A comparative study of median sternotomy and standard thoracotomy wound skin closure methods

Complications from skin closure after median sternotomy or standard thoracotomy incision, although uncommon, may be the source of undesireable morbidity and even death. A prospective randomized study of 3 different methods of wound skin closure has been carried out in 205 patients undergoing cardiothoracic surgery. These methods were: 1. continuous nylon vertical mattress suture; 2. continuous subcuticular absorbable (Dexon) suture; 3. adhesive sutureless skin closure (Op-Site). All wounds were examined by independent observers at 5, 10 and 45 days after operation, and the findings were graded from 0 to 4. At 5 days, assessments were made of inflammation, edema, discharge and infection. At 10 days, attention was paid to the state of wound healing, and at 45 days to the final cosmetic appearance. The use of continuous subcuticular Dexon suture resulted in less discharge than Op-site (p less than 0.001) and less swelling or redness than nylon (p less than 0.001). Assessment of the final cosmetic appearance of the wound 6 weeks following surgery showed subcuticular Dexon to be superior to either nylon (p less than 0.01) or Op-site (p less than 0.01).     

Muscle carnitine deficiency in patients with severe peripheral vascular disease

BACKGROUND. This study was designed to evaluate the effect of severe peripheral arterial insufficiency on carnitine concentrations and carnitine acetyltransferase and palmitoyltransferase activities in the ischemic skeletal muscles of patients with severe peripheral vascular disease. METHODS AND RESULTS. Nine biopsy specimens of ischemic muscles were obtained from five patients undergoing reconstructive vascular surgery. Biopsies from 35 normal subjects served as controls. Ischemic muscles showed a significant reduction in total carnitine from the control value of 20.9 +/- 5.2 to 11.6 +/- 6.2 nmol/mg noncollagen protein (p less than 0.01). A significantly lower free carnitine and acylcarnitine content contributed to this reduction. Similarly, carnitine acetyltransferase activity was reduced in the ischemic muscles from the control value of 102.1 +/- 41.2 to 52.9 +/- 22.1 nmol/min/mg noncollagen protein (p less than 0.01). On the contrary, carnitine palmitoyltransferase activity did not show any change (0.29 +/- 0.05 nmol/min/mg noncollagen protein in the ischemic muscles and 0.28 +/- 0.07 nmol/min/mg noncollagen protein in controls). Carnitine, acylcarnitines, and enzyme activities were also measured in the ischemic muscles in four additional patients 2 days after intravenous administration of L-propionylcarnitine (1.5 g as a single bolus followed by an infusion of 1 mg/kg/min for 30 minutes). Treatment restored normal levels of carnitine and its esters in the ischemic muscles but did not affect enzyme activities. CONCLUSIONS. Demonstration of carnitine deficiency in severe peripheral vascular disease substantiates previous findings showing the efficacy of carnitine supplementation to ischemic muscles. Furthermore, the feasibility of restoring carnitine homeostasis with L-propionylcarnitine provides the basis for clinical trials aimed at assessing the efficacy of this carnitine ester in the treatment of peripheral vascular disease.     

Isomyosin redistribution in chronic pressure overload: comparison between peptide mapping and electrophoresis under non-denaturing conditions

Summary Chronic pressure overload induces a redistribution in myosin isoenzymes as demonstrated by Ca⁺⁺-activated ATPase activity, electrophoresis under non-denaturing conditions and immunohistochemistry.We compared, in two groups of renal hypertensive rats and control rats, the isoenzymic patterns obtained by electrophoresis under non-denaturing conditions with those observed after heavy chains digestion with S. Aureus V8 protease.In the hypertensive animals in which a shift towards the slow V₂ and V₃ isomyosins was evident, peptide mapping always gave origin to a band which was not present in the controls.Since we consider this peptide as a marker of the redistribution towards the slow isoforms, peptide mapping according to Cleveland appears to be a simple and useful method to assess differences in isomyosin composition, at least between hypertrophic pressure-overloaded and normal rat ventricles. Moreover, in our experience this technique is simple, the patterns obtained from highly purified substrates are very reproducible and the digestion allows easy and clear comparisons.     

Sensory, motor, and autonomic neuropathy in patients with multiple symmetric lipomatosis

Clinical evaluation of 33 male patients affected by multiple symmetric lipomatosis has revealed a previously unreported high prevalence of somatic and autonomic neuropathies. In 84% of the patients, clinical examination revealed signs or symptoms of neural disturbances, ranging from a vibratory sensory loss to severely incapacitating trophic ulcers or Charcot's arthropathy. Electrodiagnostic investigations demonstrated a significant reduction of motor and sensory conduction velocity in the peroneal and sural nerves. Morphometric studies of nerve and muscle biopsies from five patients with multiple symmetric lipomatosis revealed a significant reduction in myelinated fiber density (4435 +/- 593 fibers/mm2 in MSL vs 7660 +/- 800 in controls; p less than 0.05), a selective reduction in the large fibers of 7 to 10 micron in diameter, and signs of chronic denervation-reinnervation processes. Bedside tests for autonomic neuropathy were abnormal in 15 of 20 patients studied. Metabolic studies in these patients confirmed a significant increase in plasma high-density lipoprotein fractions consistent with the diagnosis of hyperalphalipoproteinemia, and a significant reduction in plasma low-density lipoprotein fractions (hypobetalipoproteinemia) associated with a marked enhancement of lipoprotein lipase activity in adipose tissue. Thus, a metabolic factor has to be considered in the pathogenesis of MSL neuropathy.     

