Beats Of Nonsustained Ventricular Tachycardia Research Articles

LEFT VENTRICULAR NONCOMPACTION: AN UNUSUAL CAUSE OF HEART FAILURE

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Left ventricular noncompaction (LVNC) is a cardiomyopathy characterized by prominent trabeculae and deep intertrabecular recesses in communication with the ventricular cavity. LVNC affects up to 1.3% of the population and is responsible for 3-4% of all heart failure syndromes. CASE PRESENTATION: A 76-year-old male presented to the emergency department due to increasing dyspnea. He endorsed lower extremity swelling and orthopnea. He was tachypneic and hypoxemic. Lung auscultation revealed bibasilar crackles. Bilateral pitting pedal edema was noted. BNP was elevated at 861 pg/mL and troponins were elevated at 0.6 ng/L. Electrocardiogram demonstrated normal sinus rhythm with T-wave inversions in the inferolateral leads. Chest radiograph showed cardiomegaly, vascular congestion and bilateral pleural effusions suggestive of congestive heart failure syndrome. Transthoracic echocardiogram revealed left ventricular ejection fraction of 25-30%. Prominent trabeculae and deep interventricular recesses were noted, concerning for LVNC. Coronary angiography showed moderate nonobstructive coronary artery disease without need for percutaneous coronary intervention. His clinical condition improved with diuretic therapy, blood pressure control, and initiation of guideline-directed medical therapy. During his hospitalization, telemetry captured 6 beats of non-sustained ventricular tachycardia. Lifevest was placed to evaluate need for ICD implantation after optimization of medical therapy. He was scheduled for follow up echocardiogram in 3 months and counseled on the need for family screening. DISCUSSION: LVNC is thought to be a congenital cardiomyopathy caused by failure of cardiac sinusoids to compact during embryogenesis. However, studies demonstrate development of LV trabeculations on serial echocardiograms suggesting LVNC may be an acquired cardiomyopathy. Predisposition to trabeculation development may be genetically determined, LVNC has a 30% rate of familial recurrence. Excessive preload and afterload are thought to contribute as the development of trabeculations is noted in chronic renal failure and valvular heart disease. Criteria for diagnosis of LVNC vary and are not universally agreed upon. Thus, a multi-modality imaging approach involving echocardiography and cardiac MRI is recommended. LVNC is associated with significant complications, 56% of patients will develop heart failure syndrome and up to 40% will require heart transplantation. Additionally, 11% of patients undergo ICD implantation for ventricular arrhythmias and 7.6% of patients die of sudden cardiac death. Risk of thromboembolism ranges from 21-38%, likely due to turbulent flow through intertrabecular recesses. Three-year mortality rate is estimated at 14%. CONCLUSIONS: LVNC is a relatively common cardiomyopathy with significant morbidity and mortality. We urge clinician awareness to facilitate prompt diagnosis and management. Reference #1: Bhatia, Nisha L., et al. “Isolated Noncompaction of the Left Ventricular Myocardium in Adults: A Systematic Overview.” Journal of Cardiac Failure, vol. 17, no. 9, 2011, pp. 771–778., doi:10.1016/j.cardfail.2011.05.002. Reference #2: Tian, Julia, et al. “Left Ventricular Noncompaction: A Rare Case of Nonischemic Cardiomyopathy.” Case Reports in Cardiology, vol. 2019, 2019, pp. 1–3., doi:10.1155/2019/5637638. Reference #3: Gati, Sabiha, et al. “Adult Left Ventricular Noncompaction.” JACC: Cardiovascular Imaging, vol. 7, no. 12, 2014, pp. 1266–1275., doi:10.1016/j.jcmg.2014.09.005. DISCLOSURES: No relevant relationships by Gopika Dasari, source=Web Response No relevant relationships by Anneka Hutton, source=Web Response No relevant relationships by Eli Levine, source=Web Response No relevant relationships by Shaheen Mizyed, source=Web Response

A Double-Blind, Placebo-Controlled Trial to Evaluate the Safety, Tolerability, and Pharmacokinetics of Single, Escalating Oral Doses of JDTic.

