Ventricular tachyarrhythmias

2019 ◽  
pp. 265-276
Author(s):  
Eduard Guasch ◽  
Lluís Mont
Keyword(s):  
Heart Disease ◽  
Exercise Test ◽  
Ventricular Arrhythmias ◽  
Competitive Sport ◽  
Ventricular Tachyarrhythmias ◽  
Holter Ecg ◽  
Exploratory Testing ◽  
Increased Risk ◽  
Cardiac Condition ◽  
Exercise Induced

The identification of ventricular arrhythmias in athletes should always be carefully considered because of the increased risk of SCD. The main factor determining this risk is the presence of an underlying structural or primary arrhythmic heart disease. Consequently, the identification of ventricular arrhythmias in an athlete should prompt exploratory testing, most commonly involving 24-hour Holter ECG, echocardiography, and an exercise test. Other tests should be considered on an individual basis. In general, the more frequent and complex the ventricular arrhythmias, the higher are the risks of a heart disease, and a more thorough examination is required. While most arrhythmias in athletes without heart disease are idiopathic ventricular arrhythmias, considerable attention has been paid recently to an exercise-induced substrate for ventricular arrhythmias, similar to classic forms of arrhythmogenic ventricular cardiomyopathy. Overall, the identification of a cardiac condition will determine the prognosis, therapeutic approach, and eligibility for competitive sport.

scholarly journals Impact of ranolazine on exercise tolerance and arrhythmias in patients with INOCA

2021 ◽  
pp. 10-15
Author(s):  
Vira Tseluyko ◽  
Tetyana Pylova
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Coronary Arteries ◽  
Exercise Test ◽  
Exercise Tolerance ◽  
Ventricular Arrhythmias ◽  
Ecg Monitoring ◽  
Holter Ecg ◽  
Group I ◽  
Group Ii

The aim of the study to evaluate the effect of supplementation of basic therapy by ranolazine in patients with INOCA on exercise test parameters and Holter ECG monitoring. Materials and methods. 53 patients with stable coronary heart disease were examined, including 18 men (33.9 %) and 35 (66 %) women, the average age of patients was 57 (±9.68) years. According to the results of coronary angiography all patients had non-obstructive coronary arteries. In addition to physical and laboratory examination, bicycle ergometry, Holter ECG monitoring and echocardiography were included in the examination of patients. Patients were divided into 2 groups: group I - patients who in addition to standard therapy received ranolazine at a dose of 1000 mg twice a day for 6 months, and group II patients with standard coronary heart disease therapy. After 6 months from the beginning of the observation an objective examination, echocardiography, exercise test, Holter ECG monitoring were repeated. Results. The study found that patients receiving ranolazine in addition to standard therapy had a statistically significant increase in exercise duration after 6 months compared with baseline and group II. Before treatment in group I, the duration of the exercise test was 356.51±180.24s, and after treatment 414.32±142.10s (p=0.03). In group II, the duration of the test before treatment was 361.4±160.24 c, and after 380.5±152.2 s (p=0.15). It was also found that the duration of the test differed significantly in group I after treatment of patients from group II after treatment of patients with a standard treatment regimen (p=0.04). According to the results of Holter ECG monitoring in group I found a positive effect of ranolazine on the frequency of ventricular arrhythmias: before treatment n=1142 [30; 2012], after treatment n=729 [23; 1420], while in group II a significant difference between the number of extrasystoles before treatment and after not detected (n=1026 [17; 1920], n=985 [15; 1680], respectively) p=0.18. Conclusions. The addition of ranolazine to the basic therapy of patients with non-obstructive coronary arteries disease helps to increase exercise tolerance (according to the loading stress test) and contributes to a significant reduction in the number of ventricular arrhythmias (according to Holter-ECG) compared with both baseline and group II

scholarly journals Mechanisms of ventricular arrhythmias: a dynamical systems-based perspective

2012 ◽  
Vol 302 (12) ◽  
pp. H2451-H2463 ◽  
Author(s):  
Elizabeth M. Cherry ◽  
Flavio H. Fenton ◽  
Robert F. Gilmour
Keyword(s):  
Heart Disease ◽  
Dynamical Systems ◽  
Nonlinear System ◽  
Ventricular Arrhythmias ◽  
Ventricular Tachyarrhythmias ◽  
Electrophysiological Characteristic ◽  
Myocardial Disease ◽  
Complex Nonlinear System ◽  
Potential Impact

