Utility of exercise testing to assess athletes for post COVID-19 myocarditis.

Purpose: This study assessed a functional protocol to identify myocarditis or myocardial involvement in competitive athletes following SARS-CoV2 infection. Methods: We prospectively evaluated competitive athletes (n = 174) for myocarditis or myocardial involvement using the Multidisciplinary Inquiry of Athletes in Miami (MIAMI) protocol, a median of 18.5 (IQR 16-25) days following diagnosis of COVID-19 infection. The protocol included biomarker analysis, ECG, cardiopulmonary stress echocardiography testing with global longitudinal strain (GLS), and targeted cardiac MRI for athletes with abnormal findings. Patients were followed for median of 148 days. Results: We evaluated 52 females and 122 males, with median age 21 (IQR: 19, 22) years. Five (2.9%) had evidence of myocardial involvement, including definite or probable myocarditis (n = 2). Three of the 5 athletes with myocarditis or myocardial involvement had clinically significant abnormalities during stress testing including ventricular ectopy, wall motion abnormalities and/or elevated VE/VCO2, while the other two athletes had resting ECG abnormalities. VO2max, left ventricular ejection fraction and GLS were similar between those with or without myocardial involvement. No adverse events were reported in the 169 athletes cleared to exercise at a median follow-up of 148 (IQR108,211) days. Patients who were initially restricted from exercise had no adverse sequelae and were cleared to resume training between 3 and 12 months post diagnosis. Conclusions: Screening protocols that include exercise testing may enhance the sensitivity of detecting COVID-19 related myocardial involvement following recovery from SARS-CoV2 infection.

Aerobic training does not alter CRP in apparently healthy, untrained men.

AIM: Regular aerobic exercise may reduce cardiovascular disease (CVD) risk by lowering the concentration of inflammatory markers, such as C-reactive protein (CRP). While studies in diseased populations have shown significant decreases in CRP concentrations with regular aerobic training, little has been conclusively determined regarding the effects of aerobic training on CRP concentrations in apparently healthy, untrained populations. Aim of the study was to examine the effects of a 17-wk half marathon training program (TP) on CRP concentrations, aerobic fitness, and body composition in apparently healthy, untrained men. METHODS: Twenty men (29.3±1.0 y) enrolled as training subjects (TRN) in a 17-wk half marathon TP. An additional 22 men (27.8±1.4 y) served as controls (CON). Fasting blood samples were taken at four time points over the TP and were analyzed for CRP and interleukin-6 (IL-6) concentrations. Aerobic capacity (VO2max) and body fat percent (BF%) were measured before and after the TP. RESULTS: No significant post-training changes in CRP (P=0.70) or IL-6 concentrations (P=0.67) were seen in TRN as a result of the TP, despite significant improvements in VO2max (42.2±1.9 ml∙kg-1∙min⁻¹, P<0.0001) and significant reductions in resting heart rate (P=0.004), BF% (P=0.03), and body mass index (BMI, P=0.05). No significant changes in CRP, VO2max, BMI, or BF% were detected in CON over time. CONCLUSION: Regular aerobic training does not appear to affect CRP concentrations in apparently healthy, untrained men despite significant improvements in bodyweight, BF%, BMI, and VO2max.

Clinical utility of intraatrial pacemaker stored electrograms to diagnose atrial fibrillation and flutter.

The purpose of this study was to determine if intraatrial electrograms (EGMs) are required to diagnose specific types of atrial tachyarrhythmias detected by pacemaker diagnostics. DDD pacemakers in 56 patients were programmed to store episodes of atrial tachyarrhythmias. Some episodes had a stored atrial EGM snapshot of the atrial tachyarrhythmia. The EGMs were analyzed to confirm whether the stored episodes were true atrial tachyarrhythmias or other pacemaker-sensed events. EGM confirmation of atrial tachyarrhythmias correlated with increasing duration and rate of episodes. In particular, using EGMs, 8 (18%) of 44 episodes < 10 seconds in duration confirmed atrial tachyarrhythmias compared to 16 (89%) of 18 episodes > 5 minutes in duration (P < 0.001). Only 10 (18%) of 56 detected atrial arrhythmia episodes at rates < 250 complexes per minute were confirmed by the atrial EGM as true arrhythmias compared to 33 (57%) of 58 detected episodes at rates > 250/min (P < 0.001) Twenty-nine (91%) of 32 EGM confirmed episodes of atrial fibrillation/flutter had an atrial rate > 250 complexes per minute and were a minimum of 10 seconds in duration. Fifteen (88%) of 17 episodes meeting the combined stored data criteria of > 250 complexes per minute and duration > 5 minutes were confirmed as atrial fibrillation or flutter by stored EGMs. Atrial EGMs identified that 71 (62%) of 114 stored high atrial rate (HAR) episodes were events other than true atrial tachyarrhythmias. Pacemaker diagnostic data with intraatrial EGMs can diagnose specific atrial tachyarrhythmias and identify other pacemaker-sensed events. Stored episodes > 250 complexes per minute and > 5 minutes in duration had a high correlation with atrial fibrillation and flutter.

