prospective, single-arm multicentre trial, was designed to get regulatory approval of coronary IVL. The trial recruited 431 patients at 47 sites in 4 countries. Using OCT, calcium fractures were reported in 67.4% of lesions after IVL use. The procedural success (defined as successful stent delivery with a residual stenosis < 50% by core laboratory assessment without in-hospital MACE) was reported as 92.4% and 30-day freedom from MACE (composite occurrence of cardiac death, MI, or target vessel revascularization [TVR]) was 92.2%.

IVL has been exceptionally safe and an indirect comparison to the rates of complications following high-pressure balloon dilatation, RA and OA, demonstrated a superior safety profile in dealing with heavily calcified stenotic lesions. Comparing to slow flow/no reflow seen in a contemporary series with RA[30], slow flow/no reflow was not reported in any of the published studies and reports. IVL refrains from guidewire bias and enables symmetrical luminal gain, a phenomenon unrecognized in RA[31].

In contradiction to RA or OA, which culminates in micro-fragments that embolize distally, resulting in impaired microcirculatory function[32], larger fragments of calcium produced by IVL remain in-situ, thus having no effect on the microcirculatory function.

IVL has a number of advantages over atherectomy. There is no need for a specific training to use IVL due to the fact that the device is delivered synonymous to a standard catheter-based intervention. IVL is performed at low atmospheric balloon inflation, hence minimizing the trauma to the vessel. Furthermore, whilst treating a bifurcation lesion, with IVL, the side-branch protection utilizing a guide-wire may be carried out flowingly, without the risk of wire entrapment or severing, which may transpire with RA or OA.

In some complex, clinical scenarios, the two calcium-modification techniques, RA and IVL, may be used as complementary techniques. RA helps in modifying the intimal calcium and enable crossing balloons/stents through heavily calcified lesions. However, in cases of significant circumferential deep calcium plaques, RA may not be adequate to procure optimal expansion of the devices. IVL is a fantastic tool to treat deep calcium plaques but its deliverability is limited due to it poor crossing profile. A hybrid approach, using a combination of these two techniques, known as Rota-Shock, may be conducive in treating severely calcified stenotic lesions.

As opposed to the ablation techniques, given that IVL is balloon-based, it is simple to use and the learning curve is not steep. In the foreseeable future, this calcium-modification technique is likely to become the established strategy for dealing with challenging complex, calcified lesions.

REFERENCES

1. Tintut Y, Alfonso Z, Saini T, Radcliff K, Watson K, Boström K, Demer LL. Multilineage potential of cells from the artery wall. Circulation 2003;108:2505-10. [DOI: 10.1161/01.CIR.0000096485.64373.C5]. Epub 2003 Oct 27. [PMID: 14581408]

2. Budoff MJ, Young R, Lopez VA, Kronmal RA, Nasir K, Blumenthal RS, Detrano RC, Bild DE, Guerci AD, Liu K, Shea S, Szklo M, Post W, Lima J, Bertoni A, Wong ND. Progression of coronary calcium and incident coronary heart disease events: MESA (Multi-Ethnic Study of Atherosclerosis). J Am Coll Cardiol. 2013 Mar 26;61(12):1231-9. [DOI: 10.1016/j.jacc.2012.12.035]; [PMID: 23500326]; [PMCID: PMC4148074].

3. Demer LL, Tintut Y. Vascular calcification: pathobiology of a multifaceted disease. Circulation. 2008 Jun 3;117(22):2938-48. [DOI: 10.1161/CIRCULATIONAHA.107.743161]; [PMID: 18519861]; [PMCID: PMC4431628].

4. Johnson RC, Leopold JA, Loscalzo J. Vascular calcification: pathobiological mechanisms and clinical implications. Circ Res. 2006 Nov 10;99(10):1044-59. [DOI: 10.1161/01.RES.0000249379.55535.21]. Erratum in: Circ Res. 2009 Sep 11;105(6):e8. [PMID: 17095733].

5. Lanzer P, Boehm M, Sorribas V, Thiriet M, Janzen J, Zeller T, St Hilaire C, Shanahan C. Medial vascular calcification revisited: review and perspectives. Eur Heart J. 2014 Jun 14;35(23):1515-25. [DOI: 10.1093/eurheartj/ehu163]. Epub 2014 Apr 16. [PMID: 24740885]; [PMCID: PMC4072893].

