L. Menicanti

Surgical Ventricular Restoration Improves Mechanical Intraventricular Dyssynchrony in Ischemic Cardiomyopathy

Background—In ischemic cardiomyopathy, dyssynchrony of left ventricular (LV) mechanical contraction produces adverse hemodynamic consequences. This study tests the capacity of geometric rebuilding by surgical ventricular restoration (SVR) to restore a more synchronous contractile pattern after a mechanical, rather than electrical, intervention. Methods and Results—A prospective study of the global and regional components of dyssynchrony was conducted in 30 patients (58±8 years of age) undergoing SVR at the Cardiothoracic Center of Monaco. The protocol used simultaneous measurements of ventricular volumes and pressure to construct pressure/volume (P/V) and pressure/length (P/L) loops. Angiograms were done before and after SVR to study a 600-ms cycle during atrial pacing at 100 bpm. Mean QRS duration was similar, at 100±17 ms preoperatively and 114±28 ms postoperatively (NS). Preoperative LV contraction was highly asynchronous, because P/V loops showed abnormal isometric phases with a right shifting. Endocardial time motion was either early or delayed at the end-systolic phase so that P/L loops were markedly abnormal in size, shape, and orientation. Postoperatively, SVR resulted in leftward shifting of P/V loops and increased area; endocardial time motion and P/L loops almost normalized to allow a better contribution of single regions to global ejection. The hemodynamic consequences of SVR were improved ejection fraction (30±13% to 45±12%; P =0.001); reduced end-diastolic and end-systolic volume index (202±76 to 122±48 and 144±69 to 69±40 mL/m2; P =0.001); more rapid peak filling rate (1.75±0.7 to 2.32±0.7 EDV/s; P =0.0001); peak ejection rate (1.7±0.7 to 2.6±0.9 Sv/s; P =0.0002), and mechanical efficiency (0.56±0.15 to 0.65±0.18; P =0.04). Conclusions—SVR produces a mechanical intraventricular resynchronization that improves LV performance.

Surgical Ventricular Restoration: The RESTORE Group Experience

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/m2 to 56.6 ± 34.3 ml/m2 (p < .001). Overall 5-year survival was 68.6 ± 2.8%, Logistic regression analysis identified EF ≤ 30%, LVESVI ≥ 80 ml/m2, advanced NYHA functional class, and age ≥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.

Inflammatory Activation During Coronary Artery Surgery and Its Dose-Dependent Modulation by Statin/ACE-Inhibitor Combination

Background—On-pump coronary artery bypass graft (CABG) surgery triggers an inflammatory response (IR) which may impair revascularization. The study aimed at (1) characterizing the temporal profile of the IR by assaying appropriate markers in both systemic and coronary blood, and (2) determining whether (and which doses of) cardiovascular drugs known to have antiinflammatory properties, namely statins and ACE-inhibitors (ACEI), inhibit the response. Methods and Results—Patients scheduled for CABG (n=22) were randomized to statin/ACEI combination treatment at standard doses (STD, ramipril 2.5/simvastatin 20 mg, or atorvastatin 10 mg), or at high doses (HiDo, ramipril 10 mg, or enalapril 20 mg/simvastatin 80 mg, or atorvastatin 40 mg). Plasma levels of interleukin 6, tumor necrosis factor alpha, E-selectin, von Willebrand factor (vWF), and sVCAM-1 were serially assayed (ELISA) before, during, and after CABG. Blood was drawn from an artery, a systemic vein, and the coronary sinus. Myocardial perfusion scans were obtained before and 2 months after surgery in 19 out of 22 subjects. In the STD group both IL-6 and TNF displayed striking increases which were similar at all sites and peaked 10 to 60 minutes after aortic declamping. Such increases were drastically attenuated in the HiDo group. Instead, only modest increases in venous E-selectin, vWF, and sVCAM-1 were observed. Scintigraphic ischemia scores were entirely normalized after versus before CABG in the HiDo but not in the STD treatment group. Conclusions—On-pump CABG surgery is associated with an intense systemic inflammatory response, which can be almost completely prevented by early treatment with high (but not standard) doses of ACE-inhibitors and statins.

Functional ischemic mitral regurgitation in anterior ventricular remodeling : Results of surgical ventricular restoration with and without mitral repair

Ischemic functional mitral regurgitation following ischemic cardiomyopathy is a secondary phenomenon to ventricular dilation, and therapeutic approaches to this complication are not uniform. Solutions to improve mitral function include either mitral repair or observing the effects of coronary revascularization and/or ventricular rebuilding during surgical ventricular restoration (SVR).The present study of 108 patients (comprising 18% of our 588 SVR population) reports the effects of mitral repair following SVR and CABG by comparing geometric, functional, hemodynamic and outcome changes to SVR patients without mitral repair. The degree of mitral regurgitation went from 2.9 ± 1.2 before to 0.7 ± 0.7 after SVR and mitral repair. SVR improved EF from 29 ± 7% to 34 ± 10% p 0.001; reduced end diastolic volume from 243 ± 74 to 163 ± 53 ml and end systolic volume from 170 ± 63 to 107 ± 41 ml, p 0.000. Ventricular size and shape geometric measurements improved in all patients, either with and without mitral repair. SVR improved tenting and papillary muscle width between muscle heads in all patients, but alterations in mitral annular size improved only following mitral repair.Preoperative mitral regurgitation occurred in patients with larger ventricular volume and lower ejection fraction and was an independent predictor of operative mortality risk.

