ABSTRACT
Background: Remote rhythm monitoring with wearable devices is increasingly used especially for early detection of atrial fibrillation/flutter (AF/Afl), being the access to hospital discouraged, especially for frail elderly patients, due to the burden and risk of COVID-19 pandemic. Whereas devices using photo plethysmography (PPG) may misinterpret as AF pulse irregularities due to extrasystoles, patient-directed recording of a single (usually wrist-to-wrist) lead ECG (LEAD I) with hand-held devices or smartwatches have been developed to increase accuracy in AF detection. However, although recent studies validating such devices single-lead ECG recording have shown high sensitivity and specificity, false negative findings such as those reported here are still possible and must be prevented [1]. Purpose(s): Given previous experience of diagnostic uncertainty or failure of the smartwatch ECG (SW-ECG) LEAD I to detect AF/Afl, we have tested if false negative diagnosis could be avoided by recording in addition at least one right precordial (pseudo-V1) lead analyzed by a trained healthcare professional. Method(s): Over one calendar year observation, five patients with previous history of ablated supraventricular arrhythmias suffering sudden palpitations suspected of paroxysmal AF/Afl were instructed to record with their smartwatch at least one precordial lead in addition to LEAD I, to monitor ECG until the termination of symptoms. The SW-ECG strips were sent by telephone for professional interpretation. Diagnostic accuracy based on LEAD I and pseudo-V1 were independently validated by two cardiologists (diagnostic goldstandard - DGS). Result(s): 22 AF/Afl events occurred. Pharmacological cardioversion to sinus rhythm (SR) was obtained in 64%. 192 ECG strips were transmitted. 43,7% of the strips were automatically classified as not significant (or not valid ). Compared to DGS, out of 108 valid strips, correct automatic identification of AF/Afl was obtained in 36,4% with LEAD I, in 33,3% with pseudo V1 and in 54,5% with combined leads, respectively. Interestingly, the SW algorithm has wrongly diagnosed as SR, not only LEAD I, but also 39,4% of pseudo-V1 strips, despite clear-cut evidence of typical flutter waves (Figure 1), when RR intervals were regular due to high degree (e.g., 4:1) A-V block. Conclusion(s): With simple instructions, patients (or their relatives) can easily record an additional precordial (pseudo-V1) SW-ECG lead, that may enhance sensitivity and specificity for remote detection of AF/Afl. However, at present, visual interpretation of SW-ECG by a trained healthcare professional is still needed to guarantee 100% correct diagnosis of AF/Afl, crucial to reduce thromboembolic risk and timely initiate the appropriate treatments. The automatic interpretation of SW's ECG could be improved by appropriate training of a machine learning approach to detect and analyze the atrial waveform provided by an additional pseudo-V1 lead.
