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Surgical ventricular reconstruction for ischemic or idiopathic dilated cardiomyopathy [Elektronische Ressource] / vorgelegt von Lynda Ahn-Veelken

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56 pages
Aus der Chirurgischen Universitätsklinik Abteilung für Herz- und Gefäßchirurgie der Albert-Ludwigs-Universität Freiburg i. Br. Ärztlicher Direktor: Prof. Dr. F. Beyersdorf Surgical Ventricular Reconstruction for Ischemic or Idiopathic Dilated Cardiomyopathy INAUGURALDISSERTATION zur Erlangung des Medizinischen Doktorgrades der Medizinischen Fakultät der Albert-Ludwigs-Universität Freiburg i. Br. Vorgelegt 2004 von Lynda Ahn-Veelken geboren in New York City, U.S.A. Dekan: Prof. Dr. med. Josef Zentner 1. Gutachter: Prof. Dr. med. Friedhelm Beyersdorf 2. Gutachter: Prof. Dr. med. Martin Werner Jahr der Promotion: 2004 2Table of Contents 1 Introduction.......................................................................................................4 1.1 Functional Anatomy of the Ventricular Wall......................................................1.2 Myocardial Infarction..........................................................................................6 1.2.1 Treatment ............................................................................................................9 1.2.1.1 Medical Treatment..............................................................................................1.2.1.2 Surgical Treatment............................................................................................10 1.3 Dilated Cardiomyopathy..........................................................
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 Aus der Chirurgischen Universitätsklinik Abteilung für Herz- und Gefäßchirurgie der Albert-Ludwigs-Universität Freiburg i. Br. Ärztlicher Direktor: Prof. Dr. F. Beyersdorf      Surgical Ventricular Reconstruction for Ischemic or Idiopathic Dilated Cardiomyopathy     INAUGURALDISSERTATION zur Erlangung des Medizinischen Doktorgrades  der Medizinischen Fakultät der Albert-Ludwigs-Universität Freiburg i. Br.   Vorgelegt 2004 von Lynda Ahn-Veelken geboren in New York City, U.S.A.
 Dekan:
 
1. Gutachter:
 
2. Gutachter:
 
Jahr der Promotion:
 
 
 
Prof. Dr. med. Josef Zentner
Prof. Dr. med. Friedhelm Beyersdorf
Prof. Dr. med. Martin Werner
2004  
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Table of Contents  1 Introduction .......................................................................................................4 1.1 Functional Anatomy of the Ventricular Wall......................................................4 1.2 Myocardial Infarction..........................................................................................6 1.2.1 Treatment ............................................................................................................9 1.2.1.1 Medical Treatment ..............................................................................................9 1.2.1.2 Surgical Treatment ............................................................................................10 1.3 Dilated Cardiomyopathy ...................................................................................11 1.3.1. Treatment of DCM ............................................................................................12  2 Methods............................................................................................................13 2.1 Patient Population..............................................................................................13 2.2 Preoperative Assessment ...................................................................................13 2.2.1 Assessment of Ejection Fraction, Mitral Regurgitation, Left  Ventricular End Diastolic Diameter and Dyskinesia or Akinesia .....................13 2.2.2 Cardiac Catheterization or Arteriography .........................................................14 2.3 Surgical Procedures ...........................................................................................14 2.3.1 Dor Surgical Ventricular Reconstruction (SVR) procedure and the  Modified Dor Procedure....................................................................................14 2.3.2 Batista Partial Left Ventriculectomy (PLV) procedure.....................................15 2.3.3 Concomitant Procedures ...................................................................................15 2.4 Telephone Interview..........................................................................................16 2.5 Data Analysis ....................................................................................................17  3 Results...............................................................................................................18 3.1 Preoperative Clinical Data and Surgical Procedures.........................................18 3.2 Dor SVR Procedure...........................................................................................19 3.2.1 New York Heart Association (NYHA) Status ..................................................20 3.2.2 Echocardiographic Results to Determine Effect of Operation ..........................22 3.2.3 Survival under Dor SVR Procedure ..................................................................23 3.2.4 Hospital Mortality and Late Deaths ..................................................................25 3.3 Batista PLV Procedure ......................................................................................27 3.3.1 NYHA Status.....................................................................................................27 3.3.2 Echocardiographic Results to Determine Effect of Operation ..........................27 3.3.3 Hospital Mortality and Late Deaths under Batista PLV Procedure ..................28  4 Discussion.........................................................................................................29  5 Summary..........................................................................................................40  Zusammenfassung...........................................................................................41  6 References........................................................................................................42   Curriculum Vitae............................................................................................55   Acknowledgements..........................................................................................56
 
