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Objectives The purpose of this study was to evaluate the feasibility and safety of a novel technology that uses energy transfer from an ultrasound transmitter to achieve cardiac stimulation without the use of a pacing lead in humans. Background To overcome the limitations of pacemaker leads, a new technology enabling stimulation without the use of a lead is desirable. Methods A steerable bipolar electrophysiology catheter incorporating a receiver electrode into the tip and circuitry to convert ultrasound energy to electrical energy was inserted transvenously into the heart. An ultrasound transmitting transducer was placed on the chest wall with ultrasound gel. Ultrasound energy was amplitude-adjusted and transmitted at 313 to 385 kHz. The output waveform of the receiver electrode was monitored while the transmitter was moved on the chest wall to target the receiver. The ultrasound transmission amplitude was limited to a mechanical index of 1.9, the maximum allowed for ultrasound imaging systems. Ultrasound-mediated pacing with minimum voltage but consistent capture was obtained for 12 s. Results Twenty-four patients (48 ± 12 years) were tested during or after completion of clinical electrophysiology procedures. A total of 80 pacing sites were tested (mean 3.3 sites/patient): 12 right atrial, 35 right ventricular, and 33 left ventricular (31 endocardial) sites. The transmit-to-receive distance was 11.3 ± 3.2 cm (range 5.3 to 22.5 cm). Ultrasound-mediated pacing was achieved at all 80 test sites, with consistent capture at 77 sites. The mechanical index during pacing was 0.5 ± 0.3 (range 0.1 to 1.5). The mean ultrasound-mediated capture threshold was 1.01 ± 0.64 V. There was no adverse event related to ultrasound pacing. No patient experienced discomfort during pacing. Conclusions The feasibility and safety of pacing usng ultrasound energy has been shown acutely.

Objectives We sought to evaluate the efficacy and safety of pulmonary vein (PV) isolation using transvenous cryoablation for the treatment of atrial fibrillation (AF). Background Although electrical isolation of PVs with radiofrequency energy for the treatment of AF is feasible, it is associated with a significant risk of PV stenosis. Cryoablation is a new alternative therapy allowing ablation of tissue while preserving its underlying architecture. Methods In 52 patients with paroxysmal (n = 45) or persistent (n = 7) AF, PV isolation using the CryoCor cryoablation system (CyroCor Inc., San Diego, California) with a 10F deflectable transvenous catheter was performed as guided by ostial PV potentials. Cryoablation was applied twice at each targeted site (2.5 to 5 min/application). Computed tomography (CT) of the thorax was performed at baseline and at 3 and 12 months to evaluate for PV stenosis. Results All targeted PVs were completely isolated in 49 (94%) of 52 of patients. Of 152 PVs targeted, 147 (97%) were successfully isolated (mean 3.0 PVs isolated per patient). After a mean period of 12.4 ± 5.5 months of follow-up, 37 (71%) of 52 patients had no recurrence of AF or were clinically improved, including 29 patients (56%) who had no recurrence of AF with (n = 11) or without the use of anti-arrhythmic drugs. At 3 and 12 months, the CT scan showed no evidence of PV stenosis associated with cryoablation in any patients. Conclusions Transvenous catheter cryoablation is an effective method to create PV electrical isolation for the treatment of AF. A clinically satisfactory result can be achieved in 71% of patients with AF, without the risk of PV stenosis.

