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Biomedical subjects

Michael Freeman

Publications and source records attributed to Michael Freeman.

24 records · Page 2Linked to original sources

Nutritional supplementation with MyoVive repletes essential cardiac myocyte nutrients and reduces left ventricular size in patients with left ventricular dysfunction.

BACKGROUND: Congestive heart failure depletes the myocardium of carnitine, coenzyme Q10 (CoQ10), and taurine--substances known to influence mitochondrial function and cell calcium. We hypothesized that feeding patients a nutritional supplement that contained carnitine, CoQ10, and taurine would result in higher myocardial levels of these nutrients and improve left ventricular function. METHODS: Forty-one patients who underwent aortocoronary artery bypass with an ejection fraction < or =40% at referral were randomly assigned to a double-blind trial of supplement or placebo. Radionuclide ventriculography was performed at randomization and before surgery. Surgical myocardial biopsies, adjusted for protein content, were analyzed for carnitine, CoQ10, and taurine levels. RESULTS: The groups were well matched. Minor exceptions were supplement group versus placebo group for digoxin use (7 vs 0, respectively; P =.009) and age (62 +/- 11 years vs 69 +/- 5 years, respectively; P =.04). There were significantly higher levels in the treated group compared with the placebo group for myocardial levels of CoQ10 (138.17 +/- 39.87 nmol/g wet weight and 56.67 +/- 23.08 nmol/g wet weight; P =.0006), taurine (13.12 +/- 4.00 micromol/g wet weight and 7.91 +/- 2.81 micromol/g wet weight; P =.003), and carnitine (1735.4 +/- 798.5 nmol/g wet weight and 1237.6 +/- 343.1 nmol/g wet weight; P =.06). The left ventricular end-diastolic volume fell by -7.5 +/- 21.7 mL in the supplement group and increased by 10.0 +/- 19.8 mL in the placebo group (P =.037). CONCLUSIONS: Supplementation results in higher myocardial CoQ10, taurine, and carnitine levels and is associated with a reduction in left ventricular end-diastolic volume in patients with left ventricular dysfunction before revascularization. Because the risk of death for surgical revascularization is related to preoperative left ventricular end-diastolic volume, supplementation could improve outcomes.

Aged↗

Tibiofemoral kinematics of the anterior cruciate ligament (ACL)-deficient weightbearing, living knee employing vertical access open "interventional" multiple resonance imaging.

BACKGROUND: Our current understanding of tibiofemoral kinematics in the anterior cruciate ligament (ACL)-deficient knee is very limited. Using vertical open-access MRI, it is possible to accurately analyze tibiofemoral motion in patients with isolated rupture of the ACL. STUDY: Prospective cohort study. PURPOSE: To assess if ACL rupture alters normal knee weightbearing kinematics. METHODS: Tibiofemoral motion was assessed through the arc of flexion from 0 degrees to 90 degrees in 10 patients with isolated rupture of the ACL in one knee and a normal contralateral knee. Midmedial and midlateral sagittal images were analyzed in all positions of flexion in both knees to assess the tibiofemoral relationship. RESULTS: In the lateral compartment of the knee, the tibial plateau is persistently subluxed anteriorly throughout the arc of flexion from 0 degrees to 90 degrees (flexion facet center to posterior tibial cortex distance of 15.8 mm +/- 2.9 in ACL-deficient knees compared to 21.4 mm +/- 1.4 in normal knees at 0 degrees extension, P <.0001) when compared to normal knees. The medial tibiofemoral relationship is unchanged compared to normal knees. CONCLUSION: Rupture of the ACL changes tibiofemoral kinematics producing anterior subluxation of the lateral tibial plateau. CLINICAL SIGNIFICANCE: Altered kinematics may explain, at least in part, the increased incidence of secondary osteoarthritis in patients with ACL rupture.

Adult↗