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69
Coronary artery bypass graing with concurrent transmyocardial laser revascularization
Joshua L. Chan and Keith A. Horvath
Introduction
Chronic angina pectoris represents a signicant challenge for a growing population of patients with advanced coronary artery disease. Of the estimated 7million North Americans aected by chronic angina, over 2million patients continue to be symptomatic even with maximal medical therapy. Despite the demonstrated suc­cess of conventional interventions, this subpopulation is frequently not amenable to complete revascularization with percutaneous transluminal coronary angioplasty or coronary artery bypass gra (CABG) surgery due to anatomical constraints or diuse disease.
Transmyocardial laser revascularization (TMR) has been estab­lished as a feasible surgical modality and shown to relieve angina in this patient population. Based on the success of sole therapy, TMR has been incorporated as an adjunctive modality with CABG in cases where CABG alone would not be expected to provide com­plete revascularization. is hybrid application now represents over 90% of all TMR procedures performed in the United States and has become a valuable tool in the treatment of advanced coronary artery disease.
is chapter will discuss the technological aspects of TMR and re­view the clinical evidence assessing the use of TMR in combination with CABG to treat patients with severe angina pectoris refractory to conventional treatment options.
Historical perspective andmechanism
Early pioneers attempted to treat angina pectoris with direct myocar­dial revascularization. However, initial eorts with cardiomyopexy (Beck), cardio-omentopexy (O’Shaughnessy), and direct implant­ation of the internal thoracic (mammary) artery (Vineberg) were generally ineective. Later, Sen and associates proposed a model of creating direct vascular channels, mirroring observations in reptilian hearts of a transmural sinusoidal perfusion network. Experimental
attempts involved a number of static mechanical methods, but were hampered by limited success. It was not until the emergence of laser technologies that TMR was able to achieve signicant symptomatic relief and technical replicability.
Although the creation of vascular channels was initially assumed to provide direct myocardial perfusion, clinical work has since dem­onstrated that it is unlikely to be the principal mode of action for TMR in providing angina relief. In an autopsy series by Sigel, it was observed that the carbon dioxide (CO) laser channels were quickly occluded with granulation tissue in the early postoperative period, placing signicant doubt on the assertion that these channels pro­vided substantial and continued perfusion.
Instead, it appears that post-treatment angiogenesis is the pri­mary driving force following TMR, as it parallels clinical improve­ment over time and corresponds to changes in myocardial perfusion proles. Multiple studies have demonstrated histological evidence of neovascularization following TMR therapy, and have been sub­stantiated with evidence of upregulation of multiple growth factors within treated myocardium. While degrees of neovascularization can occur from other forms of mechanical energy, as previously shown with acupuncture needles directed into the myocardium, such methods can result in substantial scar formation, thereby lim­iting ultimate functional improvement. erefore, the key benet of TMR laser energy is its ability to limited collateral damage and scar formation, allowing for maximum angiogenesis to achieve functional recovery and cardioprotection.
Choice oflasermedium
Several types of solid-state lasers consisting of either a single laser-active dopant or in combination with an yttrium aluminium garnet (YAG) gain medium have been assessed for TMR use. However, only CO (Novadaq Technologies Inc., Mississauga, ON, Canada) and holmium (Ho):YAG (CryoLife, Inc., Kennesaw,
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CO2 laser Ho:YAG laser
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0.5 ms 1 ms 2 ms 4 ms
11 ms10 ms8 ms
Fig.69.1 Time-stop imaging capturing pulse emittance, operating characteristics, and mechanical effects of CO
systems in water.
GA, USA) mediums have been clinically approved by the Food and Drug Administration (FDA) in the United States. The re­sultant tissue interaction differs based on the chosen technology, as each particular laser type is unique in its operating character­istics and mechanical effects (Fig. 69.1).
can be created with a single emitted pulse, which is synchronized with the r wave. ese properties are believed to be advantageous as the characteristics of this single, short laser pulse does not cause ex­plosive tissue ablation, thereby minimizing the extent of myocardial trauma, and diminishes the risk of arrhythmias.
