scholarly journals Non-invasive detection of exercise-induced cardiac conduction abnormalities in sudden cardiac death survivors in the inherited cardiac conditions

EP Europace ◽  
2020 ◽  
Author(s):  
Kevin Ming Wei Leong ◽  
Fu Siong Ng ◽  
Matthew J Shun-Shin ◽  
Michael Koa-Wing ◽  
Norman Qureshi ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Recovery Period ◽  
Lower Score ◽  
Cardiac Conduction ◽  
Protective Mechanism ◽  
Significant Difference ◽  
Exercise Treadmill ◽  
Inherited Cardiac Conditions ◽  
Exercise Induced

Abstract Aims  Rate adaptation of the action potential ensures spatial heterogeneities in conduction across the myocardium are minimized at different heart rates providing a protective mechanism against ventricular fibrillation (VF) and sudden cardiac death (SCD), which can be quantified by the ventricular conduction stability (V-CoS) test previously described. We tested the hypothesis that patients with a history of aborted SCD due to an underlying channelopathy or cardiomyopathy have a reduced capacity to maintain uniform activation following exercise. Methods and results  Sixty individuals, with (n = 28) and without (n = 32) previous aborted-SCD event underwent electro-cardiographic imaging recordings following exercise treadmill test. These included 25 Brugada syndrome, 13 hypertrophic cardiomyopathy, 12 idiopathic VF, and 10 healthy controls. Data were inputted into the V-CoS programme to calculate a V-CoS score that indicate the percentage of ventricle that showed no significant change in ventricular activation, with a lower score indicating the development of greater conduction heterogeneity. The SCD group, compared to those without, had a lower median (interquartile range) V-CoS score at peak exertion [92.8% (89.8–96.3%) vs. 97.3% (94.9–99.1%); P < 0.01] and 2 min into recovery [95.2% (91.1–97.2%) vs. 98.9% (96.9–99.5%); P < 0.01]. No significant difference was observable later into recovery at 5 or 10 min. Using the lowest median V-CoS scores obtained during the entire recovery period post-exertion, SCD survivors had a significantly lower score than those without for each of the different underlying aetiologies. Conclusion  Data from this pilot study demonstrate the potential use of this technique in risk stratification for the inherited cardiac conditions.

scholarly journals Protection against severe hypokalemia but impaired cardiac repolarization after intense rowing exercise in healthy humans receiving salbutamol

2018 ◽  
Vol 125 (2) ◽  
pp. 624-633 ◽  
Author(s):  
Tania Atanasovska ◽  
Robert Smith ◽  
Claus Graff ◽  
Cao T. Tran ◽  
Jacob Melgaard ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Plasma Potassium ◽  
Protective Mechanism ◽  
Cardiac Repolarization ◽  
Early Recovery ◽  
Double Blind ◽  
Healthy Humans ◽  
Increased Risk ◽  
Exercise Induced

Intense exercise induces pronounced hyperkalemia, followed by transient hypokalemia in recovery. We investigated whether the β2 agonist salbutamol attenuated the exercise hyperkalemia and exacerbated the postexercise hypokalemia, and whether hypokalemia was associated with impaired cardiac repolarization (QT hysteresis). Eleven healthy adults participated in a randomized, counterbalanced, double-blind trial receiving either 1,000 µg salbutamol (SAL) or placebo (PLAC) by inhalation. Arterial plasma potassium concentration ([K+]a) was measured at rest, during 3 min of intense rowing exercise, and during 60 min of recovery. QT hysteresis was calculated from ECG ( n = 8). [K+]a increased above baseline during exercise (rest, 3.72 ± 0.7 vs. end-exercise, 6.81 ± 1.4 mM, P < 0.001, mean ± SD) and decreased rapidly during early recovery to below baseline; restoration was incomplete at 60 min postexercise ( P < 0.05). [K+]a was less during SAL than PLAC (4.39 ± 0.13 vs. 4.73 ± 0.19 mM, pooled across all times, P = 0.001, treatment main effect). [K+]a was lower after SAL than PLAC, from 2 min preexercise until 2.5 min during exercise, and at 50 and 60 min postexercise ( P < 0.05). The postexercise decline in [K+]a was correlated with QT hysteresis ( r = 0.343, n = 112, pooled data, P = 0.001). Therefore, the decrease in [K+]a from end-exercise by ~4 mM was associated with reduced QT hysteresis by ~75 ms. Although salbutamol lowered [K+]a during exercise, no additive hypokalemic effects occurred in early recovery, suggesting there may be a protective mechanism against severe or prolonged hypokalemia after exercise when treated by salbutamol. This is important because postexercise hypokalemia impaired cardiac repolarization, which could potentially trigger arrhythmias and sudden cardiac death in susceptible individuals with preexisting hypokalemia and/or heart disease. NEW & NOTEWORTHY Intense rowing exercise induced a marked increase in arterial potassium, followed by a pronounced decline to hypokalemic levels. The β2 agonist salbutamol lowered potassium during exercise and late recovery but not during early postexercise, suggesting a protective effect against severe hypokalemia. The decreased potassium in recovery was associated with impaired cardiac QT hysteresis, suggesting a link between postexercise potassium and the heart, with implications for increased risk of cardiac arrhythmias and, potentially, sudden cardiac death.

