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A 55-year-old man complaining of worsening dyspnea on exertion was diagnosed with restrictive interventricular septal defect, left ventricular noncompaction (LVNC), mild aortic valve stenosis and aorto-right ventricular fistula. He underwent surgical aortic valve replacement with a mechanical bileaflet valve (St. Jude n. 23) and contextual direct suture of interventricular septal defect and closure of aorto-right ventricular fistula. At 2 years of follow-up, the patient was in good general condition. A complete echocardiographic examination showed normalization of left ventricular dimensions and ejection fraction. Furthermore, left ventricular trabeculations became less evident and no longer met the diagnostic criteria for noncompaction. In our case, the expected left ventricular reverse remodeling after cardiac surgery was associated with a significant reduction in LVNC features. In conclusion, physicians should be careful in avoiding overdiagnosis of LVNC, whose features may indeed reflect only the hypertrabeculated morphology of a normal or pathological heart.

Atrial standstill is characterized by failure of atrial excitation, either spontaneous or induced by atrial electric stimulation. We report the case of a 38-year-old man with severe bradycardia and junctional escape rhythm associated with dilative cardiomyopathy. Electroanatomic mapping showed the absence of atrial viability in almost the entire right atrial endocardial surface and excluded the feasibility of atrial pacing.

MicroRNAs are key, recently discovered, regulators of gene expression. They are involved in many physiological cellular pathways so it is not surprising that an altered microRNA expression pattern can be involved in the pathogenesis of many disease states. The possibility to manipulate microRNAs to obtain a therapeutical effect is very attractive since they represent specific targets in a particular cellular pathway and because it is quite easy to synthesize short oligonucleotides with the ability to interfere with microRNA mechanism of action. The main problem for microRNA-based therapy is represented by delivery. In the last two years many studies have underlined the involvement of microRNAs in many aspects of ischemic heart disease, the leading cause of morbidity and mortality in the Western World. MiR-29 is involved in fibrotic reaction after myocardial infarction while miR-21 may exert a fundamental role in post-angioplasty restenosis. MiR-208 is involved in the shift toward a fetal gene expression pattern in contractile proteins in heart failure. MiR-1 influences susceptibility to cardiac arrhythmias after myocardial infarction. This review will focus on microRNAs involvement in multiple aspects of ischemic heart disease and on their promising novel therapeutic applications including some recent patents.

Omega-3 fatty acids are essential substances for the development and function of human organism. They cannot be synthesized in humans, and consequently have to be acquired from food, almost exclusively from fish. Omega-3 fatty acids exert potent anti-inflammatory and anti-atherosclerotic actions by interfering with the metabolism of arachidonic acid, modifying lipid composition (mainly lowering triglycerides), improving hemodynamics and reducing cardiac hypertrophy. Recently, clinical and experimental studies demonstrated an anti-arrhythmic effect and a significant impact on survival after myocardial infarction (MI). It follows that omega-3 fatty acids have been widely accepted for clinical use in patients with dyslipidemia or with atherosclerotic disease and in survivors of acute MI. This review briefly explores the metabolic mechanisms and the clinical effects of this class of substances and considers their use in patients with cardiovascular disease.

Background.Discomfort related to low-energy internal cardioversion (LEIC) represents a real problem in patients (pts) with atrial fibrillation (AF). The aim of our study was to verify if a single shock could restore sinus rhythm (SR) with a lower discomfort for the pt. Methods. Thirty pts with chronic AF were randomized to receive a single 350 V shock (15 pts) or multiple shocks of increasing energy (15 pts). Three leads were positioned, respectively, in the coronary sinus and in the lateral right wall for shock delivery, and in the right ventricular apex for R wave synchronization. Truncated, biphasic shocks were used. In the first group a single 350 V shock was directly delivered and a second 400 V shock was given only if SR has not been restored. In the second group, beginning at 50 volts the voltage was increased in steps of 50 volts until SR restoration. No patient was sedated. After each shock the pts were asked to rate their discomfort on a scale of 1 to 5 (1 = not perceived, 5 = severe discomfort) Results. SR was restored in all the subjects. In group 1 SR was obtained in 12/15 (80%) pts with the first 350 V (8.1±0.8 joules) shock, while the remaining 3 patients required the second 400 V (10.2±10.3 joules) shock. In group 2 the mean atrial defibrillation threshold was 346.7±29.7 volts (8.0±1.5 joules). Then discomfort score was 2.5±0.6 in group 1 and 3.3±0.6 in group 2 (p < 0.01). Conclusions. A single shock of 350 V restores SR in the majority of pts with chronic AF; by use this new approach, LEIC is tolerated better than the multiple shocks step-up protocol.