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1 INTRODUCTION  1.1 Functional Anatomy of the Ventricular Wall In 1660, Lower described clockwise and counterclockwise spiral patterns of the myocardium at the apex of the heart. These helical structures appeared to be the basis for the elliptical shape of the heart. According to Torrent-Guasp (99), the myocardial fibers actually originate and end at the basis of the heart and form long, intertwined loops. The final orientation of the loops is circumferential around the heart base and helical at the apex (Figure 1).
Figure 1. Two views of the spiral patterns at the apical vortex of the heart. (Cook TA. The curves of life, 1979. Dover publications, Inc.).
 This difference in orientation is the anatomical basis for an efficient cardiac ejection fraction: During systole, contraction of the basal region of the ventricle first results in constriction, followed by contraction of the apical loop which shortens the ventricle and ejects the intraventricular volume directionally towards the base. The overall motion pattern thus resembles the wringing of water out of a wet cloth, an observation made first by Borelli, a student of Galileo in 1680 (De Motu Animalium, Rome. 1681) (Figure 2).  
 
Ejection Suction
Figure 2.At the beginning of systole, a clockwise and counter-clockwise twisting similar to the wringing of a rag leads to ejection. During diastole, the upper part of the ventricle twists in the opposite direction to produce lengthening and filling (99)
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This anatomical arrangement and physiological coordination is the fundamental mechanism how a systolic shortening of an individual myocardial fiber of 15% can be translated into a 60% ventricular ejection fraction (16). Any alteration of the functional cardiac anatomy, also referred to as "ventricular remodeling", will therefore severely impair ventricular function and cardiac output (Figure 3). When structural disorder changes the physiological elliptical geometry of the myocardium (top) to that of dilated enlarged ventricle (bottom), the result is a transverse fiber orientation. The same 15% fiber shortening will therefore result only in a 30% ejection fraction as opposed to the normal 60% (16) (Figure 4). When these structural alterations of the ventricle impair the functional capacity of the ventricle to fill with and to eject blood, the result is progressive cardiac failure. Important pathological conditions that alter the heart shape are myocardial infarction and dilated cardiomyopathy of any etiology.  
Figure 3.Top figure is of a normal elliptical ventricle. When the chamber dilates and the ventricle becomes enlarged (bottom figure), the result is a transverse fiber orientation, and the loss of contraction efficiency (18).
 
Figure 4.Normal fiber shortening of 15% results in a 60% ejection fraction (left). The same 15% fiber shortening results in a 30% ejection fraction in a remodeled, spherical ventricle (19).
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1.2 Myocardial Infarction Myocardial infarction is defined as regional necrosis of cardiac tissue due to acute ischemia. Shortly after myocyte necrosis, edema and inflammation occur in the infarcted area. Eventually, a scar develops and is characterized by fibroblast proliferation and collagen deposition. Before definite scar formation, however, the infarcted area can thin and dilate. Eaton and Sutton define this process infarct expansion (46, 93). Within 72 hours, serine proteases such as plasmin and matrix metalloproteinases released from neutrophils degrade the intermyocyte collagen that acts as structural frame (93). Histologically, the thinning of the infarcted area is characterized by slippage between muscle bundles caused by collagen degradation (93). This results in a decreased myocyte density across the infarcted region (81). This vulnerable period for developing an expansion has been demonstrated to begin as early as 24 hours after myocardial infarction and continues before scar formation is completed (72). Structural changes as a result of expansion may lead to the formation of a left ventricular aneurysm which has been associated with an approximately 60% one-year mortality (72). Eaton et al. reported a 50% mortality within eight weeks after development of regional expansion and ventricular dilatation (46). Anatomically, aneurysms are composed of fibrotic tissue that replace the myocardium in the infarcted zone. Functionally, ventricular aneurysms are characterized by a local expansile or paradoxical wall motion. Complications associated with an aneurysm are arterial embolism, ventricular arrhythmias and congestive heart failure that often occur within weeks to months. The 1-year mortality rate patients who have developed an aneurysm shortlyis much higher in after an anterior infarct than in those patients without an aneurysm (46, 71, 81). When the noncontractile area involves more than 20-25% of the surface area of the left ventricle, the result is a noncompensatory ventricular enlargement and mycardial decompensation (62), defined as an impaired contractile function due to the distortion of the ventricle and its structural configuration. The development of an infarct expansion and aneurysm formation has been characterized as the early postinfarction remodeling phase (93). The late remodeling phase involves myocyte hypertrophy and a global alteration in the ventricular shape. The process of cardiac structural and functional disorder is initated by myocyte injury. In the case of an infarction, the acute loss of myocardium leads to a diminished cardiac output, increased end-systolic volume, and a secondary increase in end-diastolic pressure caused by the increase in ventricular volume. The increase in radius leads to the elevation of diastolic and systolic wall stresses. The wall tension can be calculated according to Laplace's law, K = P x r/2d [N x m-2] and rises proportionally to the ventricular diameter r when the same
 