Brugada Syndrome: Fatal Consequences of a Must-Not-Miss Diagnosis

2021 ◽  
Vol 41 (5) ◽  
pp. 15-22
Author(s):  
L. Douglas Smith ◽  
Sarah Gast ◽  
Danielle F. Guy
Keyword(s):  
At Risk ◽  
Critical Care ◽  
Sudden Cardiac Death ◽  
Ventricular Arrhythmia ◽  
Brugada Syndrome ◽  
Cardiac Death ◽  
Lifestyle Modification ◽  
Genetic Disorder ◽  
Cardiac Conduction ◽  
St Segment Elevation

Background Brugada syndrome is a genetic disorder of cardiac conduction that predisposes patients to spontaneous ventricular arrhythmia and sudden cardiac death. Although Brugada syndrome is one of the most common causes of sudden cardiac death, patients presenting with the syndrome often go misdiagnosed. This error has potentially fatal consequences for patients, who are at risk for sudden cardiac death without appropriate management. Objective To increase the critical care professional’s knowledge of Brugada syndrome through detailed description of the characteristic electrocardiographic findings, an algorithmic approach to electrocardiogram evaluation, and a case report of a patient with a previously missed diagnosis of Brugada syndrome. The essential concepts of epidemiology, pathophysiology, clinical presentation, risk stratification, and management are reviewed for critical care professionals who may encounter patients with the syndrome. Diagnosis Patients typically present with syncope or cardiac arrest and an abnormal electrocardiographic finding of ST-segment elevation in the precordial leads. The diagnosis of Brugada syndrome centers on identification of its electrocardiographic characteristics by critical care professionals who routinely evaluate electrocardiograms. Critical care professionals, especially nurses and advanced practice nurses, should be proficient in recognizing the electrocardiographic appearance of Brugada syndrome and initiating appropriate management. Interventions Management strategies include prevention of sudden cardiac death through lifestyle modification and placement of an implantable cardioverter-defibrillator. Critical care professionals should be aware of commonly used medications that may exacerbate ventricular arrhythmia and place patients at risk for sudden cardiac death. Conclusion Increased awareness of Brugada syndrome among critical care professionals can decrease patient morbidity and mortality.

scholarly journals Exercise-induced ventricular arrhythmias and risk of sudden cardiac death in patients with hypertrophic cardiomyopathy

2009 ◽  
Vol 30 (21) ◽  
pp. 2599-2605 ◽  
Author(s):  
Juan R. Gimeno ◽  
Maite Tomé-Esteban ◽  
Carla Lofiego ◽  
José Hurtado ◽  
Antonios Pantazis ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Exercise Induced

Abstract P130: QTc Prolongation in Acute Medullary Infarction Maps to the Dorsal Vagal Nucleus

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Goun Je ◽  
Yuyao Sun ◽  
Kiandokht Keyhanian ◽  
Nils Henninger
Keyword(s):  
Ischemic Stroke ◽  
Sudden Cardiac Death ◽  
Cardiac Arrhythmia ◽  
Cardiac Death ◽  
Spatial Relationship ◽  
Causal Link ◽  
Qtc Prolongation ◽  
Significant Difference ◽  
Segmentation Approach ◽  
Medullary Infarction