Little is known about the efficacy and medium-term outcomes of primary percutaneous coronary intervention (PCI) in very old patients. We evaluated in-hospital and 6-month outcomes in a retrospective cohort of nonagenarian patients presenting at our hospital with ST-segment elevation myocardial infarction (STEMI) and treated by primary PCI from January 2003 to May 2012. During this period, primary PCI was performed in 1598 consecutive patients; twenty-seven patients (age, 92.5 ± 2.5 years) were enrolled in the study. Four patients (15%) were in advanced Killip class at presentation. STEMI location was anterior in 44%. Patients received aspirin, 300 mg clopidogrel loading dose, and heparin. Abciximab was given to 41% of patients. Coronary angiography showed multivessel disease in 52% of patients. Pain-to-balloon and door-to-balloon times were 375.0 ± 410.2 minutes and 107.3 ± 47.6 minutes, respectively. Intra-aortic balloon pump was implanted in 1 patient. An average of 1.3 ± 0.7 stents (95% bare-metal stents) were implanted per patient. Procedural success rate, defined as Thrombolysis in Myocardial Infarction (TIMI) flow grade ≥ 2 and residual stenosis20%, was 89%. Hospital mortality was 18.5%. TIMI major bleeding and acute renal failure, defined as an absolute increase of 0.5 mg/dL serum creatinine, occurred in 7% and 22% of patients, respectively. Overall 6-month survival rate was 67%. Our data suggest that primary PCI can be performed in nonagenarian patients with high success rate and with an acceptable bleeding risk, even when aggressive antithrombotic drugs, such as glycoprotein IIb/IIIa inhibitors, are given.

A series of in vivo trials were carried out in order to verify whether the electromagnetic field radiated by GSM (Groupe Systemes Mobiles) mobile cellular phones might affect implanted pacemakers. Two European GSM phones of 2-watt power were tested and trials conducted on 101 pacemaker implanted outpatients attending day hospital for routine check-up, who volunteered for trials. Forty-three pacemaker models from 11 manufacturers were tested in all. When the sensing threshold of the pacemakers was set at a minimum and the antenna of the phone was in direct contact with the patient's chest, interference was detected for 26 implanted pacemakers. Specifically, pulse inhibition in 10 of 101 cases, ventricular triggering in 9 of 46 DDD-VDD pacemakers, and asynchronous pacing in 4 of 52 devices. Pulse inhibition was also observed combined with asynchronous pacing in 1 of 52 cases and with ventricular triggering in 2 of 46 cases. Minimum effect duration was ca. 3 seconds but in 6 cases effects continued as long as the interfering GSM signal was on. No permanent malfunctioning or changes in the programmed parameters were detected. Whenever interference was detected, trials were repeated to determine the maximum sensing threshold at which interference persisted (with the antenna in contact with the skin over the pacemaker). Then maximum distance between antenna and pacemaker at which interference occurred was determined at pacemaker maximum and minimum sensing threshold. Under our experimental conditions electromagnetic interference effects were detected at a maximum distance of 10 cm with the pacemaker programmed at its minimum sensing threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of oral propafenone therapy on pacing threshold were studied in 36 patients chronically paced for sick sinus syndrome or AV block. The pacemakers, all unipolar models and with noninvasive threshold measurement facilities, were: 9 VVI, 15 AAI, and 12 DDD. Each patient received an initial propafenone dose of 450 mg/day, that in 18 cases was increased to 900 mg/day. Threshold was tested at baseline and at each dosage after 7 days of therapy. With the lower propafenone dosage the threshold, measured at 2.5 V, rose from 0.14 +/- 0.10 to 0.21 +/- 0.16 msec (+55%) in the atrium (P less than 0.0001) and from 0.10 +/- 0.08 to 0.15 +/- 0.09 msec (+63%) in the ventricle (P less than 0.0001). In the 18 patients who received both dosages, the mean atrial and ventricular threshold increased from 0.12 +/- 0.10 to 0.17 +/- 0.14 msec with the lower dose and to 0.27 +/- 0.22 msec (+125%) with the higher dose (P less than 0.0001 for both increments). With the 900 mg/day dose, a threshold increment greater than or equal to 300% was observed in 15% of the stimulated chambers. A good linear correlation (r = 0.76) was found between the ventricular threshold increment and the drug induced QRS widening. In conclusion, treatment with oral propafenone increases atrial and ventricular stimulation threshold in pacemaker patients. Threshold increment is dose dependent and proportional to the drug induced QRS widening. In the majority of the cases the threshold increment is not clinically significant, but caution must be used in prescribing high doses of the drug to patients with high baseline threshold.

