Autonomic patterns preceding and following accelerated idioventricular rhythm in acute myocardial infarction.

INTRODUCTION: We have investigated the potential relationship between cardiac autonomic activity and accelerated idioventricular rhythm (AIVR) in response to reperfusion in the setting of an acute myocardial infarction (AMI) through spectral analysis of heart rate variability (HRV). METHODS AND RESULTS: We studied 16 patients with AMI who developed spontaneous sustained AIVR after initiation of intravenous thrombolysis. Sympathovagal interactions were evaluated by analysis of the low- (LF) and high-frequency (HF) spectral components of HRV for each 5-min interval over the 30-min periods preceding and following AIVR. The occurrence of AIVR was related to the ST-segment elevation resolution and the angiographic evidence of restored coronary flow to assess timely reperfusion and sustained coronary artery patency. The analysis of spectral components over time revealed combined responses of both autonomic limbs preceding and following AIVR, which were not followed by corresponding changes in heart rate. Ten minutes before AIVR, there was a characteristic continuous increase in LF, in the setting of a concomitant withdrawal of HF, suggestive of a progressive sympathetic predominance. After the end of AIVR, the opposite pattern was found with an increased HF and decreased LF, indicative of parasympathetic rebound overactivity. All patients showed signs of fast reperfusion and complete restoration of coronary flow. CONCLUSION: Our results indicate that reperfusion-induced AIVR is modulated by sympathetic stimulatory effects, whereas a counterregulatory vagal response seems to exert a profound effect upon its suppression. Clinically, the occurrence of early sustained AIVR appears to offer reliable information about both timely reperfusion and sustained and effective coronary artery patency.

In-vivo testing of digital cellular telephones in patients with implantable cardioverter-defibrillators.

AIMS: To investigate the susceptibility of implantable cardioverter defibrillators to electromagnetic interference generated by digital cellular telephones, functioning in both international transmission technologies: the Global System for Mobile Communication (GSM) and the Digital Cellular System (DCS 1800). METHODS AND RESULTS: In 36 patients with transvenous implantable cardioverter defibrillators from two manufacturers (Medtronic and Guidant/CPI), cellular telephones with different levels of minimal and maximal power output were tested in the transmitting and receiving mode. Evaluation was performed in activated implantable defibrillators during spontaneous cardiac activity and continuous VVI or DDD pacing to assess possible electromagnetic interference. In two patients, appropriateness of ventricular fibrillation detection and therapy was judged during telephone testing. There was no damage, reprogramming, inappropriate shock therapy or pacing inhibition during the tests. In seven pre-pectoral Medtronic implantable defibrillators, transient electromagnetic interference caused 19 erroneous sensing events, when the operating phone was held in close vicinity to the programmer head. These 'pseudo-oversensing' events, which did not result in logging of arrhythmia episodes in the device counter, were interpreted as an adverse interaction between the telephone and the programming device. CONCLUSION: Digital cellular telephones do not represent a risk to Medtronic and Guidant/CPI recipients of the specific implantable defibrillator models herein tested.

Intravenous magnesium sulfate versus diltiazem in paroxysmal atrial fibrillation.

BACKGROUND: Drugs currently available for the acute treatment of paroxysmal atrial fibrillation have significant limitations. We assessed the safety and effectiveness of intravenous magnesium sulfate versus diltiazem therapy in patients with prolonged episodes of paroxysmal atrial fibrillation. METHODS: In a prospective randomized trial, 46 symptomatic patients presenting with paroxysmal atrial fibrillation were given intravenous magnesium sulfate (n=23) or diltiazem (n=23) therapy. Primary outcome measures were effects on ventricular rate control and proportion of patients restored to sinus rhythm at 6 h after initiation of treatment. RESULTS: There were no differences in baseline characteristics between the two groups. Both forms of treatment were well tolerated, with no adverse clinical events. Both drugs had similar efficacy in reducing the ventricular rate at the first hour of treatment (P<0.05) with a tendency toward a further decrease during infusion times of 2 (P<0.01), 3, 4, 5 and 6 h, respectively (P<0.001). However, at the end of the 6-h treatment period, restoration of sinus rhythm was observed in a significantly higher proportion of patients in the magnesium group compared with the diltiazem group [13 of 23 patients, (57%), versus five of 23 patients, (22%), P=0.03]. CONCLUSIONS: Magnesium sulfate favorably affects rate control and seems to promote the conversion of long lasting episodes of paroxysmal atrial fibrillation to sinus rhythm, representing a safe, reliable and cost-effective alternative treatment strategy to diltiazem.

