**2. Theorotical reason of avoiding the pump**

It is logical to suppose that avoiding CPB would abolish the SIRS (systemic inflammatory response syndrome)and its untoward physiological impact. [Gu Y.J, 1999]. Gu Y.J, investigated the inflammatory response with OPCAB, and found that complement activation and consequently systemic inflammatory response occurred (due to surgical trauma) but the extent and severity were curtailed.

Comparison with on-pump CABG confirms a limited and less severe form of inflammatory response. Strüber [Strüber M.,et al,1999&, Matata B.M.et al,2000] and Matata and their coworkers reported significant increases in the levels of specific biological markers of inflammation following on-pump CABG compared to OPCAB. The inflammatory indicators that were evaluated in both studies and their results are summarized:


By the end of the 90's, most of the surgeons in India and in the far east had been performing OPCAB in 90% of their Coronary artery patients, but by early 2000, there was a sharp decline in the numbers, as most of the surgeons did not find the comfort zone in OPCAB surgery, and that their patency rates were being questioned. In the 1990s the visibility of coronary anastomosis was again a doubtful proposition, and also converting, and going on to the pump became a recipe for disaster. Then came the comparative trials of OPCAB and ONCAB , which obviously brought in results which showed that both the techniques produce nearly the same results, and that the patency was a question of concern[Kim KB,et al,2001&.Puskas JD.et al,2001] The Rooby trial showed that, at 1 year of follow-up, patients in the off-pump group had worse composite outcomes and poorer graft patency than did patients in the on-pump group[A. Laurie Shroyer,et al,NEJM,2009]. The surgeons had then come to a conclusion that OPCAB is good in experienced hands and the results in that group

The appeal of avoiding cardiopulmonary bypass with its direct and indirect physiological insult, the prospect of improved clinical outcomes, and the favorable economic impact gives OPCAB the potential of preference that may mark the dawn of a new era in our search for

OPCAB has been performed in many different ways. It's like different ways of skinning a cat. Ultimately, the gold standard of a perfect patent coronary anastomosis remains the corner stone of a good surgeon and a good operation. It is to be emphasized here that Coronary artery bypass surgery has a come a long way from performing them off pump, then on pump and now going back to off pump. But the most important point, one has to bear in mind is that , the surgeon has to do what he is most comfortable with and by which

The topic of Re-engineering in OPCAB came up , because, there was an engineering that was done during the early phase of OPCAB by the great pioneers of this procedure. But what happened along the way was that these procedures were not reproducible by lesser

It is logical to suppose that avoiding CPB would abolish the SIRS (systemic inflammatory response syndrome)and its untoward physiological impact. [Gu Y.J, 1999]. Gu Y.J, investigated the inflammatory response with OPCAB, and found that complement activation and consequently systemic inflammatory response occurred (due to surgical

Comparison with on-pump CABG confirms a limited and less severe form of inflammatory response. Strüber [Strüber M.,et al,1999&, Matata B.M.et al,2000] and Matata and their coworkers reported significant increases in the levels of specific biological markers of inflammation following on-pump CABG compared to OPCAB. The inflammatory indicators

 Activated complement factor 3a (C3a) demonstrated between 5- and 12-fold rise over the preoperative level after commencement of CPB, and minimal rise in the OPCAB

Proinflammatory interleukin 8 (IL-8) increased 5-folds with CPB whilst the level was

the optimal surgical strategy for the treatment of coronary artery disease.

mortals like us and hence we had to re-engineer this procedure to suit us.

that were evaluated in both studies and their results are summarized:

of people have been outstanding.

he would be able to give the best result.

**2. Theorotical reason of avoiding the pump** 

trauma) but the extent and severity were curtailed.

only slightly altered with OPCAB.

patients.


The other variables of CPB such as haemodilution, non-pulsatile flow, and aortic crossclamping, which may act in concert with SIRS to increase postoperative morbidity, are eliminated by the avoidance of CPB.