Objective: To determine the spatial relationship between acute medullary infarction and QTc prolongation. Background: Ischemic stroke has been associated with QTc-prolongation which increases the risk of cardiac arrhythmia and sudden cardiac death. In particular, pathological arrhythmia and unexpected sudden cardiac death has been described after acute medullary infarction (AMI). Nevertheless, it is not well understood why only as subset of patients with AMI develop significant cardiac arrhythmia. To gain insight into this issue, we sought to determine the possible anatomical structures relating to QTc-prolongation in patients. Methods: We retrospectively reviewed 1072 consecutive adult patients admitted for an acute ischemic stroke or a transient ischemic attack, who presented within 4.5 hours from the last known well time and had an admission ECG available. 724 patients had brain MRIs and among these, 13 (1.8 %) patients had an AMI and were included. For an unbiased lesion analyses, medullary infarcts were manually outlined on diffusion weighted MRI and manually co-registered with an anatomical atlas. Infarct lesions were then superimposed on each other as stratified by normal versus prolonged (men > 430 ms, women > 450 ms) QTc to determine the area of greatest degree of congruence. Results: 76.9 % of patients (10 out of 13, 9 men and 1 woman) had a prolonged QTc (476.9 ± 43.3 ms for men, 515 ms for women). There was no significant difference in electrolyte levels and preexisting comorbidities between subjects with normal and prolonged QTc. Among patients with QTc prolongation, the greatest degree of congruence of the infarct location was the dorsal vagal nucleus (DVN, 7 out of 10 patients). Conclusions: Our unbiased lesion segmentation approach identified the DVN a key anatomical substrate related to QTc-prolongation. Biological plausibility of our data and the presence of a causal link between the DVN and cardiac arrhythmia stems from the prior animal experimental data showing that selectively silencing the DVN via a pharmacogenetic approach caused QTc-prolongation in the rat. Further studies with more patients and high-resolution, volumetric MRI are needed to confirm our findings.

scholarly journals Electrically-Induced Ventricular Fibrillation Alters Cardiovascular Function and Expression of Apoptotic and Autophagic Proteins in Rat Hearts

2019 ◽  
Vol 20 (7) ◽  
pp. 1628 ◽  
Author(s):  
Andras Czegledi ◽  
Agnes Tosaki ◽  
Alexandra Gyongyosi ◽  
Rita Zilinyi ◽  
Arpad Tosaki ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Ventricular Fibrillation ◽  
Cardiac Death ◽  
Caspase 3 ◽  
Recovery Period ◽  
Heart Rhythm ◽  
Heart Tissue ◽  
Altered Expression ◽  
Cardiac Functions ◽  
Rat Hearts

Background: The pathological heart contractions, called arrhythmias, especially ventricular fibrillation (VF), are a prominent feature of many cardiovascular diseases leading to sudden cardiac death. The present investigation evaluates the effect of electrically stimulated VF on cardiac functions related to autophagy and apoptotic mechanisms in isolated working rat hearts. Methods: Each group of hearts was subjected to 0 (Control), 1, 3, or 10 min of spacing-induced VF, followed by 120 min of recovery period and evaluated for cardiac functions, including aortic flow (AF), coronary flow (CF), cardiac output (CO), stroke volume (SV), and heart rate (HR). Hearts were also evaluated for VF effects on infarcted zone magnitude and Western blot analysis was conducted on heart tissue for expression of the apoptotic biomarker cleaved-caspase-3 and the autophagy proteins: p62, P-mTOR/mTOR, LC3BII/LC3BI ratio, and Atg5-12 complexes. Results: Data revealed that VF induced degradation in AF, CF, CO, and SV, which prominently included-variable post-VF capacity for recovery of normal heart rhythm; increased extent of infarcted heart tissue; altered expression of cleaved-caspase-3 suggesting potential for VF-mediated amplification of apoptosis. VF influence on expression of p62, LC3BII/LC3BI, and Atg5-12 proteins was complex, possibly due to differential effects of VF-induced expression on proteins comprising the autophagic program. Conclusions: VF was observed to cause time-dependent changes in autophagy processes, which with additional analysis under ongoing investigations, likely to yield novel therapeutic targets for the prevention of VF and sudden cardiac death.

scholarly journals P859 Can we connect intraventricular exercise induced gradients to sudden cardiac death?