50 μs 200 μs 400 μs
800 μs700 μs600 μs500 μs
(left) and Ho:YAG (right) laser
2
Ho:YAG lasers employ a wavelength of 2120mm, delivering se­quential pulses at 5 Hz utilizing 1–2 J and 6–8 W/pulse (Fig. 69.2a). e laser itself is housed within a exible 1mm bre bundle, which
Surgicaltechnique
is advanced manually through the myocardium over multiple car­diac cycles. Pulse activation is unsynchronized to the cardiac cycle. However, separating successive pulses by time is essential in the Ho:YAG system to ensure adequate thermal dissipation; if this is not allowed to occur, accumulated heat may cause excessive tissue trauma and thermocoagulation.
In contrast, the CO laser wavelength is 10,600mm (Fig. 69.2b). is system utilizes a single 15–20 J pulse for 25–40 ms. e channel
Patients undergoing TMR are frequently candidates for combination therapy with CABG and commonly undergo a standard incision with a median sternotomy. e use of TMR itself does not mandate con­current use of cardiopulmonary bypass or anticoagulation. When implemented as adjunctive therapy, the time point at which TMR is performed in relation to CABG may be based on the surgeon’s prefer­ence, such as prior to CABG, following distal coronary anastomosis
Fig.69.2 Two FDA-approved TMR systems commercially available, based on the specific solid-state laser medium:(a) Ho:YAG (CardioGenesis
SolarGen 2100s; CryoLife, Inc., Kennesaw, GA, USA) or (b)CO2 (Heart Laser System™; Novadaq Technologies Inc., Mississauga, ON, Canada).
®
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(a) (b)
Fig.69.3 Creation of transventricular channels shown here following (a)application of TMR hand piece at an angle perpendicular to the epicardium.
(b)Placement of channels are typically in 1cm2 increments.
on cardiopulmonary bypass circuit support, or aer cross-clamp re­moval. Typically, however, adjunct TMR therapy is performed fol­lowing cardiac arrest while on cardiopulmonary bypass support, as it facilitates manipulation of the heart, enables easier access to treat­ment regions, and eliminates immediate post-treatment arrhythmia concerns.
A transoesophageal echocardiographic probe can be useful in conrming adequate channel creation, which can be visualized with the characteristic liquid vaporization. However, transmurality can also be determined by additional cues, including auditory pitch change, pulsatile bleeding from the channel, or tactile feedback with substantial reduction in resistance upon entry into the ventricular cavity.
e TMR hand piece is applied at an angle perpendicular to the epicardium for channel creation, with the location of subse­quent channels typically at a distance of every squared centimetre (Fig. 69.3). Caution is noted against placing TMR channels in exces­sively close proximity to one another, referred to ‘over-channelling’, as it may lead to excessive myocardial trauma and increase the risk of postoperative arrhythmia. Although mild intraoperative bleeding may occur at the focal ring channel locations, these are not typic­ally substantial in nature and frequently become haemostatic spon­taneously without the need for secondary temporizing measures. If persistent bleeding is observed, manual pressure can be applied intermittently over tracts; placement of temporizing epicardial su­tures is rarely necessary.
Association (ACC/AHA) and Society of oracic Surgeons (STS) have additionally reinforced the use of adjunctive TMR for these spe­cic indications.
Mortality
In the largest prospective, multicentre, randomized trial, Allen and associates observed a signicant decrease in inotropic sup­port required for patients treated with TMR plus CABG compared to CABG-only treatment (30% vs 55%; P= 0.001). e rate of major adverse cardiac events within the 30-day postoperative pe­riod was also reduced in the TMR plus CABG treatment arm (3% vs 9%; P=0.04). Survival was noted to be superior in the hybrid revascularization cohort with decreased mortality rates in both the immediate perioperative period (1.5% vs 7.6%; P=0.02) and at 1year (5% vs 11%; P= 0.05). In this series, multivariable pre­dictors of operative mortality were CABG-only (odds ratio (OR)
5.3; P=0.04) and advanced age (OR 1.1; P=0.03). Alongitudinal follow-up of this same study noted comparable survival between groups at 6years (76% vs 80%; P=0.90).
