The variability of automated QRS duration measurement.

AIMS: Previous studies have demonstrated substantial variability in manual assessment of QRS complex duration (QRSd). Disagreements in QRSd measurements were also found in several automated algorithms tested on digitized electrocardiogram (ECG) recordings. The aim of our study was to investigate the variability of automated QRSd measurements performed by two commercially available electrocardiographs. METHODS AND RESULTS: Two GE MAC 5000 (GE-1 and GE-2) electrocardiographs and two Mortara ELI 350 (Mortara-1 and Mortara-2) electrocardiographs were used in the study. Participants for the study were recruited from patients hospitalized in the department of cardiology of a university hospital. Participants underwent up to four recording sessions within a single day with a different electrocardiograph at each session when two to four immediately successive ECG recordings were undertaken. In 76 patients, 683 ECGs were recorded; the mean QRSd was 109.0 ± 26.1 ms. The QRSd difference ≥10 ms between the first and second intra-session ECG was found in 7, 3, 20, and 14% of ECG pairs for GE-1, GE-2, Mortara-1, and Mortara-2, respectively. No inter-session difference in QRSd was found within both manufacturers. In individual patients, Mortara calculated the mean QRSd to be longer by 7.3 ms (95% CI: 6.2-8.5 ms, P < 0.0001) with a 2.1-times (95% CI: 1.9-2.4) greater standard deviation of the mean QRSd (7.1 vs. 3.3 ms, P < 0.001). CONCLUSION: Electrocardiographs from two manufacturers measured QRSd values with a systematic difference and a significantly different level of precision. This may have important clinical implications in selection of suitable candidates for cardiac resynchronization therapy.

Carney complex: a clinicopathologic and molecular biological study of a sporadic case, including extracutaneous and cutaneous lesions and a novel mutation of the PRKAR1A gene.

BACKGROUND: Carney complex (CNC) is an autosomal dominant disorder associated with multiple neoplasms. OBJECTIVE: We report a case of a 40-year-old Caucasian man with a sporadic form of CNC. METHODS: This is a clinicopathologic description and molecular biological study with an emphasis on histopathologic findings. RESULTS: The patient presented with multiple cutaneous myxomas, cardiac myxomas, and spotty pigmentation at typical sites. Additionally, a blue nevus, a lipoma, multiple calcifications in both testes, and hypoechogenic areas suspected of being adenomas in the thyroid gland were found. Microscopically, the 2 cardiac and 6 cutaneous myxomas studied manifested a typical appearance, being composed of scattered polygonal, stellate, plump and/or spindle cells in a mucinous matrix containing small, sometimes dilated blood vessels. Of the 6 cutaneous myxomas, only in one lesion was there an abnormal epithelial component (tiny basaloid buds and a horn cyst). Molecular biologic study revealed a heterozygous shift mutation c.796dupA in exon 10 of the PRKAR1A gene. Physical examination and genetic testing of family members (both parents and two brothers) for the PRKAR1A mutation were negative, as was analysis of the peripheral blood of 110 randomly selected, unrelated healthy individuals for the above mutation. These findings suggest sporadic disease and a novel mutation in our patient. LIMITATIONS: None. CONCLUSION: Herein we report a case of sporadic CNC in which a novel mutation in PRKAR1A was identified.

Treatment of hyperhomocysteinemia with folic acid: effects on homocysteine levels, coagulation status, and oxidative stress markers.

The aim of the study was to determine whether folic acid treatment in subjects with homocysteinemia would change their coagulation and oxidative status. Thirty-three patients with peripheral vascular disease and 26 elderly subjects with no symptoms of atherosclerosis, all of whom had total homocysteine >20 microM, were treated with folic acid (5 or 10 mg) for 3 months. In the 33 patients with peripheral vascular disease, homocysteine levels decreased from a median of 26.7 microM at baseline to 20.0 microM (p < 0.0001), whereas in the 26 asymptomatic elderly subjects, homocysteine level decreased from 24.4 microM to 18.6 microM (p < 0.0001). Plasma fibrinogen decreased whereas plasminogen and anti-thrombin increased; the differences between pre- and posttreatment values were significant in both patients and healthy subjects. Oxidative status markers showed a shift toward lower oxidative stress. This effect was observed in both study groups. An association of the therapeutic effect with the genetic polymorphism of 5,10-methylenetetrahydrofolate reductase was not detected. Folic acid supplementation to hyperhomocysteinemic subjects resulted in a decrease in total blood homocysteine concentrations; moreover, there was a tendency to reverse the coagulation status and oxidative stress.