Objectives We sought to evaluate the long-term effects of alternative right ventricular pacing sites on myocardial function and perfusion. Background Previous studies have demonstrated that asynchronous ventricular activation due to right ventricular apical (RVA) pacing alters regional myocardial perfusion and functions. Methods We randomized 24 patients with complete atrioventricular block to undergo permanent ventricular stimulation either at the RVA (n = 12) or right ventricular outflow (RVOT) (n = 12). All patients underwent dipyridamole thallium myocardial scintigraphy and radionuclide ventriculography at 6 and 18 months after pacemaker implantation. Results After pacing, the mean QRS duration was significantly longer during RVA pacing than during RVOT pacing (151 ± 6 vs. 134 ± 4 ms, p = 0.03). At six months, the incidence of myocardial perfusion defects (50% vs. 25%) and regional wall motion abnormalities (42% vs. 25%) and the left ventricular ejection fraction (LVEF) (55 ± 3% vs. 55 ± 1%) were similar during RVA pacing and RVOT pacing (p > 0.05). However, at 18 months, the incidence of myocardial perfusion defects (83% vs. 33%) and regional wall motion abnormalities (75% vs. 33%) were higher and LVEF (47 ± 3 vs. 56 ± 1%) was lower during RVA pacing than during RVOT pacing (all p 0.05). Conclusions This study demonstrates that preserved synchronous ventricular activation with RVOT pacing prevents the long-term deleterious effects of RVA pacing on myocardial perfusion and function in patients implanted with a permanent pacemaker.

Secondhand smoke (SHS) may act as a smoking cue and prime dose of nicotine by activating acetylcholine receptors in brains to trigger smoking [(1)][1]. SHS exposure at home and having a smoking spouse or peers predicted a lower likelihood of smoking cessation in cancer patients [(2)][2]. Similar

Almost a half-century after the initial description of the use of a transvenous endocardial lead for pacing in humans ([1][1]), the right ventricular (RV) apex has been selected as the traditional site for lead positioning. This is because of the easy accessibility of the RV apical site and because

Objectives. The objectives of this study were 1) to evaluate the effect of different right atrial electrode locations on the efficacy of low energy transvenous defibrillation with an implantable lead system; and 2) to qualitate and quantify the discomfort from atrial defibrillation shocks delivered by a clinically relevant method.Background. Biatrial shocks result in the lowest thresholds for transvenous atrial defibrillation, but the optimal right atrial and coronary sinus electrode locations for defibrillation efficacy in humans have not been defined.Methods. Twenty-eight patients (17 men, 11 women) with chronic atrial fibrillation (AF) (lasting ≥1 month) were studied. Transvenous atrial defibrillation was performed by delivering R wave-synchronized biphasic shocks with incremental shock levels (from 180 to 400 V in steps of 40 V). Different electrode location combinations were used and tested randomly: the anterolateral, inferomedial right atrium or high right atrial appendage to the distal coronary sinus. Defibrillation thresholds were defined in duplicate by using the step-up protocol. Pain perception of shock delivery was assessed by using a purpose-designed questionnaire; sedation was given when the shock level was unacceptable (tolerability threshold).Results. Sinus rhythm was restored in 26 of 28 patients by using at least one of the right atrial electrode locations tested. The conversion rate with the anterolateral right atrial location (21 [81%] of 26) was higher than that with the inferomedial right atrial location (8 [50%] of 16, p < 0.05) but similar to that with the high right atrial appendage location (16 [89%] of 18, p > 0.05). The mean defibrillation thresholds for the high right atrial appendage, anterolateral right atrium and inferomedial right atrium were all significantly different with respect to energy (3.9 ± 1.8 J vs. 4.6 ± 1.8 J vs. 6.0 ± 1.7 J, respectively, p < 0.05) and voltage (317 ± 77 V vs. 348 ± 70 V vs. 396 ± 66 V, respectively, p < 0.05). Patients tolerated a mean of 3.4 ± 2 shocks with a tolerability threshold of 255 ± 60 V, 2.5 ± 1.3 J.Conclusions. Low energy transvenous defibrillation with an implantable defibrillation lead system is an effective treatment for AF. Most patients can tolerate two to three shocks, and, when the starting shock level (180 V) is close to the defibrillation threshold, they can tolerate on average a shock level of 260 V without sedation. Electrodes should be positioned in the distal coronary sinus and in the high right atrial appendage to achieve the lowest defibrillation threshold, although other locations may be suitable for certain patients.

