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Background Hypertrophic cardiomyopathy (HCM) is commonly associated with atrial fibrillation (AF), but its impact on outcomes in real-world practice is uncertain. years) were enrolled in the EURObservational Research Programme (EORP) Cardiomyopathy/Myocarditis Registry. Methods Overall, 1739 adult patients with HCM (40.9%
Then I always look to see if the initial deflection of the QRS has a lot of voltage change per change in time (seen in tachycardias that are initiated from above the ventricle because the propagate through fast conducting purkinje fiber. Patient has an ICD, which is primarily placed in patients with cardiomyopathy.
(MedPage Today) -- CHICAGO -- For patients with ventricular tachycardia (VT) and ischemic cardiomyopathy, going right to catheter ablation improved outcomes compared with trying antiarrhythmic drugs first, the VANISH2 trial showed. Death or.
Among patients with ventricular tachycardia and ischemic cardiomyopathy, catheter ablation as an initial therapy led to a lower risk of adverse outcomes than antiarrhythmic drug therapy.
BackgroundHypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder characterized by asymmetric hypertrophy of the ventricles and the ventricular septum, leading to subsequent left ventricular outflow tract (LVOT) obstruction and diastolic dysfunction.
A prehospital 12-lead was recorded: There is a regular wide complex tachycardia. The computer diagnosed this as Ventricular Tachycardia. There is a wide complex regular tachycardia at a rate of 226. Toothache, incidental Wide Complex Tachycardia Could it be fascicular VT or Bundle Branch VT ( i.e., idiopathic VT )?
male with pertinent past medical history including Atrial fibrillation, atrial flutter, cardiomyopathy, Pulmonary Embolism, and hypertension presented to the Emergency Department via ambulance for respiratory distress and tachycardia. Description : Regular Wide Complex Tachycardia at a rate of about 160. SVT with aberrancy?
And of course Ken's comments at the bottom) An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status. I do not see OMI here and all trops were only minimally elevated, consistent with either chronic injury from cardiomyopathy or with acute injury from sepsis.
She had a single chamber ICD/Pacemaker implanted several years prior due to ventricular tachycardia. Answer : The ECG above shows a regular wide complex tachycardia. Said differently, the ECG shows a rather slow ventricular tachycardia with a 2:1 VA conduction. Cardiac output (CO) was being maintained by the tachycardia.
DCM had higher T1 and lower vGLNU than HC. When compared with TIC, DCM showed significantly higher LVEDV and LVEDVi. ROC analysis revealed that LVEDV and vGLNU provided high specificity for differentiating DCM from the other etiologies.ConclusionNative T1 mapping and its texture analysis may be valuable for differentiating between DCM and HC.
A patient in the ICU with significant underlying cardiac disease [HFrEF 30%, non-ischemic cardiomyopathy, LBBB s/p CRT-D (biventricular pacer), AVNRT s/p ablation a few yrs ago, hx sinus tachycardia while on max tolerated BB therapy] went into a regular wide-complex tachycardia after intubation for severe COPD exacerbation.
The goal of the VANISH2 trial was to compare endocardial catheter ablation with conventional antiarrhythmic drug (AAD) therapy as a first-line treatment for infarct-related ventricular tachycardia (VT) in ischemic cardiomyopathy.
She was awake, alert, well perfused, with normal mental status and overall unremarkable physical exam except for a regular tachycardia, possible rales at both bases, some mild RUQ abdominal tenderness. Thus, I believe it is a regular, monomorphic, wide complex tachycardia. Or it could simply still be classic VT. RVEF 100 ml/m2.
Implantable cardioverter defibrillator (ICD) prevents sudden cardiac death (SCD) in patients with ischemic cardiomyopathy (ICM). Catheter ablation has been shown to effectively reduce ventricular tachycardia (VT) recurrence, yet its efficacy in patients without an ICD implantation remains uncertain.
The best approach for ablating ventricular tachycardia (VT) targeting right ventricular free wall (RVFW) aneurysms in arrhythmogenic right ventricular cardiomyopathy (ARVC) remains undefined.
Tachycardia-induced cardiomyopathy (TIC) is a unique cardiomyopathy, which is potentially reversible. Due to the presence of tachyarrhythmias in various cardiomyopathies, differentiating TIC from other non-reversible conditions can be challenging.
The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. My THOUGHTS on the ECG in Figure-1: The rhythm is sinus tachycardia at ~105/minute ( ie, The R-R interval is regular — and just under 3 large boxes in duration ).
Patients with non-ischemic left ventricular dilated cardiomyopathy (NIDCM) and ventricular tachycardia (VT) typically have a basal perivalvular substrate adjacent with specific distribution dependent on the genetic background.1-4 1-4 Isolated apical substrate responsible for VT in NIDCM with perivalvular sparing is rare.
Tachycardia-induced cardiomyopathy refers to changes in cardiac structure and function that result from rapid arrhythmia and can manifest as a continuous or recurrent event. Cardiomyopathy induced by atrial ta.
Tachycardia-induced cardiomyopathy (TICM) is a reversible impairment of the left ventricular (LV) systolic function caused by persistent tachyarrhythmias. It is often difficult to identify macroscopic scar in patients with TICM by cardiac magnetic resonance imaging (MRI).
The ventricular tachycardia (VT) substrate in patients with non-ischemic cardiomyopathy (NICM) is complex in distribution and intramural location. Myocardial lipomatous metaplasia (LM) is vital to post-infarct VT circuitry, but not investigated in NICM VT circuitry yet.