6. Vengrenyuk Y, Carlier S, Xanthos S, Cardoso L, Ganatos P, Virmani R, Einav S, Gilchrist L, Weinbaum S. A hypothesis for vulnerable plaque rupture due to stress-induced debonding around cellular microcalcifications in thin fibrous caps. Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14678-83. [DOI: 10.1073/pnas.0606310103]. Epub 2006 Sep 26. [PMID: 17003118]; [PMCID: PMC1595411].

7. Zhang YJ, Zhu LL, Bourantas CV, Iqbal J, Dong SJ, Campos CM, Li MH, Ye F, Tian NL, Garcia-Garcia HM, Serruys PW, Chen SL. Impact of everolimus versus other rapamycin derivative-eluting stents on clinical outcomes in patients with coronary artery disease: a meta-analysis of 16 randomized trials. J Cardiol. 2014 Sep;64(3):185-93. [DOI: 10.1016/j.jjcc.2014.01.007]. Epub 2014 Feb 20. [PMID: 24560821].

8. Qi L, Tang LJ, Xu Y, Zhu XM, Zhang YD, Shi HB, Yu RB. The Diagnostic Performance of Coronary CT Angiography for the Assessment of Coronary Stenosis in Calcified Plaque. PLoS One. 2016 May 5;11(5):e0154852. [DOI: 10.1371/journal.pone.0154852]; [PMID: 27149622]; [PMCID: PMC4858195].

9. Giustino G, Mastoris I, Baber U, Sartori S, Stone GW, Leon MB, Serruys PW, Kastrati A, Windecker S, Valgimigli M, Dangas GD, Von Birgelen C, Smits PC, Kandzari D, Galatius S, Wijns W, Steg PG, Stefanini GG, Aquino M, Morice MC, Camenzind E, Weisz G, Jeger RV, Kimura T, Mikhail GW, Itchhaporia D, Mehta L, Ortega R, Kim HS, Chieffo A, Mehran R. Correlates and Impact of Coronary Artery Calcifications in Women Undergoing Percutaneous Coronary Intervention With Drug-Eluting Stents: From the Women in Innovation and Drug-Eluting Stents (WIN-DES) Collaboration. JACC Cardiovasc Interv. 2016 Sep 26;9(18):1890-901. [DOI: 10.1016/j.jcin.2016.06.022]; [PMID: 27659564].

10. Huisman J, van der Heijden LC, Kok MM, Louwerenburg JH, Danse PW, Jessurun GA, de Man FH, Löwik MM, Linssen GC, IJzerman MJ, Doggen CJ, von Birgelen C. Two-year outcome after treatment of severely calcified lesions with newer-generation drug-eluting stents in acute coronary syndromes: A patient-level pooled analysis from TWENTE and DUTCH PEERS. J Cardiol. 2017 Apr;69(4):660-665. [DOI: 10.1016/j.jjcc.2016.06.010]. Epub 2016 Jul 28. [PMID: 27476343].

11. Copeland-Halperin RS, Baber U, Aquino M, Rajamanickam A, Roy S, Hasan C, Barman N, Kovacic JC, Moreno P, Krishnan P, Sweeny JM, Mehran R, Dangas G, Kini AS, Sharma SK. Prevalence, correlates, and impact of coronary calcification on adverse events following PCI with newer-generation DES: Findings from a large multiethnic registry. Catheter Cardiovasc Interv. 2018 Apr 1;91(5):859-866. [DOI: 10.1002/ccd.27204]. Epub 2017 Jul 19. [PMID: 28722295].

12. Bourantas CV, Zhang YJ, Garg S, Iqbal J, Valgimigli M, Windecker S, Mohr FW, Silber S, Vries Td, Onuma Y, Garcia-Garcia HM, Morel MA, Serruys PW. Prognostic implications of coronary calcification in patients with obstructive coronary artery disease treated by percutaneous coronary intervention: a patient-level pooled analysis of 7 contemporary stent trials. Heart. 2014 Aug;100(15):1158-64. [DOI: 10.1136/heartjnl-2013-305180]. Epub 2014 May 20. [PMID: 24846971].