Defining the cellular electrophysiological mechanisms for ventricular tachyarrhythmias is difficult, given the wide array of potential mechanisms, ranging from abnormal automaticity to various types of reentry and kk activity. The degree of difficulty is increased further by the fact that any particular mechanism may be influenced by the evolving ionic and anatomic environments associated with many forms of heart disease. Consequently, static measures of a single electrophysiological characteristic are unlikely to be useful in establishing mechanisms. Rather, the dynamics of the electrophysiological triggers and substrates that predispose to arrhythmia development need to be considered. Moreover, the dynamics need to be considered in the context of a system, one that displays certain predictable behaviors, but also one that may contain seemingly stochastic elements. It also is essential to recognize that even the predictable behaviors of this complex nonlinear system are subject to small changes in the state of the system at any given time. Here we briefly review some of the short-, medium-, and long-term alterations of the electrophysiological substrate that accompany myocardial disease and their potential impact on the initiation and maintenance of ventricular arrhythmias. We also provide examples of cases in which small changes in the electrophysiological substrate can result in rather large differences in arrhythmia outcome. These results suggest that an interrogation of cardiac electrical dynamics is required to provide a meaningful assessment of the immediate risk for arrhythmia development and for evaluating the effects of putative antiarrhythmic interventions.

scholarly journals Exercise recommendations in patients with valvular heart disease

Heart ◽  
2018 ◽  
Vol 105 (2) ◽  
pp. 106-110 ◽  
Author(s):  
Sabiha Gati ◽  
Aneil Malhotra ◽  
Sanjay Sharma
Keyword(s):  
Physical Activity ◽  
Heart Disease ◽  
Ventricular Function ◽  
Functional Capacity ◽  
Valvular Heart Disease ◽  
Stress Test ◽  
Exercise Stress ◽  
Competitive Sport ◽  
Increased Risk ◽  
The Impact

Valvular heart disease affects 1%–2% of young individuals, many of whom aspire to partake in competitive sport or high intensity recreational exercise. There are limited reports on the impact of intensive physical activity on the progression of valvular heart disease; therefore, current recommendations are based on consensus opinion. The management of exercising individuals with valvular heart disease requires a structured approach that incorporates several key factors including symptomatic status, functional capacity, type and nature of the valvular lesion, impact on ventricular structure and function and effect on pulmonary artery pressure. Asymptomatic individuals with minor valvular abnormalities may engage in all forms of competitive sport, whereas those with lesions of moderate severity may exercise intensively if an exercise stress test tailored to the relevant physical activity reveals good functional capacity without myocardial ischaemia, haemodynamic disturbances or arrhythmia. Symptomatic athletes and those with severe valvular heart disease, impaired ventricular function, pulmonary hypertension and arrhythmias should refrain from most competitive sports. Athletes with a bicuspid aortic valve and aortic root diameter >40 mm should avoid sport with a strong isometric component even with minimal valvular dysfunction. There is an association between mitral valve prolapse and sudden cardiac death in the general population; however, there is limited evidence of increased risk with competitive sport. Athletes undergoing corrective surgery may return to exercise after 3 months if ventricular function and exercise capacity are preserved. Individuals anticoagulated for mechanical bioprosthetic valves should avoid contact or collision sport to minimise the risk of bleeding.

Ventricular Arrhythmias

2013 ◽  
Author(s):  
Roy M. John ◽  
William G Stevenson
Keyword(s):  
Heart Disease ◽  
Catheter Ablation ◽  
Sudden Death ◽  
Ventricular Arrhythmias ◽  
Systolic Heart Failure ◽  
Left Ventricular ◽  
Polymorphic Ventricular Tachycardia ◽  
Left Ventricular Ejection ◽  
Implantable Cardioverter Defibrillators ◽  
Increased Risk