We describe the case of a 78-year-old patient, admitted to our hospital with an acute coronary syndrome. Coronary angiography showed multivessel coronary artery disease and an anomalous coronary vessel branching from the right coronary artery. After successful percutaneous revascularization and discharge, the anomalous vessel was diagnosed by contrast enhanced 64-multidetector computed tomography as a coronary-to-bronchial fistula. Since the patient was asymptomatic, conservative treatment was selected.

ALTAMURA, G., ET AL.: Transcutaneous Cardiac Pacing for Termination of Tachyarrhythmias. Transcutaneous cardiac pacing (TCP) was used for interruption of tachyarrhythmias in 31 patients: 20 with ventricular tachycardia (VT); eight with atrioventricular reentrant tachycardia (AVRT) and three had atrioventricular nodal tachycardia (AVNT). The stimulators used (Pace Aid 50/52) allow pacing at programmable rates (50–160 ppm) and output (10–200 mA at 20-msec pulse duration), when possible overdrive pacing was used. Short bursts of stimuli were delivered with increasing current intensity until interruption of the arrhythmia or to the maximum energy tolerated by the patient. VTs were interrupted in eight of the 20 patients: four of the six (67%) treated by overdrive pacing and four of the 14 (29%) were treated by underdrive pacing. Supraventricular tachycardias (SVT) were terminated in eight of the 11 patients: seven out of eight (88%) AVT, and one out of three AVNT (33%). We observed two cases of arrhythmia worsening: a VT acceleration and induction of ventricular fibrillation in a patient with AVNT. TCP was well tolerated by the majority of the patients. We conclude that TCP is an effective method for interruption of ventricular and supraventricular reentrant tachycardias, but the risk of arrhythmia worsening must be considered.

The effects of transcutaneous cardiac pacing (TCP) on cardiac activation were evaluated by endocavitary recording (HRA, RVA) in eight patients, in order to test the possibility to obtain a simultaneous atrial and ventricular stimulation. The transcutaneous pacemaker used was the Pace Aid 52 (pacing rate 50-160 ppm, current output 10-150 mA, pulse width 20 sec). The two skin electrodes (surface area 50 cm2) were placed on the chest in anteroposterior position. Ventricular capture was observed in all patients (threshold = 74 +/- 14 mA), simultaneous atrial capture was obtained in only four cases (threshold = 138 +/- 25 mA). In conclusion, our data show that four-chamber simultaneous stimulation by TCP is possible, but only with pacing energies much higher than those usually required to capture the ventricle. The ability of TCP to simultaneously pace the atria and ventricles, though not relevant in the emergency cardiac stimulation for symptomatic severe bradyarrhythmias, could be useful in the treatment of reentrant supraventricular tachycardias.

