Eduardo Franco

Circadian variations of infarct size in acute myocardial infarction

Background The circadian clock influences a number of cardiovascular (patho)physiological processes including the incidence of acute myocardial infarction. A circadian variation in infarct size has recently been shown in rodents, but there is no clinical evidence of this finding. Objective To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size. Methods A retrospective single-centre analysis of 811 patients with STEMI admitted between 2003 and 2009 was performed. Infarct size was estimated by peak enzyme release. The relationship between peak enzyme concentrations and time-of-day were characterised using multivariate regression splines. Time of STEMI onset was divided into four 6-hour periods in phase with circadian rhythms. Results Model comparisons based on likelihood ratio tests showed a circadian variation in infarct size across time-of-day as evaluated by peak creatine kinase (CK) and troponin-I (TnI) concentrations (p=0.015 and p=0.012, respectively). CK and TnI curves described similar patterns across time, with a global maximum in the 6:00–noon period and a local minimum in the noon–18:00 period. Infarct size was largest in patients with STEMI onset in the dark-to-light transition period (6:00–noon), with an increase in peak CK and TnI concentrations of 18.3% (p=0.031) and 24.6% (p=0.033), respectively, compared with onset of STEMI in the 18:00–midnight period. Patients with anterior wall STEMI also had significantly larger infarcts than those with STEMI in other locations. Conclusions Significant circadian oscillations in infarct size were found in patients according to time-of-day of STEMI onset. The infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00–noon). If confirmed, these results may have a significant impact on the interpretation of clinical trials of cardioprotective strategies in STEMI.

Acute myocardial infarction secondary to direct myocardial infiltration by a malignant neoplasia

A 24-year-old male, with a previous history of osteosarcoma with cerebral and pulmonary metastasis, presented to the emergency room with severe chest pain, dyspnoea, and diaphoresis. Physical examination revealed an apical S4 gallop, abolition of left breath sounds, and right hemiparesia. On electrocardiogram, …

Ventricular Fibrillation Caused by 1:1 Atrial Flutter

It is broadly accepted that atrial flutter (AFL) with 1:1 atrioventricular conduction can lead to sudden cardiac death due to hemodynamic compromise and the onset of ventricular fibrillation (VF). In the absence of pre-excitation, evidence for this is limited and only circumstantial. We present a case in which a 1:1 AFL led to VF in a patient without preexcitation. A 12-year-old boy with Down syndrome, a surgically corrected partial atrioventricular canal defect, and carrier of a normofunctioning 23-mm mechanical mitral valve prosthesis was admitted to the electrophysiology laboratory to undergo AFL ablation. No residual lesions were present and biventricular ejection fraction was preserved. Twelve-lead electrocardiogram showed a typical AFL with variable atrioventricular conduction (Fig. 1). Twenty minutes after general anesthesia with sevoflurane, propofol, and remifentanil,

Narrow QRS Tachycardia in a Patient with Spongiform Cardiopathy and Preexcitation: What is the Mechanism?

A 19-year-old man diagnosed with spongiform cardiomyopathy and ventricular preexcitacion was referred to our hospital for electrophysiological (EP) testing after a syncopal episode. Baseline electrocardiogram (ECG) showed ventricular preexcitation consistent with the presence of a superior paraseptal, anteroseptal, accessory pathway (AP). After triple femoral vein puncture, a decapolar catheter was placed in the coronary sinus, a tetrapolar catheter in the His bundle region (with no clear His deflection recorded through the EP study), and a 4-mm-tip irrigated ablation catheter initially at the RV apex. Programmed atrial extrastimuli from the coronary sinus reproducibly induced nonsustained and sustained episodes of an irregular narrow QRS tachycardia with apparent atrioventricular dissociation in the surface ECG (Fig. 1). Intracardiac recording during ongoing tachycardia are also shown (Figs. 2 and 3). What is the involved mechanism?

Macroreentrant atrial tachycardia around the native common atrioventricular valve in a surgically corrected complete atrioventricular septal defect

A 24-pole catheter (OrbiterR ; Bard Medical) was placed around the right-sided part of the common atrioventricular valve with its distal part within the coronary sinus. Post-pacing intervals along the coronary sinus matched the tachycardia cycle length. Left atrial activation map (Figure, Panel A, top; EnSite Precision navigator) showed a clockwise rotation around the left-sided part of the common atrioventricular valve. As left atrial electrograms comprised only 50% of the cycle length, the right atrium was also mapped. Panel B displays concealed entrainment and post-pacing intervals similar to the tachycardia cycle length, from the lateral ends of both right-sided (top) and leftsided (bottom) parts of the common atrioventricular valve (entrainment from points #1 and #2 in Panel A, respectively). With the diagnosis of macroreentrant atrial tachycardia around the native common atrioventricular valve (online supplementary video shows propagation map), a line of ablation along the theoretical cavo-tricuspid isthmus was performed (red spheres in Panel A), successfully terminating the arrhythmia.

