Abstract Background The ECG is widely used in pre-participation evaluation (PPE) of athletes (ATH). While it is assumed that greater than normal QRS voltages reflect physiologically increased left ventricular mass (LVM), this has not been adequately demonstrated in ATH. Purpose To examine the relation between QRS voltage on surface ECG and LVM and explore if the distance from the chest wall to mid-LV (CWLVdis) affects QRS voltage in ATH. Methods We examined digitized ECG data and echocardiograms in college ATH, obtained as part of routine PPE in years 2010–16. ECG parameters included R and S-wave voltage components of the Sokolow-Lyon (S-L) and Cornell criteria for LV hypertrophy (i.e. SV1 + RV5-V6 and RaVL + SV3, respectively). Transthoracic 2D echocardiography was used to determine LVM (area-length method) and the CWLVdis (detailed in Fig1A). S-L positive (SV1 + RV5-V6 >35 mV or RaVL >11 mV) ATH were compared to S-L negative by t-test, and univariate correlation and multivariable regression analysis was used to explore independent effects of body characteristics, sex, LVM and CWLVdis on QRS voltage. Results Included were 227 ATH (age 18.6±0.7 yr; 85% male; 60%/33% Caucasian/Afro-american). Of these, 66% played American football, 18% volleyball and 16% basketball. Overall, mean LVM was 174±37 g (range 96–284 g), and BSA-indexed LVM was 78±12 g/m2 (range 49–108 g/m2). Mean CWLVdis was 8.5±1.1 cm (range 5.6–11.3 cm) and was greater in males (p<0.001, Fig1B). Forty-six ATH (24%, all male) were S-L positive and no ATH were positive according to Cornell criteria. S-L positive ATH had lower BMI (25.3±3.5 vs 26.9±4.9, p=0.012), greater absolute LVM (189.1±31.3 vs. 170.1±37.4 g, p=0.002) and greater BSA-indexed LVM (85.3±10.3 vs. 76.6±11.7 g/m2, p<0.001) than S-L negative ATH. The CWLVdis was similar between S-L positive and negative ATH (8.4±1.2 vs. 8.6±1.1, respectively, p=0.213). CWLVdis was more strongly correlated to body mass (r=0.73, p<0.001, Fig. 1C) than to height (r=0.34, p<0.001). LVM correlated weakly to ECG voltage as combined in the S-L or Cornell criteria (Fig. 1C). CWLVdis was weakly correlated with R in aVL, V5 and V6 (r=0.21, 0.16 and 0.16, all p<0.02). In multivariate analysis, male sex (β=0.31), LVM (β=0.45) and body mass index (β=-0.37) were independently associated with the S-L summed voltage (R2 0.26, p<0.001). For Cornell summed voltage, only sex was an independent predictor (β=0.48, R2 0.22, p<001). Figure 1 Conclusion The R and S wave ECG amplitudes used in the two most common ECG criteria for LV hypertrophy were weakly related in the highest to lowest order to sex, LVM, body size and the distance from the LV to the chest wall in our college ATH.
We present the angiographic findings of a case of myocardial infarction associated with COVID-19 with a heavy burden of thrombus, despite only minor obstructive coronary disease.
