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SECTION XI

CARDIAC SURGERY

727

Chapter 88 Surgical Option for the ‘No-Option’ Coronary Artery Disease AJEET BANA • MUKTA TIWARI

artery disease, since it is the most widely studied and describe various surgical options for this subset of patients.

TRANSMYOCARDIAL LASER REVASCULARIZATION

A number of therapeutic procedures have been de-veloped to improve the quality of life of ‘no-option’ patients. Out of those, one is transmyocardial laser revascularization (TMR). Earlier it was believed that myocardial perfusion could be achieved by the cre-ating transmyocardial channels communicating with the left ventricular cavity. This is seen in the physiology of blood fl ow in reptilian hearts 10 . How-ever, these newly formed pathways were later closed by fi brosis and scarring. TMR utilizes a laser to create channels within the myocardium either via the sur-gical approach through epicardium or percutane-ously through endocardial. This procedure can be done in persistently symptomatic unrevasculariz-able patients due to CAD 11 .

TECHNIQUE

TMR is a surgical procedure performed under epidural anaesthesia (to prevent coronary spasm) or as an ad-junct to CABG. Patient is placed in the left lateral position; anterolateral left thoracotomy incision is made in the fourth or fi fth intercostal space to expose the anterior and lateral wall, respectively. The muscles are then retracted, pericardium opened and retracted by stay sutures. The laser probe is placed directly on the epicardial surface and fi red until the probe enters the ventricular cavity. The completion of the proce-dure is indicated by bubbles on transoesophageal echocardiography (TEE) or pulsatile spurts of blood which indicate entry into the ventricular cavity.

INTRODUCTION

Refractory angina remains a major clinical challenge in management of cardiovascular diseases. An in-crease in life expectancy in patients with ischaemic heart disease (IHD) seen with evolved therapeutic strategies has led to more patients presenting in advanced stages of the condition. Technological ad-vances have further made it possible to offer coro-nary revascularization (coronary bypass grafting [CABG] and percutaneous coronary interventions [PCI]) to a wide spectrum of high-risk patients. Drug-eluting stents have been instrumental in re-ducing the restenosis rates 1 , 2 , and extending the in-dications of PCI to those patients that were initially not considered fi t for this surgery such as those with unprotected left main stenosis or those with diabe-tes and diffuse small vessel disease. A signifi cant improvement in surgical outcomes is also seen with introduction of newer techniques such as off-pump CABG and arterial grafts, endarterectomy 3 .

Despite these advances, it has been observed that a large number of patients (5%–21%) with isch-aemic coronary artery disease are not optimal can-didates for revascularization (PCI/CABG) or they cannot be revascularize completely by these proce-dures 4–8 , and many have residual angina despite maximal medical therapy. Thus, an alternative treatment strategy is needed.

Until recently, the natural history of refractory an-gina has not been widely studied. In the USA, an esti-mated 12 million patients have chronic angina and as many as 1.8 million may have refractory angina 9 .

It is important to defi ne the no-option patient population for alternative therapies and to discuss available and experimental strategies that may pro-vide relief to these patients. In this chapter, we will concentrate on end-stage ischaemic coronary

728 SECTION XI — Cardiac Surgery

Manual compression is done to achieve haemostasis of the pulsatile fl ow. A few sutures may be needed in some cases to stop the bleeding. A total of 25–40 chan-nels are made each 1 cm apart in the left ventricle.

COMPLICATIONS

Complications are seen in up to 30% of the patients undergoing TMR. The 30-day mortality of up to 20% was reported in earlier studies; however, in random-ized trial, mortality of only 1%–5% has been re-ported 12 , 13 . This improvement has been attributed to selection of only clinically stable patients for the procedure. For unstable patients, fi rst medical opti-mization and then CABG�TMR after 2–4 weeks is recommended 12 . Other complications of the proce-dure include atrial fi brillation (10%) and ventricular arrhythmias (12%), pericardial effusion with or with-out tamponade (6%), and postoperative heart failure (4%–29%). Peterson et al. conducted a study across 173 centres and reported a 30-day mortality of 6.4% after TMR in 3717 patients. The rate of occurrence of complications such as renal failure was 4.8% and that of stroke was 0.8% in this patient group 14 .

