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Although Chagas disease is a rare entity in North America, it is associated with significant cardiac morbidity. It is estimated that 20-30% of those who are infected will eventually develop cardiovascular disease secondary to Chagas disease. We review the literature and share our experience on the surgical management of this challenging patient population.

Background: Attempts to prolong life or to improve the quality of life by partial left ventriculectomy in patients suffering from dilated cardiomyopathy have yielded strikingly variable results in leading surgical centers. Hypothesis: The outcome of patients after partiat left ventriculectomy depends on intraoperative myocardial protection together with appropriate long-term pharmacotherapy. We further assume that partial removal of the fibrotic ventricular wall may lead to a particularly inhomogeneous pattern of wall stress, giving rise to the potential of a paradoxical increase in wall stress and the creation of arrhythmogenic foci. Methods: During surgery in 24 patients, local mesh tension was measured using needle-force probes in up to five sites within the left ventricular wall before and after resection of the interpapillary mural segment. The data were used to calculate regional peak developed force and to identify any differences in the timing of local mechanical activity between the measured regions. Results: Mean decrease in regional wall stress was 42% (76 sites of measurement). However, we discovered a paradoxicat increase of 42% in 18 sites of measurement. The time delay in the onset of force development between the measured regions prior to surgery was 0 msec in 10 patients, up to 30 msec in 7 patients, and beyond 80 msec in 7 patients. After resection, the time delay increased considerably in incidence and duration. Conclusion: Ventriculectomy is an effective means of reducing wall stress. The unexpectedly high incidence of inhomogeneities in wall stress after asymmetrical surgical ventricular remodeling, currently typical for the classical Batista procedure, together with the asynchronous regional ventricular function that we found to increase after partial left ventriculectomy, needs further elucidation by electrophysiological investigations.

At its introduction, partial left ventriculectomy was seen as a promising option. 1 As initially used, its main drawback was its unpredictable effect on cardiac function. The size, shape, and location of the segment to be resected were at the discretion of the surgeon. Once the segment had been resected, any disadvantageous results were irreversible. Resection, and subsequent coaptation of the incision, often compromised coronary perfusion. 2 Experience showed that insufficient narrowing of the ventricular base could cause late postoperative mitral valvular incompetence. 3 Right ventricular function was also impaired by extensive resections from the left ventricle. 4 A further reported complication is sudden death from ventricular fibrillation, which reportedly occurred within 6 months of the intervention. 5 Encouraging initial clinical results 1,6-8 nonetheless have shown that the basic concept of partial left ventriculectomy is sound, at least when conceived as a bridging procedure. To validate the technique and improve its results, we have devised an off-pump strategy that permits reduction of ventricular radius by plication of a chosen segment of ventricular wall. By using aspirator cups, we avoid an open procedure. The technique permits initial sequestration in trial fashion, allowing us to assess ventricular function. Only if it is judged satisfactory do we then perform the definitive ventricular plication. Our new technique of sutured splinting for the definitive plication preserves the coronary vasculature.

Surgical strategies recently introduced to improve ventricular function have been based on the concepts of reduction of ventricular diameter, synchronization of myocardial activity, passive support of diastolic ventricular shape, and active support of systolic ventricular constriction. They have depended on several established theoretical assumptions, not all of which are totally valid. Clinical results have proved markedly variable. This is especially true for procedures designed to reduce the radius of the left ventricle. Some have reported up to 80% mortality, whereas others achieve results comparable with those for heart transplantation. Because of this, the method runs the risk to be rejected, or else, its more widespread application will be postponed until essential details concerning the basic concepts have been elucidated. It is these details which we discuss in this review.

Nine months after partial ventriculectomy, a 53-year-old man died of progressive heart failure. His heart was examined to determine the alignment of the muscle fibers around the ventricular scar, which was 11 cm long, 1.3 cm thick and 4 cm wide. The scar reached 2 to 12 mm beyond the surgical suture line. The fibers in the middle and subendocardial layers were malaligned, resulting in convergence, compression and regional necrosis.

Background —Partial left ventriculectomy (PLV) is a novel surgical treatment for severe heart failure consisting of resection of a large wedge of myocardium to reduce wall stress and restore the normal mass-volume ratio. Although ejection fraction (EF) has been shown to improve after PLV, few other physiological data describing its immediate effects on left ventricular (LV) performance are available. Methods and Results —Eight patients, 58±5 years old, with severe clinical heart failure and EF of 12±3% were studied before and immediately after PLV. LV performance was assessed by the predominantly load-insensitive measures of pressure-area relations with high-fidelity pressure catheters and transesophageal automated echocardiographic measures of cross-sectional area as a surrogate for volume. LV end-diastolic volume decreased from 200±60 to 89±17 mL, EF increased from 12±3% to 41±8%, and right ventricular (RV) fractional area change increased from 24±12% to 37±16% (all P 2 and preload recruitable stroke work, 33±16 to 34±19 mm Hg ( P =NS versus before). End-diastolic stiffness increased from 0.13±0.06 to 0.19±0.07 mm Hg/cm 2 ( P Conclusions —PLV resulted in reductions in LV volumes, increases in EF and RV ejection, but increases in LV stiffness. Estimates of LV performance revealed variable results associated with the degree of myocardial fibrosis. Further study of these effects in relation to patient outcome is warranted.

Background . It is reasoned that reducing left ventricular diameter (Laplace's law) in patients with dilated cardiomyopathy, will improve ventricular function. Methods . Partial left ventriculectomy was performed in 120 patients with end-stage dilated cardiomyopathies of varying causes. Most patients were in New York Heart Association functional class IV. The procedure consisted of removal of a wedge of left ventricular muscle from the apex to the base of the heart. Depending on the distance between the two papillary muscles, the mitral valve apparatus was either preserved, repaired, or replaced with a tissue prosthesis. Results . The 30-day mortality was 22% and the 2-year survival was 55%. Although 10% of surviving patients showed no improvement in New York Heart Association functional class, most of the surviving patients were in either class I (57%) or II (33.3%), and the others were in class III and IV. Conclusions . Partial left ventriculectomy can be used to treat end-stage dilated cardiomyopathy. Further studies and a longer follow-up period are needed to fully assess the effects of this procedure.

Recent morphological studies provide evidence that the ventricular walls are arranged as a 3D meshwork of aggregated cardiomyocyte chains, exhibiting marked local structural variations. In contrary to previous findings, up to two-fifths of the chains are found to have a partially transmural alignment, thus deviating from the prevailing tangential orientation. Upon contraction, they produce, in addition to a tangential force, a radial force component that counteracts ventricular constriction and aids widening of the ventricular cavity. In experimental studies, we have provided evidence for the existence of such forces, which are auxotonic in nature. This is in contrast to the tangentially aligned myocytes that produce constrictive forces, which are unloading in nature. The ventricular myocardium is, therefore, able to function in an antagonistic fashion, with the prevailing constrictive forces acting simultaneously with a dilatory force component. The ratio of constrictive to dilating force varies locally according to the specific mural architecture. Such antagonism acts according to local demands to preserve the ventricular shape, store the elastic energy that drives the fast late systolic dilation and apportion mural motion to facilitate the spiralling nature of intracavitary flow. Intracavitary pressure and flow dynamics are thus governed concurrently by ventricular constrictive and dilative force components. Antagonistic activity, however, increases deleteriously in states of cardiac disease, such as hypertrophy and fibrosis. β-blockade at low dosage acts selectively to temper the auxotonic forces.