13. Zeng Y, Tateishi H, Cavalcante R, Tenekecioglu E, Suwannasom P, Sotomi Y, Collet C, Nie S, Jonker H, Dijkstra J, Radu MD, Räber L, McClean DR, van Geuns RJ, Christiansen EH, Fahrni T, Koolen J, Onuma Y, Bruining N, Serruys PW. Serial Assessment of Tissue Precursors and Progression of Coronary Calcification Analyzed by Fusion of IVUS and OCT: 5-Year Follow-Up of Scaffolded and Nonscaffolded Arteries. JACC Cardiovasc Imaging. 2017 Oct;10(10 Pt A):1151-1161. [DOI: 10.1016/j.jcmg.2016.11.016]. Epub 2017 Mar 15. [PMID: 28330651].

14. Arad Y, Spadaro LA, Roth M, Newstein D, Guerci AD. Treatment of asymptomatic adults with elevated coronary calcium scores with atorvastatin, vitamin C, and vitamin E: the St. Francis Heart Study randomized clinical trial. J Am Coll Cardiol. 2005 Jul 5;46(1):166-72. [DOI: 10.1016/j.jacc.2005.02.089]. Erratum in: J Am Coll Cardiol. 2011 Oct 18;58(17):1832. [PMID: 15992652].

15. Motro M, Shemesh J. Calcium channel blocker nifedipine slows down progression of coronary calcification in hypertensive patients compared with diuretics. Hypertension. 2001 Jun;37(6):1410-3. [DOI: 10.1161/01.hyp.37.6.1410]; [PMID: 11408386].

16. Chertow GM, Burke SK, Raggi P; Treat to Goal Working Group. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int. 2002 Jul;62(1):245-52. [DOI: 10.1046/j.1523-1755.2002.00434.x]; [PMID: 12081584].

17. Qunibi W, Moustafa M, Muenz LR, He DY, Kessler PD, Diaz-Buxo JA, Budoff M; CARE-2 Investigators. A 1-year randomized trial of calcium acetate versus sevelamer on progression of coronary artery calcification in hemodialysis patients with comparable lipid control: the Calcium Acetate Renagel Evaluation-2 (CARE-2) study. Am J Kidney Dis. 2008 Jun;51(6):952-65. [DOI: 10.1053/j.ajkd.2008.02.298]. Epub 2008 Apr 18. [PMID: 18423809].

18. Manson JE, Allison MA, Rossouw JE, Carr JJ, Langer RD, Hsia J, Kuller LH, Cochrane BB, Hunt JR, Ludlam SE, Pettinger MB, Gass M, Margolis KL, Nathan L, Ockene JK, Prentice RL, Robbins J, Stefanick ML; WHI and WHI-CACS Investigators. Estrogen therapy and coronary-artery calcification. N Engl J Med. 2007 Jun 21;356(25):2591-602. [DOI: 10.1056/NEJMoa071513]; [PMID: 17582069].

19. Dini CS, Nardi G, Ristalli F, Mattesini A, Hamiti B, Di Mario C. Contemporary Approach to Heavily Calcified Coronary Lesions. Interv Cardiol. 2019 Nov 18;14(3):154-163. [DOI: 10.15420/icr.2019.19.R1]; [PMID: 31867062]; [PMCID: PMC6918474].

20. Kassimis G, Raina T, Kontogiannis N, Patri G, Abramik J, Zaphiriou A, Banning AP. How Should We Treat Heavily Calcified Coronary Artery Disease in Contemporary Practice? From Atherectomy to Intravascular Lithotripsy. Cardiovasc Revasc Med. 2019 Dec;20(12):1172-1183. [DOI: 10.1016/j.carrev.2019.01.010]. Epub 2019 Jan 10. [PMID: 30711477].

21. Shavadia JS, Vo MN, Bainey KR. Challenges With Severe Coronary Artery Calcification in Percutaneous Coronary Intervention: A Narrative Review of Therapeutic Options. Can J Cardiol. 2018 Dec;34(12):1564-1572. [DOI: 10.1016/j.cjca.2018.07.482]. Epub 2018 Aug 14. [PMID: 30527144].

22. Gioia GD, Morisco C, Barbato E. Severely calcified coronary stenoses: novel challenges, old remedy. Postepy Kardiol Interwencyjnej. 2018;14(2):115-116. [DOI: 10.5114/aic.2018.76400]. Epub 2018 Jun 19. [PMID: 30008761]; [PMCID: PMC6041832].