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intraventricular pressure P is maintained and the wall thickness d does not increase. Simultaneously, infarct expansion occurs in response to elevated wall stresses, particularly since the necrotic myocardium predominates and scar tissue has not yet formed. Infarct expansion would increase systolic and diastolic volumes with resultant increase in wall tension. The increase in wall tension leads to a higher strain and oxygen requirement on the remote noninfarcted myocardium. To maintain a normal cardiac output, activation of the adrenergic system, with secretion of catecholamines by the adrenal glands and the renin-angiotensin-aldosterone system (RAAS) are invoked. This neurohormonal activation then leads to two pathways, one that leads to molecular and phenotypic changes that have direct effects on cardiac myocyte growth (77, 93) and a second pathway that leads to an increasing afterload due to vasoconstriction. The increases in preload and ventricular afterload lead to an increased ventricular radius and diastolic pressure that result in greater wall tension. When adaptive responses are no longer able to counteract these distending forces, volume-overload hypertrophy in the remote noninfarcted myocardium develops which leads to progressive cavity enlargement and global dilatation. This process is known as ventricular remodeling (52, 71, 93). Cardiac hypertrophy occurs, however, not only in response to RAAS but also to increasing wall tension (93). Mechanical strains induced by rising wall tension activate a range of intracellular signals, including secretion of angiotensin II, that lead to protein synthesis and myocyte hypertrophy (77, 93).  The complex process of ventricular remodeling with its various contributing factors is described in the diagram on the next page.
 
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Myocyte injury
Loss of contractile function
Decreased cardiac out ut
Increased end-diastolic ressure
Increased wall stress
Hypertrophy of remote noninfarcted tissue with pathological phenotype of cardiomyocytes
VENTRICULAR REMODELING
Neurohormonal activation
Water and NaCl retention
 
 
Figure 5.schematic illustration of interactive forces and components that lead toA ventricular remodeling after regional infarction. 
 Since elevated wall stresses are a major stimulus for ventricular remodeling (71, 81), it is important to decrease wall stress by limiting the radius. In patients studied for 3 years after first myocardial infarction, development of progressive dilatation and severe ventricular dysfunction was found in 20% of patients (52). The consequence is an increase in left ventricular volume, the development of chronic heart failure and an adverse prognosis.
 
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1.2.1 Treatment Therapeutic options that exist for patients with ventricular remodeling include pharmacotherapy, cardiac transplantation for heart failure, the surgical ventricular reconstruction according to Dor and aneurysmectomy for patients who develop a left ventricular aneurysm during the early remodeling phase. Understanding the pathophysiology, the goal of therapy is to alleviate symptoms and to improve survival by preventing the progression of the remodeling process by minimizing risk factors.   1.2.1.1 Medical Treatment Pharmacological intervention include the use of angiotensin-converting enzyme inhibitors (ACE-I), beta blockers (b-blockers) and digitalis glycosides. ACE-I are used to inhibit the activation of the renin-angiotensin-aldosterone system which become activated in heart failure. Indeed, the Studies of Left Ventricular Dysfunction (SOLVD) trial has shown that ACE-I may reverse the remodeling process (53, 64, 90, 93). However, the incidence of sudden death has not been reduced with the use of ACE-I (24). Randomized trials have hitherto failed to define the optimal dose of ACE-I (59). Moreover, the side effects of ACE-I, which include hyperkalemia, azotemia, angioedema or severe coughing may also prevent their long-term use in individual patients. B-blockers are used to decrease sympathetic stimulation due to ventricular failure and are indicated for patients after a heart attack. However, for patients with reactive airway disease, diabetes, bradyarrhythmias and heart block without a pacemaker, the use of b-blockers is contraindicated. Digitalis glycosides (primarily digoxin) are used for symptomatic patients with heart failure who have a low ejection fraction. Recently, a randomized placebo-controlled study of digoxin showed that the rate of a deteriorating heart and hospitalization decreased with the digoxin group. However, there was no difference in mortality between the two groups (35). Furthermore, for patients with renal failure, there are contraindications for the use of digoxin and potentially life threatening side effects. Ventricular tachycardia or fibrillation, supraventricular arrhythmia, and atrioventricular block also continue to pose significant problems with the use of digoxin. Although medical treatment has prolonged the life expectancy in which 50% of patients with heart failure now live 8 years (17), the number of deaths has increased steadily despite the advances in treatment (55). For patients categorized in NYHA III or IV status, there remains an adverse 3-year prognosis, despite the improvement of symptoms (74, 103). Past and recent clinical trials have demonstrated that intervention with ACE-I and b-blockers may attenuate remodeling (15, 53, 93), however the overall mortality rate is higher than surgical intervention
 