Ventricular arrhythmias are common in all forms of heart disease and are an important cause of cardiac arrest and sudden death. Many ventricular arrhythmias are benign but may serve as a marker for underlying disease or its severity. Others are life threatening. The significance of an arrhythmia is determined by the specific characteristics of the arrhythmia and the associated heart disease, and these features guide evaluation and therapy. This review discusses various mechanisms and types of ventricular arrhythmias and management based on clinical presentation (including patients with symptomatic arrhythmia and increased risk of sudden death without arrhythmia symptoms). Genetic arrhythmia syndromes, such as abnormalities of repolarization and the QT interval, catecholaminergic polymorphic ventricular tachycardia (VT), and inherited cardiomyopathies, are discussed in depth. Under the rubric of management of ventricular arrhythmias, drug therapy for ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs), and catheter ablation for VT are also covered. Tables chart out guideline recommendations for ICD therapy, drugs for the management of ventricular arrhythmias, and indications and contraindications for catheter ablation of ventricular arrhythmias. Electrocardiograms are provided, as well as management algorithms for ventricular arrhythmias based on patient presentation, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection less than or equal to 35% who are candidates for consideration of an ICD for primary prevention of sudden cardiac death. This review contains 5 highly rendered figures, 3 tables, and 60 references.

scholarly journals Atropine-induced sinus tachycardia protects against exercise-induced ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia

EP Europace ◽  
2020 ◽  
Vol 22 (4) ◽  
pp. 643-648
Author(s):  
Prince J Kannankeril ◽  
M Benjamin Shoemaker ◽  
Kathryn A Gayle ◽  
Darlene Fountain ◽  
Dan M Roden ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Exercise Test ◽  
Ventricular Arrhythmias ◽  
Sinus Bradycardia ◽  
Recovery Period ◽  
Catecholaminergic Polymorphic Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia ◽  
Ventricular Ectopy ◽  
Ectopic Beats ◽  
Exercise Induced

Abstract Aims Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmia syndrome characterized by exercise-induced ventricular arrhythmias, sudden death, and sinus bradycardia. Elevating supraventricular rates with pacing or atropine protects against catecholaminergic ventricular arrhythmias in a CPVT mouse model. We tested the hypothesis that increasing sinus heart rate (HR) with atropine prevents exercise-induced ventricular arrhythmias in CPVT patients. Methods and results We performed a prospective open-label trial of atropine prior to exercise in CPVT patients (clinicaltrials.gov NCT02927223). Subjects performed a baseline standard Bruce treadmill test on their usual medical regimen. After a 2-h recovery period, subjects performed a second exercise test after parasympathetic block with atropine (0.04 mg/kg intravenous). The primary outcome measure was the total number of ventricular ectopic beats during exercise. All six subjects (5 men, 22–57 years old) completed the study with no adverse events. Atropine increased resting sinus rate from median 52 b.p.m. (range 52–64) to 98 b.p.m. (84–119), P = 0.02. Peak HRs (149 b.p.m., range 136–181 vs. 149 b.p.m., range 127–182, P = 0.46) and exercise duration (612 s, range 544–733 vs. 584 s, range 543–742, P = 0.22) were not statistically different. All subjects had ventricular ectopy during the baseline exercise test. Atropine pre-treatment significantly decreased the median number of ventricular ectopic beats from 46 (6–192) to 0 (0–29), P = 0.026; ventricular ectopy was completely eliminated in 4/6 subjects. Conclusion Elevating sinus rates with atropine reduces or eliminates exercise-induced ventricular ectopy in patients with CPVT. Increasing supraventricular rates may represent a novel therapeutic strategy in CPVT.

Ventricular Arrhythmias

2020 ◽  
Author(s):  
Roy M. John ◽  
William G Stevenson
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Catheter Ablation ◽  
Sudden Death ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Polymorphic Ventricular Tachycardia ◽  
Left Ventricular Ejection ◽  
Premature Ventricular Contractions ◽  
Increased Risk

Ventricular arrhythmias are common in all forms of heart disease and are an important cause of cardiac arrest and sudden death. Many ventricular arrhythmias are benign but may serve as a marker for underlying disease or its severity. Others are life threatening. The significance of an arrhythmia is determined by the specific characteristics of the arrhythmia and the associated heart disease, and these features guide evaluation and therapy. This review discusses various mechanisms and types of ventricular arrhythmias and management based on clinical presentation (including patients with symptomatic arrhythmia and increased risk of sudden death without arrhythmia symptoms). Genetic arrhythmia syndromes, such as abnormalities of repolarization and the QT interval, catecholaminergic polymorphic ventricular tachycardia (VT), and inherited cardiomyopathies, are discussed in depth. Under the rubric of management of ventricular arrhythmias, drug therapy for ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs), and catheter ablation for VT are also covered. Tables chart out guideline recommendations for ICD therapy, drugs for the management of ventricular arrhythmias, and indications and contraindications for catheter ablation of ventricular arrhythmias. Electrocardiograms are provided, as well as management algorithms for ventricular arrhythmias based on patient presentation, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection less than or equal to 35% who are candidates for consideration of an ICD for primary prevention of sudden cardiac death. This review contains 5 figures, 8 tables, and 61 references. Keywords: Ventricular arrhythmias, implanted cardioverter-defibrillator (ICD), Ventricular tachycardia (VT), Premature Ventricular Contractions (PVC), Myocardial Infarction (MI), Brugada syndrome, Arrhythmogenic right ventricular cardiomyopathy (ARVC), electrocardiographic (ECG)