MECHANISM OF ACTION

A. Open channel hypothesis It has been discussed earlier in the chapter that

TMR creates sinusoids to promote direct perfu-sion of the myocardium by oxygenated blood from the left ventricular cavity 10 . However, these channels created quickly fi lled up with necrotic debris in the postoperative period los-ing their patency and hence do not provide the assumed benefi t. Also, over time there is scar formation in these channels with loss of communication with the ventricular cavity 15 .

B. Angiogenesis Further insight into the potential mechanism of

effect of TMR has been suggested by histologi-cal evidence of angiogenesis in the areas of laser injury. An increase in neovascularization in the region of the channels was reported by Hardy et al. 16 , and later confi rmed by subse-quent studies 17–19 . With immunohistochemical staining, the presence of CD31 and factor VIII antibody has been demonstrated, thereby con-fi rming the presence of endothelial linings by virtue of evidence of angiogenesis. Almost a threefold increase in the new blood vessels with the use of TMR has been seen in ischaemic regions (near the channels) as compared to controls 20 .

C. Myocardial denervation TMR has also been hypothesized to lead to dam-

age the epicardial sympathetic nerves and have antianginal effects. There are studies reporting loss of tyrosine hydroxylase, a neural-specifi c enzyme, and decreased uptake of PET tracer C11 hydroxyephedrine which support this hypothesis 21 , 22 . However, denervation theory has been questioned because heart has dual in-nervation by both sympathetic and parasympa-thetic systems. Some studies conducted in dogs with SA node denervation and vagotomy have reported no change in the refl ex response to epicardial or intracoronary bradykinin after TMR 23 . Also, it has been seen that there is rein-nervation of the sympathetic fi bres in the chronic phase post-TMR 24 . Hence, myocardial denervation is unlikely the sole mechanism for the antianginal effect of TMR.

EVIDENCE OF CLINICAL EFFICACY OF TMR

Various outcome measures such as the patient re-ported changes in severity of symptoms and quality of life, functional capacity, rates of hospitalization and cardiovascular mortality have been studied to assess the effi cacy of TMR. The outcomes can be measured by a variety of imaging modalities, in-cluding sestamibi and thallium nuclear studies, PET, stress echocardiography and MRI. All these studies were done on patients with at least class II or III angina and who were not candidates for tradi-tional revascularization ( Table 88-1 ) 73,75 .

TMR has been associated with a signifi cant im-provement in symptomatology as well as quality of life, particularly in patients with class III/IV angina. These positive results have also been sustained at long-term follow-up, thus also a reduction in cardiac-related hospitalization rate.

CORONARY VENOUS BYPASS GRAFTING

INTRODUCTION

At present CABG is an important and commonly performed revascularization procedure in blocked coronary arteries. However, in patients with diffuse disease, this may not be the best option or clinically suitable. In these cases, endarterectomy is a better option. However, managing thin coronary arteries with immature plaque is a diffi cult task and hence in these cases retrograde coronary venous bypass grafting (CVBG) is one of the better therapeutic

729Chapter 88 — Surgical Option for the ‘No-Option’ Coronary Artery Disease

TABLE 88-1 CLINICAL TRIALS WITH TRANSMYOCARDIAL LASER REVASCULARIZATION (75 OR MORE PATIENTS)

Trial Type of Trial

Number of Patients

Change in Angina Class

Change in Exercise Duration

Change in Myocardial Perfusion

Change in Left Ventricular Ejection Fraction

Change in Quality of Life

Change in Survival

Burkhoff et al., 1999 (see ref 19)

Prospective randomized nonblinded

182 Yes Yes No Small decrease

Yes No

Schofi eld et al., 1999 (see ref 13)


188 Yes Yes No – Yes No

Allen et al., 1999 and 2004 (see refs 22, 70)


275 Yes Yes No Yes No at 1 year but yes at 5 years

Frazier et al., 1999 (see ref 12)


192 Yes – Yes (rest-redistribution thalium)

– Yes No

Stone et al., 2002 (see ref 68)

Prospective randomized blinded (placebo-controlled)

141 No No – – – No

Aaberge et al., 2000 and 2002 (see ref 69, 70)


100 Yes No – No – No

Horvath et al. 2001 (see ref 71)

Nonrandomized prospective

78 Yes – – – Yes –

Spertus et al., 2000 (see ref 72)

Prospective randomized (intention to treat)

99 Yes – – – Yes –

Allen et at., 2004 (see ref 74) a

Prospective randomized blinded

218 Yes – – – – No

Oesterle et al., 2000 (see ref 76)

Prospective randomized nonblinded (percutaneous)

221 Yes Yes – – – No

a Patients underwent coronary artery bypass grafting also; all other trials included patients undergoing only transmyocardial laser revascularization.

options, where retrograde perfusion is achieved via cardiac venous system.

