Prophylactic mitral reconstruction for mitral regurgitation.

BACKGROUND: Mitral regurgitation (MR) will produce myocardial dysfunction. The goal of this study was to review outcomes of mitral valve reconstruction in asymptomatic patients with severe MR. METHODS: From 1992 to 2000, 93 asymptomatic patients with degenerative disease and severe MR underwent mitral valve reconstruction. Mean preoperative left ventricular internal diameter diastole was 56 +/- 8 mm and ejection fraction was 60% +/- 6%. Mean age was 47 +/- 10 years and mean follow-up 23 +/- 27 months. All patients underwent complex reconstruction. RESULTS: There were no deaths and two late reoperations. One was for systolic anterior motion of the anterior leaflet of the mitral valve requiring valve replacement and one for hemolysis requiring re-repair. There was one perioperative transient ischemic attack and no late thromboembolic events. At follow-up all but 1 patient remains in NYHA class I and all had no MR except in 2 patients at 63 and 89 months. CONCLUSIONS: Mitral valve reconstruction for "asymptomatic" MR can be performed with no mortality and low morbidity before development of left ventricular dysfunction. Early prophylactic repair is advocated in the presence of severe MR if valve reparability is assured.

Surgical alternatives for heart failure.

Heart failure is one of the leading causes of hospitalization in the United States. Congestive heart failure is a chronic, progressive disease and its central element is remodeling of the cardiac chamber associated with ventricular dilation. Secondary mitral regurgitation is a complication of end-stage cardiomyopathy and is associated with poor prognosis. Historically, these patients were not considered operative candidates because of their high morbidity and mortality. Heart transplantation is now considered standard treatment for select patients with end-stage heart disease; however, it is applicable only to a small number of patients. In an effort to address this problem, newer and alternative surgical approaches are evolving, including mitral valve annuloplasty, the Batista procedure, and other left ventricular shape changing technologies. Using these operative techniques to alter the shape of the left ventricle, in combination with optimal medical management for heart failure, improves survival, and patients may avoid or postpone transplantation.

Reoperation for Freestyle stentless aortic valves.

Ten patients who initially underwent Freestyle stentless aortic valve implantation required reoperation. The goal of this study was to describe the reoperative techniques used and to review the outcomes of reoperation in patients with Freestyle stentless aortic valves. From September 1992 to April 2001, at the University of Michigan, a total of 552 Freestyle stentless aortic valves were implanted, and in 10 (1.8%) of these patients (7 men, 3 women) a reoperation was required. The mean age at the time of the initial implantation was 53.5 +/- 14.1 years. Implantation techniques included both modified inclusion root (7) and inclusion root (3). Reasons for reoperation included endocarditis (7), aortic aneurysm (1), valve dehiscence (1), and subvalvular outflow tract obstruction (1). Eight patients underwent homograft reimplantations and in 2 Freestyle reimplantations. In all cases, the previous aortotomy was re-entered, the pseudoendothelial layer over the distal suture line of the noncoronary sinus was incised and continued into the other 2 sinuses. Utilizing a ganglion knife, the Freestyle valve was freed from the native aortic tissue to the proximal suture line. The Dacron sewing ring was then separated using sharp dissection and the lower suture line excised. No calcification was noted in any case. The mean time interval between the first and second operative procedure was 13.4 +/- 21.5 months. There were no operative deaths and only one late death. Mean long-term follow-up was 43 +/- 29 months. Reoperation on a Freestyle stentless aortic valve, when necessary, can be accomplished without increased operative risk and with excellent survival.

Mitral valve repair in heart failure.

Mitral regurgitation (MR) is a frequent complication of end-stage heart failure. Historically, these patients were either managed medically or with mitral valve replacement, both associated with poor outcomes. Mitral valve repair via an 'undersized' annuloplasty repair is safe and effectively corrects MR in heart-failure patients. All of the observed changes contribute to reverse remodeling and restoration of the normal left-ventricular geometric relationship. Mitral valve repair offers a new strategy for patients with MR and end-stage heart failure.

Surgical approaches to dilated cardiomyopathy.

Heart failure is one of the leading causes of hospitalization in the United States today. Congestive heart failure is a chronic progressive disease with the common central element being the remodeling of the cardiac chamber associated with ventricular dilation. Secondary mitral regurgitation is a complication of end-stage cardiomyopathy and is associated with a poor prognosis. Historically, these patients were not considered operative candidates due to the high morbidity and mortality in this patient population. Heart transplantation is now considered the standard of treatment for select patients with end-stage heart disease, however, it is only applicable to a small number of patients. In an effort to address this problem, newer and alternative surgical approaches are evolving, including mitral valve annuloplasty, the Batista myoplasty, and cardiomyoplasty. When these operative techniques that alter the shape of the left ventricle are utilized, in combination with optimal medical management for heart failure, survival is improved and patients can avoid or postpone transplantation.