23. Généreux P, Bettinger N, Redfors B, Lee AC, Kim CY, Lee MS, Shlofmitz RA, Moses JW, Stone GW, Chambers JW. Two-year outcomes after treatment of severely calcified coronary lesions with the orbital atherectomy system and the impact of stent types: Insight from the ORBIT II trial. Catheter Cardiovasc Interv. 2016 Sep;88(3):369-77. [DOI: 10.1002/ccd.26554]. Epub 2016 Apr 16. [PMID: 27084293].

24. Brinton TJ, Ali ZA, Hill JM, Meredith IT, Maehara A, Illindala U, Lansky A, Götberg M, Van Mieghem NM, Whitbourn R, Fajadet J, Di Mario C. Feasibility of Shockwave Coronary Intravascular Lithotripsy for the Treatment of Calcified Coronary Stenoses. Circulation. 2019 Feb 5;139(6):834-836. [DOI: 10.1161/CIRCULATIONAHA.118.036531]; [PMID: 30715944].

25. Ali ZA, Nef H, Escaned J, Werner N, Banning AP, Hill JM, De Bruyne B, Montorfano M, Lefevre T, Stone GW, Crowley A, Matsumura M, Maehara A, Lansky AJ, Fajadet J, Di Mario C. Safety and Effectiveness of Coronary Intravascular Lithotripsy for Treatment of Severely Calcified Coronary Stenoses: The Disrupt CAD II Study. Circ Cardiovasc Interv. 2019 Oct;12(10):e008434. [DOI: 10.1161/CIRCINTERVENTIONS.119.008434]. Epub 2019 Sep 25. [PMID: 31553205].

26. Hill JM, Kereiakes DJ, Shlofmitz RA, Klein AJ, Riley RF, Price MJ, Herrmann HC, Bachinsky W, Waksman R, Stone GW; Disrupt CAD III Investigators. Intravascular Lithotripsy for Treatment of Severely Calcified Coronary Artery Disease. J Am Coll Cardiol. 2020 Dec 1;76(22):2635-2646. [DOI: 10.1016/j.jacc.2020.09.603]. Epub 2020 Oct 15. [PMID: 33069849].

27. Yeoh J, Hill J. Intracoronary Lithotripsy for the Treatment of Calcified Plaque. Interv Cardiol Clin. 2019 Oct;8(4):411-424. [DOI: 10.1016/j.iccl.2019.06.004]; [PMID: 31445725].

28. Brodmann M, Werner M, Brinton TJ, Illindala U, Lansky A, Jaff MR, Holden A. Safety and Performance of Lithoplasty for Treatment of Calcified Peripheral Artery Lesions. J Am Coll Cardiol. 2017 Aug 15;70(7):908-910. [DOI: 10.1016/j.jacc.2017.06.022]; [PMID: 28797363].

29. De Silva K, Roy J, Webb I, Dworakowski R, Melikian N, Byrne J, MacCarthy P, Hill J. A Calcific, Undilatable Stenosis: Lithoplasty, a New Tool in the Box? JACC Cardiovasc Interv. 2017 Feb 13;10(3):304-306. [DOI: 10.1016/j.jcin.2016.11.048]; [PMID: 28183471].

30. Tomey MI, Sharma SK. Interventional Options for Coronary Artery Calcification. Curr Cardiol Rep. 2016 Feb;18(2):12. [DOI: 10.1007/s11886-015-0691-8]; [PMID: 26768738].

31. Shockwave Medical Inc. Clinical Evidence: PAD II. https:// shockwavemedical.com/clinicians/international/peripheral/clinical-evidence/pad-ii. Accessed Dec 26, 2020.

32. Karimi Galougahi K, Shlofmitz RA, Ben-Yehuda O, Généreux P, Maehara A, Mintz GS, Stone GW, Moses JW, Ali ZA. Guiding Light: Insights Into Atherectomy by Optical Coherence Tomography. JACC Cardiovasc Interv. 2016 Nov 28;9(22):2362-2363. [DOI: 10.1016/j.jcin.2016.09.028]; [PMID: 27884364].

Refbacks

  • There are currently no refbacks.


Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.