Introduction The Intermountain Risk Score (IMRS) was developed and validated to predict short-term and long-term mortality in hospitalised patients using demographics and commonly available laboratory data. In this study, we sought to determine whether the IMRS also predicts all-cause mortality in patients hospitalised with heart failure with preserved ejection fraction (HFpEF) and whether it is complementary to the Get with the Guidelines Heart Failure (GWTG-HF) risk score or N-terminal pro-B-type natriuretic peptide (NT-proBNP). Methods and results We used the Stanford Translational Research Integrated Database Environment to identify 3847 adult patients with a diagnosis of HFpEF between January 1998 and December 2016. Of these, 580 were hospitalised with a primary diagnosis of acute HFpEF. Mean age was 76±16 years, the majority being female (58%), with a high prevalence of diabetes mellitus (36%) and a history of coronary artery disease (60%). Over a median follow-up of 2.0 years, 140 (24%) patients died. On multivariable analysis, the IMRS and GWTG-HF risk score were independently associated with all-cause mortality (standardised HRs IMRS (1.55 (95% CI 1.27 to 1.93)); GWTG-HF (1.60 (95% CI 1.27 to 2.01))). Combining the two scores, improved the net reclassification over GWTG-HF alone by 36.2%. In patients with available NT-proBNP (n=341), NT-proBNP improved the net reclassification of each score by 46.2% (IMRS) and 36.3% (GWTG-HF). Conclusion IMRS and GWTG-HF risk scores, along with NT-proBNP, play a complementary role in predicting outcome in patients hospitalised with HFpEF.
Abstract Myalgic Encephalomyelitis or Chronic Fatigue Syndrome (ME/CFS) is a heterogeneous syndrome in which patients often experience severe fatigue and malaise following exertion. Immune and cardiovascular dysfunction have been postulated to play a role in the pathophysiology. We therefore, examined whether cytokine profiling or cardiovascular testing following exercise would differentiate patients with ME/CFS. Twenty-four ME/CFS patients were matched to 24 sedentary controls and underwent cardiovascular and circulating immune profiling. Cardiovascular analysis included echocardiography, cardiopulmonary exercise and endothelial function testing. Cytokine and growth factor profiles were analyzed using a 51-plex Luminex bead kit at baseline and 18 hours following exercise. Cardiac structure and exercise capacity were similar between groups. Sparse partial least square discriminant analyses of cytokine profiles 18 hours post exercise offered the most reliable discrimination between ME/CFS and controls (κ = 0.62(0.34,0.84)). The most discriminatory cytokines post exercise were CD40L, platelet activator inhibitor, interleukin 1-β, interferon-α and CXCL1. In conclusion, cytokine profiling following exercise may help differentiate patients with ME/CFS from sedentary controls.
HISTORY: A 50-year-old male suffered a cardiac arrest after an endurance cycling event. After prompt cardiopulmonary resuscitation and electrical cardioversion, coronary angiography demonstrated severe intermediate vessel stenosis treated with percutaneous coronary intervention. Echocardiography showed mildly reduced Left Ventricular (LV) systolic function and wall motion abnormalities discordant with coronary angiography. Magnetic Resonance Imaging demonstrated interventricular septum, mid-inferolateral wall and LV apex hypokinesis. Positron Emission Tomography showed normal myocardial metabolism. After diagnostic work up, an Automatic Implantable Cardioverter Defibrillator (AICD) was implanted. Recurrent palpitations on return to high intensity exercise were investigated with Cardiopulmonary Exercise Testing (CPET). PHYSICAL EXAMINATION: Unremarkable AICD site and no clinical signs of heart failure. DIFFERENTIAL DIAGNOSES: Anxiety, Supraventricular Arrhythmia, Progressive Cardiomyopathic process with Ventricular Arrhythmia, Inappropriate anti-tachy pacing TEST AND RESULTS:CPET: Maximal effort with RER of 1.11 and excellent exercise capacity (Figure 1). Abrupt increase in HR coinciding with the respiratory compensation point was observed from 135 bpm (79% max HR) to 155 bpm (91% max HR) with a subsequent plateau and no variability suspicious of an atrial paced rhythm. Stress Echocardiogram: Normal contractile reserve. No evidence of inducible myocardial ischemia by symptom, ECG or echocardiogram criteria. Resting LVEF 55 +/- 5% despite multi coronary territory hypokinesis.FINAL DIAGNOSIS: Inappropriate Rate Adaptive Pacing in an AICD TREATMENT AND OUTCOMES: Rate adaptive pacing was ceased with no further palpitations. Shared decision making resulted in graded return to high intensity exercise. Medical management of heart failure. Process initiated to further investigate etiology of cardiomyopathic process.
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