Out-of-hospital cardiac arrest occurs at home in 65-80% of cases and is often witnessed. We designed a study to explore the feasibility of a home defibrillation program (a) evaluating the retention of cardiopulmonary resuscitation and automated external defibrillators (AED) use skills (BLSD) (b) assessing the impact on anxiety, depression, and quality of life and (c) recording the critical issues emerging from program implementation.Thirty-three post-myocardial infarction patients and their 56 relatives received BLSD training and an AED. Assessment of BLSD skills, levels of anxiety, and depression and quality of life were scheduled every 3 months for 1 year or until a common stopping date.Overall BLSD score was 26 +/- 3 at baseline vs. 22 +/- 5 at 3 months (P.0001), 21 +/- 6 at 6 months (P.0001), 22 +/- 4 at 9 months (P.0001) and 23 +/- 5 at 12 months (P = .001). Conversely, the BLSD component AED use" remained stable throughout the study. Quality of life, anxiety, and depression scores remained constant. Compliance to BLSD retraining sessions and AEDs checks decreased over time and was influenced by a concomitant clinical appointment.BLSD performance of families of post-myocardial infarction patients decreases over time, even though the ability to operate AEDs appears to be the least affected component. Compliance with retraining sessions and AED checks declines over time and is improved if they are combined with clinical appointments. The implementation of a home defibrillation program does not affect anxiety, depression, or the quality of life.

The effects of omega-3 fatty acids on membrane stabilization are well known. Reduction of ventricular arrhythmias and sudden death has been reported; fewer data exist regarding the effects on atrial arrhythmias. The object of this report is to evaluate the reduction of atrial arrhythmia-fibrillation after treatment with omega-3, in patients with dual-chamber pacemakers.We have examined 40 patients with paroxysmal atrial tachyarrhythmia recorded at the periodic pacemaker controls. At the study entry, all patients were treated with omega-3 (1 g/die); no changes in the device programmation and in the previous pharmacological therapy were allowed. The devices were interrogated after 4 months of treatment to evaluate the number of episodes and the burden of atrial tachyarrhythmia. At this time, the treatment was discontinued and the patients were reevaluated 4 months later.Two patients discontinued the treatment complaining of adverse gastroentheric effects. The episodes of atrial tachyarrhythmia in the pre-treatment period resulted 444 +/- 1161, and the burden 3.89% of time; in the treatment period resulted respectively 181 +/- 436 (-59%, p = 0.037) and 1.06% (-67%, p = 0.029). After drug withdrawal, the episodes of atrial tachyarrhythmia raised to 552 +/- 1717 (p = 0.065) and the burden to 2.69% (p = 0.003).Our data suggest a powerful effect of omega-3 fatty acids in the reduction of atrial tachyarrhythmia-fibrillation in these patients, without significant adverse effects.

New technologic development of implantable cardioverter-defibrillators (ICDs) keeps up with the exponential increase of their use for primary and secondary prevention of sudden cardiac death. The first-generation ICD with limited shock capability alone could be considered adequate in most cardiac arrest victims, but it was not suitable for sudden death prevention in all high-risk patients with cardiac disease. The second-generation ICD was comprised of hybrid pacemaker-defibrillator systems that provided on-demand ventricular antibradycardia pacing. The third-generation devices include additional functions, such as antitachycardia pacing for ventricular tachycardia (VT) reversion and low-energy ventricular cardioversion, in addition to ventricular defibrillation and single-chamber ventricular demand pacing. In the near future, advanced dual-chamber atrioventricular (AV) pacing and defibrillating systems will also be available. The dual chamber ICD will allow atrial inhibited/dual-chamber (AAI/DDD) rate-responsive pacing, simultaneous atrial and ventricular sensing to optimize the arrhythmia identification, and ICD shock delivery in the proper arrhythmia-related chamber. Clinical benefits of these devices compared with their cost and complexity will require careful evaluation.