Animal studies suggest that kappa opioid receptor antagonists (KORAn) potentially could treat a wide variety of addictive and depressive disorders. We assessed the KORAn JDTic for safety, tolerability, and pharmacokinetics in a double-blind, placebo-controlled, randomized trial evaluating single oral doses in healthy adult males. Predose and postdose safety assessments included orthostatic vital signs; 6-lead continuous telemetry monitoring (approximately 16 h predose to 24 h postdose); 12-lead electrocardiograms (ECGs); clinical chemistry, hematology, coagulation, and urinalysis; psychomotor functioning (using the Wayne Saccadic Fixator (WSF)); and adverse events. As a potential indicator of JDTic effects on affect, the POMS Standard instrument was administered predose and daily postdose Days 1–6. At 1 mg, 2 of the 6 JDTic (and 0/6 placebo) subjects experienced a single, asymptomatic event of multiple beats of nonsustained ventricular tachycardia (NSVT). Their events were temporally similar with respect to time postdose (and the postdose timing of an NSVT event in a monkey). These events triggered a study stopping rule. No differences were observed between the placebo and JDTic subjects with respect to clinical chemistry, hematology, coagulation, urinalysis, orthostatic vital signs, WSF, or 12-lead ECG parameters. Plasma JDTic levels were below the lower limit of quantitation (0.1 nM) in all subjects. There were no significant differences in POMS scores between the placebo and JDTic groups. Although the evidence is circumstantial, it suggests that NSVT is a potential JDTic toxicity in humans. Given the therapeutic potential of KORAn, further investigation is needed to determine whether a significant JDTic human cardiac effect indeed exists, and if so, whether it is specific to JDTic or represents a KORAn class effect.

Abstract 18457: Outpatient Milrinone Therapy as a Bridge to Pediatric Heart Transplantation: A Large Single Center Experience

Objective: Milrinone infusion as treatment of end stage heart failure in children is well established. Previous reports of outpatient milrinone therapy (tx) are limited by small numbers. Our objective was to evaluate the safety of outpatient milrinone tx as a bridge to heart transplant (HT). Methods: We retrospectively reviewed the records of all patients (pt) at our institution that have received outpatient milrinone tx between February 2000 and June 2013. Results: A total of 53 pt received outpatient milrinone tx, all had failed milrinone weaning, all began milrinone as an inpatient, and all had an indication of bridge to HT. The median age was 9.7 years [IQR 2-16] and 27 (51%) were male. The diagnosis prior to HT was congenital heart disease (15), cardiomyopathy (21; 16 dilated and 5 restrictive), and graft failure (17). Successful HT was performed in 52 and 1 pt is alive waiting. The median length of stay (LOS) for initiation of milrinone was 7 days (d) [IQR 2-16]. There were 2737 d of outpatient milrinone tx without a death and the median duration of tx was 28 d [IQR 15-62; range1-377]. The mean dose was 0.5 ± 0.02 mcg/kg/min. Arrhythmias occurred in 2 pt (atrial flutter and 3 beats of non-sustained ventricular tachycardia). There were 27 rehospitalizations in 16 pt for a total 97 inpatient days with a median LOS of 2d [IQR 1-3]. Indications for rehospitalization were atrial flutter (1pt, 3d),worsening heart failure (4pt, 26d, median LOS=3d [IQR 1-11]), central venous line (CVL) malfunction (10 pt, 23d, median LOS = 1d [IQR 1-2], CVL infection (2 pt, 5d, mean LOS = 2.5d +/- 0.71, and other (16pt,10 admissions, 40d, median LOS=2d [IQR 1-6]. One pt with worsening heart failure was admitted for additional inotropic support with dopamine and remained an inpatient until HT. Conclusion: There was no mortality in patients on milrinone awaiting HT. Arrhythmias were rare and catheter related complications were infrequent. The outpatient use of milrinone in children is safe and effective when initiated in the inpatient setting and it may reduce costs and improve quality of life in children awaiting HT.