Thus avoiding the heart lung machine would be a logical solution in performing coronary artery bypass surgery

## **3. Myocardial preservation**

Adequate myocardial preservation is crucial in CABG operations. Preoperative resuscitation of ischemic myocardium enables recruitment of hibernating myocardium and forms an important component of any myocardial protection strategy. The intraoperative strategy varies (within physiological boundaries) as much from patient to patient as it is from surgeon to surgeon, to the extent that a good clinical outcome becomes the ultimate determinant of the optimal strategy. Even with the same surgeon, the strategy is adapted to the patient and clinical scenario that a prescriptive regimen is not standard. The objective of intraoperative myocardial preservation is to enable efficient myocardial energy management by reducing cardiac metabolic demands on the one hand, while improving myocardial oxygen supply and utilization on the other [Buckberg G.D et.al,1996].

In on-pump CABG, cardioplegia or cross-clamp fibrillation are conventional methods of intraoperative myocardial protection. Cardioplegia favorably affects myocardial energy metabolism but results in the alteration of both the intra- and extracellular milieu and, together with CPB can precipitate changes in cardiac performance postoperatively [Mehlhorn U.,1995]. Cross-clamp fibrillation can increase the endocardial viability ratio and lead to similar changes in cardiac function. In both strategies of myocardial protection, a period of global myocardial ischemia is followed by reperfusion with oxygen-rich blood predisposing to reperfusion injury which manifests as myocardial stunning and arrhythmias in the early postoperative period.

Since deliberate induction of global ischemia is unnecessary in OPCAB, it is logical to suppose that iatrogenic biochemical injury to the myocardium would not occur. More so, the blunted inflammatory response with avoidance of CPB is characterised by low production of IL-8 which is involved in myocardial injury . In fact, Atkins et al. first suggested that OPCAB preserved cardiac function in 1984 [Atkins C.W .et al,1984]. In different prospective randomized studies, Ascione [Ascione R.et al,1999], Penttilä [Penttilä H.J.,et al,2001], Van Dijk [Van Dijk D..et al,2001], Czerny [Czerny M.,et al 2001], Bennetts [Bennetts J.S.et al,2002], and Masuda [Masuda M.et al,2002], and their collaborators reported minimal change in the biochemical markers of myocardial injury (troponin T and/or creatinine kinase-MB isoenzyme), and in some cases, better myocardial function after OPCAB compared to on-pump CABG. Changes in myocardial metabolism indicative of oxidative stress due to local ischemia when the target coronary artery is occluded to enable visualization for distal anastomoses have been reported in OPCAB [Matata B.M. et al 2002]. Compared to on-pump CABG, OPCAB is associated with better myocardial energy preservation, less oxidative stress and minimal myocardial damage [Penttilä H.J et al.2001].

Re-Engineering in OPCAB Surgery 185

Fig. 1. Photo showing the operation table with the head end elevated and tilted to the side of

ended up having inotropes and vasoconstrictors to maintain hemodynamics. Ischemic

What we had re-engineered here, was to increase the heart rate .To attain that, we use intermittent boluses of Injection Atropine (0.6mgs per milliliter), which is only a Chronotropic agent and not an Inotrope. Thus, avoiding unnecessary strain on the myocardium. We aim at a rate above 100 per minute and this keeps the heart briskly

We do not use vasopressors or vasodilators in any of our patients undergoing OPCAB.The only drug the patient would be given intermittently is the Atropine injection. We use Glycerol trinitrate(GTN) in our patients after the distal anastomosis, and that too as an

Mueller et al. found no change in the hemodynamics during exposure of the posterior and anterior wall arteries, and only marginal change for the lateral wall artery with a 'no compression' technique [Mueller X.M et al,2002]. It has been suggested that the use of left ventricular apical suction device for cardiac positioning provokes less hemodynamic

The technique which we have developed is to cut down the pericardium on the right side, down to the inferior vena cava, and to leave the right pleura opened. We routinely open the left pleura to help in the mammary dissection. Hence, in all our patients we have all the three chambers- the

patients when given either of them, they develop further ischemia and become bad.

contracting and avoiding the usual hemodynamic collapse seen in the early days.

instability compared with pericardial retraction sutures [Sepic J.et al,2002].

mediastinum and both the pleural cavity, remaining in continuity with each other.

the surgeon.

antihypertensive only.