The purpose of this study was to evaluate the feasibility and safety of a novel technology that uses energy transfer from an ultrasound transmitter to achieve cardiac stimulation without the use of a pacing lead in humans.To overcome the limitations of pacemaker leads, a new technology enabling stimulation without the use of a lead is desirable.A steerable bipolar electrophysiology catheter incorporating a receiver electrode into the tip and circuitry to convert ultrasound energy to electrical energy was inserted transvenously into the heart. An ultrasound transmitting transducer was placed on the chest wall with ultrasound gel. Ultrasound energy was amplitude-adjusted and transmitted at 313 to 385 kHz. The output waveform of the receiver electrode was monitored while the transmitter was moved on the chest wall to target the receiver. The ultrasound transmission amplitude was limited to a mechanical index of 1.9, the maximum allowed for ultrasound imaging systems. Ultrasound-mediated pacing with minimum voltage but consistent capture was obtained for 12 s.Twenty-four patients (48 +/- 12 years) were tested during or after completion of clinical electrophysiology procedures. A total of 80 pacing sites were tested (mean 3.3 sites/patient): 12 right atrial, 35 right ventricular, and 33 left ventricular (31 endocardial) sites. The transmit-to-receive distance was 11.3 +/- 3.2 cm (range 5.3 to 22.5 cm). Ultrasound-mediated pacing was achieved at all 80 test sites, with consistent capture at 77 sites. The mechanical index during pacing was 0.5 +/- 0.3 (range 0.1 to 1.5). The mean ultrasound-mediated capture threshold was 1.01 +/- 0.64 V. There was no adverse event related to ultrasound pacing. No patient experienced discomfort during pacing.The feasibility and safety of pacing usng ultrasound energy has been shown acutely.

ObjectivesThe purpose of this research was to investigate the effect of using rate-adaptive pacing and atrioventricular interval (AVI) adaptation on exercise performance during cardiac resynchronization therapy (CRT).BackgroundThe potential incremental benefits of using rate-adaptive pacing and AVI adaptation with CRT during exercise have not been studied.MethodsWe studied 20 patients with heart failure, chronotropic incompetence (70% AP-HR, patients with 70% AP-HR. The percentage HR changes during exercise positively correlated with exercise time (r = 0.67, p < 0.001), METs (r = 0.56, p < 0.001), and Vo2max (r = 0.55, p < 0.001).ConclusionsIn heart failure patients with severe chronotropic incompetence as defined by failure to achieve >70% AP-HR, appropriate use of rate-adaptive pacing with CRT provides incremental benefit on exercise capacity during exercise.

OBJECTIVES We sought to investigate the effect of aspirin resistance on the incidence of myonecrosis after non-urgent percutaneous coronary intervention (PCI) among patients pretreated with clopidogrel. BACKGROUND Oral antiplatelet therapy using aspirin and a thienopyridine is the standard of care for preventing thrombotic complications of PCI. The effect of aspirin resistance on the outcomes of patients undergoing PCI is unknown. METHODS We used the Ultegra Rapid Platelet Function Assay-ASA (Accumetrics Inc., San Diego, California) to determine aspirin responsiveness of 151 patients scheduled for non-urgent PCI. All patients received a 300-mg loading dose of clopidogrel >12 h before and a 75-mg maintenance dose in the morning of the PCI. The incidence of myonecrosis was measured by creatine kinase-myocardial band (CK-MB) and by troponin I (TnI) elevations after PCI. RESULTS A total of 29 (19.2%) patients were noted to be aspirin-resistant. There was a significantly higher incidence of female subjects in the aspirin-resistant versus aspirin-sensitive groups. The incidence of any CK-MB elevation was 51.7% in aspirin-resistant patients and 24.6% in aspirin-sensitive patients (p = 0.006). Elevation of TnI was observed in 65.5% of aspirin-resistant patients and 38.5% of aspirin-sensitive patients (p = 0.012). Multivariate analysis revealed aspirin resistance (odds ratio [OR] 2.9; 95% confidence interval [CI] 1.2 to 6.9; p = 0.015) and bifurcation lesion (OR 2.8; 95% CI 1.3 to 6.0; p = 0.007) to be independent predictors of CK-MB elevation after PCI. CONCLUSIONS Despite adequate pretreatment with clopidogrel, patients with aspirin resistance as measured by a point-of-care assay have an increased risk of myonecrosis following non-urgent PCI.

