Emilio García-Morán

Inappropriate tachycardia detection by a biventricular implantable cardioverter defibrillator

GARCIA‐MORAN, E., et al.: Inappropriate Tachycardia Detection by a Biventricular Implantable Cardioverter Defibrillator. This case describes “double counting” of intrinsic conduction due to the combination of intraventricular conduction delay and the merging of the electrograms from the right and left ventricle (coronary sinus) leads in a biventricular cardioverter defibrillator. This situation prompted asymptomatic antitachycardia pacing. Lengthening of AV conduction by betablocker solved the problem.

Angina inestable en el anciano: perfil clínico, manejo y mortalidad a los tres meses. Datos del registro PEPA

Introduccion y objetivos Son escasos los datos publicados sobre las caracteristicas y el manejo de la angina inestable en el paciente anciano en nuestro pais. El objetivo fue analizar las caracteristicas clinicas y la utilizacion de recursos diagnosticos y terapeuticos en los pacientes con edad ≥ 70 anos. Pacientes y metodos El grupo estudiado esta compuesto por 1.551 pacientes con edad ≥ 70 anos de un total de 4.115 pacientes incluidos en el registro PEPA, con un seguimiento de 90 dias, que se han comparado con los 2.564 pacientes Resultados Entre los pacientes de edad avanzada (76 ± 5 anos), comparados con los mas jovenes (58 ± 8,5 anos), existe una significativa mayor proporcion de mujeres (el 43 frente al 27%), diabeticos (el 30 frente al 23%) e hipertensos (el 60 frente al 49%) y menor (p Conclusion En pacientes con edad avanzada y angina inestable se aprecia un patron diferente en los factores de riesgo cardiovascular y un perfil clinico mas desfavorable. Su manejo es menos agresivo y su mortalidad es mayor. La diabetes, la insuficiencia cardiaca y la desnivelacion del segmento ST al ingreso son predictores independientes de mal pronostico en este grupo de edad avanzada.

Kearns-Sayre Syndrome: Recurrent Syncope and Atrial Flutter

Kearns-Sayre syndrome is a rare disease linked to mitochondrial inheritance. The characteristic diagnostic triad consists of progressive external ophthalmoplegia, pigmentary degeneration of the retina, and atrioventricular block. It may also be associated with mental retardation, ataxia, deafness, muscle weakness, and endocrine disorders, such as diabetes mellitus or hypothyroidism. We present the case of a 37-yearold man with a noticeable phenotypic manifestation (Figure 1). From childhood, he had progressively presented photophobia, progressive loss of vision, external ophthalmoplegia, neurosensory deafness, Addison’s syndrome, muscle weakness, and ataxia. His present clinical symptoms consisted of recurrent syncope and atrial flutter. The association of Kearns-Sayre syndrome with atrial flutter has not been described. Twelve years before the current episode, he had been cardiologically assessed and diagnosed with Kearns-Sayre syndrome. At that time, the patient was asymptomatic, but the electrocardiogram showed right bundle-branch block and left anterior fascicular block. Periodic follow-up was prescribed. In the successive follow-ups, the patient remained asymptomatic with no changes in the electrocardiogram. The onset of the current clinical symptoms started during the postoperative of a cholecystostomy, when the patient presented several episodes of syncope. The electrocardiogram disclosed atypical flutter rhythm and regular conduction with an approximate ventricular frequency of 106 bpm, right bundle-branch block, and left anterior fascicular block (Figure 2). The echocardiogram was normal. An electrophysiological study established the diagnosis of cavotricuspid isthmusdependent flutter and counterclockwise rotation around the tricuspid valve. Isthmus ablation was performed successfully. After recovery of sinus rhythm, the atrioventricular conduction study showed prolongation of the HV interval and a short LETTERS TO THE EDITOR

Predictors of Lack of Clinical Improvement at Mid-Term Follow-up With Cardiac Resynchronization Therapy

