CABG (see Table 9). This real-world experience of a huge number of patients arguably provides a much more reliable and realistic guide for pa- tient treatment than the super-selected small sub- set of patients randomized in the AWESOME trial. An analysis of the Canadian APPROACH database (Alberta Provincial Project for Outcomes Assessment in Coronary Heart Dis- ease) [57] that began in 1995 and followed patients for up to 7 years included 4228 patients who had heart failure who underwent a cardiac catheteriza- tion: 2538 patients underwent revascularization by CABG or PCI and 1690 patients were treated with medical management alone. No direct comparison between CABG and PCI was made. Risk-adjusted survival curves for CABG seem superior to PCI (adjusted hazard ratio for CABG 0.44, 95% CI 0.38–0.52 versus 0.58 for PCI, 95% CI 0.49–0.69, both calculated against medical management group) (Fig. 12). Surgical revascularization for patients who have low LVEF remains a challenging procedure and in general should be attempted in centers able and willing to provide mechanical assist or heart transplant services. The oft-cited operative mor- tality of 5% to 8% is the mortality of centers with significant experience in handling such patients. Summary From the analysis of clinical series presented above we learn that selected patients who have low LVEF and CAD clearly benefit from coronary revascularization with CABG, and that CABG offers a 5-year survival of 60% to 70% and a life extension of close to a year at 5 years’ follow-up compared with a strategy of initial medical man- agement, with an average perioperative mortality between 5% to8% in experienced hands (twice that of patients who have normal ejection fraction). Clinical improvement should be expected in most patients who undergo CABG. This is important for patients who have a limited life span thatthey could spend with a good functional status rather than being hospitalized for multiple repeat PCIs or symptomatic deterioration. Clinical variables, the use of HAVOC score, and myocardial viability testing are tools that can help refine patient selection. The weight the clinical information available suggests that re- vascularization by CABG seems to be superior to PCI in most patients who have low ejection fraction, particularly in patients who have low LVEF and symptoms of angina. There are situa- tions, however, in which PCI may be helpful, such as in patients who have low ejection fraction and one or more previous cardiac operations, or in those whose severe noncardiac comorbidities preclude major surgery. References [1] Bourassa MG, Gurne O, Bangdiwala SI, et al. Nat- ural history and patterns of current practice in heart failure. The studies of left ventricular dysfunction (SOLVD) investigators. J Am Coll Cardiol 1993; 4(Suppl A):14A–9A. [2] Anonymous (The CONSENSUS trial Study group). Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987;316: 1429–35. [3] Anonymous (The SOLVD Investigators). Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991;325:293–302. [4] Packer M, Bristow MR, Cphn JN, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. N Engl J Med 1996;334: 1349–55. [5] Anonymous (MERIT-HF Study Group). Effect of metoprolol CR/XL in chronic heart failure: meto- prolol CR/XL randomized intervention trial in congestive heart failure (MERIT-HF). Lancet 1999;353:2001–7. [6] Pitt B, Zannad F, Remme WJ, et al. The effect of spi- ronolactone on morbidity and mortality in patients with severe heart failure. Randomized aldactone evaluation study investigators. N Engl J Med 1999; 341:709–17. [7] Miller WL, Tointon SK, Hodge DO, et al. Long- term outcome and the use of revascularization in patients with heart failure, suspected ischemic heart disease, and large reversible myocardial perfusion defects. Am Heart J 2002;143:904–9. [8] Halkin A, Singh M, Nikolsky E, et al. Prediction of mortality after primary percutaneous coronary intervention for acute myocardial infarction the CADILLAC risk score. J Am Coll Cardiol 2005; 45:1397–405. [9] Eagle KA, Guyton RA, The American College of Cardiology/American Heart Association Task Force on ACC/AHA PRACTICE GUIDELINES (Committee to Update the 1999 Guidelines for Cor- onary Artery Bypass Graft Surgery). ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association task force on practice guidelines developed in collaboration with the American association for thoracic surgery 225 REVASCULARIZATION FOR HF: CORONARY BYPASS OR PCI? Revascularization in Heart Failure: The Role of Percutaneous Coronary Intervention Ajay J. Kirtane, MD, SM a,b , Jeffrey W. Moses, MD a, * a Columbia University Medical Center, New York, NY, USA b Cardiovascular Research Foundation, New York, NY, USA Ischemic heart disease is the leading cause of heart failure in North America, accounting for approximately two thirds of heart failure cases [1]. Patients who have ischemic heart failure suffer from higher rates of ischemic events, arrhythmic events, and increased mortality compared with patients who have normal ventricular function. Although there are inadequate clinical trial data in this patient population, coronary revasculariza- tion, either by way of percutaneous coronary inter- vention (PCI) or coronary artery bypass grafting (CABG), has the potential to provide relief of symptoms, improve ventricular performance, and possibly improve mortality in patients who have potentially revascularizable and viable myocar- dium [2–4]. Although the performance of coronary revascularization in patients who have depressed ventricular function is associated with a greater overall risk for adverse periprocedural events [5– 7] compared with similar patients who have nor- mal ventricular function, performance of PCI or CABG in this particular subset of patients may also be associated with the greatest absolute bene- fit afforded through revascularization [6,8]. Criteria for revascularization in heart failure patients For a patient with heart failure to be consid- ered a suitable candidate to truly benefit from coronary revascularization, ischemic heart disease should be at least a significant cause of the patient’s depressed ventricular function and clin- ical heart failure. Although this statement may seem trite, its importance cannot be overstated. Because