ABSTRACT
Background: Identification of athletes with cardiac inflammation following COVID-19 can prevent exercise fatalities. The efficacy of pre and post COVID-19 infection electrocardiograms (ECGs) for detecting athletes with myopericarditis has never been reported. We aimed to assess the prevalence and diagnostic significance of novel 12-lead ECG patterns following COVID-19 infection in elite soccer players. Method(s): We conducted a multicentre study over a 2-year period involving 5 centres and 34 clubs and compared pre COVID and post COVID ECG changes in 455 consecutive athletes. ECGs were reported in accordance with the International recommendations for ECG interpretation in athletes. The following patterns were considered abnormal if they were not detected on the pre COVID-19 infection ECG: (a) biphasic T-waves;(b) reduction in T-wave amplitude by 50% in contiguous leads;(c) ST-segment depression;(d) J-point and ST-segment elevation >0.2 mV in the precordial leads and >0.1 mV in the limb leads;(e) tall T-waves >=1.0 mV (f) low QRS-amplitude in >3 limb leads and (g) complete right bundle branch block. Athletes exhibiting novel ECG changes underwent cardiovascular magnetic resonance (CMR) scans. One club mandated CMR scans for all 28 (6%) athletes, despite the absence of cardiac symptoms or ECG changes. Result(s): Athletes were aged 22+/-5 years (89% male and 57% white). 65 (14%) athletes reported cardiac symptoms. The mean duration of illness was 3+/-4 days. The post COVID ECG was performed 14+/-16 days following a positive PCR. 440 (97%) athletes had an unchanged post COVID- 19 ECG. Of these, 3 (0.6%) had cardiac symptoms and CMRs resulted in a diagnosis of pericarditis. 15 (3%) athletes demonstrated novel ECG changes following COVID-19 infection. Among athletes who demonstrated novel ECG changes, 10 (67%) reported cardiac symptoms. 13 (87%) athletes with novel ECG changes were diagnosed with inflammatory cardiac sequelae;pericarditis (n=6), healed myocarditis (n=3), definitive myocarditis (n=2), and possible/probable myocarditis (n=2). The overall prevalence of inflammatory cardiac sequelae based on novel ECG changes was 2.8%. None of the 28 (6%) athletes, who underwent a CMR, in the absence of cardiac symptoms or novel ECG changes revealed any abnormalities. Athletes revealing novel ECG changes, had a higher prevalence of cardiac symptoms (67% v 12% p<0.0001) and longer symptom duration (8+/-8 days v 2+/-4 days;p<0.0001) compared with athletes without novel ECG changes. Among athletes without cardiac symptoms, the additional yield of novel ECG changes to detect cardiac inflammation was 20% (n=3). Conclusion(s): 3% of elite soccer players demonstrated novel ECG changes post COVID-19 infection, of which almost 90% were diagnosed with cardiac inflammation during subsequent investigation. Most athletes with novel ECG changes exhibited cardiac symptoms. Novel ECGs changes contributed to a diagnosis of cardiac inflammation in 20% of athletes without cardiac symptoms.
ABSTRACT
Background: We have previously described the prognostic utility of QRS amplitude diminution (LoQRS) in predicting mortality and clinical decompensation in patients with COVID-19. However, whether and how COVID-19 vaccination status modulates risk prediction is not currently known. Objective: To assess any effect vaccination status may have on prevalence or risk prediction of LoQRS. Methods: We performed a retrospective analysis of patients admitted with laboratory confirmed COVID-19. Patients were excluded if the ECG was not acquired within 72 hrs of admission. Low QRS Amplitude (LoQRS) was defined by a composite of QRS amplitude <5mm in the limb leads or <10mm in the precordial leads (a composite of V1-V3 and V4-V6), or a ≥ 50% reduction in QRS amplitude. LoQRS was considered present even if found only in leads V1-V3 or V4-V6. Results: Among 3,365 patients, 11% were vaccinated and 89% were unvaccinated. LoQRS occurred in 30.9% of patients (33.5% of vaccinated patients and 30.5% in unvaccinated patients). Mortality occurred in 20.4% of patients without LoQRS compared to 30.2% in patients with LoQRS. The same pattern was seen in ICU admission, with 23.5% of patients without LoQRS being admitted to the ICU compared to 33.4% of patients with LoQRS. In multivariable models, LoQRS was independently associated with mortality and ICU admission regardless of vaccination status (or for mortality in unvaccinated patients: 1.24, 95% CI 1.03-1.49, P<0.01 vs 1.27 (95% CI 1.05-1.52, p<0.01). LoQRS also predicts ICU admission (OR 1.7, 95%CI 1.4-2.0) in unvaccinated patients vs. 1.73 (95%CI 1.5-2.1). In a survival analysis, vaccinated patients demonstrated improved mortality over unvaccinated counterparts, with a marked increase in mortality with, and stratification by, the presence of LoQRS in the unvaccinated. Conclusion: QRS amplitude on either the presenting or follow-up ECG independently predicts mortality and ICU admission in hospitalized patients with COVID-19 regardless of vaccination status. Patients who were vaccinated overall had better outcomes. [Formula presented]
