[Creatine kinase (CK)].

Myoglobin has been described as an early marker of myocardial injury. It increases within 1 to 3 hours of myocardial injury, and falls back to normal early after the event. Few data suggest that myoglobin can be used to triage patients with chest pain. To assess the diagnostic utility of second myoglobin levels drawn within 2 to 3 hours after presentation to the emergency department for detecting myocardial infarction, we prospectively collected myoglobin levels in 368 patients aged > or = 30 years who were admitted with chest pain. Myoglobin levels were measured at admission and 2 to 3 hours later. Sensitivity and specificity for detecting acute myocardial infarction for a twofold increase in myoglobin level from baseline were 39% and 98%, respectively. The early diagnostic performance of myoglobin at admission, the second level drawn 2 to 3 hours later, and creatine kinase-MB mass drawn at admission were similar (receiver-operating characteristic curves 0.80, 0.86, and 0.85). The diagnostic performance of each of these markers was significantly superior to the absolute change from baseline to second myoglobin (receiver-operating characteristic curve 0.77). In patients who presented within 4 hours of symptom onset, myoglobin drawn 2 to 3 hours later had the highest yield for detecting myocardial infarction. These results suggest that serial myoglobin measurement aiming to detect changes over time is not superior to single marker determinations. Myoglobin measured in 2 to 3 hours from admission may be helpful in triaging patients who present within 4 hours from onset of symptoms.

Creatine Kinase↗

PubMed1999

Gene shifting: a novel therapy for mitochondrial myopathy.

Mutations in mitochondrial DNA (mtDNA) are the most frequent causes of mitochondrial myopathy in adults. In the majority of cases mutant and wild-type mtDNAs coexist, a condition referred to as mtDNA heteroplasmy; however, the relative frequency of each species varies widely in different cells and tissues. Nearly complete segregation of mutant and wild-type mtDNAs has been observed in the skeletal muscle of many patients. In such patients mutant mtDNAs pre-dominate in mature myofibers but are rare or undetectable in skeletal muscle satellite cells cultured in vitro. This pattern is thought to result from positive selection for the mutant mtDNA in post-mitotic myofibers and loss of the mutant by genetic drift in satellite cells. Satellite cells are dormant myoblasts that can be stimulated to re-enter the cell cycle and fuse with existing myofibers in response to signals for muscle growth or repair. We tested whether we could normalize the mtDNA genotype in mature myofibers in a patient with mitochondrial myopathy by enhancing the incorporation of satellite cells through regeneration following injury or muscle hypertrophy, induced by either eccentric or concentric resistance exercise training. We show a remarkable increase in the ratio of wild-type to mutant mtDNAs, in the proportion of muscle fibers with normal respiratory chain activity and in muscle fiber cross-sectional area after a short period of concentric exercise training. These data show that it is possible to reverse the molecular events that led to expression of metabolic myopathy and demonstrate the effectiveness of this form of 'gene shifting' therapy.

Creatine Kinase↗