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Eur J Cardiothorac Surg 2004;26:S42-S47
© 2004 Elsevier Science NL

Review

Surgical left ventricle reconstruction, pathophysiologic insights, results and expectation from the STICH trial

Department of Cardiac Surgery, Istituto Policlinico San Donato, Milano, Italy

^* Corresponding author. Address: Department of Cardiac Surgery, Istituto Policlinico San Donato, Via Morandi 30, 20097 San Donato Milanese, Milano, Italy. Tel.: +39 02 5277 4521; fax: +39 02 5277 4327. (Email: menicanti{at}libero.it).

	Abstract

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

 
Post-infarction ischemic cardiomyopathy is the most frequent cause of clinical heart failure in the western society. Despite aggressive early revascularization, myocardial infarction leaves shape and function abnormalities in a consistent number of patients with increased risk of death and ischemic events. Alternative treatment strategies are therefore advisable in these high-risk patients. Surgical ventricular restoration (SVR) is a safe and effective surgical option for post-infarction ischemic cardiomyopathy resulting in improvement of pump function, functional class and survival. Observational data now need to be confirmed by randomized data and the multicenter international randomized surgical treatment of ischemic heart failure (STICH) trial will definitely assess if SVR adds benefit to coronary bypass alone in patients with left ventricular dysfunction and dilated ventricle.

Key Words: Myocardial infarction • Left ventricular remodeling • Left ventricular shape • Surgical ventricular reconstruction

	1. Introduction

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

 
Coronary artery disease (CAD) is the most frequent cause of heart failure (HF) in the western societies and HF can be the only mode of CAD presentation associated with increasing HF incidence and higher mortality.

The increasing number of patients suffering from HF largely derives from the enhancement in survival due to the improved therapies for other manifestation of CAD, especially acute myocardial infarction. However, survival is often accompanied by some degree of myocardial damage which progressively causes LV remodeling and initiates a vicious circle that leads to clinical HF.

Post-infarction left ventricle remodeling is in fact a complex phenomenon which involves molecular, neurohormonal, genetic factors that ultimately leads to chamber dilatation, shape abnormalities and ventricular dysfunction. Studies have demonstrated that early reperfusion salvages subepicardial layer but may fail to salvage the subendocardium [1,2].

The incidence of the classic thin-walled left ventricle with a clear demarcated zone between the contractile muscle and the diseased tissue is therefore declining due to the aggressive, successful initial management of acute myocardial infarction which can interrupt the process before it reaches the trans-mural stage.

There are few reports dealing with the function of the left ventricle after a successful early revascularization. In an old publication Goudron (1992) stated that a dilatation of the LV is present in 20% of infarcted patients treated with conventional therapy [3]. In a recent paper Bolognese observed that in 30% of patients successfully treated with primary PTCA, left ventricle dilatation (defined as >20% end diastolic volume increase) is present 6 months after the procedure. Cardiac death and combined events rate were significantly higher among patients than among those without LV dilatation [4]. In a series of 79 patients with successfully reperfused anterior MI (primary PTCA within 5 h from the beginning of symptoms) we observed that 6 months after PTCA, despite persistence of LAD patency, 30% of patients showed LV shape/function abnormalities with ventricular dilatation and a clear picture of dilated ischemic cardiomyopathy in 10% and a picture of classic akinetic or dyskinetic aneurysm in 20% (unpublished observations). (Fig. 1 ) Myocardial regional or global dysfunction can persist after successful early reperfusion leading to adverse remodeling and clinical HF in a consistent number of patients. Treating the culprit lesion of acute MI may not therefore be sufficient to guarantee the cure of that patient and it is necessary to check for the size and the function of the ventricle to assess prognosis. Intensive medical management reduces symptoms and improves survival but patients in high functional class (NYHA III–IV) still have a poor 3 years prognosis despite improved medical therapy, with very high social end economical impact.

View larger version (30K): [in this window] [in a new window]   Fig. 1. Wall motion and curvature analysis. Shadow areas represent the normal mean values±SD. Curvature values are expressed as the reciprocal of the radius (1/r); on the abscissa the five regions identified by the centerline method. AB, antero-basal; AL, antero-lateral; AP, apical; DI, diaphragmatic; PB, postero-basal Right: B% indicates the extent of systolic bulging in respect to LV perimeter A% indicates the extent of wall motion abnormalities (differing at least 2 SD from normal) in respect to LV perimeter.

