Can Smartwatch Prevent Sudden Cardiac Deaths? A Case Of Smartwatch Failure in Arrhythmogenic Right Ventricular Dysplasia.

Arrhythmogenic right ventricular dysplasia (ARVD) is caused by mutations in genes coding for components of desmosomes in the myocardium. Mutations in these genes make desmosomes dysfunctional and account for myocyte detachment, followed by inflammation and apoptosis when it encounters undue mechanical stress. This is why ARVD is a common cause of sudden cardiac death in athletes with undiagnosed ARVD, as increased physical activity exacerbates this progression of ARVD and associated arrhythmias. We describe a case of ARVD in a 36-year-old woman who presented with an unusual sensation in her chest due to non-sustaining ventricular tachycardia, which her smartwatch failed to pick up. Many smartwatches use photoplethysmography (PPG) to monitor heart rate (HR). A typical PPG device contains two light sources (green light and infrared) and a photodetector to measure the reflected light, proportional to the beat-to-beat variation in blood volume. HR is then calculated from these variations. In ambulatory settings, smartwatches underestimate HR in most tachyarrhythmias, mainly when the HR is more than 100 beats/min. Patients using smartwatches for ambulatory heart monitoring should know that the absence of an irregular pulse notification does not exclude possible arrhythmias. Management of ARVD is mainly focused on the prevention of syncope and cardiac arrest through antiarrhythmic medications and an implantable cardioverter defibrillator.

Relation of Coronary Flow Reserve to Other Findings on Positron Emission Tomography Myocardial Perfusion Imaging and Left Heart Catheterization in Patients With End-stage Renal Disease Being Evaluated for Kidney Transplant.

Cardiovascular disease is the leading cause of death in patients with end-stage renal disease (ESRD) and often goes undetected. Abnormal coronary flow reserve (CFR), which predicts increased risk of cardiac death, may be present in patients with ESRD without other evidence of coronary artery disease (CAD). We prospectively studied 131 patients who had rest and dipyridamole pharmacologic stress N13-ammonia positron emission tomography myocardial perfusion imaging (PET MPI) for kidney transplant evaluation. Thirty-four patients also had left heart catheterization. Abnormal PET MPI was defined as qualitative ischemia or infarct, stress electrocardiogram ischemia, or transient ischemic dilation. CFR was calculated as the ratio of stress to rest coronary blood flow. Global CFR < 2 was defined as abnormal. Of 131 patients who had PET MPI (66% male, 55.6 ± 12.1 years), 30% (39 of 131) had abnormal PET MPI and 59% (77 of 131) had abnormal CFR. In a subset of 34 patients who had left heart catheterization (66% male, 61.0 ± 12.1 years), 68% (23 of 34) had abnormal CFR on PET MPI, and 68% (23 of 34) had ≥70% obstruction on left heart catheterization. Abnormal CFR was not significantly associated with abnormal PET MPI (p = 0.13) or obstructive CAD on left heart catheterization (p = 0.26). In conclusion, in the first prospective study of PET MPI in patients with ESRD, abnormal CFR is highly prevalent and is independent of abnormal findings on PET MPI or obstructive CAD on left heart catheterization.

Utility of near-infrared spectroscopy for detection of thin-cap neoatherosclerosis.

AIMS: Near-infrared spectroscopy (NIRS) has been employed to assess the composition of the atherosclerotic plaques in native coronary arteries. However, little is known about the detection of neoatherosclerosis by NIRS in in-stent restenosis (ISR). The aim of the study was to assess the relationship between the distribution of lipid determined by NIRS and morphology of ISR on optical coherence tomography (OCT). METHODS AND RESULTS: We performed both NIRS and OCT in 39 drug-eluting stents with ISR. Values of lipid-core burden index (LCBI) derived by NIRS were compared with the OCT-derived thickness of the fibrous cap covering neoatherosclerotic lesions. A total of 22 (49%) in-stent neointimas were identified as lipid rich by both NIRS and OCT. There was good agreement between OCT and NIRS in identifying lipid within in-stent neointima (kappa = 0.60, 95% CI: 0.34-0.86). OCT identified thin-cap neoatheromas (TCNA) (<65 µm) in 12 stents (23%). The minimal cap thickness of in-stent neoatherosclerotic plaque measured by OCT correlated with the maxLCBI4mm (maximal LCBI per 4 mm) within the stent (r = -0.77, P< 0.01). Moreover, maxLCBI4mm was able to accurately predict TCNA with a cut-off value of >144. CONCLUSION: NIRS correlates with OCT identification of lipids in stented vessels and is able to predict the presence of thin fibrous cap neoatheroma.

Effects of baseline and early acquired thrombocytopaenia on long-term mortality in patients undergoing percutaneous coronary intervention with bivalirudin.

AIMS: Bivalirudin use as a procedural anticoagulant in patients undergoing percutaneous coronary intervention (PCI) is associated with a lower incidence of thrombocytopaenia compared to other antithrombotic agents. We aimed to evaluate the prognostic impact of baseline thrombocytopaenia and early changes in platelet counts among patients undergoing PCI with exclusive use of bivalirudin. METHODS AND RESULTS: We evaluated 7,505 patients who underwent PCI over a period of eight years. Patients who received unfractionated heparin and glycoprotein IIb/IIIa receptor inhibitors were specifically excluded. Eight hundred and fifty-eight (11.4%) patients had baseline thrombocytopaenia and 451 (6.0%) developed acquired thrombocytopaenia. After adjustment for potential covariates, moderate to severe acquired thrombocytopaenia was the strongest independent predictor (HR 4.34, 95% CI: 2.13-8.84; p<0.001) of in-hospital net adverse clinical events, which included major adverse cardiac events and major bleeding complications. Age, male gender, baseline platelet count and intra-aortic balloon pump (IABP) insertion were independent predictors of in-hospital acquired thrombocytopaenia. After a mean follow-up of 2.6±1.7 years, moderate to severe baseline thrombocytopaenia (HR 2.42, 95% CI: 1.79-3.29; p<0.001), moderate to severe acquired thrombocytopaenia (HR 2.37, 95% CI: 1.13-4.97; p=0.02) and severe changes in platelet count (>67 k) were significant predictors of mortality. CONCLUSIONS: In patients undergoing PCI with bivalirudin, moderate to severe baseline and acquired thrombocytopaenia along with severe changes in platelet count are associated with higher long-term mortality.