Opportunities for sudden death prevention: directions for new clinical and basic research.

Sudden cardiac death (SCD) represents an enormous public health problem in all developed countries of the world, yet its magnitude and precise incidence in different populations and disease subgroups remains unclear. There also remain major questions and research challenges in establishing the sensitive and specific markers of SCD risk needed for optimizing therapeutic strategies and allocation of resources, such as implantable defibrillators. In the past, risk factors for coronary artery disease (CAD) have been heavily relied on to identify risk for SCD. However, although a majority of SCD events continue to occur in the context of this disease etiology, risk factors for CAD appear to have relatively limited ability to predict risk in specific individuals and subgroups with enhanced progressive or inherited susceptibility to lethal arrhythmias. This commentary is intended to assess potentials for progress in developing improved approaches to SCD prediction and prevention through new clinical and basic research on the fundamental causes of ventricular arrhythmias, the development of new markers of electrical instability, and better understanding of the role of genetic variability in their origin.

Sudden cardiac death: exploring the limits of our knowledge.

Despite progress in epidemiology, clinical profiling, and interventions, sudden cardiac death remains a major clinical and public health problem. There remain important unresolved issues that are challenges for future progress. Among these are a better understanding of the magnitude of the problem and methods of profiling risk for individuals, the etiology and mechanisms of cardiac arrest in individuals with and without previously identified structural heart disease, clinical strategies for primary and secondary prevention of sudden cardiac death, and further development of community programs for improving cardiac arrest survival in the out-of-hospital environment. Each of these areas of endeavor and potential progress are reviewed and discussed.

Prediction of sudden cardiac death by fractal analysis of heart rate variability in elderly subjects.

OBJECTIVES: The aim of this study was to test the hypothesis that abnormal scaling characteristics of heart rate (HR) predict sudden cardiac death in a random population of elderly subjects. BACKGROUND: An abnormality in the short-term fractal scaling properties of HR has been observed to be related to a risk of life-threatening arrhythmias among patients with advanced heart diseases. The predictive power of altered short-term scaling properties of HR in general populations is unknown. METHODS: A random sample of 325 subjects, age 65 years or older, who had a comprehensive risk profiling from clinical evaluation, laboratory tests and 24-h Holter recordings were followed up for 10 years. Heart rate dynamics, including conventional and fractal scaling measures of HR variability, were analyzed. RESULTS: At 10 years of follow-up, 164 subjects had died. Seventy-one subjects had died of a cardiac cause, and 29 deaths were defined as sudden cardiac deaths. By univariate analysis, a reduced short-term fractal scaling exponent predicted the occurrence of cardiac death (relative risk [RR] 2.5, 95% confidence interval [CI], 1.9 to 3.2, p < 0.001) and provided even stronger prediction of sudden cardiac death (RR 4.1, 95% CI, 2.5 to 6.6, p < 0.001). After adjusting for other predictive variables in a multivariate analysis, reduced exponent value remained as an independent predictor of sudden cardiac death (RR 4.3, 95% CI, 2.0 to 9.2, p < 0.001). CONCLUSIONS: Altered short-term fractal scaling properties of HR indicate an increased risk for cardiac mortality, particularly sudden cardiac death, in the random population of elderly subjects.

Paradoxical behavior of PR interval dynamics during exercise and recovery and its relationship to cardiac memory at the atrioventricular node.

This preliminary study deals with the dynamics of the PR interval during exercise testing by using a Bruce protocol in 31 nonmedicated, normal patients with ages of 33 +/- 14 years. The behavior of the PR interval permitted its categorization into 2 groups. In Group I (27 of 31, 87.1% of patients) the PR interval showed the expected biphasic behavior with a gradual shortening with increasing exercise and a gradual lengthening during recovery. In contrast, the PR interval in Group II (4 of 31, 12.9% of patients) showed a triphasic behavior since, toward the end of recovery, there was a second decrease in duration. Because of this temporal relation to the phases of exercise, this paradoxical response, in analogy to what happened to the QT interval during exercise, could have been caused by a form of short-term memory or to varying, but normal, intergroup differences in autonomic function. However, further studies involving a greater number of patients are required to reach definite conclusions.

Patterns of acute inferior wall myocardial infarction caused by hyperkalemia.