	2. Pathophysiology of post-infarction LV remodeling

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

The classic aneurysm is characterized by a dyskinetic portion of the ventricle demarcated by a neck which separates scarred from sound tissue. Nowadays, this type of lesion is no longer or very rarely seen after MI because of the early reperfusion which often leaves the scar only at the subendocardium.

Surgical ventricular restoration (SVR) is considered a surgical alternative option for the treatment of ischemic heart disease when MI leaves regional asynergy which determines dilatation and dysfunction of the LV. Observational results have shown that the technique is safe and effective in improving LV pump function, functional status and survival [6–8]. The term SVR is often considered synonym of aneurysmectomy, creating some confusion in interpreting the results and patients selection in that aneurysmectomy approaches the classic aneurysm (i.e. dyskinetic lesions) while SVR applies also to akinetic lesions.

Di Donato demonstrated that surgical outcome in a large series of patients treated with SVR is linked to the extent of asynergy rather than to the type (akinetic vs dyskinetic) [9].

This observation has helped to advance the belief that remodeling operation may be applied as surgical treatment in post-infarction dilated cardiomyopathy.

	3. Drivers for change

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

 
3.1 Pathophysiologic insight of surgical ventricle restoration
The success of this surgical procedure is based on several aspects:

(a) Complete revascularization: grafting the LAD is important despite this coronary feeding the scarred anterior wall. In fact, the upper part of the septum, which is almost always functioning, needs to be well perfused to improve ejection.

(b) Diminishing ventricular volume: the volume should be reduced in its septal, anterior and inferior components; in this way left ventricular wall stress will be reduced and the portion that it is not involved in the infarcted area (remote zone) will improve its mechanical efficiency, consequently. Dor procedure completely achieves this goal and this is the difference with other techniques all based on volumetric reduction. The classical linear resection in fact, doesn't correct the septal component; Batista procedure resects the lateral portion which can often be the only functioning area in such patients.

(c) If volume reduction is excessive, the probability of determining diastolic dysfunction is high, but now with the introduction of sizing devices this problem is minimized.

(d) Restore the shape: this is an important issue because the physiological elliptical shape of the LV is important to optimize mechanical efficiency. It was demonstrated that if the LV is amputated at the apical level diastolic dysfunction worsens. Moreover, a residual spherical cavity brings an incorrect position of the papillary muscles which may result in post-operative mitral regurgitation.

As already mentioned, these data arise from observational study and this operation is now sufficiently mature to justify a randomized trial to evaluate whether appropriately performed SVR actually adds value to CABG in patients with regional dysfunction.

	4. Observational results obtained with SVR

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

 
The larger experience with SVR is from the Cardiothoracique Center of Monaco and from our Center with more than 1000 patients who have been treated in each Center. Another important contribution is given by the RESTORE team, a group of 10 international Centers performing the procedure since 1998 [10]. Concordant results show the improvement in LV function parameters (Table 1 ), in NYHA functional class (Fig. 2 ) and in survival (Fig. 3 ). Patients with advanced HF have a poor prognosis, especially if secondary mitral regurgitation is present. Grigioni reported a 5-year survival rate from 38 to 29% in patients with ischemic mitral regurgitation according to the ERO< or >20 [11]. Our data show a survival rate of 62% at 5 years in a high risk population treated with SVR and mitral repair [12].

View larger version (29K): [in this window] [in a new window]   Fig. 2. Kaplan Meyer survival curve according to pre-operative NYHA class in 365 patients. Operative mortality is included. Survival is excellent in classes I, II and III. Overall, class IV patients have a 5-year survival rate >60%.

View larger version (12K): [in this window] [in a new window]   Fig. 3. With permission from the RESTORE group. Distribution of NYHA functional class before and after SVR.