Additional observational data with the STS National Adult Cardiac Database assessing nearly 940,000 patients over a 4-year pe­riod observed an overall mortality rate of 3.8% in TMR plus CABG patients compared to 2.7% in those treated with CABG alone (P <0.001). However, TMR plus CABG patients in this series were identied to have signicant baseline dierences, reecting a pre­dilection for diuse arterial disease based on their preoperative demographics (Table 69.1). When patients with unstable angina were removed, risk-adjustment analysis revealed an observed-to-
Clinical results oftransmyocardial laser revascularization plus CABG combination therapy
Indications
Data from multiple retrospective and prospective, randomized trials have assessed the safety and ecacy of TMR plus CABG. Based on the cumulative clinical evidence, the use of TMR with CABG has been recommended for patients with angina pectoris having at least one myocardial territory not amenable to adequate revascularization with CABG alone. A consensus statement from the International Society of Minimally Invasive Cardiac Surgery (ISMICS) as well as practice guidelines from the American College of Cardiology/American Heart
expected mortality ratio in patients treated with TMR plus CABG of 0.87. Based on these ndings, the addition of TMR to CABG in order to achieve a more complete revascularization was not shown to impact the short-term mortality rate compared to treatment with CABG alone (5.2% vs 4.3; P=0.13).
Konstanty-Kalandyk recently published actuarial data on 10-year survival rates in a cohort of patients with severe disseminated cor­onary atherosclerosis who were treated with CABG and/or TMR. is retrospective review of 86 patients revealed a cumulative sur­vival of 78.3% at 10years in the CABG plus TMR group compared to 72.5% in the single-therapy group (P= 0.535). Single therapy was identied as an independent predictor of late mortality (OR
1.736; P=0.264), potentially further highlighting the importance of achieving complete revascularization in patients with disseminated
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Table69.1 Baseline demographics ofTMR plus CABG and CABG-
only patients enrolled inthe STS National Adult Cardiac Database
Characteristics CABG only
Body surface area, m2 (SD) 1.96 (0.24) 1.99 (0.23) <0.001
Diabetes (all types) 34% 50% <0.001
Insulin-dependent diabetes 10% 19% <0.001
Renal failure 5% 7% <0.001
Haemodialysis 1% 2% <0.001
Cerebrovascular accident 7% 9% <0.001
Chronic lung disease 14% 17% <0.001
Peripheral vascular disease 16% 20% <0.001
Cerebral vascular disease 12% 17% <0.001
Myocardial infarction 46% 49% <0.001
Reoperation 9% 26% <0.001
Three-vessel CAD 71% 80% <0.001
Hypercholesterolaemia 62% 73% <0.001
Hypertension 72% 80% <0.001
CABG, coronary artery bypass graft surgery; CAD, coronary artery disease; SD, standard deviation; TMR, transmyocardial laser revascularization.
n=932,715
TMR + CABG
n=5,618
P-value
angina scores revealed that there was a signicant reduction in the number of patients with CCS angina scores of III or IV following hybrid therapy (0% vs 10%; P=0.009) with a notable trend towards a greater percentage reporting being angina-free (78% vs 63%; P=0.08). Of interest, a signicantly greater proportion of diabetic patients, who are more susceptible to diuse microvascular disease, were angina free following TMR plus CABG (93% vs 63%; P=0.02). e incidence of additional need for CABG and percutaneous cor­onary intervention were similar in each group, with statistically signicant long-term angina improvement (P=0.04) and freedom from angina (P=0.04) maintained in a multivariate analysis.
Resourceutilization
A retrospective review of 255 patients compared the use of adjunctive TMR to CABG alone and assessed the potential savings with com­bination therapy. In this study, patients treated in the adjunctive treatment arm were observed to have signicantly decreased inten­sive care unit times (1.6 ± 0.2days vs 2.1 ± 0.2days; P <0.01) and total hospital lengths of stay (7.1 ± 0.6days vs 8.2 ± 0.4days; P <0.001). Additionally, 30-day readmission rates were substantially reduced (2.8% vs 7.8%; P <0.05). Other factors, such as operative times and ventilator requirement, were similar in both cohorts. Separately, long-term evaluation of TMR plus CABG in a multicentre trial involving 44 patients revealed greater event-free survival (dened as
freedom from repeat revascularization, angina, and death) at 4years coronary atherosclerosis. Of interest, subanalysis based on anatom­ical location of interventions (anterior vs lateral vs posterior) was additionally performed. In those with treatment to the anterior wall, there was a signicant improvement in survival with TMR plus CABG compared to single therapy (100% vs 72.2%; P=0.027), as well as in freedom from cardiac death (100% vs 76.4%; P=0.044).