HISTORY

Pratt in 1898 first proposed the idea that myocar-dial perfusion in some cases can be achieved by means of a flow of blood from the coronary ve-nous system which would not be affected by atherosclerosis 25 . In 1948, Beck and colleagues first carried out retroperfusion by CVBG through coronary sinus 26 .

The Beck II procedure consisted of a free vein graft from the aorta to the coronary sinus, with a second operation 2–3 weeks later to ligate the coronary sinus. Remarkable success was reported with this

procedure in revascularization of the heart. However, related mortality of 26.1% and development of CABG led to the abandonment of this procedure. Arealis and colleagues in 1973, studied the effect of selective CVBG only for region of ischaemic myocar-dium. Normal refl ux was kept for the rest of the myocardial veins. Great cardiac vein parallel to LAD and middle cardiac vein parallel to PDA were selected as goal vessels.

PRECLINICAL STUDY AND ANIMAL TRIALS

Studies in some animal models 27 indicate that retrograde venous revascularization is possible and improves cardiac function in a state of acute


ischaemia. In these experimental studies, retroper-fusion of the coronary sinus has been used to improve myocardial perfusion and postischaemic systolic and diastolic function in many surgical pro-cedures. In addition, animal trials have also shown that arterialization of cardiac veins also decreases the infarct size 28 , 29 .

CLINICAL STUDY

Gu-Cheng et al. studied the role of CVBG in diffuse coronary artery in right coronary system 30 . In one group, CVBG was done using internal mammary artery (IMA) as sequential graft to middle cardiac vein after ligating its proximal end, whereas in other group, no graft was put on diffuse disease right coronary system. They found at 3 months af-ter discharge that CVBG group was asymptomatic and had no evidence of ischaemia, whereas 40% of nongrafted group had evidence of ischaemia and were symptomatic. They also noticed improvement in left ventricular ejection fraction in CVBG group.

PROCEDURE OF CVBG

Saphenous vein could be used to arterialization of great or middle cardiac vein with ligation of proxi-mal portion of grafted vein so that blood will not go to coronary sinus ( Fig. 88-1 ).

It has been shown that blood fl ow of less than 50 mL/min in grafted vessel can led to ischaemia or infarction. On the other hand, if blood fl ow in cardiac vein increases more than 60 mL/min, chances of myo-cardial oedema and even intramural haemorrhage will increase 31 . So in CVBG procedures, it is important to measure the fl ow by ultrasound fl ow probe, and if it is high, reduce the diameter of vein by putting ligatures so that cardiac vein pressure becomes optimal.

Internal mammary artery, as one kind of muscu-lar artery materials, can enlarge or contract to lumen to adjust the blood fl ow with strong adaptability

and IMA can be used to graft cardiac veins to avoid excessive blood fl ow 32 .

CVBG surgery is indicated in patients suffering from diffuse coronary heart disease for both the re-lief of symptoms and the improvement of life expec-tancy 27 , 33 , 34 . Selective CVBG should be considered in patients with CAD not amenable to traditional revascularization strategies 35–38 . The indications for selective CVBG include patients with tenuous right coronary artery or diffuse lesions. CVBG may also be considered in patients requiring repeat CABG 39–41 . Signifi cant improvement in the long-term prognosis can be expected with more precise anastomosis.

TEMPORARY CARDIAC SYMPATHECTOMY

The sympathetic efferent nerves to thoracic struc-tures including heart are brought by the stellate ganglion or the cervicothoracic ganglion. Afferent sympathetic fi bres originating from the stellate gan-glion are primarily noradrenergic neurons. The postganglionic fi bres from the cervical and thoracic ganglions split into a complex interconnecting net-work that is essential for the mediation of cardio-cardiac refl exes and reaches either the heart or the intrinsic cardiac ganglia.