OBJECTIVES We sought to determine the electrophysiologic actions of sotalol in the remodeled atrium of humans. BACKGROUND In experimental studies, sotalol has limited class III action in the electrically remodeled atrium and did not prevent atrial fibrillation (AF) induction. METHODS We determined the effective refractory periods (ERPs) at three pacing cycle lengths (400, 500, and 600 ms) in the high right atrium (HRA) and distal coronary sinus (DCS) before and after intravenous infusion of dl-sotalol in 10 patients with persistent AF who underwent internal cardioversion. The same protocols were performed in 10 control subjects in sinus rhythm. RESULTS In the HRA and DCS, the atrial ERPs at different drive cycle lengths were significantly shorter in patients with AF than in control subjects (p < 0.05). In patients with AF, the atrial ERP's adaptation to rate was nearly normal in the HRA, but was poor in the DCS. In both groups, dl-sotalol significantly increased the atrial ERPs at both the HRA and DCS, as compared with baseline (p < 0.05). However, the prolongation of atrial ERPs was significantly less at a drive cycle length of 600 ms in patients with AF versus control subjects (p < 0.05). After infusion of dl-sotalol, the atrial ERP's adaptation to rate at both the HRA and DCS was poor in patients with AF, and AF was still easily inducible in the majority of them, but not in control subjects. CONCLUSIONS The results of the present study demonstrate that the electrophysiologic actions of dl-sotalol are significantly attenuated in the chronically remodeled human atrium, and these changes might represent a probable explanation for the low efficacy of dl-sotalol to prevent early AF recurrence after electrical cardioversion.

We sought to evaluate the long-term effects of alternative right ventricular pacing sites on myocardial function and perfusion.Previous studies have demonstrated that asynchronous ventricular activation due to right ventricular apical (RVA) pacing alters regional myocardial perfusion and functions.We randomized 24 patients with complete atrioventricular block to undergo permanent ventricular stimulation either at the RVA (n = 12) or right ventricular outflow (RVOT) (n = 12). All patients underwent dipyridamole thallium myocardial scintigraphy and radionuclide ventriculography at 6 and 18 months after pacemaker implantation.After pacing, the mean QRS duration was significantly longer during RVA pacing than during RVOT pacing (151 +/- 6 vs. 134 +/- 4 ms, p = 0.03). At six months, the incidence of myocardial perfusion defects (50% vs. 25%) and regional wall motion abnormalities (42% vs. 25%) and the left ventricular ejection fraction (LVEF) (55 +/- 3% vs. 55 +/- 1%) were similar during RVA pacing and RVOT pacing (p0.05). However, at 18 months, the incidence of myocardial perfusion defects (83% vs. 33%) and regional wall motion abnormalities (75% vs. 33%) were higher and LVEF (47 +/- 3 vs. 56 +/- 1%) was lower during RVA pacing than during RVOT pacing (all p0.05). Patients with RVA pacing had a significant increase in the incidence of myocardial perfusion defects (p0.05) and a decrease in LVEF (p0.01) between 6 and 18 months, but patients with RVOT pacing did not (p0.05).This study demonstrates that preserved synchronous ventricular activation with RVOT pacing prevents the long-term deleterious effects of RVA pacing on myocardial perfusion and function in patients implanted with a permanent pacemaker.