Efficacy and symptomaticrelief
A retrospective study consisting of 169 high-risk patients identi­ed a sustained improvement in Canadian Cardiovascular Society (CCS) angina class following TMR plus CABG. At 12months post treatment, the study cohort was found to have signicant improve­ment in severe angina (CCS classIII/IV) compared to baseline (4% vs 90%; P <0.001). Symptomatic relief appears to correlate with in­dependent ndings by Trehan and colleagues, who observed an in­crease in average exercise tolerance at 12months postoperatively when this technique was applied to 77 patients (5.2 minutes to 9.7 minutes). Myocardial segments treated with TMR were addition­ally analysed with thallium perfusion scanning, which revealed a linear trend of improvement by 25% during the same time period.
Long-term symptomatic relief was conrmed by Allen in a 5-year follow-up of their prospective, multicentre study of 263 cases. In the initial study, patients scheduled to undergo CABG who also
compared to isolated CABG (39% vs 14%; P <0.064). During this time period, the rate of repeat revascularization interventions was 0% with TMR plus CABG and 24% with CABG alone (P <0.05).
Emerging applications withstem cell-basedtherapies
Research has been carried out evaluating the use of stem cell­based therapies combined with the traditional modalities high­lighted in this chapter. In a study of six patients undergoing CABG, co-treatment with mesenchymal stem cells in non-revascularized segments at time of surgery was found to produce signicant im­provements in regional tissue perfusion (from 12.29% ± 0.44% to
15.86% ± 0.77%; P=0.02), and contractility (from −17.26 ± 1.97 to −22.01 ± 2.42; P=0.04). An FDA phase Itrial has also been conducted investigating direct intramyocardial injection of bone marrow stromal stem cells in conjunction with TMR. Regional contractility in the cell-treated areas improved at 12 months postoperatively (from −0.4% ± 1.4% to −5.1% ± 1.6%; P= 0.02). Patients additionally reported signicant symptomatic improve­ment with a reduction of CCS angina scores (3.3 ± 0.5 vs 1.3 ± 1.2; P <0.01). ese preliminary studies highlight recent innovations to address ischaemic myocardial regions not amenable to conventional techniques alone to achieve a more complete revascularization
through a multifaceted, synergistic approach. had additional areas of ungraable disease were enrolled. Patients were randomized and blinded to receive CABG alone or CABG with TMR. While not all centres participated in the subsequent follow-up
Conclusion
study, 83% (218/263) of the original cohort was evaluable and the baseline demographics were similar between groups. CCS angina class at baseline was comparable between treatment arms (2.9 ± 1.3 vs 2.8 ± 1.3; P=0.50). Patients in the TMR plus CABG treatment arm reported a signicantly greater improvement in overall CCS an­gina severity from baseline compared to CABG alone (0.4 ± 0.7 vs
0.7 ± 1.1; P=0.05). Further characterization of the distribution of
Chronic refractory angina pectoris remains a complex challenge, es-
pecially in those patients with anatomical constraints limiting trad-
itional revascularization. is scenario is becoming more common
as extensive repeated percutaneous coronary intervention has led to
‘full metal jackets’ in the coronary arteries of an increasing number
of patients referred for CABG. Its management is of particular
69 Coronary artery bypass grafting with concurrent transmyocardial laser revascularization 473
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relevance as incomplete revascularization is a predictor for poor clin­ical outcomes and the number of patients with advanced coronary artery disease is only anticipated to increase. e hybrid application of TMR and CABG represents one of the few modalities available for cases not completely amenable to coronary revascularization tech­niques alone. Overall, the clinical evidence demonstrates that the adjunctive utilization of TMR with CABG has multiple advantages in this specic population, including angina relief, increased exer­cise performance, decreased morbidity, and improved survival. As reected by multiple recommendations from the STS, ISMICS, and ACC/AHA, consideration for TMR plus CABG is warranted for se­lect patients with chronic refractory angina pectoris secondary to diuse disease despite optimal pharmacological and interventional therapies.
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2. Mirhoseini M, Muckerheide M, Cayton MM. Transventricular revascularization by laser. Lasers Surg Med. 1982;2(2):187–98.
3. Sen PK, Udwadia TE, Kinare SG, Parulkar GB. Transmyocardial acupuncture:a new approach to myocardial revascularization. J orac Cardiovasc Surg. 1965;50:181–9.