The aims of the study were to verify the efficacy and safety of low energy internal cardioversion (LEIC) in patients with persistent atrial fibrillation (AF) and to identify the factors affecting the atrial defibrillation threshold (ADT). Forty-nine patients with persistent (lasting > or = 10 days) AF underwent LEIC. In each patient, two 6 Fr custom-made catheters with large active surface areas were positioned in the coronary sinus (cathode) and the lateral right wall (anode), respectively, for shock delivery, and a tetrapolar lead was placed in the right ventricular apex for R wave synchronization. Truncated, biphasic (3 ms + 3 ms), exponential shocks were used, beginning at 50 V and increasing in steps of 50 V until sinus rhythm had been restored. Mild sedation (diazepam 5 mg i.v.) was administered to 12 patients. Sinus rhythm was restored in all the subjects with mean voltage and energy levels of 352.0 +/- 80.3 V and 8.2 +/- 3.4 J, respectively. The ADT in patients pretreated with amiodarone (6.4 +/- 1.8 J) was lower than that of patients who had not received any antiarrhythmic drugs (9.2 +/- 3.7) (P = 0.04). No ventricular arrhythmias were induced by any of the atrial shocks, and no other complications were observed. During a mean follow-up of 162.9 +/- 58.7 days, AF recurred in 21 (43%) patients; 71% of these occurred in the first week after cardioversion. LEIC is effective in restoring sinus rhythm in patients with persistent AF. The technique seems to be safe and does not require general anesthesia or, in most cases, sedation. Patients pretreated with amiodarone have lower ADTs.

Background —In animal models, induced atrial fibrillation shortens the atrial effective refractory period (ERP) and reverses its physiological adaptation to rate. It is not clear whether this process, known as “electrical remodeling,” occurs in humans. Methods and Results —We determined the ERPs, at 5 pacing cycle lengths (300 to 700 ms) and in 5 right atrial sites, after internal cardioversion of chronic atrial fibrillation in 25 patients (14 in pharmacological washout and 11 on amiodarone). The ERPs were 195.5±18.8 ms in the washout and 206.3±17.9 ms in the amiodarone patients ( P r =0.95 in the washout and r =0.94 in the amiodarone group), and slope values indicating a normal (≥0.07) or nearly normal (0.05 to 0.06) adaptation of ERP to rate were found in 77% of the 84 paced sites. The mean ERP was shorter in the lateral wall (198.1±17.9 ms) than in the atrial roof (203.3±21.5 ms) and in the septum (210.5±20.0 ms) ( P P Conclusions —After cardioversion of chronic atrial fibrillation, (1) atrial ERP adaptation to rate was normal or nearly normal in the majority of the cases, (2) a significant dispersion of refractoriness between different right atrial sites was present, and (3) ERPs were significantly increased after 4 weeks of sinus rhythm in both washout and amiodarone patients.

Background Atrial fibrillation (AF) is considered to be maintained by multiple reentrant circuits without or with a very short excitable gap. However, the possibility of local atrial capture has been shown recently in experimental AF or induced AF in humans. Methods and Results This study was undertaken to evaluate the feasibility of atrial capture—suggestive of an excitable gap—in spontaneous chronic AF. Decremental pacing was performed in 47 right atrial sites in 14 patients with chronic AF, not taking antiarrhythmic drugs. A Franz catheter (for pacing and monophasic action potential recording) and a recording quadripolar catheter positioned about 10 mm apart were used. Local capture was achieved in 41 (87.2%) sites for a total of 100 captures. In 71 episodes the capture was lost within 15 seconds, while in the remaining 29, pacing was stopped after 15 seconds of stable capture. The AF types immediately before capture were type 1 in 83 and type 2 in 17 episodes. Type 3 AF was never captured. Pacing cycle at capture was 175.7±20.9 ms. The baseline atrial interval (FF) was 185.4±24.5, significantly longer than the FF recorded during pacing immediately before capture (176.0±19.8 ms) ( P Conclusions During spontaneous chronic AF in humans, (1) local capture by atrial pacing is possible up to at least 15 mm from the pacing site, (2) regional entrainment is possible during type 1 and type 2 AF but not type 3 AF, and (3) pacing before capture accelerates AF, probably by transient or local capture. These findings suggest that an excitable gap is present in chronic AF, therefore supporting the hypothesis that leading circle reentry is not the unique electrophysiological mechanism maintaining the arrhythmia.

