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 |
REPOSITORIES: biostudies-literature
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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.
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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.
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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.
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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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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.
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Project description:BackgroundDiaphragmatic pacemakers are used to assist respiration in ventilator-dependent patients. Electromagnetic interference with intrinsic cardiac electrical activity is a theoretical risk but has never been reported in the literature. This case highlights a serious complication of cardiac arrest as a result of diaphragmatic pacing.Case summaryWe report a quadriplegic patient with recent diaphragmatic pacemaker implantation who presented with ventricular tachycardia leading to cardiac arrest. Extensive workup was negative for other aetiologies for ventricular arrhythmias. Reduction of the left-sided diaphragmatic pacemaker voltage resulted in cessation of ventricular ectopy.DiscussionDiaphragmatic pacing at high voltages can cause unwanted transmission of impulses to the cardiac myocytes as a rare complication. This should be noted as a possible complication of intramuscular diaphragmatic pacing, and efforts should be taken to circumvent this risk in the future.
| S-EPMC8440889 | biostudies-literature
Project description:IntroductionCoronary vasospasm is an uncommon but important cause of myocardial ischaemia and ventricular arrhythmias.Case presentationIn this report, we present a striking example of vasospasm manifesting as ST-segment elevation and ventricular tachycardia on Holter monitoring. Later, spasm occurred during a procainamide challenge performed for suspected Brugada syndrome. The patient underwent implantable cardioverter-defibrillator insertion and was successfully treated with oral calcium channel blocker.DiscussionWe review contemporary data regarding management and outcomes in coronary vasospasm and discuss the use of implantable defibrillator therapy in patients who have sustained a significant arrhythmic event.
| S-EPMC6426052 | biostudies-literature
Project description:BackgroundCoronavirus disease 2019 (COVID-19) has been associated with myocardial involvement. Among cardiovascular manifestations, cardiac arrhythmias seem to be fairly common, although no specifics are reported in the literature. An increased risk of malignant ventricular arrhythmias and electrical storm (ES) has to be considered.Case summaryWe describe a 68-year-old patient with a previous history of coronary artery disease and severe left ventricular systolic disfunction, who presented to our emergency department describing cough, dizziness, fever, and shortness of breath. She was diagnosed with COVID-19 pneumonia, confirmed after three nasopharyngeal swabs. Ventricular tachycardia (VT) storm with multiple implantable cardioverter defibrillator (ICD) shocks was the presenting manifestation of cardiac involvement during the COVID-19 clinical course. A substrate-based VT catheter ablation procedure was successfully accomplished using a remote navigation system. The patient recovered from COVID-19 and did not experience further ICD interventions.DiscussionTo date, COVID-19 pneumonia associated with a VT storm as the main manifestation of cardiac involvement has never been reported. This case highlights the role of COVID-19 in precipitating ventricular arrhythmias in patients with ischaemic cardiomyopathy who were previously stable.
| S-EPMC7337657 | biostudies-literature
Project description:In patients with coronary artery disease, ventricular tachycardia (VT) is usually related to left ventricular (LV) post-infarction scars. A case of a 78-year-old man with post-infarction VT originating from the right ventricular (RV) free wall is described. Following recurrent episodes of VT with left bundle branch block morphology and left superior axis deviation, a patient with prior myocardial infarction was submitted to catheter ablation. Two areas of abnormal bipolar electrograms were observed at 3D electroanatomical mapping: one located at the basal aspect of the posterior and postero-septal LV, and the other one extending from the antero-lateral to the posterior mid-basal RV free wall. Ventricular late potentials (LPs) were recorded within both scars, but only pacing from those located in the RV resulted in long stimulus-to-QRS latency and optimal pace-mapping. Accordingly, this substrate was deemed the culprit of the clinical VT. Radiofrequency catheter ablation aimed at eliminating all LPs recorded from both scars was effective in preventing VT recurrences at follow-up. A post-infarction RV free-wall scar may exceptionally be responsible of VT occurrence. Right ventricular mapping should be considered in selected cases based on 12-lead electrocardiogram VT morphology and prior RV infarct.
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Project description:In the electrophysiological laboratory, orthodromic atrioventricular reciprocating tachycardia (ORT) can be distinguished from atrial tachycardia and atrioventricular node reentry tachycardia by identifying orthodromic and antidromic wavefront fusion during ventricular overdrive pacing (VOP). Previous work has shown that basal VOP near the accessory pathway (AP) increases the likelihood of observing fusion; however, in a third of cases, fusion is not appreciable regardless of VOP location.To explore the hypothesis that pacing near His-Purkinje system (PS) end points reduces fusion quality, which may explain patients with nonresponsive ORT.In a novel computer model of ORT, simulations were performed with a variety of AP locations and pacing sites; results were analyzed to assess factors influencing fusion quality in pseudo-electrocardiogram signals.Entrainment by basal VOP near the AP was more likely to produce fusion visible on simulated electrocardiograms compared to entrainment by apical VOP, but this advantage was dramatically diminished when the pacing site was also near PS end points. Prediction of fusion quality based on AP proximity alone was dramatically improved when corrected to penalize for PS proximity.These results suggest that basal VOP near the AP and far from the PS is optimal; this could be tested in patients. A denser basal ramification of PS fibers is known to exist in a minority of human hearts; our findings indicate that this unusual PS configuration is a plausible explanation for ORT cases where fusion is never observed in spite of entrainment by basal VOP near the AP.
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