Mitral-Aortic Flow Reversal in Cardiac Resynchronization Therapy

Background— Flow entering the left ventricle is reversed toward the outflow tract through rotating reversal flow around the mitral valve. This was thought to facilitate early ejection, but had not been proved to date. We hypothesized that perfect coupling between reversal and ejection flow would occur at optimal atrioventricular delay (AVD), contributing to its hemodynamic superiority, and evaluated its applicability for AVD optimization. Methods and Results— Forty consecutive patients with cardiac resynchronization therapy underwent intracardiac flow analysis and AVD optimization. Reversal and ejection flow curves were studied. The presence and duration of reversal-ejection discontinuity were assessed for all programmed AVD. Reproducibility of each optimization method was evaluated through interobserver variability. Discontinuity between reversal and ejection flow was observed in all patients with longer than optimal AVD, increasing linearly with excess duration in AVD (linear R2=0.976, P<0.001). Longer discontinuities implied progressive decreases in pre-ejection flow velocity in the left ventricular outflow tract, with consequent loss of flow momentum. The equation optimal AVD=programmed AVD–[1.2(discontinuity duration)]+4 accurately predicted optimal AVD. Short AVD systematically compromised reversal flow because of premature ejection. Agreement over optimal AVD was superior when assessed by flow reversal method (intraclass correlation coefficient =0.931; P<0.001) over both iterative and aortic velocity–time integral methods. Conclusions— Perfect coupling between mitral-aortic flow reversal and ejection flow in the left ventricle occurs at optimal AVD. As a result, full blood momentum in the outflow tract is used to facilitate early ejection. This can be measured and provides a new method for AVD optimization.

Challenging Lead Implantation Guided by Voltage Map.

The patient was a 16-year-old boy who had been born with pulmonary atresia and ventricular septal defect, for which he had undergone complete repair. He had a Melody pulmonary valve and stents in both pulmonary artery branches. He underwent placement of a dualchamber cardioverter defibrillator for syncope and nonsustained ventricular tachycardia. The implantation was performed in the Department of Pediatric Cardiac Surgery. It was complicated by the tremendous complexity involved in placing the ventricular lead, due to inadequate capture and sensing (R wave) thresholds, making it necessary to evaluate several positions, until an apical position was chosen. Three months later, a very high ventricular capture threshold (6.5 V 1 ms) and an R wave = 4 mV were observed. Fluoroscopic examination ruled out lead displacement, and we were consulted with regard to its replacement. Given the difficulties of the initial implantation and to minimize the duration of the open surgery (due to the risk of infection), we decided to begin by constructing an endocardial voltage map of the right ventricle with the EnSite Velocity navigation system (St. Jude Medical) (Figure A, video of the supplementary material), using contact mapping with a sensor-equipped catheter to avoid recording floating points in the interior. After evaluating 203 points, we observed extensive regions with voltage < 5 mV (grays), inadequate for implantation, and others 10 mV that were suitable (violet). The previously implanted lead was in one of the gray regions (asterisk). The direct connection of the new ventricular lead to the navigation system itself made it possible to guide it for implantation in a healthy region. Figure A shows the final position of the lead (arrow), and Figure B corresponds to its fluoroscopic image. In this position, an adequate capture threshold (0.75 V 0.5 ms) and an R wave = 9 mV were achieved, and have been maintained after more than 1 month.

Prehospital activation of cardiac catheterization teams in ST-segment elevation myocardial infarction

INTRODUCTION AND OBJECTIVES Current clinical guidelines for ST-segment elevation myocardial infarction (STEMI) suggest prehospital activation of the cardiac catheterization team. In previous protocols in our center activation occurred once patients arrived at the hospital. In January 2011, we initiated a new primary angioplasty activation protocol from prehospital locations. Our objective was to quantify the influence of this change on reperfusion times. METHODS A total of 173 consecutive STEMI patients (n=73/100 before/after initiation of the new protocol), diagnosed in a prehospital setting within 12 hours of symptom onset, were analyzed. The time between the patients arrival at the hospital and beginning of the angioplasty procedure was termed the cath lab activation delay. RESULTS The new protocol resulted in a 37-min reduction in system delay (166 [132-235] min before vs. 129 [105-166] min after, p<0.001), mostly driven by a 64% reduction in cath lab activation delay (55 [0-79] min before vs. 20 [0-54] min after, p=0.001). This reduction was mainly observed outside working hours. The percentage of patients treated with a system delay ≤ 120 min increased from 14.5% before the new protocol to 41.8% afterwards (p=0.001). CONCLUSIONS Prehospital activation of the cardiac catheterization team resulted in earlier reperfusion of STEMI patients.

Three-Dimensional Echocardiographic Left Ventricular Curvature Analysis: A New Approach to Left Ventricular Remodeling with Clinical Applications to Be Discovered

Left ventricular (LV) remodeling is a serious process that may lead to fatal heart failure and can be caused by many cardiovascular diseases, such as ischemic cardiomyopathy, dilated cardiomyopathy, myocarditis, valvular disease, and others. 1 Several pathophysiologic processes have been demonstrated to take part in this complex process. 2 For instance, cardiomyocyte apoptosis is increased in remodeled ventricles in patients with ischemic and dilated cardiomyopathy, with as much as 2% of cardiomyocyte nuclei being apoptotic at the same time. 3 Myocyte hypertrophy and increased interstitial collagen are also found. The main features of a remodeled ventricle are a large volume, poor contractility (which leads to a decreased ejection fraction [EF]), and an altered geometry. 2 Larger volumes correlate with patient outcomes, and current therapeutic efforts aim to decrease LV volumes to prevent adverse events. Two-dimensional echocardiographic volume measurements have shown good correlation with the incidence of outcomes, 4 but threedimensional (3D) echocardiography provides more accurate analyses of LV volumes and EFs and correlates better with magnetic resonance imaging values, and its measurements have less intraobserver and interobserver variability. 5,6 Moreover, it has been shown to identify parameters associated with the way LV function declines as the left ventricle dilates, such as ventricular mechanical dyssynchrony. 7