Surgical ventricular restoration improves ventricular function and is highly effective therapy in the treatment of ischemic cardiomyopathy with excellent five-year outcome.

Ventricular torsion and untwisting are essential for normal ventricular function and their mechanisms are related to the temporal responses of the helical and circular muscle fibers that comprise cardiac architecture. Explanation of the presystolic isovolumic contraction (IVC) period is essential for analysis of these interactions. Structural and imaging studies by magnetic resonance, speckle tracking, velocity vector encoding, and sonomicrometer crystals are described to define why and how different muscular components contract asynchronously. Mechanical and functional relationships are described for pre-systolic IVC, torsion, postejection isovolumic interval, and rapid and slow filling. Circular fibers dominate to cause pre- and posttwisting global counterclockwise and clockwise movement, and helical fibers govern torsion whereby the base rotates clockwise and apex counterclockwise; untwisting cannot begin until torsion is completed. Prolonged torsion extends into the postejection isovolumic interval and delays untwisting, and is caused by prolonged contraction of the right-handed helical arm or descending segment of the helical ventricular myocardial band that narrows the ∼80 ms "timing hiatus" between end of shortening of the descending and the ascending segment or left-handed arm of the helical muscle. Longer torsion duration by this mechanism becomes the common theme for unbalanced torsion and untwisting in diastolic dysfunction, physiological, structural, and electrical disease processes, whose management may be guided by changing the interconnected reasons for these adverse mechanical and timing factors.

Despite a more spherical postoperative left ventricular chamber, systolic pump function improves after the Dor procedure, mainly for the improvement in inferior wall shortening. The presence of late mitral regurgitation is relatively frequent in this series of patients, and this emphasizes the importance of a more accurate quantitative evaluation of preoperative functional mitral regurgitation to repair the valve when appropriate. Geometric correlates of late mitral regurgitation appeared to be greater chamber sphericity and larger ventricular volumes preoperatively.

Congestive heart failure may be caused by late left ventricular (LV) dilation following anterior infarction. Early reperfusion prevents transmural necrosis, and makes the infarcted segment akinetic rather than dyskinetic. Surgical ventricular restoration (SVR) reduces LV volume and creates a more elliptical chamber by excluding scar in either akinetic or dyskinetic segments. The international RESTORE group applied SVR in a registry of 1198 post-infarction patients between 1998 and 2003. Early and late outcomes were examined and risk factors identified.Concomitant procedures included coronary artery bypass grafting in 95%, mitral valve repair in 22%, and mitral valve replacement in 1%. Overall 30-day mortality after SVR was 5.3% (8.7% with mitral repair vs. 4.0% without repair, p < .001) Perioperative mechanical support was uncommon (< 9%). Global systolic function improved postoperatively, as ejection fraction increased from 29.6 +/- 11.0% to 39.5 +/- 12.3% (p < .001) and left ventricular end systolic volume index decreased from 80.4 +/- 51.4 ml/m(2) to 56.6 +/- 34.3 ml/m(2) (p < .001). Overall 5-year survival was 68.6 +/- 2.8%, Logistic regression analysis identified EF < or = 30%, LVESVI > o = 80 ml/m(2), advanced NYHA functional class, and age > or =75 years as risk factors for death. Five-year freedom from hospital readmission for CHF was 78%. Preoperatively, 67% of patients were class III or IV, and postoperatively 85% were class I or II.SVR improves ventricular function and is highly effective therapy in the treatment of ischemic cardiomyopathy with excellent 5-year outcome.

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Surgical anterior ventricular endocardial restoration is a safe and effective operation in the treatment of the remodeled dilated anterior ventricle after anterior myocardial infarction.

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