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J Thorac Cardiovasc Surg 2004;128:21-26
© 2004 The American Association for Thoracic Surgery
Editorial |
a Department of Surgery, Division of Cardiothoracic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, Calif, USA
b Option of Bioengineering, California Institute of Technology, Pasadena, Calif, USA
Received for publication November 26, 2003; accepted for publication March 16, 2004.
* Address for reprints: Gerald D. Buckberg, MD, David Geffen School of Medicine at UCLA, Division of Cardiothoracic Surgery, PO Box 951741, 62-258 Center for the Health Sciences, Los Angeles, CA 90095-1741, USA
gbuckberg{at}mednet.ucla.edu
| See related article on page 27.
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Left ventricular aneurysms with a thin wall were commonplace before treatment of acute infarction with reperfusion by either thrombolysis or percutaneous angioplasty. The classic surgical approach to this region was made by collapse of the scarred region, and the procedure on the free wall was described in 1959 by Cooley and colleagues1 and in 1985 was enlarged to the septum by Jatene2 and Dor and associates.3 The report in this issue4 follows the Mickleborough group's earlier presentation in 20005 and refocuses attention on the role of chamber rebuilding in patients with thin-walled ventricles after either anterior or inferior infarctions. There is general avoidance of mitral procedures and exclusion of patients with pulmonary hypertension. The long-term results and hospital mortality were excellent in this subset of patients with congestive heart failure (CHF), especially because 83% of patients were in New York Heart association functional III or IV class. Conventional medical management has been associated with high mortality in this class.
The evaluation for candidacy has become more critical, with magnetic resonance imaging (MRI) recently used to measure end-systolic volume index, directly correlates with prognosis.6 Such vital data help to identify restrictions inherent in visualizing only motion by ejection fraction, as well as defining previous echocardiographic limitations. For example, they look at the distal third of the ventricle, rather than left ventricular end-diastolic diameter. This is useful, because ischemic disease causes nonhomogeneous dilation from anterior infarction beyond the bases of the papillary muscles used for left ventricular end-diastolic diameter calculations. Evaluations of size that use traditional left ventricular end-diastolic diameter values may be misleading in ischemic disease and are more useful for homogeneous global dilatation that follows aortic or mitral valve disorders or nonischemic disease.
Furthermore, use of endocardiectomy in 41% of patients decreased late antiarrhythmic deaths and is a critical finding to support the leadership role for Mickleborough, who joins with Dor7 in making leading contributions to this approach. The absence of sudden cardiac death among the survivors is a powerful indicator of the importance of this finding. Furthermore, the MRI illustrations of the restored elliptical shape are excellent and focus on how restoration alters size and shape when the heart is rebuilt toward a conic form.
The ventricle or the wall?
Although the database reinforces "traditional results," the authors do not appear to recognize that "the field has moved." This has occurred because reperfusion has changed the thin scar to a thickened wall that does not collapse during ventricular venting. Consequently, this article fails to address relevant issues about the septum and thickened nonfunctional muscle that affect the huge CHF population. I specified thin-walled chambers in the title of this editorial because only the thin-walled scar subset was studied. My subtitle "Is This our Patient Population?" reminds us of patients who have reperfusion by percutaneous transluminal angioplasty, thrombolysis, or coronary artery bypass grafting (CABG) and occupy a predominant position in today's CHF cohort.
The database shows a 10-year survival of 61% in a population with limited incidence of sudden death and brings clear focus to bear on the operative decision to deal with the septum only when it is thin. Transplants and recurrence of CHF were considered poor results and will contribute to higher death rate in the interval studied and in the near future. These poor results happened more often in the larger hearts, and we must know which of these patients had septal rebuilding, rather than falling into the larger category (78%) with no septal exclusion. The preoperative and postoperative end-systolic volume indices are now added in a small subset, and these values must be contrasted with those in patients with and without septal exclusion to make a contrast in their own series. Furthermore, this MRI evaluation will allow these data to be compared with the 5-year results reported by Di Donato and Dor,8 in which volume was reported and septal exclusion always was done. I suspect that comparable data will be seen in the cohort with septal exclusion, but higher ventricular volumes will persist when septal retention is done.
