scholarly journals 1Non-invasive detection of exercise induced cardiac conduction abnormalities in sudden cardiac death survivors in the inherited arrhythmic syndromes

EP Europace ◽  
2017 ◽  
Vol 19 (suppl_1) ◽  
pp. i1-i1
Author(s):  
KMW Leong ◽  
FS Ng ◽  
MJ Shun-Shin ◽  
N Davies ◽  
DP Francis ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Cardiac Conduction ◽  
Conduction Abnormalities ◽  
Exercise Induced

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.

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

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 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.

Pathologic Changes of the Cardiac Conduction Tissue in Sudden Cardiac Death

1995 ◽  
Vol 16 (3) ◽  
pp. 193-202 ◽  
Author(s):  
M. Paz Suarez-Mier ◽  
Lourdes Fernandez-Simón ◽  
Carlos Gawallo
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Cardiac Conduction

scholarly journals Loss of the transcription factor Meis1 prevents sympathetic neurons target-field innervation and increases susceptibility to sudden cardiac death

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Fabrice Bouilloux ◽  
Jérôme Thireau ◽  
Stéphanie Ventéo ◽  
Charlotte Farah ◽  
Sarah Karam ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Association Studies ◽  
Sympathetic Neurons ◽  
Premature Death ◽  
Trophic Factors ◽  
Cardiac Conduction ◽  
Genome Wide Association Studies ◽  
Target Field ◽  
Cardio Vascular

Although cardio-vascular incidents and sudden cardiac death (SCD) are among the leading causes of premature death in the general population, the origins remain unidentified in many cases. Genome-wide association studies have identified Meis1 as a risk factor for SCD. We report that Meis1 inactivation in the mouse neural crest leads to an altered sympatho-vagal regulation of cardiac rhythmicity in adults characterized by a chronotropic incompetence and cardiac conduction defects, thus increasing the susceptibility to SCD. We demonstrated that Meis1 is a major regulator of sympathetic target-field innervation and that Meis1 deficient sympathetic neurons die by apoptosis from early embryonic stages to perinatal stages. In addition, we showed that Meis1 regulates the transcription of key molecules necessary for the endosomal machinery. Accordingly, the traffic of Rab5+ endosomes is severely altered in Meis1-inactivated sympathetic neurons. These results suggest that Meis1 interacts with various trophic factors signaling pathways during postmitotic neurons differentiation.

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