Project description:In this case with antidromic atrioventricular reciprocating tachycardia via the atriofascicular pathway, entrainment from the right ventricular apex showed minor constant fusion. This may indicate that an atriofascicular pathway with distal arborization can connect to the branch of the right bundle and partly to the working myocardium.
Project description:BackgroundThe majority of ventricular tachycardias (VTs) occurs in patients with structural heart disease and is associated with an increased risk of sudden cardiac death. These VT are scar-related and may develop in patients with ischaemic or non-ischaemic cardiomyopathies.Case summaryWe describe a 44-year-old patient without any pre-existing cardiovascular disease, presenting with the first documentation of a haemodynamically unstable sustained fast VT with a cycle length of 250 ms. He reported a suicidal attempt with a self-made handgun aged 16 when he had shot himself in the thorax and had injured the myocardium. After presenting with the VT coronary artery disease was excluded through cardiac catheterization. A cardiovascular magnetic resonance study showed a localized myocardial scar in the left ventricular free wall starting from the subepicardium and correlating to the scar described 28 years ago by the thoracic surgeons. In an electrophysiological study, non-sustained VT were easily inducible. Presuming a causal relationship between the fast VT and the epicardial scar, a single-chamber implantable cardioverter-defibrillator was implanted and beta-blocker therapy was initiated.DiscussionScar-related VT often occur many years after an acute event, e.g. an acute myocardial infarction. This case highlights, that any cardiac trauma, even a superficial epicardial projectile-related damage with subsequent scarring, may cause a VT after many years and to our knowledge for the first time describes the occurrence of a VT due to mechanical damage to the myocardium by a gunshot.
Project description:Cardiovascular diseases account for nearly 31% of global deaths. Ventricular arrhythmia cause 1-2 in 1000 sudden cardiac deaths. Patient with a known case of coronary artery disease presented with complaints of heaviness in the chest with pain radiating to the left shoulder joint with sweating and dizziness for 6 months. The patient was diagnosed as monomorphic ventricular tachycardia (mVT) and left ventricular hypertrophy (LVH) based on electrocardiograph (ECG) findings. Treatment planned to bring Agni, Rasa, Vata Dosha into homeostasis. mVT is completely cured in 24 days of Ayurvedic treatment. The electrocardiograph was normal after the course of treatment. In this case report, we treated the patient with monomorphic ventricular tachycardia with Ayurvedic treatment. This case report provides guidance for heart disease management with Ayurveda.
Project description:BackgroundFabry disease is an inherited rare metabolic disease caused by mutation in the GLA gene, encoding lysosomal enzyme alpha-galactosidase A. The disorder is a systemic disease that manifests as cerebrovascular and cardiac disease, chronic renal failure, skin lesion, peripheral neuropathy, and other abnormalities. Ventricular tachycardia as a Fabry disease presentation is very rare.Case summaryA 36-year-old man self-presented to a general practitioner complaining of episodes of shortness of breath together with a 6-month history of malaise. The 12-lead electrocardiogram (ECG) prompted a decision to transfer him immediately to a percutaneous coronary intervention (PCI) capable hospital under the suspicion of acute coronary syndrome. Whilst awaiting transport, he experienced acute onset of dyspnoea together with non-specific chest heaviness. A repeat ECG monitor strip showed ventricular tachycardia transforming to ventricular fibrillation. The patient was successfully defibrillated. Coronary angiography was performed upon arrival at hospital and demonstrated unobstructed coronary arteries. Transthoracic echocardiography revealed concentric left ventricular hypertrophy (LVH) and normal systolic function, with severe diastolic dysfunction. Magnetic resonance imaging (MRI) confirmed the LVH, and did not demonstrate any late gadolinium enhancement.DiscussionOur case illustrates the pivotal role of critical clinical thinking in the diagnosis of rare but treatable hereditary cardiomyopathy. The uncommon cardiac presentation of Fabry disease promotes further research linking different phenotypes of Fabry disease with different pathogenic mutations.
Project description:Background Papillary muscles are an important source of ventricular tachycardia (VT). Yet little is known about the role of the right ventricular (RV) endocavity structure, the moderator band (MB). The aim of this study was to determine the characteristics of the MB that may predispose to arrhythmia substrates. Methods Ventricular wedge preparations with intact MBs were studied from humans (n=2) and sheep (n=15; 40-50 kg). RV endocardium was optically mapped, and electrical recordings were measured along the MB and septum. S1S2 pacing of the RV free wall, MB, or combined S1-RV S2-MB sites were assessed. Human (n=2) and sheep (n=4) MB tissue constituents were assessed histologically. Results The MB structure was remarkably organized as 2 excitable, yet uncoupled compartments of myocardium and Purkinje. In humans, action potential duration heterogeneity between MB and RV myocardium was found (324.6±12.0 versus 364.0±8.4 ms; P<0.0001). S1S2-MB pacing induced unidirectional propagation via MB myocardium, permitting sustained macroreentrant VT. In sheep, the incidence of VT for RV, MB, and S1-RV S2-MB pacing was 1.3%, 5.1%, and 10.3%. Severing the MB led to VT termination, confirming a primary arrhythmic role. Inducible preparations had shorter action potential duration in the MB than RV (259.3±45.2 versus 300.7±38.5 ms; P<0.05), whereas noninducible preparations showed no difference (312.0±30.3 versus 310.0±24.6 ms, respectively). Conclusions The MB presents anatomic and electrical compartmentalization between myocardium and Purkinje fibers, providing a substrate for macroreentry. The vulnerability to sustain VT via this mechanism is dependent on MB structure and action potential duration gradients between the RV free wall and MB.