Anatomically, left anterior artery occlusion will routinely infarct the septum, yet this structure was approached in only 22% of patients. This limited attention to the damaged region matches their previously mentioned restriction of rebuilding only with thin walls.9 Failure to deal with this critical structure was addressed in my accompanying editorial,10 which called attention to the functional commonality of wall events after coronary occlusion that produces either dyskinesia to akinesia, depending upon use of reperfusion. Both muscles are nonfunctional. Thickness may differ, because reflow causes thickening of bulging ischemic muscle but only salvages the epicardial surface of noncontracting muscle (Figure 1).
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The MRI analysis shows comparable end-systolic volume indices between akinetic and dyskinetic hearts. All measurements were at least 30% lower than those summarized by Dor and coworkers11 when they focused our attention on rebuilding nonfunctional segments, whether they bulged or not. The time frames between infarction and operation are comparable in this series, whereas Dor and coworkers’11 previous analysis showed that akinetic hearts were larger and underwent restoration 1 year later than dyskinetic hearts. Their summary presumes the remote muscle continued to stretch and secondarily impaired function of the viable compensating region. This process is well defined in Figure 2, which shows how a dyskinetic ventricle became akinetic and had advanced failure develop by subsequent stretch.
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The basic surgical issue is how our interventions can return global contraction and improve cardiac output when addressing regions that lose this capacity after infarction. Should the noncontractile region be left in place or excluded? This decision process needs an approach that both understands viability and can restore global contraction. These issues are different, and the perfect example is the viable muscle of patients with globally dilated muscle after valvular heart disease, with 10-year mortality of 70% when valve replacement is done in patients with 40% or lower ejection fraction.12 Sudden cardiac death and progressive heart failure are causal events, matching the responsible factors in ischemic disease, so ventricular volume and shape are critical factors.
MRI contribution
Our newer diagnostic tools are helpful in the ischemic population, and some of them were used in this study. The distinction between viable muscle, despite its thickness, can be made by gadolinium scan during MRI analysis13 rather than by measuring tissue distance by needle pointing to size transmural scar. An example is shown in Figures 3 and 4, where thick wall muscle is nonfunctional and displays late enhancement, indicating nonviability of a significant part of the wall. Although the report by Mickleborough and associates4 is supplemented by recent MRI volume analysis, these newer viability tests were not included.
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The concept of akinesia and dyskinesia must also be considered, because both regions are asynergic (do not function) and cause stretch of remote muscle to compensate to ensure cardiac function. In the past, dyskinesia followed acute infarction without reperfusion. The compensating remote muscle then gradually became akinetic as part of the global process of progressive distension. Availability of reperfusion by either thrombolysis or percutaneous transluminal angioplasty immediately produces akinesia by making the thin dyskinetic nonfunctioning segment thicken to shrink ventricular volume.6 Consequently, the bulging of dyskinesia is lost early, and the akinetic reperfused segment within a smaller ventricular volume allows the remote muscle to remodel more slowly than does a nonreperfused dyskinetic region. The surgical objective is to exclude the nonfunctional region. Decision-making in the operating room is linked to understanding this process and is not related to either dyskinesia or akinesia of the nonfunctioning region to be excluded.
Surgical decisions
The traditional approach to ventriculotomy has used the concept of dimpling from transmural scar, and ventricular incision is avoided if there is no collapse during venting. This shrinking happens with thin-walled scar but is absent when the thick-walled region is akinetic. If the deciding factor for entry in this series was free wall collapse, then patients without free wall collapse were excluded from a restoration procedure. Mickleborough and associates4 took a similar approach to septal rebuilding but used a needle rather than vision to determine its thickness, because collapse cannot be observed. This wall thickness restriction is completely different from criteria for restoration that are used in reperfused infarcted muscle that remains thick14,15; there is no reliance on either dimension or dimpling during venting, because the restoration decision has been made preoperatively by evidence of nonfunction on ventriculography or echocardiography.
Mickleborough and associates' use of the beating heart during the restoration procedure has distinct advantages if the procedure is done in thick-walled hearts that are akinetic.4 The reperfusion process per se avoids transmural scarring and often causes trabecular scarring in a nonhomogeneous way. Consequently, visual demarcation between whitened scar and pink interceding muscle is difficult, and distinction of the junction between the contracting and damaged region by vision may be impossible if the heart is arrested by cardioplegia. Conversely, palpation of the beating heart makes this differentiation simple to accomplish, as shown in the accompanying image (Figure 5).
