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This article discusses a case of misdiagnosis from a smartwatch. A 60-year-old man received alerts on his wearable electronic device indicating that he may have atrial fibrillation. However, further testing revealed that he had a rare arrhythmia known as dual AV node non-reentrant tachycardia, or double fire. This condition can be misdiagnosed as supraventricular ectopy, ventricular ectopy, or atrial fibrillation. The article emphasizes the importance of careful physician review of rhythm strips to confirm the diagnosis, especially in cases where wearable devices are used. Treatment for double fire tachycardia typically involves radiofrequency ablation of the slow pathway. [Extracted from the article]

Introduction: Serial increases in high-sensitivity cardiac troponin (hs-cTnT) have been associated with death in community-dwelling adults, but the association remains uninvestigated in those with ambulatory coronary artery disease (CAD). Hypothesis: An increase in hs-cTnT over 5 years predicts subsequent all-cause mortality in ambulatory CAD. Methods: We measured hs-cTnT at baseline and after 5 years in 635 participants with ambulatory CAD. We defined "undetectable" levels of hs-cTnT as < 5 pg/mL, "detectable" as between 5 and 14 pg/mL, and "elevated" as >14 pg/mL. We used an unadjusted and a multivariable-adjusted Cox proportional hazards model to evaluate the association between 5-year change in hs-cTnT and subsequent all-cause mortality. Results: There were 386 participants (61%) who had an increase in hs-cTnT levels between baseline and year 5 measurements (median increase 5.6 pg/mL, IQR 3.2-9.9 pg/mL). There were 182 deaths after a mean 4.2 years of follow-up after year 5. After adjusting for clinical variables, a > 50% increase in hs-cTnT between baseline and year 5 was associated with a nearly 2-fold increased risk of death from any cause (HR 1.7, 95% CI 1.1-2.7). Additional hazard ratios for death from any cause, categorized by levels of baseline and year 5 hs-cTnT, are displayed in the figure. Conclusion: In ambulatory CAD, serial increases in hs-cTnT predict death, suggesting that preventive strategies may be warranted in this setting. Figure: Hazard ratios for death from any cause, categorized by levels of baseline and year 5 high-sensitivity cardiac troponin (hs-cTnT), adjusted for clinical variables. Error bars represent 95% confidence intervals. Data for patients who had detectable baseline but undetectable year 5 levels, as well as patients with elevated baseline but undetectable year 5 levels are not displayed due to small numbers of deaths in these categories. [ABSTRACT FROM AUTHOR]

Mavacamten is a first-in-class cardiac myosin ATPase inhibitor, approved by the United States Food and Drug Administration for the treatment of hypertrophic cardiomyopathy with obstructive physiology (oHCM). Here, we present the real-world use of mavacamten in 50 patients with oHCM at a tertiary care referral center. In both our highlighted case and in our aggregate data, we report significant improvement in wall thickness, mitral regurgitation, left ventricular outflow tract obstruction and New York Heart Association symptom class. Moreover, in our center's experience, neither arrhythmia burden, nor contractility have worsened in the vast majority of patients: we note a clinically insignificant mean decrease in left ventricular ejection fraction (LVEF), with only two patients requiring temporary mavacamten discontinuance for LVEF < 50%. Adverse events were rare, unrelated to mavacamten itself, and seen solely in patients with disease too advanced to have been represented in clinical trials. Moreover, our multidisciplinary pathway enabled us to provide a large number of patients with a novel closely-monitored therapeutic within just a few months of commercial availability. These data lead us to conclude that mavacamten, as a first-in-class cardiac myosin inhibitor, is safe and efficacious in real-world settings., Competing Interests: VP has consulting and advisory relationships with BioMarin, Lexeo Therapeutics and Viz.ai and receives funding from BioMarin, the John Taylor Babbitt Foundation. MW reports research grant and in kind support from Bristol Myers Squibb, consulting for Leal Therapeutics, outside the submitted work. EA reports advisory board fees from Apple and Foresite Labs. EA has ownership interest in SVEXA, Nuevocor, DeepCell, and Personalis, outside the submitted work. EA is a board member of AstraZeneca. CW reports consultancy fees from AiRNA Bio and Avidity Biosciences. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Kim, Chu, Keamy-Minor, Paranjpe, Tang, O'Sullivan, Desai, Liu, Munsey, Hecker, Cuenco, Kao, Bacolor, Bonnett, Linder, Lacar, Robles, Lamendola, Smith, Knowles, Perez, Kawana, Sallam, Weldy, Wheeler, Parikh, Salisbury, Ashley and the Stanford Center for Inherited Cardiovascular Disease.)