Ventricular Arrhythmias

2020 ◽  
Author(s):  
Roy M. John ◽  
William G Stevenson
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Catheter Ablation ◽  
Sudden Death ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Polymorphic Ventricular Tachycardia ◽  
Left Ventricular Ejection ◽  
Premature Ventricular Contractions ◽  
Increased Risk

Ventricular arrhythmias are common in all forms of heart disease and are an important cause of cardiac arrest and sudden death. Many ventricular arrhythmias are benign but may serve as a marker for underlying disease or its severity. Others are life threatening. The significance of an arrhythmia is determined by the specific characteristics of the arrhythmia and the associated heart disease, and these features guide evaluation and therapy. This review discusses various mechanisms and types of ventricular arrhythmias and management based on clinical presentation (including patients with symptomatic arrhythmia and increased risk of sudden death without arrhythmia symptoms). Genetic arrhythmia syndromes, such as abnormalities of repolarization and the QT interval, catecholaminergic polymorphic ventricular tachycardia (VT), and inherited cardiomyopathies, are discussed in depth. Under the rubric of management of ventricular arrhythmias, drug therapy for ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs), and catheter ablation for VT are also covered. Tables chart out guideline recommendations for ICD therapy, drugs for the management of ventricular arrhythmias, and indications and contraindications for catheter ablation of ventricular arrhythmias. Electrocardiograms are provided, as well as management algorithms for ventricular arrhythmias based on patient presentation, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection less than or equal to 35% who are candidates for consideration of an ICD for primary prevention of sudden cardiac death. This review contains 5 figures, 8 tables, and 61 references. Keywords: Ventricular arrhythmias, implanted cardioverter-defibrillator (ICD), Ventricular tachycardia (VT), Premature Ventricular Contractions (PVC), Myocardial Infarction (MI), Brugada syndrome, Arrhythmogenic right ventricular cardiomyopathy (ARVC), electrocardiographic (ECG)

Exercise-Induced Muscle Vasodilatation and Treadmill Exercise Test Responses in Individuals without Overt Heart Disease

Cardiology ◽  
2014 ◽  
Vol 127 (1) ◽  
pp. 38-44 ◽  
Author(s):  
Rafael Amorim Belo Nunes ◽  
Viviana Giampaoli ◽  
Humberto Felício Gonçalves de Freitas ◽  
Alexandre da Costa Pereira ◽  
Fernando Araújo ◽  
...  
Keyword(s):  
Heart Disease ◽  
Exercise Test ◽  
Treadmill Exercise ◽  
Treadmill Exercise Test ◽  
Exercise Induced

Advanced imaging for risk stratification of sudden death in hypertrophic cardiomyopathy

Heart ◽  
2020 ◽  
Vol 106 (11) ◽  
pp. 793-801 ◽  
Author(s):  
Jay Ramchand ◽  
Agostina M Fava ◽  
Michael Chetrit ◽  
Milind Y Desai
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Risk Stratification ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Small Subset ◽  
Imaging Features ◽  
Icd Implantation ◽  
Increased Risk ◽  
Cardiac Condition

Hypertrophic cardiomyopathy (HCM) is a common inherited cardiac condition, which typically manifests as left ventricular hypertrophy. A small subset of patients with HCM have an increased risk of sudden cardiac death (SCD) from ventricular arrhythmias. Risk of SCD can be effectively reduced following implantation of implantable cardiac defibrillators (ICD), although this treatment carries a risk of complications such as inappropriate shocks. With this in mind, we turn to advances in cardiac imaging to guide risk stratification for SCD and to select the appropriate individual who may benefit from ICD implantation. In this review, we have taken the opportunity to briefly summarise the role of imaging in the diagnosis of HCM before focusing on how specific imaging features influence risk of SCD in patients with HCM.

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