Current status of mitral valve reconstruction in patients with dilated cardiomyopathy.

Congestive heart failure (CHF) is one of the leading causes of hospitalization in the United States today and its incidence is increasing. Despite improvements with medical management approximately 50% of patients with CHF die within 3 years of presentation. Heart transplantation is now considered standard treatment for selected patients with severe CHF and end-stage heart disease; however, it is only applicable to a small percentage of patients. In an effort to solve this problem medical and surgical strategies are rapidly expanding and evolving. Mitral valve reconstruction represents an alternative surgical strategy in patients with dilated cardiomyopathy that will allow for preservation of the limited number of donor organs for those patients who have no other surgical or medical alternatives.

Steroid pretreatment improves graft recovery in a sheep orthotopic heart transplantation model.

BACKGROUND: Previous reports provide conflicting evidence concerning effects of steroids on recovery of cardiac function during procedures involving cardiopulmonary bypass. This study was designed to test the hypothesis that pretreatment of animals with steroids before heart transplantation improves graft hemodynamic function. METHODS: Four groups of sheep were studied: CON, nonsteroid-treated nontransplanted controls (n = 8); CON-S, steroid-treated nontransplanted controls (n = 5); TX, nonsteroid-treated transplanted animals (n = 5); and TX-S, steroid-treated transplanted animals (n = 5). Steroid-treated animals were given methylprednisolone 30 mg/kg immediately before surgery. Procedures for harvest and orthotopic transplantation were similar to those used clinically. Contractile function, left ventricular diameter, and cardiac output of control and transplanted hearts were measured for 6 hours. A 2 x 2 factorial repeated measures analysis of variance was used to determine statistical significance (p < 0.05). RESULTS: Steroid pretreatment produced significantly higher function in controls and transplanted animals compared with nonsteroid-treated animals. On average over 6 hours, significant steroid effects were observed for left ventricular peak systolic pressure, mm Hg (CON, 85 +/- 2; CON-S, 98 +/- 3; TX, 74 +/- 3; TX-S, 91 +/- 2); global stroke work, mJoule x cm(-2) (CON, 4.69 +/- 0.21; CON-S, 5.88 +/- 0.32; TX, 2.27 +/- 0.17; TX-S, 4.23 +/- 0.16); and peak rate of pressure relaxation (-dP/dt(max)), mm Hg/msec (CON, 1.23 +/- 0.05; CON-S, 1.44 +/- 0.08; TX, 0.60 +/- 0.03; TX-S, 2.04 +/- 0.13). Steroid pretreatment produced more stable recovery for transplanted animals. All five TX-S animals could be removed from inotropic support and had stable function for 6 hours. In contrast, 1 of 5 TX animals could not be removed from inotropic support, and 1 of 5 TX hearts failed 3 hours after transplant. Arterial blood PO2 values were significantly higher in steroid-treated animals than in nonsteroid treated animals. Blood systemic lactate, which was elevated after transplantation, returned to control level by 6 hours in the steroid-treated group but not in the nonsteroid-treated group. CONCLUSION: Steroid pretreatment of heart donors and recipients improved systolic and diastolic function and hemodynamic stability after transplantation. In addition, steroid pretreatment improved pulmonary gas exchange of control and transplanted animals.

Incomplete recovery of working heart function after twenty-four-hour preservation with a modified University of Wisconsin solution.

BACKGROUND AND METHODS: This study was designed to determine the function of isolated rabbit hearts after static preservation with modified University of Wisconsin solution for 24 hours. Commercially available University of Wisconsin solution, modified with CaCl2 1 mmol/L and 2,3-butanedione monoxime 30 mmol/L, was used as the preservative. After flushing the coronary vasculature with medium, hearts were submersion stored at 1 degree C to 4 degrees C. After preservation, isolated heart function at 37 degrees C was quantified for 30 minutes in a non-ejecting mode and for 4 hours ejecting at a physiologic workload. Fresh control hearts (n = 5) and University of Wisconsin solution-preserved hearts (n = 6) were studied. RESULTS: Nonworking (non-ejecting) left ventricular function of the two groups did not differ, except for peak rate of left ventricular pressure development which was higher for the University of Wisconsin solution hearts than for controls. When the hearts were subjected to a physiologic workload, however, left ventricular function of the two groups differed significantly. Three of the six University of Wisconsin solution hearts failed before the 4-hour perfusion end point, whereas all five control hearts maintained stable working function for the full 4 hours. The University of Wisconsin solution hearts, while in the ejecting mode, exhibited significantly impaired function. Mean values were as follows (p < 0.05): left ventricular systolic pressure (in millimeters of mercury), control 105 +/- 1, University of Wisconsin solution 86 +/- 4; peak rate of left ventricular pressure development (in millimeters of mercury per millisecond), control 3.33 +/- 0.11, University of Wisconsin solution 2.39 +/- 0.24; cardiac output (in milliliters per minute per gram), control 400 +/- 25, University of Wisconsin solution 288 +/- 26; stroke work (in milliJoules per gram), control 20.1 +/- 1.3, University of Wisconsin solution 11.9 +/- 1.1; left ventricular end-diastolic pressure (in millimeters of mercury), control 5.4 +/- 0.3, University of Wisconsin solution 10.2 +/- 1.3; peak aortic flow rate (in milliliters per minute), control 946 +/- 9, University of Wisconsin solution 659 +/- 44; millimoles of lactate produced in 30 min/Joule stroke work, control 0.50 +/- 0.06, University of Wisconsin solution 6.99 +/- 0.37. CONCLUSIONS: These results indicate that (1) hypothermic storage in this modified University of Wisconsin solution does not preserve hearts sufficiently to support a physiologic workload for an extended period and (2) assessment of post-preservation function with a non-ejecting heart model does not accurately predict the ability of the preserved heart to support a physiologic workload.