Taquicardia ventricular bidireccional atípica

A 75-year old male, with the sole cardiovascular risk factor of being an active smoker, was admitted with a several week history of progressive exertional dyspnea. He was not taking any medication on a regular basis. We performed a complete cardiological evaluation and diagnosed the patient with idiopathic dilated cardiomyopathy and severe left ventricular systolic dysfunction. Upon hospitalization, treatment was started with furosemide and captopril; an electrocardiogram revealed sinus rhythm with ventricular extrasystoles. Renal function parameters and serum ion concentrations were within normal limits from admission (creatinine: 0.7 mg/dL; sodium: 139 mEq/L; potassium: 4 mEq/L; magnesium: 1.6 mEq/L). We performed a continuous 24-h electrocardiogram in order to determine the density of ventricular extrasystoles as a possible cause for the cardiomyopathy, and 20% of the complexes corresponded to ventricular extrasystoles with two morphologies, as well as runs of 3-5 beats of nonsustained ventricular tachycardia. We documented one asymptomatic, at-rest episode of tachycardia at 113 bpm, which was a wide QRS tachycardia that alternated between the two morphological QRS types that had been observed in isolated extrasystoles (A). It was electrocardiographically compatible with bidirectional ventricular tachycardia. Although bidirectional ventricular tachycardia is characteristic of digitalis intoxication or familial forms of catecholaminergic ventricular tachycardia, this case was an atypical bidirectional tachycardia caused by a coupled continuous alternation of ventricular extrasystoles in the same patient (B). We started treatment with beta blockers and the ventricular extrasystole density decreased significantly (figure).

Differential Effects of Statins ( Pravastatin or Simvastatin) on Ventricular Ectopic Complexes: Gα i2, a Possible Molecular Marker for Ventricular Irritability

Retrospective studies suggest that statins might exert an antiarrhythmic effect on the heart. The mechanism of this effect is unclear. Parasympathetic stimulation of the heart has been shown to protect against ventricular arrhythmias. The goal of this study was to determine the effect of statins on ventricular arrhythmias and its correlation with changes in parasympathetic responsiveness and Galpha(i2) expression. Patients were randomized to pravastatin and simvastatin in a double-blind crossover design. Ventricular arrhythmias were determined by analysis of 24-hour Holter recordings. Spectral RR interval analysis of Holter studies determined peak high-frequency power fraction, which reflects parasympathetic modulation of heart rate. Expression of Galpha(i2), a molecular component of the parasympathetic response pathway, was determined by Western blots of patients' lymphocytes. Pravastatin treatment decreased the incidence of ventricular premature complexes by 22.5 + or - 3.4% (n = 20, p <0.05), couplets, and runs of 3 to 6 beats of nonsustained ventricular tachycardia from 9.8 + or - 2.67 to 3.9 + or - 1.25 events/patient/24 hours (n = 12, p <0.05). Pravastatin increased peak high-frequency fraction by 29.8 + or - 4.3% (n = 33, p <0.001), while Galpha(i2) expression increased by 51.3 + or - 22.5% (n = 21, p <0.05). Effects of simvastatin on ventricular premature complexes and nonsustained ventricular tachycardia were not significant. Relative changes in couplets and nonsustained ventricular tachycardia in pravastatin-treated patients correlated negatively with changes in Galpha(i2) and high-frequency fraction (rho = -0.588 and rho = -0.763, respectively, n = 12, p <0.05). In conclusion, these data suggest that pravastatin might decrease cardiac irritability via an increase in parasympathetic responsiveness and that changes in Galpha(i2) expression might serve as a molecular marker for this effect, which might play a role in the molecular mechanism of the antiarrhythmic effect of statins.

Palpitations in a Medical Intern

Palpitations in a Medical Intern

Three-dimensional mapping of the initiation of nonsustained ventricular tachycardia in the human heart.