Cardiac sarcoidosis (CS), a rare condition characterized by non-caseating granulomas, can manifest with symptoms such as atrioventricular block and ventricular tachycardia (VT), as well as mimic inherited cardiomyopathies. A 58-year-old woman presented with sustained VT with a prior diagnosis of hypertrophic cardiomyopathy (HCM).
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a family inherited cardiomyopathy associated with ventricular arrhythmias. With the development of molecular biology, histology, imaging, and other dia.
Many genetic non-ischemic dilated cardiomyopathies (NICM) cause ventricular tachycardias (VT) originating from scar substrate identified as areas of low electrogram voltage. Substrate locations vary and the causes of scar are not well defined.
Shortly after isoprenalin infusion was initiated, there were short runs of ventricular tachycardia. The granulomatous inflammation affects the heart, causing an infiltrative cardiomyopathy The most common manifestations of cardiac sarcoidosis are atrioventricular (AV) block and ventricular tachyarrhythmias (VT).
Catheter ablation is an effective tool to reduce ventricular tachycardia (VT) burden. There is a lack of robust data studying the intraprocedural characteristics and outcomes of VT ablation in patients with non-ischemic (NICM) versus ischemic cardiomyopathy (ICM).
Ventricular Tachycardia (VT) is an important cause of morbidity and mortality in structural heart Disease. Current literature is limited in direct comparison of VT in ischemic (ICM) compared to non-ischemic cardiomyopathy (NICM).
Catheter ablation (CA) is effective in the treatment of ventricular tachycardia (VT). Although some data suggest patients with non-ischemic cardiomyopathy (NCIM) have worse outcomes compared to those with an ischemic etiology (ICM), direct comparisons are scarcely reported.
He had a background of arrhythmic right ventricular cardiomyopathy. He had previously undergone the placement of a dual-chamber implantable cardioverter-defibrillator for atrioventricular block and ventricular tachycardia (VT). Clinical introduction A man in his 50s presented to the emergency department with palpitations.
A 50-something male with unspecified history of cardiomyopathy presented in diabetic ketoacidosis (without significant hyperkalemia) with a wide complex tachycardia and hypotension. Analysis: there is a wide complex tachycardia. This was the interpretation I put into the system: WIDE COMPLEX TACHYCARDIA. It is regular.
A 69-year-old man with a history of MI and cardiomyopathy presented with 2 days of dyspnea. Regular tachycardia (124 beats per min), diaphoresis, and rales were present. A diagnosis was made.
Conclusion: Assuming none of the above exceptions exist the ECG in Figure-1 has to be presumed VT until proven otherwise. == C ASE C onclusion: Today's patient was hemodynamically stable in association with the ECG in Figure-1.
The above ECGs show the initiation and continuation of a polymorphic ventricular tachycardia. Polymorphic ventricular tachycardia can be ischemic, catecholaminergic or related to QT prolongation. There was hyperkinesis of the basal segments and findings were interpreted as typical of takotsubo cardiomyopathy. Learning points: 1.
Abstract Introduction Due to its unique features, pulsed field ablation (PFA) could potentially overcome some limitations of current radiofrequency (RF) ventricular tachycardia (VT) ablation. Methods Two patients with ischemic cardiomyopathy and previously failed RF VT ablations were treated with PFA.
Objectives To describe a cohort of patients with arrhythmogenic left ventricular cardiomyopathy (ALVC), focusing on the spectrum of the clinical presentations. Twenty-one (41%) had normal echocardiogram, 13 (25%) a hypokinetic non-dilated cardiomyopathy (HNDC) and 17 (33%) a dilated cardiomyopathy (DCM).
VF should make you think of ischemia, cardiomyopathy (especially scar from old MI), or one many other cardiac but non-ischemic etiologies. Confirmation of sinus tachycardia should be easy to verify when the heart rate slows a little bit ( as the patient's condition improves ) — allowing clearer definition between the T and P waves.
Wild-type transthyretin amyloid cardiomyopathy (ATTRwt-CM) is often accompanied by atrial fibrillation (AF), atrial flutter (AFL), and atrial tachycardia (AT), which are difficult to control because beta-blockers and antiarrhythmic drugs can worsen heart failure (HF).
2. Baseline fibrotic substrate from dilated cardiomyopathy leading to VT. I interpreted the ECG as VT with two primary etiological possibilities: 1. Abrupt plaque ulceration of Type 1 ACS leading to VT. From a clinical standpoint I reconciled the first possibility as most probable since the chest discomfort came first.
Surgical disarticulation of the right ventricular (RV) free wall has been described by Guiraudon and colleagues as an effective therapy for refractory ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy (ARVC).1
In all-comers with significant VAs, the pooled rate of SHD post-CMR evaluation was 39% (24% in the subgroup of premature ventricular contractions and/or non-sustained ventricular tachycardia vs 63% in the subgroup of more complex VAs). A change in diagnosis after use of CMR ranged from 21% to 66% with a pooled average of 35% (29%–41%).
Belhassen’s ventricular tachycardia is an uncommon arrhythmia in infants. Originating near the left posterior fascicle, it is initiated by supraventricular ectopy or sinus tachycardia and is uniquely sensitive to verapamil. Use of verapamil in infants is controversial due to risk of severe hemodynamic compromise.
Supraventricular tachycardias are the most common arrhythmias that occur during pregnancy. Pharmacologic therapy is often preferred in pregnant patients. When pharmacologic therapy fails, fluoroless catheter ablation utilizing electroanatomic mapping systems and intracardiac echocardiography (ICE) may be considered.
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