The efficacy of detecting arrhythmia is higher with 7-day continuous electrocardiographic patch monitoring than with 24-h Holter monitoring.

Background: Detecting high-risk arrhythmia is important in diagnosing patients with palpitations. We compared the diagnostic accuracies of 7-day patch-type electrocardiographic (ECG) monitoring and 24-h Holter monitoring for detecting significant arrhythmias in patients with palpitations. Methods: This was a single-center prospective trial with 58 participants who presented with palpitations, chest pain or syncope. Outcomes were defined as the detection of any one of six arrhythmias, including supraventricular tachycardia (SVT), atrial fibrillation or atrial flutter lasting more than 30 s, pauses of more than 3 s, high-degree atrioventricular block, ventricular tachycardia (VT) >3 beats, or polymorphic VT/ventricular fibrillation. The McNemar test for paired proportions was used to compare arrhythmia detection rates. Results: The overall arrhythmia detection rate was higher with 7-day ECG patch monitoring than with 24-h Holter monitoring (34.5% vs. 19.0%, p = .008). Compared with the use of 24-h Holter monitors, the use of 7-day ECG patch monitors was associated with higher detection of SVT (29.3% vs. 13.8%, p = .042). No serious adverse skin reactions were reported among the ECG patch-monitored participants. Conclusions: The results suggest that a 7-day patch-type continuous ECG monitor is more effective for the detection of supraventricular tachycardia than is a 24-h Holter monitor. However, the clinical significance of device detected arrhythmia should be consolidated.

Mutation in the transcriptional regulator PhoP contributes to avirulence of Mycobacterium tuberculosis H37Ra strain.

Attenuated strains of mycobacteria can be exploited to determine genes essential for their pathogenesis and persistence. To this goal, we sequenced the genome of H37Ra, an attenuated variant of Mycobacterium tuberculosis H37Rv strain. Comparison with H37Rv revealed three unique coding region polymorphisms. One polymorphism was located in the DNA-binding domain of the transcriptional regulator PhoP, causing the protein's diminished DNA-binding capacity. Temporal gene expression profiles showed that several genes with reduced expression in H37Ra were also repressed in an H37Rv phoP knockout strain. At later time points, genes of the dormancy regulon, typically expressed in a state of nonreplicating persistence, were upregulated in H37Ra. Complementation of H37Ra with H37Rv phoP partially restored its persistence in a murine macrophage infection model. Our approach demonstrates the feasibility of identifying minute but distinct differences between isogenic strains and illustrates the consequences of single point mutations on the survival stratagem of M. tuberculosis.