However, emerging evidence suggests that intraoperative myocardial protection in OPCAB can provide an added advantage [.Guyton R.A. Et al,200 & Muraki S.et al.2001]. In their pioneering report, Trapp and Bisarya gave an exquisite description of coronary perfusion and the instantaneous improvement in the ECG and blood pressure during OPCAB. Vassiliades et al. [Vassiliades T.A .et al,2002] compared active coronary perfusion using a perfusion pump, with passive perfusion by a cannula connected from the aorta to the graft, and no coronary perfusion, after the distal anastomosis in a randomized clinical trial. They found lower troponin I levels with active and passive coronary perfusion, but cardiac performance was better with active coronary perfusion. The use of intracoronary shunt during OPCAB has also been shown to preclude left ventricular dysfunction [Yeatman M.et al 2002].

Reperfusion injury can occur from regional ischemia due to a combination of underlying coronary obstructive pathology, stabilization and anastomotic techniques, compounded by episodes of hypotension which precede revascularisation. The precarious normoxic and normothermic passive coronary perfusion may be insufficient to protect against myocardial damage in such clinical scenarios.

The concept of myocardial protection in OPCAB is less tedious. In most cases passive coronary perfusion with intracoronary shunts will suffice, but in the presence of heightened cardiac risk such as recent acute myocardial ischemia or infarction, and severely impaired left ventricular function active coronary perfusion is advantageous especially in multi-vessel revascularization.

The role of Intra-aortic balloon pump (IABP)in patients with Ischemic myocardium and in low ejection fraction would be discussed later in the chapter. As of today, apart from using intra coronary shunt, the use of aorto-coronnary shunts in some instances have been a disposable worth remembering.

**Hemodynamic instability** has been the major concern in performing OPCAB even today. Though we have been able to master the technique of positioning the heart by the use of various technique and devices, this still remains a major concern. Exposure of the coronary artery target sites requires the heart to be lifted, rotated, dislocated and displaced producing a distortion of cardiac geometry and consequently hemodynamic fluctuations frequently occur. As a result, the early reports of OPCAB described single or double grafts limited to anterior target sites. The corrective measures for these hemodynamic changes include volume loading, trendelenberg positioning, and displacement of the heart into the opened right pleura, use of inotropes, vasopressors, vasodilators, intra-aortic balloon pump, and right heart circulatory support [Mathison M.et al, 2000 &, Kim K.B. et al, 2001].

What we had **re-engineered** over the last five years is to avoid the Trendelenberg position. And we practice an **anti-Trendelenberg position** of the patient, where the patient lies on the table with the head end up. This is very useful in patients with ischemia, where the pulmonary artery (PA) pressure is high. This maneuver reduces the PA pressure, and there by reduces the left ventricular end diastolic pressure (LVEDP). This is exactly what the patient would do when he develops chest pain in his room. He sits up and tries to catch his breath. That is what we help him do in the operation theater as he is anaesthetised.

If the CVP is low and the right ventricle looks empty, then we give a fluid challenge to improve his preload. But we always try to avoid the Trendelenberg position.