Elucidation of the electrophysiological mechanisms of nonsustained ventricular tachycardia (VT) in humans is required to define the relationship between nonsustained VT and sustained VT. This goal requires, at least in part, analysis of transmural ventricular activation in patients with both sustained and nonsustained VTs. We analyzed three-dimensional intraoperative cardiac maps of extrastimuli and beats during 44 nonsustained VTs and the initiating beats of 6 sustained VTs from six patients with healed myocardial infarcts who were undergoing arrhythmia surgery. The coupling interval, total activation time, and diastolic interval of each extrastimulus and beat of nonsustained VT were compared with counterparts during sustained VT. Sites activated last during extrastimuli initiating nonsustained or sustained VTs occurred in the same region, and activation times were comparable. However, the site of earliest activation during the initial or subsequent beats of nonsustained VT was discordant from the site activated earliest during the first and subsequent beats of sustained VT in 74% of cases. The mean variance in coupling interval, but not total activation time or diastolic interval, was significantly greater for VT that terminated before the 10th cycle than for VT that sustained. When analyzed from the last extrastimulus up to the fifth VT cycle, the standard deviation of the coupling interval, but not of the total activation time, was greater for nonsustained than for sustained VTs. Electrode density was sufficient to define an arrhythmia mechanism for 36 beats of nonsustained VT. Twenty-one (58%) initiated in the subendocardium, midmyocardium, or epicardium by a macroreentrant mechanism, and 15 (42%) initiated in the subendocardium by a focal mechanism. Compared with sustained VT, nonsustained VT initiates at discordant sites, is characterized by oscillations in coupling interval but not in total activation time, and initiates by either a macroreentrant or a focal mechanism.

Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: Role of the accessory pathway

Clinical and electrophysiologic characteristics associated with spontaneous and inducible atrial fibrillation and ventricular tachyarrhythmia were assessed in 20 consecutive patients with Wolff-Parkinson-White (WPW) syndrome undergoing surgical division (n = 12) or transcatheter electrical ablation (n = 8) of accessory pathways. Patients with spontaneous atrial fibrillation were characterized by the trend (not significant) of a shorter antegrade accessory pathway effective refractory period (256 ± 26 vs 303 ± 109 msec). However, patients with and without spontaneous atrial fibrillation did not differ with respect to prevalence of structural heart disease (3 of 11 vs 2 of 9), intra-atrial conduction time (34 ± 10 vs 32 ± 10 msec), or interatrial conduction time (86 ± 21 vs 88 ± 17 msec). Thus, atrial and accessory pathway electrophysiologic properties (per se) were not clear determinants of susceptibility to atrial fibrillation. Among the 20 patients, 10 to 35 beats of nonsustained ventricular tachycardia (seven patients) or ventricular fibrillation (three patients) were induced at electrophysiologic study with one to three programmed extrastimull. Clinically, a ventricular arrhythmia (ventricular fibrillation during atrial fibrillation) had occurred in only one of these patients. The discordance of these observations was significant ( p < 0.01). Patients with and without inducible ventricular arrhythmias were not distinguished by clinical factors or by electrophysiologic properties of the accessory pathway or ventricles. Accessory pathway conduction was completely or partially eliminated by ablation procedures in 14 of 20 patients. During a mean follow-up of 27 months, atrial fibrillation recurred in two patients with failed ablation procedures and in one patient with left atrial enlargement (despite accessory pathway division) ( p = 0.019 vs pre-ablation). Ventricular arrhythmias remained inducible in two patients in whom accessory pathway ablation failed ( p = 0.01 vs initial study). However, spontaneous ventricular tachyarrhythmias did not occur during follow-up. We conclude that susceptibility to spontaneous or inducible atrial fibrillation and ventricular tachyarrhythmia in patients with WPW syndrome and no organic heart disease depends primarlly on the existence of a functional accessory pathway. These susceptibllities are eliminated by interruption of accessory pathway conduction. Ventricular tachyarrhythmias remain infrequent spontaneous events in the WPW syndrome. Their more frequent induction at electrophysiologic study is not predictive of clinical occurrence.