Minimally invasive mitral valve replacement: Port-access technique, feasibility, and myocardial functional preservation

AbstractObjective: This experiment examined the feasibility of minimally invasive port-access mitral valve replacement via a 2.5 cm incision. Methods: The study evaluated valvular performance and myocardial functional recovery in six mongrel dogs after port-access mitral valve replacement with a St. Jude Medical prosthesis (St. Jude Medical, Inc., St. Paul, Minn.). Femoro-femoral cardiopulmonary bypass and a balloon catheter system for myocardial protection with cardioplegic arrest (Heartport, Inc., Redwood City, Calif.) were used. The mitral valve was replaced through a 2.5 cm port in the left side of the chest, and the animals were weaned from bypass. Cardiac function was measured before and at 30 and 60 minutes after bypass. Left ventricular pressure and electrical conductance volume were used to calculate changes in load-independent indexes of ventricular function. Results: Each procedure was successfully completed. Recovery of left ventricular function was excellent at 30 and 60 minutes after bypass compared with the prebypass values for elastance (30 minutes = 4.04 ± 0.97 and 60 minutes = 4.27 ± 0.57 vs prebypass = 4.45 ± 0.96; p = 0.51) and for preload recruitable stroke work (30 minutes = 76.23 ± 4.80 and 60 minutes = 71.21 ± 2.99 vs prebypass = 71.23 ± 3.75; p = 0.45). Preload recruitable work area remained at 96% and 85% of baseline at 30 and 60 minutes (p = not significant). In addition, transesophageal echocardiography demonstrated normal prosthetic valve function, as well as normal regional and global ventricular wall motion. Autopsy revealed secure annular-sewing apposition and normal leaflet motion. Conclusions: These results suggest that minimally invasive mitral valve replacement using percutaneous cardiopulmonary bypass with cardioplegic arrest is technically reproducible, achieves normal valve placement, and results in complete cardiac functional recovery. Minimally invasive mitral valve replacement is now feasible, and clinical trials are indicated. (J Thorac Cardiovasc Surg 1997; 113:1022-31

Anterior leaflet procedures during mitral valve repair do not adversely influence long-term outcome

AbstractObjectives. This study was done to assess the impact of anterior mitral leaflet reconstructive procedures on initial and long-term results of mitral valve repair.Background. It has been suggested that involvement of the anterior leaflet in mitral valve disease adversely affects the long-term outcome of mitral valve repair. Our policy has been to aggressively repair such anterior leaflets with procedures that include triangular resections in some cases.Methods. From June 1979 through June 1993, 558 consecutive Carpentier-type mitral valve repairs were performed. The anterior mitral leaflet and chordae tendineae were repaired in 156 patients (mean age 58 years). The procedures included anterior chordal shortening in 78 patients (50%), anterior leaflet resections in 44 (28%), resuspension of the anterior leaflet to secondary chordae in 42 (27%) and anterior chordal transposition in 27 (17%). Concomitant cardiac surgical procedures were performed in 75 patients (48%).Results. The operative mortality rate was 2.5% (2 of 81) for isolated mitral valve anterior leaflet repair and 3.8% (6 of 156) for all mitral valve anterior leaflet repair. Freedom from reoperation at 5 and 10 years was, respectively, 89.7% (n = 160) and 83.4% (n = 24) for the entire series of 558 patients, 91.9% (n = 51) and 81.2% (n = 10) for patients with anterior leaflet procedures, 88.8% (n = 109) and 84.4% (n = 14) for patients without anterior leaflet procedures and 91.7% (n = 118) and 88.9% (n = 18) for patients without rheumatic disease. Logistic regression showed that rheumatic origin of disease (odds ratio 2.99), but not anterior leaflet repair, increased the risk for reoperation.Conclusions. These results demonstrate that expansion of mitral valve techniques to include anterior leaflet disease yields immediate and long-term results equal to those seen in patients with posterior leaflet disease

Vein graft arterialization causes differential activation of mitogen-activated protein kinases

AbstractObjectiveVascular injury results in activation of the mitogen-activated protein kinases—extracellular-signal regulated kinases, c-jun N-terminal kinase, and p38MAPK—which have been implicated in cell proliferation, migration, and apoptosis. The goal of this study was to characterize mitogen-activated protein kinase activation in arterialized vein grafts.MethodsCarotid artery bypass using reversed external jugular vein was performed in 29 dogs. Vein grafts were harvested after 30 minutes and 3, 8, and 24 hours, and 4, 7, 14, and 28 days. Contralateral external jugular vein and external jugular vein interposition vein-to-vein grafts were used as controls. Vein graft extracts were analyzed for extracellular-signal regulated kinases, c-jun N-terminal kinase, and p38MAPK activation. Proliferating cell nuclear antigen expression was investigated as a parameter of cell proliferation. Apoptosis was assessed by terminal deoxynucleotidyl transferase–mediated 2′-deoxyuridine 5′-triphosphate nick end labeling staining and intimal hyperplasia by morphometric examination of tissue sections.ResultsSignificant intimal hyperplasia was observed at 28 days. Over the time points studied, vein graft arterialization resulted in bimodal activation of both extracellular-signal regulated kinase and p38MAPK (30 minutes through 3 hours; 4 days) but did not induce activation of c-jun N-terminal kinase. Proliferating cell nuclear antigen expression increased from days 1 through 28, and apoptosis increased between 8 and 24 hours.ConclusionVein graft arterialization induces bimodal activation of extracellular-signal regulated kinase and p38MAPK; however, in contrast with what is described in arterial injury, it does not induce c-jun N-terminal kinase activation. These results provide the first comprehensive characterization of the mitogen-activated protein kinase signaling pathways activated in vein graft arterialization and identify mitogen-activated protein kinases as potential mediators of vein graft remodeling and subsequent intimal hyperplasia