ABSTRACT
Aims: We aimed to examine whether there is abnormal value of index of cardiac electrophysiological balance (iCEB=QT/QRS) in patients with confirmed coronavirus disease 2019 (COVID-19), which can predict ventricular arrhythmias (VAs), including non-Torsades de Pointes-like ventricular tachycardia/ventricular fibrillation (non- TdPs-like VT/VF) in low iCEB and Torsades de Pointes (TdPs) in high iCEB. We also investigated low voltage ECG among COVID-19 group. Methods and Results: This is a cross-sectional, single center study with a total of 53 newly diagnosed COVID-19 patients (confirmed with polymerase chain reaction (PCR) test) and 63 age and sex-matched control subjects were included in the study. Electrocardiographic marker of iCEB were calculated manually from 12-lead ECG. Low voltage ECG defined as peak-to-peak QRS voltage less than 5mm in all limb leads and less than 10mm in all precordial leads. Patients with COVID-19 more often had low iCEB, defined as iCEB below 3.24 compared to control group (56.6% vs 11.1%), (OR=10.435;95%CI 4.015 - 27.123;p=0.000). There were no significant association between COVID-19 and high iCEB, defined as iCEB above 5.24 (OR=1.041;95%CI 0.485 - 2.235;p=0.917). There were no significant difference of the number of low voltage ECG between COVID-19 and control groups (15.1% vs 6.3%), (OR=2.622;95%CI 0.743 - 9.257, p=0.123). Conclusion: In this study showed that patients with COVID-19 are more likely to have low iCEB, suggesting that patients with COVID-19 may be proarrhytmic (towards non- TdPs-like VT/VF event), due to the alleged myocardial involvement in SARS-CoV-2 infection.
ABSTRACT
Background: Transthyretin cardiac amyloidosis (ATTR-CM) is important comorbidity associated with severe aortic stenosis (AS). Multiple studies have shown that ATTR-CM was present in 10-15% of all cases with severe AS. The purpose of this quality improvement project is to raise awareness of ATTR-CM in patients who underwent transcatheter aortic valve replacement (TAVR) for severe AS amongst the healthcare providers and patients. Methods: We retrospectively reviewed all TAVR cases performed at our institution in 2019 (Total cases 87). We screened for the presence of predefined high-risk features for ATTR-CM based on prior literature (Presence of diastolic dysfunction, left ventricular hypertrophy on echocardiogram, low voltage-mass ratio, low limb lead voltage on EKG, arrhythmia/bundle branch block, or systemic symptoms of amyloidosis). We subsequently contacted the patients to discuss our clinical suspicion of ATTR-CM and offered clinical referral to a cardiac amyloid specialist. Results: Of the total of 87 patients who underwent TAVR in 2019, 12 patients were deceased at chart review. We have identified 50 patients (66.7%) who had high-risk features of ATTR-CM. A total of 17 patients (34% of 50 patients) agreed to be referred to cardiac amyloid specialist. Six patients (12%) were tested with 99m Technetium Pyrophosphate imaging, and all were negative for ATTR-CM. Eleven patients (22%) are still pending testing. Six patients did not wish for referral due to personal reasons. We were not able to reach 15 patients via phone (30%). In addition, we have found additional 12 patients who were deceased (Total mortality count of 24, 27.5%) in two years. Conclusion: Our project has increased awareness within structural cardiologists as we have implemented a prospective screening process within our institution. While we expected to diagnose ATTR-CM in 10% of severe AS who underwent TAVR, we had multiple difficulties contacting them, coordinating referrals due to the COVID-19 pandemic and higher 2-year mortality. We are hypothesizing whether the higher 2-year mortality is secondary to undetected ATTR-CM. We are planning for screening and timely referral for patients who underwent TAVR more recently.