Type 2 Diabetes Mellitus Is Associated With Faster Degeneration of Bioprosthetic Valve Results From a Propensity Score–Matched Italian Multicenter Study

BACKGROUNDnThe present study was aimed at determining the impact of type 2 diabetes mellitus (DM) on postoperative bioprosthetic structural valve degeneration.nnnMETHODS AND RESULTSnTwelve Italian centers participated in the study. Patient data refer to bioprosthetic implantations performed from November 1988 to December 2009, which resulted in 6184 patients (mean age 71.3±5.4 years, 60.1% male) being enrolled. Of these patients, 1731 (27.9%) had type 2 DM. The propensity score-matching algorithm successfully matched 1113 patients with type 2 DM with the same number of no-DM patients. The postmatching standard differences were less than 0.1 for each of the covariates, and 64.2% of DM patients were matched. The early (30 days) mortality rate was 7.8% (n=87) versus 2.9% (n=33) in patients with or without type 2 DM (P<0.001), respectively. Seven-year freedom from valve deterioration was significantly lower in patients with DM (73.2% [95% confidence interval, 61.6-85.5] versus 95.4% [95% confidence interval, 83.9-100], P<0.001). In Cox regression models with robust SEs that accounted for the clustering of matched pairs, DM was the strongest predictor of structural valve degeneration (hazard ratio 2.39 [95% confidence interval 2.28-3.52]). When we allowed for interaction between type 2 DM and other key risk factors, DM remained a significant predictor beyond any potentially associated variable.nnnCONCLUSIONSnPatients with type 2 DM undergoing bioprosthetic valve implantation are at high risk of early and long-term mortality, as well as of structural valve degeneration.Background— The present study was aimed at determining the impact of type 2 diabetes mellitus (DM) on postoperative bioprosthetic structural valve degeneration.nnMethods and Results— Twelve Italian centers participated in the study. Patient data refer to bioprosthetic implantations performed from November 1988 to December 2009, which resulted in 6184 patients (mean age 71.3±5.4 years, 60.1% male) being enrolled. Of these patients, 1731 (27.9%) had type 2 DM. The propensity score–matching algorithm successfully matched 1113 patients with type 2 DM with the same number of no-DM patients. The postmatching standard differences were less than 0.1 for each of the covariates, and 64.2% of DM patients were matched. The early (30 days) mortality rate was 7.8% (n=87) versus 2.9% (n=33) in patients with or without type 2 DM ( P <0.001), respectively. Seven-year freedom from valve deterioration was significantly lower in patients with DM (73.2% [95% confidence interval, 61.6–85.5] versus 95.4% [95% confidence interval, 83.9–100], P <0.001). In Cox regression models with robust SEs that accounted for the clustering of matched pairs, DM was the strongest predictor of structural valve degeneration (hazard ratio 2.39 [95% confidence interval 2.28–3.52]). When we allowed for interaction between type 2 DM and other key risk factors, DM remained a significant predictor beyond any potentially associated variable.nnConclusions— Patients with type 2 DM undergoing bioprosthetic valve implantation are at high risk of early and long-term mortality, as well as of structural valve degeneration.nn# Clinical Perspective {#article-title-46}

Mechanical Synchrony: Role of Surgical Ventricular Restoration in Correcting LV Dyssynchrony During Chamber Rebuilding

Cardiac failure is frequently complicated by intra and or interventricular conduction delay that results in dyssynchronized cardiac contraction and relaxation. In contrast to an electrical intervention by biventricular pacing, this study tests the capacity of geometric rebuilding by surgical ventricular restoration (SVR) to restore a more synchronous contractile pattern through mechanical reconstruction without exogenous pacing input.Thirty patients (58 ± 8 years) undergoing SVR at the Cardiothoracic Center of Monaco were prospectively evaluated with a protocol which uses simultaneous measurements of ventricular volumes and pressure to construct pressure/volume (P/V) and pressure/length (P/L) loops. Mean QRS duration was within normal limits (100± 17 ms) preoperatively. Preoperative LV contraction was highly asynchronous. Endocardial time motion was either early or delayed at the end-systolic phase, yielding P/L loops with abnormal in size, shape, and orientation. Postoperatively, SVR resulted in leftward shifting of P/V loops and increased area; endocardial time motion and P/L loops almost normalized. The hemodynamic consequences of SVR included improved ejection fraction; reduced end-diastolic and end-systolic volume index; more rapid peak filling rate; peak ejection rate and mechanical efficiency resulting in mechanical intraventricular resynchronization that improves LV performance.