In late nineties, the principle of OPCAB was to perform the coronary anastomosis at a heart rate of less than 60 per minute. Hence, the patients coming for surgery used to be well beta blocked, so that it would be easy to perform the anastomosis. But, most of these patients

However, emerging evidence suggests that intraoperative myocardial protection in OPCAB can provide an added advantage [.Guyton R.A. Et al,200 & Muraki S.et al.2001]. In their pioneering report, Trapp and Bisarya gave an exquisite description of coronary perfusion and the instantaneous improvement in the ECG and blood pressure during OPCAB. Vassiliades et al. [Vassiliades T.A .et al,2002] compared active coronary perfusion using a perfusion pump, with passive perfusion by a cannula connected from the aorta to the graft, and no coronary perfusion, after the distal anastomosis in a randomized clinical trial. They found lower troponin I levels with active and passive coronary perfusion, but cardiac performance was better with active coronary perfusion. The use of intracoronary shunt during OPCAB has also been shown to preclude left ventricular dysfunction [Yeatman M.et

Reperfusion injury can occur from regional ischemia due to a combination of underlying coronary obstructive pathology, stabilization and anastomotic techniques, compounded by episodes of hypotension which precede revascularisation. The precarious normoxic and normothermic passive coronary perfusion may be insufficient to protect against myocardial

The concept of myocardial protection in OPCAB is less tedious. In most cases passive coronary perfusion with intracoronary shunts will suffice, but in the presence of heightened cardiac risk such as recent acute myocardial ischemia or infarction, and severely impaired left ventricular function active coronary perfusion is advantageous especially in multi-vessel

The role of Intra-aortic balloon pump (IABP)in patients with Ischemic myocardium and in low ejection fraction would be discussed later in the chapter. As of today, apart from using intra coronary shunt, the use of aorto-coronnary shunts in some instances have been a

**Hemodynamic instability** has been the major concern in performing OPCAB even today. Though we have been able to master the technique of positioning the heart by the use of various technique and devices, this still remains a major concern. Exposure of the coronary artery target sites requires the heart to be lifted, rotated, dislocated and displaced producing a distortion of cardiac geometry and consequently hemodynamic fluctuations frequently occur. As a result, the early reports of OPCAB described single or double grafts limited to anterior target sites. The corrective measures for these hemodynamic changes include volume loading, trendelenberg positioning, and displacement of the heart into the opened right pleura, use of inotropes, vasopressors, vasodilators, intra-aortic balloon pump, and

What we had **re-engineered** over the last five years is to avoid the Trendelenberg position. And we practice an **anti-Trendelenberg position** of the patient, where the patient lies on the table with the head end up. This is very useful in patients with ischemia, where the pulmonary artery (PA) pressure is high. This maneuver reduces the PA pressure, and there by reduces the left ventricular end diastolic pressure (LVEDP). This is exactly what the patient would do when he develops chest pain in his room. He sits up and tries to catch his

If the CVP is low and the right ventricle looks empty, then we give a fluid challenge to

In late nineties, the principle of OPCAB was to perform the coronary anastomosis at a heart rate of less than 60 per minute. Hence, the patients coming for surgery used to be well beta blocked, so that it would be easy to perform the anastomosis. But, most of these patients

right heart circulatory support [Mathison M.et al, 2000 &, Kim K.B. et al, 2001].

breath. That is what we help him do in the operation theater as he is anaesthetised.

improve his preload. But we always try to avoid the Trendelenberg position.

al 2002].

damage in such clinical scenarios.

disposable worth remembering.

revascularization.

Fig. 1. Photo showing the operation table with the head end elevated and tilted to the side of the surgeon.

ended up having inotropes and vasoconstrictors to maintain hemodynamics. Ischemic patients when given either of them, they develop further ischemia and become bad.

What we had re-engineered here, was to increase the heart rate .To attain that, we use intermittent boluses of Injection Atropine (0.6mgs per milliliter), which is only a Chronotropic agent and not an Inotrope. Thus, avoiding unnecessary strain on the myocardium. We aim at a rate above 100 per minute and this keeps the heart briskly contracting and avoiding the usual hemodynamic collapse seen in the early days.

We do not use vasopressors or vasodilators in any of our patients undergoing OPCAB.The only drug the patient would be given intermittently is the Atropine injection. We use Glycerol trinitrate(GTN) in our patients after the distal anastomosis, and that too as an antihypertensive only.