Diagnostic superiority of continuous-loop electrocardiographic recording over other testing in a patient with recurrent syncope and underlying coronary artery disease with severe left ventricular dysfunction.

Dysrhythmic causes of syncope may elude diagnosis in postinfarction patients despite elaborate testing, including electrophysiologic study. For a correct diagnosis, capture of cardiac rhythm during patient's typical symptoms is crucial. This report describes a patient with coronary artery disease and decreased left ventricular ejection fraction who experienced recurrent syncopal episodes without obvious precipitating factors. The 12-lead electrocardiogram showed left bundle-branch block indicating a possible conduction abnormality as the underlying cause of syncope. Twenty-four-h Holter monitoring exhibited no sinus rhythm or conduction disturbances but revealed a nonsustained run of ventricular tachycardia. Findings at electrophysiologic testing led to a presumptive diagnosis of tachyarrhythmic cause of syncope; however, the correct diagnosis was only made with use of a loop monitor which documented a 15-s sinus pause during a syncopal episode.

Usefulness of reperfusion ventricular arrhythmias in non-invasive prediction of early reperfusion and sustained coronary artery patency in acute myocardial infarction.

BACKGROUND: Established tenets of occurrence of reperfusion ventricular arrhythmias in acute myocardial infarction (AMI) do not provide insight into the timing of achieving reperfusion or whether coronary artery patency is sustained. We assessed the significance of ventricular arrhythmias in the non-invasive prediction of timely reperfusion and sustained restoration of coronary patency after thrombolysis in patients with AMI. METHODS: 24-hour Holter monitors were placed in 163 patients with an AMI before administration of thrombolytic therapy. Patients were classified into 3 groups of early (within 2 hours) or late reperfusion, or no-reperfusion, according with clinical and continuous ST-segment electrocardiographic criteria. Ventricular fibrillation, ventricular tachycardia (VT) and accelerated idioventricular rhythm (AIVR) were also categorized as having occurred early (within the first 2 hours) or late (after the first 2-hour period). Angiographic confirmation of coronary patency was determined 2 to 6 days after AMI. RESULTS: Early reperfusion was predicted by early sustained AIVR in 86% of patients and early non-sustained AIVR in 62.5% of patients, with sensitivity 38% and 77%, and specificity 96% and 69%, respectively; p<0.0001. Late non-sustained AIVR was commonly seen in early and late reperfused patients (92-97%) as well as in non-reperfused patients (74%). Sustained coronary patency was predicted by early sustained AIVR in 93% of patients, as well as by early non-sustained AIVR in 86% of patients and late non-sustained AIVR in 79% of patients, with sensitivity 22%, 55% and 94%, and specificity 95%, 71% and 18%, respectively; p<0.05. CONCLUSION: Only the occurrence of sustained AIVR, and probably early non-sustained AIVR convey useful information about both early reperfusion and sustained coronary artery patency. The absence of AIVR does not preclude successful thrombolysis.

VDD pacing from the middle cardiac vein via a persistent left superior vena cava.

We report a combination of unusual features demonstrating a permanent pacemaker implantation of a single-pass VDD lead by way of an anomalous persistent left superior vena cava in the middle cardiac vein. The ventricular stimulation resembled a right bundle branch block QRS morphology and was successfully synchronized by spontaneous atrial activity. This case illustrates an alternative approach of effective VDD pacing and sensing in patients with such a venous anomaly when other standard implantation sites fail.

Significance of R-on-T phenomenon in early ventricular tachyarrhythmia susceptibility after acute myocardial infarction in the thrombolytic era.