4. Sigel JE, Abramovich CM, Lytle BW, Ratli NB. Transmyocardial laser revascularization:three sequential autopsy cases. J orac Cardiovasc Surg. 1998;115(6):1381–5.
5. Pelletier MP, Giaid A, Sivaraman S, Dorfman J, Li CM, Philip A, Chiu RC. Angiogenesis and growth factor expression in a model of transmyocardial revascularization. Ann orac Surg. 1998;66(1):12–8.
6. Horvath KA. Transmyocardial laser revascularization. J Card Surg. 2008;23(3):266–76.
7. Jones JW, Richman BW, Crigger NA, Baldwin JC. Technique of transmyocardial revascularization:avoiding complications in high-risk patients. J Cardiovasc Surg (Torino). 2001;42(3):353–7.
8. Diegeler A, Cheng D, Allen K, Weisel R, Lutter G, Sartori M, etal. Transmyocardial laser revascularization:a consensus statement of the International Society of Minimally Invasive Cardiothoracic Surgery (ISMICS) 2006. Innovations (Phila). 2006;1(6):314–22.
9. Hillis LD, Smith PK, Anderson JL, Bittl JA, Bridges CR, Byrne JG, etal. 2011 ACCF/AHA Guideline for coronary artery bypass gra surgery:executive summary:a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;124(23):2610–42.
10. Bridges CR, Horvath KA, Nugent WC, Shahian DM, Haan CK,
Shemin RJ, etal. e Society of oracic Surgeons practice
guideline series:transmyocardial laser revascularization. Ann orac Surg. 2004;77(4):1494–502.
11. Allen KB, Dowling RD, DelRossi AJ, Realyvasques F, Lefrak EA, Pfeer TA, etal. Transmyocardial laser revascularization combined with coronary artery bypass graing:a multicenter, blinded, prospective, randomized, controlled trial. J orac Cardiovasc Surg. 2000;119(3):540–9.
12. Allen KB, Dowling RD, Schuch DR, Pfeer TA, Marra S, Lefrak EA, etal. Adjunctive transmyocardial revascularization:ve-year follow-up of a prospective, randomized trial. Ann orac Surg. 2004;78(2):458–65.
13. Horvath KA, Ferguson TB, Guyton RA, Edwards FH. Impact of unstable angina on outcomes of transmyocardial laser revascularization combined with coronary artery bypass graing. Ann orac Surg. 2005;80(6):2082–5.
14. Konstanty-Kalandyk J, Piątek J, Kędziora A, Bartuś K, Drwila R, Darocha T, etal. Ten-year follow-up aer combined coronary artery bypass graing and transmyocardial laser revascularization in patients with disseminated coronary atherosclerosis. Lasers Med Sci. 2018;33(7):1527–35.
15. Stamou SC, Boyce SW, Cooke RH, Carlos BD, Sweet LC, Corso PJ. One-year outcome after combined coronary artery bypass grafting and transmyocardial laser revascularization for refractory angina pectoris. Am J Cardiol. 2002;89(12):1365–8.
16. Trehan N, Mishra Y, Mehta Y, Jangid DR. Transmyocardial laser as an adjunct to minimally invasive CABG for complete myocardial revascularization. Ann orac Surg. 1998;66(3):1113–8.
17. Wehberg KE, Julian JS, Todd JC, Ogburn N, Klopp E, Buchness M. Improved patient outcomes when transmyocardial revascularization is used as adjunctive revascularization. Heart Surg Forum. 2003;6(5):328–30.
18. Frazier OH, Tuzun E, Eichstadt H, Boyce SW, Lansing AM, March RJ, etal. Transmyocardial laser revascularization as an adjunct to coronary artery bypass graing:a randomized, multicenter study with 4-year follow-up. Tex Heart Inst J. 2004;31(3):231–9.
19. Karantalis V, DiFede DL, Gerstenblith G, Pham S, Symes J, Zambrano JP, etal. Autologous mesenchymal stem cells produce concordant improvements in regional function, tissue perfusion, and brotic burden when administered to patients undergoing coronary artery bypass graing:the Prospective Randomized Study of Mesenchymal Stem Cell erapy in Patients Undergoing Cardiac Surgery (Prometheus) trial. Circ Res. 2014;114(8):1302–10.