Effect of hemodialysis on left ventricular contractility in pediatric patients with end-stage renal disease.

Assessment of the effect of hemodialysis on myocardial contractility is complicated by variations in loading conditions that can occur during hemodialysis and by the prevalence of coronary artery disease among patients with chronic renal failure. Therefore, we used a load-independent index of left ventricular contractility, derived from analyses of the rate corrected velocity of circumferential fiber shortening (Vcfc)-end systolic wall stress (ESWS) relationship, to study the acute effects of hemodialysis on left ventricular function in the cases of 15 pediatric patients with end-stage renal disease. Prior to dialysis, Vcfc was appropriate for ESWS (102% +/- 16% of predicted) and did not differ significantly from values obtained from a group of nine normal control subjects of similar ages (103% +/- 9% of predicted), indicating that the patients' left ventricles were functioning in a normal inotropic state. After dialysis, Vcfc increased to levels beyond those expected for ESWS (118% +/- 20% of predicted, P < .05 versus control; P < .001 versus predialysis levels), indicating that dialysis was associated with enhancement of the left ventricle's inotropic state. A statistically significant increase in plasma norepinephrine levels was also observed. However, the increase in the percentage of the predicted Vcfc did not correlate with observed changes in this inotropic agent or with dialysis-induced variations in body weight or levels of electrolytes, urea nitrogen, or creatinine, and firm conclusions regarding the identity of the factors responsible for the positive inotropic effect of hemodialysis could not be drawn.

Opioids can enhance and inhibit the electrically evoked release of methionine-enkephalin.

The stimulated (40 Hz) release of enkephalin from the myenteric plexus can be modulated by multiple types of opiate receptor. The direction of the modulation is not fixed but is bimodal. Both an inhibition and an enhancement of evoked release is observed depending on the concentration of opioid agonist that is used. Each of these effects can be antagonized by naloxone. Following pretreatment of guinea pig myenteric plexus in vitro with forskolin (0.5 microM) or the lipid soluble cAMP analog 8-(4-chlorphenylthio)-cAMP (8-CPT-cAMP; 100 microM) the inhibition of stimulated Met-enkephalin release that is produced by sufentanil (10(-8) M), [D-Pen2-D-Pen5]enkephalin (DPDPE, 10(-8) M) or dynorphin (10(-7) M) is no longer observed. On the contrary, in forskolin- or 8-CPT-cAMP treated myenteric plexus a previously inhibitory concentration of the above opioids now produces an enhancement of the magnitude of the stimulated Met-enkephalin release. Excitatory responses (enhanced release) to lower concentrations of sufentanil (1 nM) or DPDPE (5 nM) are not affected by pretreatment with the same concentration of forskolin or 8-CPT-cAMP. These data suggest that the ability of opioids to enhance or inhibit evoked enkephalin release is mediated via different biochemical processes (separate second messenger systems). This could imply that the opioid enhancement of enkephalin release is due to a direct facilitation of release and not to disinhibition. The ability of opioids to enhance the release of at least some neurotransmitters should be taken into account when attempting to explain the physiological sequelae of the acute and chronic effects of narcotics.

Identification of renal calculi by computerized infrared spectroscopy.

A method is described for the assessment of renal calculi by means of a computerized IR spectrometer. A preliminary reference library of IR spectra of 34 different renal calculi of known composition has been created. The reference library used in the operation of a computerized search program indicates the closest matches in the reference library data with the IR spectrum of an unknown sample. The computerized method of characterizing renal calculi has the advantage that it greatly reduces the likelihood of introducing errors because of operator bias in the subjective interpretation of spectral data.