INTRODUCTION About 30% of all patients do not respond to cardiac resynchronization therapy for heart failure. The objective of the study was to analyze the variables that may predict the lack of response. PATIENTS AND METHOD We analyzed the results in a series of 63 patients who received cardiac resynchronization with a biventricular device. Clinical and left ventricular function parameters were evaluated at the beginning of the study and at 6 months. Responders were defined as those who were alive, had not received a heart transplant, and who achieved more than a 10% increase in distance in the 6-minute walking test. RESULTS Mean age was 68.3 (8) years, 51 patients (81%) were men, and NYHA functional class was III-IV in 79.4%. Mean left ventricular ejection fraction was 22.4% (6)%, QRS width was 177 (25) ms, and 77.8% were in sinus rhythm. Almost half (46%, n=29) had ischemic heart disease. At 6-month follow-up, 69.8% of the patients were responders. Ischemic heart disease, sustained monomorphic ventricular tachycardia and a degree of mitral regurgitation >II/IV before implantation were associated with lack of response. No association was found for any of the other baseline variables. Logistic regression analysis identified all three of the aforementioned variables as independent predictors of lack of response: ischemic heart disease OR=4.8, 95% CI, 1.2-18.3, P=.023; ventricular tachycardia OR=8.7, 95% CI, 1.8-41.3, P=.007; and mitral regurgitation OR=8.03, 95% CI, 1.7-37.1, P=.008. CONCLUSION The likelihood of responding to resynchronization therapy is lower in patients with ischemic heart disease, significant mitral regurgitation, or sustained monomorphic ventricular tachycardia.

Refractory Electrical Storm: A Role for Transient Sympathetic Blockade

Castillo J, et al.; FANTASIIA Study Investigators. Quality of anticoagulation with vitamin K antagonists. Clin Cardiol. 2015;38:357–64. 3. Kim E, Ozonoff A, Hylek EM, Berlowitz DR, Ash AS, Miller DR, et al. Predicting outcomes among patients with atrial fibrillation and heart failure receiving anticoagulation with warfarin. Thromb Haemost. 2015;114:70–7. 4. del Campo M, Roberts G. Changes in warfarin sensitivity during decompensated heart failure and chronic obstructive pulmonary disease. Ann Pharmacother. 2015. http://dx.doi.org/10.1177/1060028015590438. 5. Bridgen M, Kay C, Lee A, Adamson PB. Audit of the frequency and clinical response to excessive oral anticoagulation in an outpatient population. Am J Hematol. 1998;59:22–7. 6. Ripley TL, Harrison D, Germany RE. Effect of heart failure exacerbations on anticoagulation: a prospective, observational, pilot cohort study. Clin Therap. 2010;32:506–14.

Worsening Conduction Delay in Hypertrophic Cardiomyopathy: What Drug Is Responsible?

We present the case of a 64-year-old male who presented to the emergency room because of recent onset palpitations. He was diagnosed with a first episode of atrial fibrillation and was managed at the emergency room by direct current cardioversion. The patient’s past medical record was unremarkable, and no relevant findings were discovered during the physical examination or laboratory tests. The baseline ECG is shown in Figure 1. On discharge the patient was referred for outpatient cardiology evaluation and was eventually seen 2 months later. The ECG at the outpatient clinic is shown in Figure 2. Figure 1. Baseline ECG. Figure 2. ECG at the cardiology outpatient clinic. Which drug was most likely prescribed to the patient to account for the differences between the first and second ECGs? Please turn the page to read the diagnosis. The ECG shows an …

ECG, July 2016.

We report the case of an 86-year-old woman who presented to the emergency department with syncope and spasms in left upper extremity. She had recently undergone implantation of a dual-chamber pacemaker because of symptomatic, paroxysmal, complete atrioventricular block secondary to syncope. Figure 1 shows the electrocardiogram on her arrival at the emergency room and Figure 2, the chest radiograph.

Response to ECG, July 2016

The electrocardiogram (Figure, panel B) shows the double spikes typical of dual-chamber (DDD) pacemakers. The first beat (*1) corresponds to the native QRS following the double spikes, with a prolonged PR interval, indicating the loss of ventricular capture. This loss is not permanent; the following 4 beats show a paced QRS (——) and the fifth (*5), again a loss of capture. The P waves are evident (^), but there are no adequate data on atrial detection or capture. The diagnosis is reel syndrome (option 3), caused by lead dislodgement due to generator rotation over its sagittal axis. The lead winds around the generator as though the latter were a reel (Figure, panels A and C) (Figure, panels A and C: chest radiographs following implantation and in the emergency department, respectively). In twiddler syndrome, the rotation of the generator causes the lead to wind around itself, forming a braid. In ratchet syndrome, there is no rotation and, usually, only the lead is affected. Option 4 is a distractor; the dislodged atrial lead can be seen in the generator pocket (Figure, panel C), and caused the spasms in the upper extremity described by the patient.