coronary artery disease is so common, patients who have cardiomyopathy of nonische- mic origin frequently have coexistent and often incidental coronary artery disease. Such patients may derive some benefit from coronary revascu- larization, but the risks of PCI and CABG, including periprocedural adverse events and the requirement for long-term antiplatelet therapies, are not insignificant. The benefit of revasculariza- tion in such patients is not likely to be as great as for a patient who has cardiomyopathy wholly caused by ischemic coronary artery disease. Several factors must be present for a patient who has ischemic cardiomyopathy to be consid- ered a suitable candidate for improvement through revascularization. Patient-related factors include a reasonable life expectancy from other coexistent disease states and a relative paucity of other comorbidities (eg, chronic kidney disease, cerebrovascular disease, pulmonary disease, and so forth), particularly for patients being consid- ered for CABG. In general, patients who are good revascularization candidates have a significant amount of demonstrably ischemic or hibernating (ie, viable) myocardium, or anginal symptoms [2,9,10]. Finally, the ischemic or hibernating territory should be amenable to revascularization either through PCI or CABG. For PCI, this im- plies lesions that can be treated with a percutane- ous approach with the overall goal of maximal revascularization of ischemic or hibernating terri- tories. In the case of CABG, this generally implies the presence of distal vasculature suitable for * Corresponding author. Center for Interventional Vascular Therapy, Columbia University Medical Center and the Cardiovascular Research Foundation, New York, NY 10032. E-mail address: jmoses@crf.org (J.W. Moses). 1551-7136/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.hfc.2007.05.003 heartfailure.theclinics.com Heart Failure Clin 3 (2007) 229–235 Left Ventricular Restoration: How Important is the Surgical Treatment of Ischemic Heart Failure Trial? Lorenzo Menicanti, MD a, * , Marisa Di Donato, MD b a San Donato Hospital, San Donato Milanese, Milano, Italy b University of Florence, Firenze, Italy Chronic ischemic heart failure (CHF) is one of the major health care issues in the western world partly because of an aging population and more effective treatment of acute myocardial infarction [1,2]. Intensive medical management reduces symp- toms and improves survival in CHF but patients in high functional classes (NYHA III-IV) still have a poor 3-year prognosis despite improved medical therapy, with high social and economic impact [3]. The increase in left ventricular (LV) volume following myocardial infarction (MI) is a compo- nent of the remodeling process characterized by LV volume increase and geometry abnormalities with frequently associated mitral regurgitation that leads to heart failure (HF) progression; this progression is independent of the neurohormonal activation, according to the biomechanical model of HF recently introduced by Mann and Bristow [4]. The concept of a biomechanical model of HF reinforces the need for therapies able to reduce LV volumes and restore geometry; the model also em- phasizes the need for measuring LV volumes and geometric parameters and the importance of as- sessing the presence and the degree of mitral re- gurgitation in patients who have ischemic dilated cardiomyopathy and cardiac dysfunction. Left ventricular shape and function abnormalities following myocardial infarction A strict relationship exists between the shape of the LV and its function. The ellipsoid is the geometric form that most resembles the shape of the normal ventricle. It derives from the archi- tecture of the anatomic distribution of cardiac muscle fibers. The double spiral that constitutes the three-dimensional (3-D) architecture of the heart permits a shortening of 15% of the fibers to give an ejection fraction of 60% and the different distribution of the fibers within the wall from the epicardium to the endocardium accounts for the twisting effect of the apex that optimizes the ejection of blood into the aortic vessel. The elliptic shape enhances blood flow at the inflow and outflow tract. When disease alters the shape of the ventricle, the equilibrium of forces and of spatial orientation of the fibers in the LV is altered and loses its optimal function. The extracellular matrix (cardiac interstitium and collagen) markedly contributes to connect the myocytes in a complex array of fibers forming the 3-D architecture of the wall and coordinating the delivery of forces generated by myocytes. These forces are important determinants of diastolic and systolic stiffness and serve to resist deformation, maintain shape and wall thickness, and prevent ventricular bulging and rupture [5]. Shape changes after MI (especially if anterior) mainly consist of a reduction of curvature radius (the reciprocal of internal radius) at the apical level that creates a high local tension. The increase in tension plays a key role in activating complex neurohormonal mechanisms, including an in- crease in angiotensin II, collagen deposition, and degradation through metalloproteinase-1 and -2 activation. This activation may induce apoptosis launching the complex process called remodeling, which characterizes ischemic cardiomyopathy [5–8]. The increase in chamber volume * Corresponding author. Department of Cardiac Sur- gery, San Donato Hospital, Via Morandi 30, 20097 San Donato Milanese, Milano, Italy. E-mail address: menicanti@libero.it (L. Menicanti). 1551-7136/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.hfc.2007.04.009 heartfailure.theclinics.com Heart Failure Clin 3 (2007) 237–243 . the archi- tecture of the anatomic distribution of cardiac muscle fibers. The double spiral that constitutes the three-dimensional (3-D) architecture of the heart permits a shortening of 15% of. the myocytes in a complex array of fibers forming the 3-D architecture of the wall and coordinating the delivery of forces generated by myocytes. These forces are important determinants of diastolic. reciprocal of internal radius) at the apical level that creates a high local tension. The increase in tension plays a key role in activating complex neurohormonal mechanisms, including an in- crease in