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(17, 23, 24, 90). Furthermore, Sutton et al. (94) have reported that treatment beyond 1 year with captopril (ACE-I) for patients from the SAVE trial (Surgical and Ventricular Enlargement trial) had no affect on progressive ventricular dilatation and declining ventricular function.  1.2.1.2 Surgical Treatment Surgical intervention offers an additional option for treatment for patients with chronic heart failure and/or a remodeled ventricle. Surgical methods such as an implantable left ventricular assist device (LVAD), coronary revascularization, heart transplantation for end-stage cardiac failure, conventional aneurysmectomy and the Dor surgical ventricular reconstruction procedure are discussed below. LVAD is a mechanical device that serves to support patients with circulatory failure and ventricular arrythmias. This device, however, is a temporary and not a permanent solution. Disadvantages include high initial costs, substantial monitoring and complications such as bleeding, infection and the risk of thromboembolism, since most devices do not have an endothelial covering (98). Myocardial reperfusion may modify ventricular enlargement by restoring the remaining viable myocardium in the infarcted zone. Maintaining a patent vessel would salvage the vulnerable area of myocardium that is most open to damage and thereby limit infarct expansion. Pfeffer et al. observed a progressive ventricular enlargement over a period of one year in patients with an occluded artery in the infarct area and attributed the increase in ventricular volume of 21 +/- 8 ml to late effects on the viable myocardium at the border between infarcted and noninfarcted myocardium (82). Reperfusion has also been demonstrated to reduce infarct size and improve cardiac performance (9, 88). As a result, coronary revascularization has been used as a treatment to possibly attenuate remodeling. However, despite the benefits of myocardial reperfusion, one study noted higher mortality and the development of congestive heart failure when LVESV index was 100ml/min/m2 greater after revascularization alone (109). Among patients with a or low ejection fraction (EF) (EF<30%), the eight-year survival rate for revascularization alone was 58% (100). Furthermore, the value of revascularization in patients with left ventricular dysfunction but no detectable ischemia is unclear. Heart transplantation offers an additional therapeutic option for patients, particularly for those with end-stage heart failure. However, organ availability continues to be a limiting factor, and approximately 20% of patients on the waiting list die (69). In addition, rejection of the donor organ remains a problem. Vasculopathy of the allograft after heart transplantation is the main cause of illness and death after the first year (47).
 
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In 1984, Dor et al. recognized the importance of excluding the noncontracting segment (either of akinetic or dyskinetic nature) in the left ventricle in order to enhance cardiac function. He postulated an improvement in ventricular function when nonfunctioning myocardium is resected and replaced with an endoventricular patch which would restore the remodeled ventricle to its normal elliptical form. This geometric approach, which is usually combined with CABG, modified the first simple resection of a left ventricular aneurysm in 1958 by Cooley and later by Jatene in 1962. Conventional aneurysmectomy involves resection of the aneurysm on a non-beating heart followed by a longitudinal suturing of the opening (25) or a circular suture of the orifice with or without a Dacron patch (57). The failure to address volume reduction and ventricular reconstruction are the main disadvantages of traditional surgical methods. Dor's procedure however, should be more advantageous in the long term because the physiological distribution and pattern of the muscle fibers are taken into consideration by suturing a intraventricular patch in place of the excluded dysfunctional myocardium. The ventricular size and volume is subsequently reduced and concomitantly a CABG or repair of mitral valve is performed when necessary. CABG is an integral procedure in Dor's operation when patients present with ischemic conditions, particularly since coronary artery stenosis is an underlying disease in patients with an aneurysm and angina pectoris is a frequent indication for surgery (8, 20, 27, 34, 41, 80). Furthermore, compared to revascularization alone for patients with an EF<30%, survival at eight years was higher at a rate of 69% under the Dor SVR procedure (40).  1.3 Dilated Cardiomyopathy The theory that cardiac reconstruction prevents progressive remodeling may also pertain to other conditions of a pathologically enlarged heart, such as dilated cardiomyopathy (DCM). Ventricular remodeling in DCM is progressive global dilatation, a decrease in systolic function and a distortion of the mitral valve. The concept of reducing chamber diameter and subsequently wall tension was therefore not only limited to ventricular remodeling after a myocardial infarction, but was also performed on DCM. By etiology, there are two fundamental forms of DCM (1) a primary myocardial involvement which include idiopathic, familial; and (2) a secondary myocardial involvement which includes infective DCM as a result of viral, bacterial, fungal, protozoal myocarditis; metabolic disease; neuromuscular disease such as Duchenne's progressive muscular dystrophy; connective tissue disorders such as systemic lupus erythematosus, rheumatoid arthritis, polyarthritis nodosa, progressive systemic sclerosis and dermatomyositis; alcohol and drug toxicity, for example with
 
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