	5. Options for progress

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

Non-randomized trials compared long-tem results of medical and surgical treatment in patients with ischemic ventricular dysfunction and HF. A meta-analysis by Yusuf combined individual patient data from the CASS trial with those enrolled in the six other early-randomized trials [13]. Only 191 (7.2%) of the 2649 patients had an EF<40% and only 106 (4.0%) of these patients, who were primarily symptomatic for angina, had HF symptoms. A literature search of 326 published reports on results of CABG in patients with HF or LV dysfunction identified three well-designed cohort studies. Mortality benefit of CABG over medical therapy was 10 and 20 lives per 100 in 3 years in two studies and 29 lives per 100 patients at 5 years in the third study. Despite these results very few of these patients receive a surgical treatment in clinical practice. In the Duke Databank for Cardiovascular Diseases only 22% of similar patients are operated on, 72% are managed with medical therapy and 7% receive a PCI.

5.2 The STICH trial
These uncertainties and the need for evidence-based results led to the multicenter international randomized trial, surgical treatment for ischemic heart failure (STICH) that addresses two specific primary hypotheses in patients with chronic coronary artery disease and clinical heart failure and/or left ventricular dysfunction:

(a) The revascularization hypothesis states that coronary artery bypass grafting (CABG) with intensive medical therapy (MED) improves long-term survival compared to MED alone.

(b) The reconstruction hypothesis states that patients with anterior LV dysfunction, surgical ventricular restoration (SVR) to a more normal LV size improves survival free of subsequent hospitalization for cardiac cause in comparison to CABG alone.

Important secondary endpoints include morbidity, economics, and quality of life. Core laboratories for cardiac magnetic resonance (CMR), echocardiography (ECHO), neurohormonal/cytokine/genetic (NCG), and radionuclide (RN) studies will insure consistent testing practices and standardization of data necessary to identify eligible patients and to address specific questions related to the primary hypotheses.

Over a period of 3 years, 2800 patients with LV dysfunction or HF, LV ejection fraction (EF) <35 and CAD amenable to CABG will be enrolled. These patients will be characterized by angina intensity or presence of left main coronary stenosis as appropriate for only surgical therapy. All patients will be evaluated further for appropriateness of SVR indicated by an enlargement of LV in the antero septal portion with an akinesia >35% of the anterior wall.

The patients will be randomized in three strata A, B, and C (Fig. 4 ).

View larger version (29K): [in this window] [in a new window]   Fig. 4. The design of the STICH trial enrollment is shown.

In stratum B patients eligible for SVR are randomized but due to the absence of left main stenosis and of important angina, surgery is not an evidence-based choice.

Two-hundred patients will be treated with MED, 200 with CABG, 200 with SVR and CABG.

In stratum C patients eligible for SVR presenting with refractory angina and/or left main disease are randomized. Three-hundred will be treated with CABG and 300 patients will be treated with CABG plus SVR.

Overall, the primary hypothesis MED versus CABG will consider 1000 patients with CABG, 1000 patients with MED, and SVR versus CABG will consider 500 patients with CABG plus SVR and 500 with CABG alone.

STICH is the most important randomized medical-surgical trial after CASS in the treatment of CAD.

If the two primary hypotheses will be demonstrated and surgical therapy will be proven to be superior to medical therapy, early aggressive evaluation of CAD, as a potentially correctable etiology of new onset HF, would be the preferred strategy. This could actually, tremendously change the treatment of ischemic heart disease.

	6. Key issues

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

 
The prevalence of post-myocardial infarction heart failure is increasing in western society, especially in the elderly.

Early reperfusion after MI either with thrombolysis or primary PTCA leaves shape and function abnormalities in a consistent number of patients.

Coronary bypass surgery improves regional function only in viable myocardium.

SVR associated with CABG has the potential of decreasing wall stress and improve regional function, consequently.

LV shape is an important determinant of regional and global ventricular function.

	Appendix

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

 
Conference discussion

Dr T. Gardner (Philadelphia, PA, USA): As you may know, the STICH trial is in some jeopardy because of poor patient enrollment, and it is ironic, especially with your final conclusion, that the cardiologists, at least the US cardiologists, seem very reluctant to randomize these patients.