20. Chan JL, Miller JG, Zhou Y, Robey PG, Stroncek DF, Arai AE, etal. Intramyocardial bone marrow stem cells in patients undergoing cardiac surgical revascularization. Ann orac Surg. 2020;109(4):1142–9.
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70
Prior percutaneous coronary intervention and surgicalrevascularization
Suvitesh Luthra, Sunil K. Ohri, and David P. Taggart
Introduction
Surgical revascularization may be needed aer a prior percutaneous coronary intervention (PCI) due to further progression of de novo disease or failure of a PCI due to in-stent restenosis (ISR) or stent thrombosis. e proportion of patients referred for coronary artery bypass graing (CABG) with prior PCI varies between institutions from 5% to 30%.
Magnitude and scope oftheproblem
According to the National Cardiovascular Data CathPCI Registry that was set up in 1998 to provide a mechanism for centres to identify opportunities for quality improvement on the basis of ev­idence-based performance feedback, there were 667,424 PCIs per­formed in 1612 centres in the United States in 2014. Overall, 41.2% of patients had undergone a prior PCI. Among those presenting without an acute coronary syndrome, only 53.5% were deemed ap­propriate according to the appropriate use criteria. Similarly, data from the Duke Databank for Cardiovascular Disease from July 2009 to March 2015 showed that repeat PCI accounted for 39% of interventions and in whom PCI was performed for ISR (7.5% of all PCI procedures). In the Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) trial at 5 years, repeat revascularization occurred dramatically more oen aer initial PCI than aer initial CABG (25.9% vs 13.7%, re­spectively; P <0.001), and more oen consisted of multiple repeat revascularizations (9.0% vs 2.8%, respectively; P=0.022). Repeat PCI procedures were more frequently performed for de novo le­sions in the PCI than CABG group (33.3% vs 13.4%, respectively; P <0.001). ese patients had signicantly higher rates of the com­posite safety end point of death, stroke, and myocardial infarction aer initial PCI than aer initial CABG (33.8% vs 16.6%; P <0.001). Any repeat revascularization was an independent predictor of the composite safety end point aer both initial PCI (hazard ratio (HR)
2.2, 95% condence interval (CI) 1.6–3.0; P <0.001) and initial CABG (HR 1.8, 95% CI 1.2–2.9; P=0.011).
Cassese etal., in one of the largest PCI series for de novo lesions, reported that 26.4% of patients had angiographic restenosis by 6–8 weeks. ey reported ISR rates of 30.1%, 14.6%, and 12.2% in pa­tients treated with bare-metal stents (BMSs), rst-generation drug­eluting stents (DESs), and second-generation DESs, respectively.
Large observational studies have been inconsistent in assessing the impact of prior PCI on outcomes aer CABG (Table 70.1).– In a retrospective analysis of 12,270 patients over 17years of whom 3% had prior PCI, Barakate etal. found no signicant dierence in 30-day mortality and post-CABG myocardial infarction rates. In one of the largest studies to date by Sánchez etal. with over 63,000 patients, previous PCI (4.9% of patients) was not an independent risk factor for in-hospital mortality (odds ratio 0.88, 95% CI 0.72–
1.07; P=0.20) nor aer adjusting for propensity score (odds ratio
0.9, 95% CI 0.75–1.08; P=0.27).
However, at least three previous editorials have armed the ad­verse eects of prior PCI on CABG outcomes.– Aprevious meta­analysis of 14 studies showed that early mortality rates were higher with prior PCI (relative risk (RR) 1.54, 95% CI 1.19–2; P=0.007), while myocardial infarction (RR 1.46, 95% CI 1.04–2.06; P=0.06) was not signicantly increased and stroke rates were comparable in both cohorts (P=0.95). e risk of renal failure was lower in the primary CABG cohort. However, survival at 3years was compar­able. Another meta-analysis of nine studies by Biancari etal. con­cluded that 30-day/in-hospital mortality was signicantly higher in patients with prior PCI (pooled rate 2.7% vs 2.0%, RR 1.39, 95% CI
1.06–1.84; P=0.02), but prior PCI did not aect late outcome (RR
1.07, 95% CI 0.90–1.28; P=0.43). Ueki etal. in their pooled ana­lysis reported that mortality was adversely aected only in the sub­group of studies with 40% or more multiple prior PCI episodes (OR
1.99, 95% CI 1.56–2.53).