Project description:BackgroundSustained forms of tachycardia especially from the left ventricular summit are rare. Adenosine sensitive outflow tachycardias, especially from the left ventricular summit, are rarer still. These arrhythmias may be exercise or stress induced as they are facilitated by catecholamines and characteristically terminate with adenosine, vagal manoeuvres, and beta-blockers. The surface 12-lead electrocardiogram can be used to localize the anatomic site of origin before catheter ablation; however, prediction of the precise origin may still be challenging due to the intimate and complex anatomy of the outflow tracts.Case summaryA 12-year-old female presented to an emergency room with frequent runs of wide complex tachycardia that terminated with adenosine but would spontaneously reinitiate. After three additional temporary terminations with adenosine and because of an inability to completely eliminate tachycardia, she was started on an esmolol infusion that resulted in an abrupt termination of tachycardia. At follow-up, she reported breakthrough episodes of tachycardia with exercise, especially associated with beta-blocker non-compliance. The rest of her cardiac testing was normal apart from an anomalous right coronary artery origin from the left coronary sinus. Given the increased frequency of symptomatic palpitations and medication non-compliance, she underwent an electrophysiology study. During the study, a ventricular tachycardia was successfully mapped to an epicardial focus at the left ventricle summit and was successfully ablated.DiscussionThe response of this patient's ventricular tachycardia to adenosine suggests a triggered mechanism. To our knowledge, this is the first unambiguous example of left ventricular tachycardia due to cAMP-mediated triggered activity in this age group.
Project description:BackgroundCatecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe genetic arrhythmogenic disorder characterized by adrenergically induced ventricular tachycardia manifesting as stress-induced syncope and sudden cardiac death. While CPVT is not associated with dilated cardiomyopathy (DCM) in most cases, the combination of both disease entities poses a major diagnostic and therapeutic challenge.Case summaryWe present the case of a young woman with CPVT. The clinical course since childhood was characterized by repetitive episodes of exercise-induced ventricular arrhythmias and a brady-tachy syndrome due to rapid paroxysmal atrial fibrillation and sinus bradycardia. Medical treatment included propranolol and flecainide until echocardiography showed a dilated left ventricle with severely depressed ejection fraction when the patient was 32 years old. Cardiac magnetic resonance imaging revealed non-specific late gadolinium enhancement. Myocardial inflammation, however, was excluded by subsequent endomyocardial biopsy. Genetic analysis confirmed a mutation in the cardiac ryanodine receptor but no pathogenetic variant associated with DCM. Guideline-directed medical therapy for HFrEF was limited due to symptomatic hypotension. Over the next months, the patient developed progressive heart failure symptoms that were finally managed by heart transplantation.DiscussionManagement in patients with CPVT and DCM is challenging, as Class I antiarrhythmic drugs are not recommended in structural heart disease and prophylactic internal cardioverter-defibrillator implantation without adjuvant antiarrhythmic therapy can be detrimental. Regular echocardiographic screening for DCM is recommendable in patients with CPVT. A multidisciplinary team of heart failure specialists, electrophysiologists, geneticists, and imaging specialists is needed to collaborate in the delivery of clinical care.
Project description:A 74-year-old woman presented with incessant wide complex tachycardia that was refractory to cardioversions. Successful radiofrequency catheter ablation was performed on the left ventricular posteromedial papillary muscle. An inaudible steam pop has occurred during the procedure, but we confirmed that there were no complications during the procedure and short-term follow-up of echocardiography. Two months after the procedure, an asymptomatic pseudoaneurysm was identified at the ablation site that had not been observed in the short-term follow-up.
Project description:BackgroundVentricular tachycardia (VT) originating in the right ventricular outflow tract (RVOT) is the most common form of idiopathic VT. Catheter ablation of right ventricular outflow tract tachycardia (RVOT-VT) is associated with high success rates. However, non-inducibility of VT on electrophysiological (EP) study can severely impact ablation outcome. We describe a novel catheter ablation strategy which proved feasible and safe in a case of highly symptomatic, non-inducible RVOT-VT.Case summaryA 51-year-old male with a history of non-sustained VT (NSVT) was referred to our hospital after two syncopal episodes resulting in collapse. Upon admission, a cluster of monomorphic NSVT (250-270 b.p.m.) resulted in haemodynamic instability and required transfer to the intensive care unit. On twelve-lead electrocardiogram, NSVT showed inferior axis and left bundle branch block, suggestive of RVOT-VT. Diagnostic workup including echocardiography, coronary angiography, and late enhancement computed tomography (CT) revealed no evidence of structural heart disease. On two EP studies, non-inducibility of clinical VT despite repeated ventricular pacing and isoproterenol infusion rendered precise mapping of triggered activity unfeasible. Therefore, a bailout ablation strategy was developed by performing a circumferential electrical RVOT isolation using a 3.5 mm irrigated-tip ablation catheter under the guidance of high-density electroanatomic mapping (CARTO® 3) and CT reconstruction of cardiac anatomy. No procedural complications occurred, and the patient remained arrhythmia-free during a 6-month follow-up period.DiscussionCatheter ablation is a first-line therapy for symptomatic and drug-refractory idiopathic RVOT-VT. Non-inducibility of RVOT-VT represents a relevant limitation for successful ablation which might be overcome by electrical RVOT isolation as a bailout ablation strategy.