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
C Cotrim ◽  
F Costa ◽  
D Severino ◽  
L Baquero ◽  
J Guardado
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Heart Diseases ◽  
Young Male ◽  
Exercise Stress ◽  
Male Athlete ◽  
First Case ◽  
History Of ◽  
Intense Training ◽  
Exercise Induced

Abstract Background Some publications, on exercise induced intraventricular gradients, admit the possibility they can be related to some cases of unexplained sudden cardiac death (SCD). Clinical case We present the case of a young male athlete (16 years) that after winning a triathlon competition has sudden cardiac death. No cardiovascular risk factors. No family history of SCD A previous episode of dizziness, accompanied by nausea and vomiting related to intense training happens 6 months before. In September 2018 about 30 minutes after winning a triathlon competition has SCD episode having been resuscitated on site by the competition physician having been defibrillated and transported to intensive care unit. After discharge, cardiac MRI, Coronary AngioTC, complete genetic study for heart diseases, flecainid test, transthoracic echocardiogram, stress echocardiogram with hyperventilation and ergometrine. All have normal results (Figure) During 24 hours Holter ECG isolated premature ventricular complexes were detected and during exercise stress echocardiography a significant intraventricular gradient without systolic anterior movement of mitral valve was detected (Figure). The athlete was disqualified for sports practice, refuses CDI implantation and started bisoprolol 2,5 mg daily. To the best of our knowledge this is the first case of association between SCD and exercise induced intraventricular gradient. This possible association should be studied in the future. Abstract P859 Figure. Intraventricular gradient in SCD athlete

scholarly journals 217 Why it is important to recognize Brugada syndrome in athletes: a case report

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Lidia Colangelo ◽  
Maria Colangelo ◽  
Luca Stefanini
Keyword(s):  
High Risk ◽  
Sudden Cardiac Death ◽  
Effective Treatment ◽  
Brugada Syndrome ◽  
Cardiac Death ◽  
Recovery Period ◽  
Young Athletes ◽  
Case Presentation ◽  
Timely Diagnosis ◽  
Increased Risk

Abstract Aims The Brugada syndrome (Brs) is an inherited disorder associated with risk of ventricular fibrillation and sudden cardiac death in a structurally normal heart. The purpose of this case presentation was to spread awareness about this condition, highlight the importance of timely diagnosis and effective treatment of this channelopathy especially in asymptomatic young athletes at high risk of sudden cardiac death. Methods and results In this report, we discuss the case of a 47-year-old male. He was a tennis player who performed a visit to the sports doctor to have issued a certificate for competitive fitness. He had no familiar history of sudden death or syncope. The patient’s electrocardiogram (ECG) revealed J-point elevation and ST-segment elevation in the right precordial leads V1 and V2 positioned in the second, third, or fourth intercostal space, showing classic type II ‘saddleback’ morphology in V2 and BrS was suspected. Hence, the patient underwent Holter ECG monitoring with evidence of spontaneous type 1 Brugada pattern (‘coved’ morphology), as well as frequent ventricular ectopic beats with left branch block morphology. Indeed, a diagnosis of BrS was made. Antiarrhythmic prophylaxis therapy with hydroquinidine was initiated and the patient was suspended from competitive activity with a 3-month follow-up. Conclusions The BrS is a hereditary disease characterized by a typical ECG pattern potentially predisposing active individuals with no patent structural heart disease to ventricular arrhythmias (VA) and sudden cardiac death (SCD). Nowadays, it is difficult to discern the true burden of BrS due to the unknown real prevalence of asymptomatic patients and the dynamic variability of the ECG pattern in individuals. The purpose of this case presentation was to spread awareness about this condition, highlight the importance of timely diagnosis, and effective treatment of this channelopathy especially in asymptomatic young athletes at high risk of SCD. Indeed, exercise may potentially worsen the ECG abnormalities in BrS patients, resulting in higher peak J-point amplitudes during the vasovagal reaction of the recovery period, possibly leading to an increased risk of cardiac events. Moreover, the enhanced vagal tone in athletes could be both a BrS risk factor and an exercise effect. For this reason, athletic pre-participation screening is essential for minimizing the risk for SCD in athletes participating in either competitive or leisure sporting activities.

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