Reconsidering the utility of manifest entrainment pacing in macroreentrant ventricular tachycardia: A case report.
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ABSTRACT:
SUBMITTER: Okada M
PROVIDER: S-EPMC7498511 | biostudies-literature | 2020 Sep
REPOSITORIES: biostudies-literature
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Reconsidering the utility of manifest entrainment pacing in macroreentrant ventricular tachycardia: A case report.
Okada Masato M Tanaka Nobuaki N Oka Takafumi T Tanaka Koji K Hirao Yuko Y Inoue Koichi K
HeartRhythm case reports 20200603 9
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Project description:BackgroundAnti-tachycardia pacing (ATP) is a pain-free alternative to defibrillation shock for monomorphic ventricular tachycardia (VT). Intrinsic ATP (iATP) is a novel algorithm of auto-programmed ATP. However, the advantage of iATP over conventional ATP in clinical cases is still unknown.Case summaryA 49-year-old man with no significant past medical history was transferred to our institution with sudden-onset fatigue from working on a farm. A 12-lead electrocardiogram showed monomorphic sustained wide QRS tachycardia with a right bundle branch block pattern and superior axis deviation with a cycle length (CL) of 300 ms. Sustained monomorphic VT originating from the left ventricle due to underlying vasospastic angina was diagnosed by contrast-enhanced cardiac magnetic resonance imaging, coronary angiography, and the acetylcholine stress test, and implantable cardioverter defibrillator implantation was performed. Nine months later, a clinical VT episode with a CL of 300 ms was observed, which could not be terminated by three sequences of conventional burst pacing. Ventricular tachycardia was finally terminated by a third iATP sequence without any acceleration.DiscussionAlthough standard burst pacing by conventional ATP reached the VT circuit, it failed to terminate the VT. Using the post-pacing interval, iATP automatically calculated the appropriate number of S1 pulses required to reach the VT circuit. In iATP, the S2 pulses are delivered with a calculated coupling interval based on the estimated effective refractory period during tachycardia. In this case, iATP might have led to less aggressive S1 stimulation, followed by aggressive S2 stimulation, which probably helped terminate the VT without any acceleration.
| S-EPMC10328381 | biostudies-literature
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.
| S-EPMC9347201 | biostudies-literature
Project description: Not available
| S-EPMC4671300 | biostudies-literature
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.
| S-EPMC8188868 | biostudies-literature
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.
| S-EPMC7661046 | biostudies-literature
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.
| S-EPMC6439386 | biostudies-literature
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.
| S-EPMC10307682 | biostudies-literature
Project description: Not available
| S-EPMC10506732 | biostudies-literature
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.
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