5'-Nucleotidase activity is decreased in seminal plasma and spermatozoa from varicocele patients

5'-Nucleotidase is involved in sperm capacitation via the cAMP-adenosine pathway and in sperm motility via direct adenosine production from AMP. Since these functions are reduced in varicocele, the aim of this study was to investigate whether the enzyme levels were altered in sperm from varicocele patients. The mean (SD) international units (IU) of 5'-nucleotidase activity in seminal plasma from 35 varicocele III patients was 0.16(0.09) IU ml(-1) vs 0.35(0.13) IU ml(-1) in 53 controls, this decrease being statistically significant at p < or = 0.001. A significant decrease in activity, expressed as international units per mg of protein concentration in spermatozoa homogenates, was also observed with spermatozoa: 0.0018(0.0017) IU mg(-1) in varicocele III vs 0.0081(0.0060) IU mg(-1) in controls, at p < or = 0.001. Compared to controls, the activity decrease observed both in spermatozoa and seminal plasma from 45 men with varicocele I was not statistically significant at p < or = 0.05. To determine the diagnostic value of 5'-nucleotidase in assessing sperm fertility in varicocele III, we used the likelihood ratios method and best cut-offs were identified in receiver operating characteristic curves. With a prevalence of 36%, the post-test probability of infertility was 91% in spermatozoa and 78% in seminal plasma. The cut-off values of 5'-nucleotidase activity discriminating for fertile/unfertile semen were 0.2 IU ml(-1) in seminal plasma and 0.003 IU mg(-1) of protein in spermatozoa. Overall, determination of 5'-nucleotidase activity, especially in spermatozoa, can be useful to characterize different varicocele degrees as well as the sperm fertility potential.     

Role of kinin B2 receptor signaling in the recruitment of circulating progenitor cells with neovascularization potential

Reduced migratory function of circulating angiogenic progenitor cells (CPCs) has been associated with impaired neovascularization in patients with cardiovascular disease (CVD). Previous findings underline the role of the kallikrein-kinin system in angiogenesis. We now demonstrate the involvement of the kinin B2 receptor (B(2)R) in the recruitment of CPCs to sites of ischemia and in their proangiogenic action. In healthy subjects, B(2)R was abundantly present on CD133(+) and CD34(+) CPCs as well as cultured endothelial progenitor cells (EPCs) derived from blood mononuclear cells (MNCs), whereas kinin B1 receptor expression was barely detectable. In transwell migration assays, bradykinin (BK) exerts a potent chemoattractant activity on CD133(+) and CD34(+) CPCs and EPCs via a B(2)R/phosphoinositide 3-kinase/eNOS-mediated mechanism. Migration toward BK was able to attract an MNC subpopulation enriched in CPCs with in vitro proangiogenic activity, as assessed by Matrigel assay. CPCs from cardiovascular disease patients showed low B(2)R levels and decreased migratory capacity toward BK. When injected systemically into wild-type mice with unilateral limb ischemia, bone marrow MNCs from syngenic B(2)R-deficient mice resulted in reduced homing of sca-1(+) and cKit(+)flk1(+) progenitors to ischemic muscles, impaired reparative neovascularization, and delayed perfusion recovery as compared with wild-type MNCs. Similarly, blockade of the B(2)R by systemic administration of icatibant prevented the beneficial effect of bone marrow MNC transplantation. BK-induced migration represents a novel mechanism mediating homing of circulating angiogenic progenitors. Reduction of BK sensitivity in progenitor cells from cardiovascular disease patients might contribute to impaired neovascularization after ischemic complications.     

Coronary cardiac allograft vasculopathy versus native atherosclerosis: difficulties in classification

Cardiac allograft vasculopathy is regarded as a progressive and diffuse intimal hyperplastic lesion of arteries and veins that leads to insidious vessel narrowing and to allograft ischemic disease, such as acute myocardial infarction or sudden cardiac death. The coronary lesions in transplanted hearts are considered as a particular type of arteriosclerosis with many similarities but also significant differences compared to native coronary atherosclerosis. It is particularly difficult for pathologists to systematically classify the lesions and to elucidate their origins, since over time, the allograft immune responses cause vascular pathology characterized by not only the onset of de novo fibrocellular lesions but also remodeling of already-existing native atherosclerotic lesions in the donor heart. Intraplaque hemorrhages, which result from newly formed leaky microvessels, may cause rapid increase of stenosis and generate a substrate for plaque destabilization. Comparing cardiac allograft vasculopathy from explanted hearts at autopsy with native coronary atherosclerosis from hearts removed at transplantation has revealed that ongoing intraplaque hemorrhages are also an important feature of cardiac allograft vasculopathy and may be important factors in the rapid progression of cardiac allograft vasculopathy.