Left stellate blockade is usually practiced, as it is well known that anatomically the sympathetic af-ferents are predominant on the left side. Heart has no known nociceptor nerve ending and cardiac pain is transmitted to the CNS via these afferent sympathetic nerves. They carry the pain signal from the heart, converge at cervical and stellate ganglion fi nally reaching the intermediolateral grey column between T2 and T6. Ultimately, the pain signal reaches the central nervous system via spinotha-lamic tracts. Since the end of seventeenth century, the analgesic effect of sympathetectomy has been known and the fi rst surgical sympathectomy to treat angina was reported by Jonnesco in 1916 42 . In 1966, Wiener et al. compared stellate ganglion blockade (SGB) to placebo for the control of an-gina 43 . However, this has never been studied in a randomized trial and hence is not a widely advo-cated treatment for refractory angina.

About 15 mL of 0.5% bupivacaine was used for either left SGB or paravertebral blockade in one of the largest prospective cohort studies with 59 unre-vascularizable patients treated with 44 . Patients with syndrome X, or microvascular angina, were ex-cluded. The results showed that after the fi rst injec-tion, left SGB relieved angina for 3.5 weeks (SD � 3.4 weeks). There was an overall response rate of 67%, and nearly half of the patients were treated

Figure 88-1. Coronary venous bypass graft to middle car-diac vein.


with four or more blockades. None of the patients presented with any serious complications.

Although there is a lack of randomized con-trolled trials, selected centres do perform SGB. Complications have been reported between 0.2% and 3%, and include vertigo, hypotension, frozen shoulder and local haematoma 44 , 45 .

SPINAL CORD STIMULATION

Spinal cord stimulation (SCS) is a novel treatment strategy for end-stage IHD patients with intractable angina ( Fig. 88-2 ) 50 . The effi cacy of SCS on the relief of intractable angina pectoris was studied in a 1-year follow-up randomized study. The outcome measures included quality of life parameters, cardiac para-meters and complications. A total of 24 patients selected for the study were either randomized to group A (actively treated n � 12, device received within 2 weeks) or group B (n � 10, control, implan-tation received after the study period). SCS was shown to improve both the quality of life and car-diac parameters. There was reduction in ischaemia after implantation of the device in both exercise test-ing with a treadmill and 24-h ambulatory Holter re-cordings. There was also an associated improvement in exercise capacity 46 . Ten patients with intractable angina and evidence of MI on 48-h ambulatory elec-trocardiograph (ECG) recording were studied for in-dices of ischaemia with and without SCS. It was seen that the total ischaemic burden of the entire group

was signifi cantly reduced from a median of 27.9 (1.9–278.2) mm � min before SCS to 0 (0–70.2) mm � min with SCS ( P � .03) 47 .

In another study conducted in 13 treated patients and 12 control patients with chronic angina for 6 weeks, the effi cacy of SCS was evaluated as a treat-ment for chronic intractable angina pectoris. The outcome measures studied included exercise capac-ity and ischaemia, daily frequency of anginal attacks and nitrate tablet consumption, and quality of life. Compared with control, an increase in the exercise duration ( P � .03) and time to angina ( P � .01) was seen in the actively treated group. Anginal attacks and sublingual nitrate consumption ( P � .01) and ischaemic episodes on 48-h electrocardiogram ( P � .04) were decreased. There was a perceived in-crease in the quality of life ( P � .03), while a de-crease in pain was reported ( P � .01) 48 . Nineteen consecutive patients implanted for SCS were stud-ied. Hospitalization rate was 0.97/patient/year as seen after revascularization, while it was 0.27/patient/year after SCS ( P � .02). Mean hospitaliza-tion rate after revascularization was 8.3 days versus 2.5 days with SCS ( P � .04) 49 .

It has been frequently questioned whether the effects seen with SCS are indeed a revascularization strategy or just placebo effect. Does SCS provide only symptomatic relief in no-option patients without effecting survival, myocardial infarction, need for repeat revascularization or left-ventricular function? An attempt to address these questions is being made

Figure 88-2. A suggested mechanism for spinal cord stimulation–mediated pain control via effects on spinal neurophysiology. (1) SCS activates low-threshold, large diameter A� fi bres, which synapse (2) onto inhibitory (GABAergic or cholinergic) interneu-rons in the dorsal horn. (3) These inhibitory interneurons release transmitter (e.g. GABA, acting via GABA B receptors) to reduce the excitability of spinal projection neurons, such that subsequent inputs from A� and C fi bres are attenuated. (GABA, gamma-aminobutyric acid; SCS, spinal cord stimulation; STT, spinothalamic tract). (Adapted from: Prager, J. P. (2010). What does the mechanism of spinal cord stimulation tell us about complex regional pain syndrome? Pain Medicine, 11, 1278–1283.)