Dr Menicanti : Absolutely. The problem with the STICH trial is in hypothesis 1. The enrollment in the hypothesis 2 (patients that need surgery), randomization between CABG and CABG plus restoration, will be completed in a very short period. The cardiologists are reluctant to randomise patients presenting distal coronary stenonis even there is not angina. The normal attitude in this historical period is to revascularise patient in the presence of stenonsis, but doesn't not exists evidence that this treatment is superior to another one. So this is the reason why the STICH trial is going slowly. In Europe it has gone better than in the United States, because probably in Europe there is a different approach to the patients. The discussion on the type of treatment is wider in Europe than USA. In USA, the cardiologists decide; in Europe, sometimes it is not true.

So as a surgeon, I would like to really invite the people that are here to participate in this study, because it can give us great knowledge and great power. So it is true we have some problems, but we are pushing.

I suggest to read the paper published by Bolognese, because this paper, written by a cardiologist, gives us a good idea about what is angioplasty in acute myocardial infarction. I think that sometimes we need more information about the cardiologist's activity.

For example, this morning we spoke about drug-eluting stents, if you read the sirolimus study, that is one of the great studies for the drug-eluting stents, they said that there is recurrence of stenosis in a vessel bigger than 1.5 mm with focal stenosis in 8% of cases, in the control group the restenosis was present in 35% of the patients. That means that before the introduction of the drug eluting stents the restenosis of a focal lesion of a large vessel greater than 1.5 mm was present in 35% of treated population.

So I think an association like this should get public this data, because or there is a problem with this study or there was a big problem before this study.

Dr L. Bockeria (Moscow, Russia): I would like to pay attention to key issues you mentioned. There is the last one, ‘left ventricle shape is an important determinant of regional and global ventricular function’. This is a point which is in fact never discussed by cardiologists, because they cannot do what surgeons do. And I would like to ask you how often you can predict the shape you like to have in this patient?

Dr Menicanti : That is a good question. When we use now this type of a sizer that keeps the normal relationship between longitudinal and transverse diameter, we know quite good how the final shape will be, because in this way we are sure that we respect the longitudinal diameter and we avoid the amputation of the left ventricle.

For example, if I have a case like that with the dilatation that starts from this point and arrives to that point, so we have a transitional zone that is between A and B and the transitional zone is parallel to the mitral valve, I have two options. I can put together A and B, so it will be an elliptical shape but too small a cavity, and that is bad. The other possibility is I put a patch between A and B. At this moment I will have good volume but my shape will be a sphere. So if I have a sizer inside that tells me how long must be the longitudinal diameter, I can decide where I put my new apex. Surely in a case like that there is a gap between this point and that point, and this gap can be overcome with a small plication. It is enough, 1, 1-1/2 cm, just to lift up a small portion of the scar tissue towards the new apex. In this way we can have as a final result a good shape.

And if you look at this slide, it is a patient with occlusion of the left anterior descending, as you can see, and if you look at the shape of the ventricle that we had before the procedure, we will see that the transitional zone is here and that it is parallel to the mitral valve. So if you follow this zone, surely we will amputate the ventricle. But if I know where I have to put my new apex, I can plicate this portion just to lift up the new apex. In effect, if you look after the procedure, you see that we have a relatively good shape, and here, there is a small plication towards the new apex. So at the end we know which kind of shape we will leave.

Dr Bockeria : We know that the previous approach in such a case coming from Vincent Dor was to put a patch just on the border of the alive myocardium and fibrotic. Is it the same approach nowadays?

Dr Menicanti : It changed a little, because the idea to use a shape and to use a volume guide was published by Vincent Dor. The only thing that changed with this type of shaper is the shaper has a longitudinal diameter that is a physiological one. So if you respect the longitudinal diameter, you leave a small amount of scar sometimes on the inferior wall, but this small amount can be plicated, and so it changes the shape of the ventricle.

And in the data that we have when we used the shaper, we can see that when we don't use the shaper, the sphericity intext, the relationship between longitudinal and transverse diameters, it is approaching one, it is approaching the sphere. If you use this shaper, we remain in the physiological range, that is, 0.6, 0.5.

Dr J. Vaage (Oslo, Norway): I can observe that we have left the future and are now discussing surgical techniques. If we return to the future, don't you think that if the future is 10 years or more, we will actually treat this condition with cell transplantation and gene therapy, and maybe also tissue engineering that we will hear about in the next session?