Nature ofdisease and impact onfutureprognosis
In patients with prior PCI, CABG may be required for either stent failure (thrombosis or ISR) or progression of de novo disease in other territories and disease progression by either mechanism
Table70.1 Studies comparing impact ofprior PCI overthe last 20years
https://t.me/medicina_free
First author, year (ref)
Kalaycioğlu,
6
1998
Barakate,
7
2003
Hassan,
8
2005
Van den Brule, 2005
Gürbüz,
10
2006
Thielmann,
11
2006
Pliam,
12
2007
Alcázar,
13
2008
Number of patients FU (years) Stent type Survival MACCE Conclusions
PCI Control % Prior PCI Type PCI No PCI P-value Outcome PCI No PCI P-value
40 40 50 3 PTCA ‘Early’
‘Late’
1 (0.4) 2 (0.8)
1 (0.4) 1 (0.4)
Higher cross-clamp, bypass times, in-hospital stay, and angina at 3years with previous PTCA
361 11,909 2.9 17 PTCA 30-day 6 (2) 195 (2) NS No difference on 30-day
mortality Higher in-hospital stay (8 vs 9.1) in no PTCA group
919 5113
(919 PM)
113 1141 9 1 PTCA (most
9
15.2 4 Unknown In-hospital 33 (3.6) PM 25 (2.7)
not stented)
In-hospital 1-year cardiac
4 (3.5) 0 (0 )
related
87 (1.7) PM 7 (0.8)
24 (2.1) 13 (1.2)
0.01
0.003
0.32
0.25
Prior PCI is a significant predictor of in-hospital mortality
No difference in cardiac mortality at 1year High OR of hospital mortality:age, pulmonary disease, NYHA, LVEF, preop MI, reintervention, renal complications, stroke
190 421 31.1 2.45
(median)
Unknown Event-free
survival
19 (10) 15 (3.6) 0.0001 Preop PCI is an independent risk
factor for symptom recurrence, cardiac events, and increased overall mortality Overall worse outcomes in failed PCI
360 single 289 Multi
2626 19.8 BMS > DES In-hospital 12 (3.3) single
17 (5.9) multi
53 (2) <0.0001 MACE
Stroke SCD Cardiac death LCOS Periop MI
1:24 (6.6) ≥2:41 (14.1) 1:8 (2.2) ≥2:6 (2.1) 1:4 (1.1) ≥2:5 (1.7)
144 (5.5) 56 (2.1) 11 (0.4) 42 (1.6) 60 (2.3) 126 (4.8)
<0.001
1.00 <0.02 <0.001 <0.04 <0.007
Multiple PCI increase perioperative risk for in-hospital mortality and MACE
1:9 (2.5) ≥2:15 (5.1) 1:9 (2.5) ≥2:13 (4.5) 1:18 (5) ≥2:26 (9)
137 (1–3) 17 (>3)
1317 10.5 5 BMS and
DES
In-hospital 5-year
0 (0 )1–3 1 (5.9) >3 21 (15.3) 1–3 5 (27.4) >3
22 (1.7) 236 (17.9)NS>0.05
MACE Stroke MI IABP
5 (3.2) 0 (0 ) 0 (0 ) 1 (0.6)
68 (5.2) 32 (2.4) 14 (1.1) 3 (0.2)
NS <0.05 NS NS
Stented patients had more complications, longer hospital stays No difference in survival Trend to worse survival if >3 stented vessels
116 680 14.6 3 BMS and
DES
30-day 11 (9.5)
BMS:3 (6.8) DES:5 (10.4)
29 (4.3) 95%CI
(1.6–8.34)
MACE Perioperative MI Cardiac death Stroke
32 (21.9) 25 (22.6) 9 (7.8) 0 (0 )
114 (16.8) 67 (9.9) 16 (2.4) 5 (0.7)
RR:1.65 (1.17–2.31) RR:2.19 (1.44–3.31) RR:3.3
Patients with PCI have more MI, cardiac death and all cause death Type of stent has no significant difference in survival
(1.49–7.28) RR:0.16 (0.14–9.86)
Chocron,