We investigated the clinical significance and mechanism of the R-on-T phenomenon in the current thrombolytic era as potential precipitant of R-on-T-induced early ventricular tachyarrhythmias in patients with a thrombolysed acute myocardial infarction. We also examined the role of QT dispersion on ventricular vulnerability and its association with R-on-T-initiated ventricular tachyarrhythmias. A total of 93 patients underwent 24-hour Holter monitoring starting at hospital admission before thrombolysis. Patients were classified into 2 groups: those with (n = 76) and those without (n = 17) reperfusion according to electrocardiographic criteria. All R-on-T ventricular premature complexes (VPCs) and R-on-T-initiated arrhythmic events (ventricular tachycardia [VT], ventricular fibrillation) were counted to estimate arrhythmia density and severity in 2 time periods during and after completion of thrombolysis. Measurements of QT and QTc intervals and dispersion parameters were obtained on the 12-lead electrocardiogram before thrombolysis and at 24 hours in patients with and without R-on-T VTs. Overall, R-on-T VPCs were rarely observed (1.8% of total VPCs over 24 hours), occurring more frequently during than after thrombolysis (at a rate of 8 vs 0.6 VPCs/hour, p = NS) and at a higher rate during thrombolysis in nonreperfused than in perfused patients (15 vs 8/hour, p = NS). Three VF episodes were observed in 1 reperfused patient, and all were R-on-T initiated. Episodes of nonsustained R-on-T VTs (3.3% of total VTs over 24 hours) appeared more frequent during than after thrombolysis (at a rate of 0.8 vs 0.05 VPCs/ hour, p = NS), and compared with non-R-on-T VTs they were significantly faster (374 +/- 56 ms vs 411 +/- 69 ms; p < 0.05), with a trend toward longer duration. Our findings indicate that R-on-T VPCs and R-on-T VTs are early rare features in acute myocardial infarction, and do not serve as triggers of severe ventricular tachyarrhythmia. The study of ventricular repolarization did not elicit an identifiable risk factor of R-on-T VT susceptibility.

Effects of early captopril therapy after myocardial infarction on the incidence of late potentials.

BACKGROUND: Late potentials (LP) on signal-averaged electrocardiography (SAECG), recorded 6 to 30 days after an acute myocardial infarction (AMI), identify patients at risk for late arrhythmic events. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce ventricular remodeling and cardiovascular mortality after AMI. HYPOTHESIS: The aim of this study was to investigate the effect of early (< 24 h) administration of captopril on the presence of LP on Days 6-30 after AMI. METHODS: The study included 117 patients with a first AMI; 63 patients (53 men and 10 women, aged 59 +/- 12 years), 35 with an anterior and 28 with an inferior AMI (44 thrombolyzed), received early captopril therapy. The control group consisted of 54 age-matched patients (39 men and 15 women, aged 60 +/- 12 years), 19 with an anterior and 35 with an inferior AMI (31 thrombolyzed, p = NS), who did not receive early therapy with an ACE inhibitor. The mean left ventricular ejection fraction was similar in both groups (48 vs. 46%). Time domain analysis of SAECG was performed using a band-pass filter of 40-250 Hz. Late potentials were considered present if any two of three criteria were met: (1) Filtered QRS duration (QRSD) > 114 ms, (2) root-mean-square voltage of the last 40 ms of the QRS complex (RMS) < 20 microV, and (3) duration of low amplitude (< 40 microV) signal of the terminal portion of the QRS (LAS) > 38 ms. RESULTS: In the two groups of patients there were no differences in mean values of SAECG parameters. No patient was receiving any antiarrhythmic drugs. In the captopril group LPs were present in 9 of 63 patients (14%) and in the control group in 17 of 54 patients (31%) (p = 0.046). There was no difference in the number of patients with a patent infarct-related artery in the two groups (76 vs. 59%). CONCLUSION: Captopril treatment early after an AMI reduces the incidence of LPs recorded on Days 6-30 and may thus favorably affect the arrhythmogenic substrate.

Unusual features of right and left idiopathic ventricular tachycardia abolished by radiofrequency catheter ablation.