Mueller et al. found no change in the hemodynamics during exposure of the posterior and anterior wall arteries, and only marginal change for the lateral wall artery with a 'no compression' technique [Mueller X.M et al,2002]. It has been suggested that the use of left ventricular apical suction device for cardiac positioning provokes less hemodynamic instability compared with pericardial retraction sutures [Sepic J.et al,2002].

The technique which we have developed is to cut down the pericardium on the right side, down to the inferior vena cava, and to leave the right pleura opened. We routinely open the left pleura to help in the mammary dissection. Hence, in all our patients we have all the three chambers- the mediastinum and both the pleural cavity, remaining in continuity with each other.

Re-Engineering in OPCAB Surgery 187

Fig. 3. Showing the heart totally verticalized by the use of the positioner, and the stabilizer

Performing vascular anastomoses on small arteries on a beating heart can be a daunting and frustrating adventure, and so far, no available method of target vessel stabilization can achieve a steady bloodless field comparable to an arrested heart. This was a major concern with OPCAB. The beating heart with a bloody operating field poses a major challenge to delicate tissue handling, and casts a shadow of uncertainty about the quality of the distal anastomosis. However, with the application of effective target vessel stabilization, and efficient visualization systems the early and mid-term patency of OPCAB has been

The stabilizers we use are the suction stabilizers. The position of the stabilizer is very. important to achieve a very stable anastomotic site to perform a good coronary anastomosis. We have tried all types of suction stabilizers, from the Medtronic -Octopus II, III and the Octopus IV. We are now using the Maquet, which was the previous Guidant – Acrobat

in position around the PDA.

encouraging

**4. Quality of distal anastamosis** 

Fig. 2. Showing the Positioner verticalising the heart and the stabilizer used on the marginal circumflex.

We too routinely use the Positioner for lifting the apex of the heart. The suction pressure used is not more than 150-200 mm of Hg. The positioner is always used in an off apex position, so as to avoid sucking the Left anterior descending (LAD) coronary artery. We use this pressure to avoid excessive damage to the apex. We also watch the suction tube, to see if any blood is being sucked. In such cases , the positioner is removed and repositioned in a different place. In case of grafting of the circumflex and the Posterior descending artery (PDA) this heart is only Verticalized and not tilted to the right side. This lifting of the apex, increases the left and the right ventricular volume. And in case the PDA, is being grafted, then we tilt the head end down, so as to increase the visibility of the PDA. This probably would be the only time when the Trendelenberg position is used. By this time the LAD is already perfused, and this has relieved the ischemia. If the visibility of the circumflex is bad, then the table is dropped down to its maximum and the positioner moved to right a bit. With this maneuver, even the Atrioventricular groove could be visualized.

Fig. 2. Showing the Positioner verticalising the heart and the stabilizer used on the marginal

We too routinely use the Positioner for lifting the apex of the heart. The suction pressure used is not more than 150-200 mm of Hg. The positioner is always used in an off apex position, so as to avoid sucking the Left anterior descending (LAD) coronary artery. We use this pressure to avoid excessive damage to the apex. We also watch the suction tube, to see if any blood is being sucked. In such cases , the positioner is removed and repositioned in a different place. In case of grafting of the circumflex and the Posterior descending artery (PDA) this heart is only Verticalized and not tilted to the right side. This lifting of the apex, increases the left and the right ventricular volume. And in case the PDA, is being grafted, then we tilt the head end down, so as to increase the visibility of the PDA. This probably would be the only time when the Trendelenberg position is used. By this time the LAD is already perfused, and this has relieved the ischemia. If the visibility of the circumflex is bad, then the table is dropped down to its maximum and the positioner moved to right a bit.

With this maneuver, even the Atrioventricular groove could be visualized.

circumflex.

Fig. 3. Showing the heart totally verticalized by the use of the positioner, and the stabilizer in position around the PDA.