Dr Menicanti : Surely, gene therapy is one option. The data that we have published by Menasche and others are not so nice, and we know that to put stem cells in scar tissue can really be a problem and if they have a lot of arrhythmias after that.

This is the old procedure that was published in '84, but surely it has a future, because, as you can see, the indication is large and large. It is not perfect, because every surgery can do better. Surely if they will arrive to substitute the scar with a beating heart, that is perfect. The future is also this afternoon and for a patient that need to be operated this afternoon probably to wait some years it is not possible. I will remind you that there are some companies that are thinking about a contractile patch. So this is another option that probably will be better.

Dr Bockeria : But you cannot get the results from stem cell therapy if you don't bring the shape of the heart to normal. That is very well known and widely discussed, and now there are no two opinions about that. That is why I guess until you don't bring the shape to the normal physiological shape, you cannot get results, even using stem cells.

Dr G. Buckberg (Los Angeles, CA, USA): I think another answer to Dr Bockeria's question must center on ventricular geometry. For example, consider patients with dilated valvular cardiomyopathy, where there is no region with ischemia. The underlying form is a spherical or circular ventricle, rather than the normal elliptical contour. This shape change is the common theme of heart failure, and prognosis can be adverse despite the absence dead cells in patients with dilated valvular cardiomyopathy with <40% ejection fraction. Even if we successfully replace the valve without hospital mortality, there is a 70% mortality in 10 years. The underlying reason is that we only looked at the valve, yet left the abnormal ventricular form in place.

Lorenzo (Lorenzo Menicanti), you have talked predominantly about ischemic disease, but my question relates to where the dilated spherical geometry fits into the spectrum of patients with non-ischemic disease from chronic valvular insufficiency or myogenic origin of non-valvular disease. Here, distribution of damage is non-uniform, and Suma used the concept of site selection to exclude damaged regions in patients with non-ischemic disease, just as we exclude the find out the bad area in ischemic patients, and reports good late survival.

I think there is an enormous future in the broad spectrum of dilated cardiomyopathy patients that need ventricular restoration. We must learn to think of ventricular ‘form’ in a three-dimensional fashion, and then learn how to change ‘form’, just like you have done for ischemic disease of the inferior wall.

Dr Menicanti : We speak about ischemia because of our experience, and it is proven that it works in ischemia. For other pathology, as cardiomyopathy, personally I have no experience. The only surgeon that has experience is Suma, and he started with really high mortality in the beginning, with 50% mortality. Now he is reducing mortality to around 30%. So it is a sort of surgery that seems promising but in my opinion is still in testing time.

Dr R. Dion (Leiden, Netherlands): Just a short comment to support what Lorenzo has explained to us. We started three years ago in Leiden being very aggressive to resect not only aneurysms but also large akinesia's, and we also are taking a lot of care to get an elliptic shape.

This strategy and its very promising results led to an impressive increase in referral from 3 to 5 cases a year when we started in January 2000—as this was the case also in Brussels at my former institution—to more than 20 (and still increasing) at the present time. Ventricular restoration certainly represents a large reservoir of patients for the interested surgeons, provided that the strategy and indications rest on a multidisciplinary approach.

My second comment is about the price of the sizer that you use (the mannequin of Chase): it should be stressed that it costs 1400 Euros per (disposable) unit!

Dr Menicanti : I spoke about the shaper. I didn't cite Chase Medical. There are other shapers in the market. Some are the same concept, to maintain the longitudinal diameter relationship. Others are different. Surely it costs, but turns the procedure easier and faster, avoiding some possible error, and it can be resterilized.

Dr Dion : Well, we use a huge condom which is less spherical than a balloon, and certainly much less expensive than your sizer, even if not resterilizable.

	Footnotes

 
Presented at the EACTS Symposium for the Future of Cardiac Surgery, Frankfurt, Germany, July 1–2, 2004.

	References

Top Abstract 1. Introduction 2. Pathophysiology of post... 3. Drivers for change 4. Observational results... 5. Options for progress 6. Key issues Appendix References

 

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