Aβ- fibers1

Aδ- and C-fibers

STT

SCS1

-2

4-

33


by a randomized Medtronic-sponsored study and in a another planned study.

CELL-BASED THERAPY

In ‘no-option’ patients with chronic refractory angina, cell-based therapy for therapeutic angiogen-esis holds great promise 51 , 52 . Although the exact mechanisms underlying how and which stem cells contribute to angiogenesis remain controversial, clinical investigation have been started with unfrac-tionated bone marrow cells (BMCs), which contain both haematopoetic and mesenchymal stem cells, and circulating endothelial progenitor cells (EPCs). EPCs are known to directly contribute to blood ves-sel formation 53–55 . The action of stem cells in angio-genesis is not yet known to occur directly or via paracrine effect or both 56 , 57 . The preliminary results of phase 1 trials using unselected BMCs have reported good initial safety with encouraging results 58–63 . How-ever, effi cacy was not assessed in any of these trials. Losodo et al. conducted a double-blind, placebo-controlled randomized phase 1 trial in 24 patients with intramyocardial injections of granulocyte colony-stimulating factor (G-CSF)-mobilized CD34� cells 64 . A reduction of angina episodes and nitroglyc-erin use was reported in the preliminary results. Thus, a phase 2 double-blind, prospective, randomized, placebo-controlled study, ACT34-CMI has been planned thereafter to determine the tolerability, effi -cacy, safety and dose range of intramyocardial injec-tion of G-CSF-mobilized autologous CD34� cells in patients with refractory chronic MI for reduction of episodes of angina pectoris. Similar to the phase 1 trial, subcutaneous G-CSF 5 mcg/kg/day was given for 5 days followed by leukapheresis of CD34� cells fol-lowed by intramyocardial injection of the CD34� cells using NOGA (R)

guidance. A total of 150 patients with frequency of angina episodes as the primary end point will be enrolled 65 . Wilson et al. also conducted a phase 1 trial in 2005, using higher dose G-CSF or GM-CSF as a single agent. They reported an increase in acute coronary syndromes with the use of these agents 66 . Therefore, the preferred approach currently appears to be mobilization of cells followed by direct injection of those cells.

CARDIAC TRANSPLANTATION FOR ISCHAEMIC HEART DISEASE

Patients with severe left ventricular dysfunction hav-ing evidence of myocardial viability and target ves-sels for revascularization have a better prognosis with surgical revascularization as opposed to medical

management 51 , 67 . However, surgical revasculariza-tion does not provide any benefi t in patients who reach end-stage ischaemic cardiomyopathy without evidence of viability 51 . Thus, cardiac transplantation can be considered as treatment of choice for these patients with end-stage ischaemic cardiomyopathy. Although the indications for cardiac transplantation have been clearly defi ned, the ever changing status of the patient’s heart and multiple medical and surgi-cal options make the decision a diffi cult one.

Patients diagnosed with ischaemic cardiomyopathy and visiting a transplant centre should be evaluated for myocardial viability testing. Once the viability is established, the decision regarding revascularization versus transplant needs to be made. The question that needs to be addressed is whether the patient is too sick for revascularization or rather, when does the mortal-ity of a revascularization procedure outweigh the mor-tality of waiting on the transplant list?

But if viability is established but patient does not have revascularizable target, the scenario changes and patient can be listed early in transplant list. To conclude, cardiac transplantation continues to be the best long-term option for end-stage ischaemic cardiomyopathy. However, the preoperative evalua-tion and exhaustion of all other treatment options are essential when managing this population.

In past, treatment options for patients with re-fractory angina were limited to traditional antiangi-nal therapy and secondary risk factor modifi cation. At present, with advancement in techniques of re-vascularization number of no-option patients is in-creasing. Hence, the need of time is to develop specialized clinics with multidisciplinary approach to treat this subset of patients.

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