The SHM is accurate in measuring QTc interval in sinus rhythm when compared to 12-lead ECG in healthy volunteers. For patients receiving QT prolonging antiarrhythmics, SHM is capable of detecting QTc prolongation, and lead-I of the SHM is most accurate in measuring the QTc if < 500 milliseconds.
Cardiac resynchronization therapy may be superior to RV pacing in patients undergoing AVJ ablation for AF. Further studies, adequately powered to detect clinical outcomes, are required.
Angiotensin-converting enzyme 2 (ACE2), a homologue of angiotensin-converting enzyme (ACE), converts angiotensin (Ang) I to Ang(1-9) and Ang II to Ang(1-7), but does not directly process Ang I to Ang II. Cardiac function is compromised in ACE2 null mice; however, the importance of ACE2 in the processing of angiotensin peptides within the murine heart is not known. We determined the metabolism of angiotensins in wild-type (WT), ACE (ACE −/− ) and ACE2 null mice (ACE2 −/− ). Angiotensin II was converted almost exclusively to Ang(1-7) in the cardiac membranes of WT and ACE −/− strains, although generation of Ang(1-7) was greater in the ACE −/− mice (27.4 ± 4.1 versus 17.5 ± 3.2 nmol −1 mg h −1 for WT). The ACE2 inhibitor MLN4760 significantly attenuated Ang II metabolism and the subsequent formation of Ang(1-7) in both strains. In the ACE2 −/− hearts, Ang II metabolism and the generation of Ang(1-7) were significantly attenuated; however, the ACE2 inhibitor reduced the residual Ang(1-7)-forming activity in this strain. Angiotensin I was primarily converted to Ang(1-9) (WT, 28.9 ± 3.1 nmol −1 mg h −1 ; ACE −/− , 49.8 ± 5.3 nmol −1 mg h −1 ; and ACE2 −/− , 35.9 ± 5.4 nmol −1 mg h −1 ) and to smaller quantities of Ang(1-7) and Ang II. Although the ACE2 inhibitor had no effect on Ang(1-9) formation, the carboxypeptidase A inhibitor benzylsuccinate essentially abolished the formation of Ang(1-9) and increased the levels of Ang I in cardiac membranes. In conclusion, our studies in the murine heart suggest that ACE2 is the primary pathway for the metabolism of Ang II and the subsequent formation of Ang(1-7), a peptide that, in contrast to Ang II, exhibits both antifibrotic and antiproliferative actions.
The use of smartphones for arrhythmia monitoring is another leap for ECG utilization and arrhythmia detection - effectively taking the technology to any smartphone user. Smart wearable technology, while very common, is limited mostly to activity tracking and exercise motivation. Rhythm strip generating smartphone products (Kardia Mobile by AliveCor and ECG Check by Cardiac Designs) are more powerful at arrhythmia detection than wearable monitors. These products, which have been studied in a variety of situations, rely on an external device with metal sensors to create a rhythm strip, which is usually Lead I. A different subset of smartphone products use photoplethysmography through a phone camera and light to detect atrial fibrillation. Together, these products are creating a paradigm shift in rhythm detection and monitoring.
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