Objectives. We sought to analyze in patients with chronic atrial fibrillation (AF) the change in the intracardiac atrial defibrillation threshold (ADT) at rest and during exercise, to quantify the effective risk of low energy endocavitary cardioversion during the effort and to compare the ADT of chronic and reinduced AF.Background. Low energy endocavitary cardioversion is a new alternative to transthoracic shock in patients with chronic AF. Nevertheless, patient discomfort and possible induction of ventricular arrhythmias should be further evaluated.Methods. Sixteen patients with chronic AF were included in the study. Two 6F custom-made catheters (Electro-Catheter, Inc.) were used for shock delivery and one tetrapolar lead for ventricular synchronization. Without sedation and in a random order, patients underwent two sequences of shocks to determine the ADT at rest and during exercise. Exercise was performed isometrically by the superior limbs. Atrial fibrillation was reinduced by atrial pacing. After each shock, the patients were requested to grade their discomfort with a score from 1 to 5. The power of the study was >90% in detecting a 25% difference in the ADT between groups.Results. Patients were classified into two groups: Nine patients (group A) underwent the first cardioversion during exercise; seven patients (group B) underwent the first cardioversion at rest. In total, the mean (±SD) ADT was 6.70 ± 1.54 J during exercise and 7.02 ± 1.82 J at rest (p = 0.59). A significantly lower ADT was observed in the second shock sequence than the first one (6.32 ± 2.09 J vs. 7.40 ± 0.87 J, p < 0.05). The discomfort score was 3.25 ± 0.86 at rest and 2.94 ± 0.77 during exercise (p = 0.09). No complications occurred.Conclusions. Low energy endocavitary cardioversion is a safe and effective procedure in patients with chronic AF. Discomfort is not generally severe enough to result in procedure termination. The ADT is not influenced by exercise and is higher in chronic than in reinduced AF.(J Am Coll Cardiol 1997;29:576–81)

ALTAMURA, G., ET AL.: Emergency Cardiac Pacing for Severe Bradycardia. Our study included the treatment of transcutaneous cardiac pacing (TCP) in 32 patients: (A) 19 patients were treated in the emergency area for complete symptomatic AV block before endocavitary pacing; (B) five patients were in asystole following DC shock or out-of-hospital cardiac arrest; and (C) eight patients were affected by bifascicular block undergoing emergency surgery and were treated in order to prevent complete AV block. Two transcutaneous stimulators were used. PaceAid-CRC model 50/52 with 20-msec pulse width; the electrodes were positioned on the V, ECG position and on the back. Results: in all but two patients, it was possible to obtain stable cardiac capture; in one patient arrived in hospital in asystole after prolonged cardiac arrest and in the other one was affected by complete AV block, TCP was ineffective. In groups A and B, TCP was maintained for a mean time of 15 minutes; in group C, TCP was tested in all patients, but performed in only one patient during surgery. Mean threshold was 81 mA. Stimulation was well tolerated in all but five patients. TCP is a reliable, noninvasive method that offers the possibility to initiate pacing within seconds and can be used by medical staff. In our opinion, it should be considered as the first choice emergency treatment of severe symptomatic bradycardia. In asystole, beneficial effects can be obtained only if TCP is performed early enough after the onset of arrhythmia.

The efficacy of noninvasive transcutaneous cardiac pacing (TCP) in the treatment of tachyarrhythmic events was tested in 24 patient: 14 with ventricular tachycardia, seven with supraventricular tachycardia and three with atrial flutter. Six (42.9%) ventricular tachycardias were interrupted: in two of the ten patients on whom underdrive pacing was attempted and in all four cases in which overdrive stimulation was possible. Five of the six supraventricular tachycardias utilizing an atrioventricular bypass tract were interrupted, while the TCP was unsuccessful on the only patient with atrioventricular nodal reentrant tachycardia. TCP failed to interrupt the arrhythmia in the three cases of atrial flutter. No clinically significant untoward effects (in particular tachycardia acceleration or ventricular fibrillation) were observed, except for a tolerable thumping sensation on the chest during pacing. In four patients, TCP effects on cardiac activation was evaluated by endocavitary recording: while the mean ventricular threshold was 70 mA, atrial capture was possible on only two patients at a current intensity of 140 and 150 mA. We consider our preliminary experience with TCP in the treatment of tachycardias encouraging. The technique was easily and rapidly usable and it was immediately successful in the majority of atrioventricular reentrant tachycardias and in a relevant percentage of ventricular tachycardias. In this latter setting TCP was mostly effective in the slower tachycardias where overdrive pacing was possible. A further experience with devices provided by higher pacing rates is warranted.