Two unusual cases are presented with idiopathic right and left ventricular tachycardia (IVT) with intriguing clinical and electrophysiological characteristics. The first patient with a sustained IVT of right ventricular outflow tract origin, and an electrophysiological mechanism suggesting reentry, had been resuscitated from cardiac arrest. The second patient had an IVT with a left bundle branch block morphology, which originated from the basal-septal region of the left ventricle (left ventricular outflow tract tachycardia). Both patients were cured with radiofrequency catheter ablation, guided by endocardial activation sequence and pace mapping.

Successful radiofrequency catheter ablation of automatic atrial tachycardia with regression of the cardiomyopathy picture.

Ectopic atrial tachycardia (EAT) is often refractory to pharmacological suppression, and if uncontrolled, it can lead to cardiomyopathy. Although RF current catheter ablation therapy has been effective in eliminating the arrhythmia, there is limited information, particularly in adult patients with regard to the reversal of the tachycardia induced cardiomyopathy. Four adult patients, 20-56 years of age, and a 6-year-old boy, were referred with refractory EAT. Four patients had heart failure and three had depressed LV function by echocardiographic criteria. All patients underwent electrophysiological study, and RF ablation was successful in abolishing the arrhythmogenic foci. Of these, four were located in the right atrium and one in the left atrium, and were identified by recording of the earliest atrial activation. No complications occurred. Termination of the EAT resulted in symptomatic improvement. Serial echocardiographic assessment of LV function indicated a significant reversal of the cardiomyopathy picture with reduction in chamber size and recovery in systolic function; indices of diastolic dysfunction persisted in one patient. Chronic, uncontrolled EAT can cause tachycardia induced cardiomyopathy. The picture of the cardiomyopathy resolves after elimination of the focus. RF ablation is both effective and safe, and may be considered as early therapy, particularly in patients with incessant EAT and ventricular dysfunction.

Abnormal signal-averaged electrocardiograms in patients with incomplete right bundle-branch block.

BACKGROUND AND HYPOTHESIS: A hypothesis was formulated that regional delayed activation of the right ventricle, as seen in incomplete right bundle-branch (IRBBB) aberrancy, may simulate late potential activity and may be responsible for abnormal signal-averaged electrocardiograms (SAECGs). No previous studies have specifically addressed this issue in this particular group of patients (with IRBBB). Therefore, the aim of the present study was to investigate the incidence of abnormal SAECGs in patients with IRBBB. If this were confirmed, our purpose would further be to investigate ways of reducing the false positive results. METHODS: The study group included 53 patients (28 men and 25 women), aged 53 +/- 13 years, with no history of previous myocardial infarction or ventricular tachycardia and who had an electrocardiogram (ECG) showing IRBBB. An SAECG was also performed in a control group of 19 age-matched individuals with a normal ECG. Time domain analysis was performed using a band pass filter of 40-250 Hz. The following parameters were considered normal: filtered QRS duration (QRSD) < 114 ms, root mean square of the voltage of the last 40 ms of the QRS complex (RMS) > 20 microV, and the duration of the low amplitude signal (< 40 microV) at the terminal portion of the QRS (LAS) < 38 ms. An SAECG was considered abnormal if any two of these criteria were abnormal. RESULTS: The mean values of the SAECG parameters were: QRSD 101 +/- 11 ms, RMS 32 +/- 20 microV, LAS 32 +/- 12 ms, and noise 0.29 +/- 0.13 microV. Abnormal SAECGs with at least two criteria satisfied were present in 16 of 53 (30%) patients compared with 0 (0%) of 19 individuals in the control group (p = 0.02). Abnormal values included the combination of RMS and LAS in 12 patients and all three parameters in 4 patients. However, if the definition of late potentials were limited to the combination of abnormal QRSD and either RMS or LAS values, the incidence of false positive results (4 patients) (7.5%) would be significantly decreased (p = 0.007). At 21 months of follow-up, no arrhythmic events occurred. CONCLUSIONS: Delayed terminal conduction observed in IRBBB may cause a high incidence of false positive late potentials on SAECGs. Based on this study, we propose that this can be largely remedied if the optimal criteria for the presence of late potentials in patients with IRBBB always include the combination of QRSD and either RMS or LAS.