https://t.me/medicina_free
14
2008
Gaszewska­Zurek,
15
2009
430 2059 17.3 5 PTCA, BMS,
DES
162
149 52.1 3 BMS In-hospital (PCI <2years prior to
5-year cardiac death
3-year
CABG)
Yap, 2009161457 11,727 11.1 7 Unknown In-hospital
1-year 3-year 5-year
Kinoshita,
17
2009
Massoudy,
18
2009
Bonaros,
19
2009
Tran, 200920221 1537 12.6 5 (3.6
Stevens,
21
2010
79 196 (all
28.7 6 Unknown Surgical mortality 6 (7.6) 2 (1) 0.008 Previous PCI increased surgical
off-pump)
3078 (1)
25,752 14 5 Unknown In-hospital death 80 (2.6) 1098 (≥2)
306 452 40.4 5 BMS and
DES
Unknown Operative
median)
823 809 (PM)
8819
2427 (PM)
8.5 5 Unknown 30-day
Perioperative 30-day
2-year
Remote PCI: 1-year 2-year 3-year 4-year 5-year Recent PCI: 1-year 2-year 3-year 4-year 5-year
9 (2.1) 23 (1.1) 1.91
(0.86–4.26) PM:1.72 (0.78–3.77)
1 (0.6) 4 (2.5)
24 (1.65) 39 (2.7) 82 (5.6) 130 (8.9)
1 (0.7) 5 (3.4)
182 (1.55) 410 (3.5) 797 (6.8) 797 (6.8)
NS NS
0.78
0.013
1159 (4.5) 0.03 MACE Single:265 (8.6)
25 (2.3)
12 (4.4) 10 (3.3)
6 (2.7) 15 (6.6)
11 (2.4) 8 (1.8)
15 (1) 194 (12.6)
<0.001 <0.001
2.65 (1.03–6.85)
0.017
9 (1.1) 32 (3.9) 56 (6.8) 73 (8.9) 91 (11.1) 110 (13.4) 77 (9.5) 96 (11.9) 116 (14.3) 139 (17.2) 160 (19.8)
168 (1.9) 503 (5.7) 723 (8.2) 970 (11) 1217 (13.8) 1508 (17.1)
138 (5.7) 199 (8.2) 267 (11) 335 (13.8)
0.432
0.004
0.555 (PM)
0.073
0.353 (PM)
415 (17.1)
MACE MI Cardiac death Stroke Angina UA Revascularization Cardiac arrest CHF
73 (17) 8 (1.9) 9 (2.1) 6 (1.4) 32 (7.4) 26 (6) 24 (5.6) 2 (0.5) 8 (1.9)
240 (11.6) 28 (1.4) 23 (1.1) 23 (1.1) 128 (6.2) 53 (2.6) 66 (3.2) 3 (0.1) 19 (0.9)
0.0016 HR:1.38 (0.63–3.03) HR:1.91 (0.88–4.13) HR:1.28 (0.52–3.14) HR:1.22 (0.83–1.8)
Increase in overall MACE composite in PCI arm as well as unstable angina and need for revascularization
HR:2.43 (1.52–3.89) HR:1.8 (1.13–2.87) HR:3.2 (0.53–19.17) HR:2.01 (0.88–4.60)
No difference in death at 3years or in-hospital Higher rate of chest pain with PCI (P=0.04)
MACE 40 (3) 350 (3) 0.99 Prior PCI was not associated with
higher in-hospital mortality or MACE rates
mortality after off-pump in diabetics with multivessel disease
2517 (8.4) 0.0003 Multiple previous PCI (≥2) had
≥2:131 (11.9)
increased in-hospital death and MACE
MACE LCOS IABP Stroke MI
24 (7.9) 4 (6.7) 7 (11.7) 6 (1.7) 5 (8.3)
19 (4.3) 4 (3.6) 10 (8.9) 1 (0.9) 2 (1.8)
<0.001
0.031
0.034
0.58
0.002
PCI has increased perioperative and 30-day death, MACE, bleeding complications, need for transfusion, and renal failure
PCI pretreated had an increased risk of operative death, MACE, and AF At 2year:increased mortality with PCI Low EF increased mortality in CABG only
MACE Perioperative MI
334 (41) 21 (2.6)
963 (40) 76 (3.1)
0.385
0.444
Prior PCI did not affect 30-day mortality and overall mortality in matched cohorts Recent (<14days) vs remote (>14days) PCI did not affect survival.
(continued)