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The infrastructure of ischemic CHF is coronary artery obstruction, and part of management is to do CABG to reduce recurrent angina. However, despite successful revascularization that correctly approaches viability, the 10-year mortality is 60% to 80% from the consequences of CHF after CABG alone in ischemic patients with left ventricular dysfunction whose preoperative ejection fraction is less than 35% or 25%, and this occurs despite absence of recurrent angina16.
The concept of hibernation has been raised. This concept is related to viability rather than thickness. Was MRI evaluation of the thick-walled muscle used to check for viability, or was the absence of visual collapse during venting the only criteria applied to apply revascularization rather than exclusion? Furthermore, the limitation of viability to prognosis in the dilated heart has been shown previously by the study of Vanoverschelde and colleagues17 in which when left ventricular end-systolic volume index was greater than 75 mL/m2, thick-walled viable muscles did not recover function after revascularization alone. This report of CABG alone brings attention to the surgical role of restoring global contractility by rebuilding, rather than only treating viability by reperfusion in thick, dilated hearts. This observation may be a preview of future events, in which restoration may become a consideration in dilated hearts with multiple mini-infarctions that subsequently present in CHF without a focal event. Such dilation may develop more commonly after multiple angioplasties with distal embolization.
If the concept of a thick wall became a vital reason to avoid ventricular exclusion, this then would necessitate the operative rather than preoperative distinction of how patients with CHF were treated by either CABG or CABG and restoration. Consequently, there must be a series of patients in Toronto with extensive infarctions who did not have rebuilding, as well as those with a thick septum that was not treated. The late follow-up of both cohorts is essential to allow subsequent single-institution comparisons. This may be possible because the recent series included a cohort of patients who underwent MRI testing to determine the thickness of the anterior wall as well as the septum.
The future population
This report4 provides an excellent follow-up for these narrowly selected patients with thin-walled aneurysm but not the larger CHF population. The reader must know what happened to the broader scale of patients with a thicker septum that failed to beat after infarct reperfusion. This subset is dealt with in almost 100% of patients undergoing restoration9 where septal thinness is not a consideration for septal exclusion in dilated hearts after infarction.
Consequently, although this article is useful for a discrete cohort, the described approach is highly restricted and will fail to deal with the commonplace disease if applied only according to the selection criteria of a focal area of ventricular thinning. The selection bias becomes misleading, because a broader view of this process will expand the use of a valid operation in more than 1,500,000 ischemic patients with class III or IV disease. More importantly, it places into the "contraindicated" category a large population who can safely undergo procedures.11,15,18
Aside from considerations about thickness, this is an important article that adds to the many contributions from Mickleborough on ventricular reconstruction. Simultaneously, this article brings attention to recent advances in our understanding of how reperfusion makes akinesia replace dyskinesia in the failing heart. The tradition of dealing only with thin-walled scar must change, to foster our recognition and subsequent management of nonfunctional muscle. Attention only to the thin-walled heart may become a barrier to our progress.
We must move forward from traditional consideration of thickness alone to exclude thick and damaged nonfunctional regions to test whether restoration of geometry will effect cardiac function. The alternate process of retention of a damaged thickened segment may allow ongoing stretching of remote muscle. The consequence may retain the current limitation imposed by revascularization alone in the natural history of ischemic dilated cardiomyopathy.
References
This article has been cited by other articles:
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  N. D. Patel, J. A. Williams, L. U. Nwakanma, E. S. Weiss, and J. V. Conte Impact of Lateral Wall Myocardial Infarction on Outcomes After Surgical Ventricular Restoration Ann. Thorac. Surg., June 1, 2007; 83(6): 2017 - 2028. [Abstract] [Full Text] [PDF]
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 S. A.F. Tulner, P. Steendijk, R. J.M. Klautz, J. J. Bax, M. J. Schalij, E. E. van der Wall, and R. A.E. Dion Surgical ventricular restoration in patients with ischemic dilated cardiomyopathy: Evaluation of systolic and diastolic ventricular function, wall stress, dyssynchrony, and mechanical efficiency by pressure-volume loops. J. Thorac. Cardiovasc. Surg., September 1, 2006; 132(3): 610 - 620. [Abstract] [Full Text] [PDF]
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 M. G. Crespo-Leiro and J. J. Cuenca-Castillo Surgical treatment of heart failure: heart transplantation and ventricular restoration surgery Eur. Heart J. Suppl., September 1, 2006; 8(suppl_E): E39 - E42. [Abstract] [Full Text] [PDF]
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