This is one of the first published articles dealing with two patients with hyperkalemia showing, not only a pattern of acute anteroseptal myocardial infarction, but of inferior myocardial infarction as well. This was attributed to uneven effects of high potassium in different regions of the heart. Marked reduction of resting potential of a large group of cells from the most affected regions could produce areas of inexcitability, capable of generating abnormal q waves. Likewise, ST-segment elevation could be attributed to a hyperkalemic diastolic current of injury (due to depolarization of resting potential) and to a combination of diastolic and systolic current of injury (due to a reduction of action potential amplitude). In addition, current flowing down voltage gradients on either side (epicardial and endocardial) of the M cell region could be responsible for the T wave, and even, to some extent, to the ST-segment changes. However, it cannot be excluded that the previously described changes may have resulted from coronary spasm without chest pain. In fact, an intriguing possibility, namely that hyperkalemia could trigger coronary spasm has to be considered also.

Fractal analysis and time- and frequency-domain measures of heart rate variability as predictors of mortality in patients with heart failure.

Time-domain measures of heart rate (HR) variability provide prognostic information among patients with congestive heart failure (CHF). The prognostic power of spectral and fractal analytic methods of HR variability has not been studied in the patients with chronic CHF. The aim of this study was to assess whether traditional and fractal analytic methods of HR variability predict mortality among a population of patients with CHF. The standard deviation of RR intervals, HR variability index, frequency-domain indexes, and the short-term fractal scaling exponent of RR intervals were studied from 24-hour Holter recordings in 499 patients with CHF and left ventricular ejection fraction < or =35%. During a mean follow-up of 665 +/- 374 days, 210 deaths (42%) occurred in this population. Conventional and fractal HR variability indexes predicted mortality by univariate analysis. For example, a short-term fractal scaling exponent <0.90 had a risk ratio (RR) of 1.9 (95% confidence interval [CI] 1.4 to 2.5) and the SD of all RR intervals <80 ms had an RR of 1.7 (95% CI 1.2 to 2.1). After adjusting for age, functional class, medication, and left ventricular ejection fraction in the multivariate proportional-hazards analysis, the reduced short-term fractal exponent remained the independent predictor of mortality, RR 1.4 (95% CI 1.0 to 1.9; p <0.05). All HR variability indexes were more significant univariate predictors of mortality in functional class II than in class III or IV. Among patients with moderate heart failure, HR variability measurements provide prognostic information, but all HR variability indexes fail to provide independent prognostic information in patients with the most severe functional impairment.

Dynamics of the uncorrected QT interval during vagal-induced lengthening of RR intervals.

Analysis of 21 episodes of vagal-induced atrioventricular block showed that the uncorrected QT intervals at the end of the corresponding RR pauses were not prolonged, in reference to the pre-block QT intervals, with pauses shorter than 1,280 ms. Subsequently, they gradually lengthened as the RR pauses progressively increased to 13,710 ms. This dynamic behavior of the QT interval in subjects without structural heart disease could have resulted from a complex interaction between the cumulative effects of previous cycle lengths (memory effect?) and the autonomic nervous system.

Spontaneous paroxysmal atrioventricular block in patients with positive tilt tests and negative electrophysiologic studies.

A subgroup of patients with neurocardiogenic syncope and negative electrophysiologic studies and adenosine tests (in 5 of 6 cases), who developed symptomatic paroxysmal atrioventricular block in the natural, ambulatory state, had positive tilt tests without advanced block. Lack of concordance between electrocardiographic changes may have reflected differential effects of the autonomic nervous system in the sinus and atrioventricular nodes, occurring in diverse circumstances and less likely because of the protocol used for tilt testing.

[Ischemic sudden death: critical analysis of risk markers. Part VIII]. / Muerte súbita isquémica: análisis crítico de los marcadores de riesgo. Parte VIII.

Coronary artery disease is responsible for approximately 75-80% of sudden cardiac deaths in most industrialized countries. Risk factors can be divided in those which suggest structural heart disease and those reflecting abnormal physiological markers. Therapeutic strategies for primary prevention of sudden cardiac death require careful scrutiny. The systematic use of risk markers to identify and stratify high risk groups may be of help to establish primary prevention measures in daily practice. Different methods to stratify risk factors using ejection fraction, ventricular arrhythmias, heart rate variability, baroreflex sensitivity, and dispersion of repolarization are discussed in this article.

An innovative application of anatomic electromagnetic voltage mapping in a patient with Ebstein's anomaly undergoing permanent pacemaker implantation.

A novel application of the Biosense CARTO System anatomic electromagnetic voltage mapping is presented, utilized as a guide for permanent pacemaker placement. The technique is illustrated in the successful implantation of an atrial lead in a patient with Ebstein's anomaly characterized by a severely dilated right atrium and extremely low-amplitude voltage signals, requiring a DDD pacemaker. Electromagnetic voltage mapping can be used in selected patients with structural heart disease to determine the optimal site for permanent pacemaker lead placement.