OBJECTIVESWe examined the feasibility and efficacy of using a single-pass, dual-electrode (Solo) lead for atrial fibrillation (AF) detection and defibrillation.BACKGROUNDThe efficacy and safety of an implantable atrial defibrillator (IAD) has been extensively studied; however, separate right atrial (RA) and coronary sinus (CS) defibrillation leads are used for the present system.METHODSWe studied the use of the Solo lead for AF detection and defibrillation in 17 patients who underwent cardioversion of chronic AF. The Solo lead with a proximal 6-cm RA electrode and a distal 6-cm spiral-shaped CS electrode were positioned into the CS with the RA electrode against the anterolateral RA wall. The RA-CS electrogram signal amplitudes were measured and the efficacy of the Solo lead for AF detection and defibrillation was assessed by using an external version of the IAD.RESULTSThe leads were inserted in all patients without complication (mean fluoroscopy time: 13.3 ± 6.8 min). The mean RA-CS signal amplitude was 484 ± 229 μV during sinus rhythm and 274 ± 88 μV during AF (p < 0.05). All patients had satisfactory atrial signal amplitude to allow accurate detection of sinus rhythm. Successful cardioversion was achieved in 16/17 (94%) patients with an atrial defibrillation threshold of 320 ± 70 V (5.5 ± 2.7 J). Insufficient interelectrode spacing resulted in suboptimal electrode locations, associated with a lower atrial signal amplitude, a higher atrial defibrillation threshold and diaphragmatic stimulation.CONCLUSIONSThese results suggest a simplified lead configuration with optimal interelectrode spacing can be used with an IAD for AF detection and defibrillation.

We sought to evaluate the prognostic implication of the CHADS2 score for prediction of new-onset atrial fibrillation (AF) in patients with palpitations but without structural heart disease. 428 patients without AF or structural heart disease undergoing 24-hour ECG monitoring for palpitations were

Objectives. This study was designed to evaluate the relation between the severity of the residual stenosis of the infarct-related artery and changes in left ventricular volume and function after a first anterior myocardial infarction. Background. Although thrombolytic therapy improves clinical outcome after acute myocardial infarction, the relations between the severity of the residual stenosis of the infarct-related artery and postinfarction left ventricular remodeling and function are unclear. Methods. Fifty-eight patients with a first anterior myocardial infarction and significant disease only in the left anterior descending coronary artery on arteriography performed after 7 to 10 days were evaluated. All patients received thrombolytic therapy. Residual stenosis of the infarct-related artery was measured with quantitative coronary arteriography. Left ventricular volumes and ejection fraction were measured by echocardiography and radionuclide angiography, respectively, 7 to 10 days, 6 months and 1 year after infarction. End-diastolic and end-systolic left ventricular volumes were measured by two-dimensional echocardiography and normalized to body surface area. Patients were classified into three groups according to baseline residual stenosis severity: total occlusion (Group I), minimal lesion diameter

Objectives. This study sought to examine the effect of mitral regurgitation (MR) on platelet activation in patients with mitral valve prolapse (MVP) or rheumatic MR.Background. MVP and rheumatic MR are associated with an increased incidence of thromboembolic events. Although the underlying causes are not clear, increased platelet activation has been suggested as one of the pathogenic mechanisms. Results of previous studies that have investigated the relation between MVP and platelet activation are controversial. Whether the presence of MR in patients with mitral valve disease is associated with platelet activation remains unclear.Methods. We studied platelet activation by measuring the plasma level of platelet factor 4 (PF4) and beta-thromboglobulin (BTG) in 16 patients with MVP, 12 patients with rheumatic MR and 25 control subjects. A detailed echocardiographic examination, including M-mode measurement and color Doppler flow mapping to detect the presence and severity of MR was performed.Results. Patients and control subjects were matched for gender, age and left ventricular ejection fraction. Eight (50%) of 16 patients with MVP had MR. Patients with MVP and MR and patients with rheumatic MR had a significantly larger left atrial diameter. Mean log plasma levels of PF4 and BTG were significantly higher in patients with MVP and MR and patients with rheumatic MR than in control subjects (1.17 ± 0.22 and 0.93 ± 0.23 IU/ml vs. 0.52 ± 0.34 IU/ml, p < 0.01; 1.70 ± 0.21 and 1.53 ± 0.15 IU/ml vs. 1.37 ± 0.15 IU/ml, p < 0.05, respectively) but were comparable in patients with MVP and no MR and control subjects. Plasma levels of PF4 and BTG were positively correlated with the severity of MR, as assessed by a semiquantitative method (r = 0.59, p = 0.0001; r = 0.60, p = 0.0001, respectively). Increasing age and left atrial enlargement were not related to platelet activation.Conclusions. MR in mitral valve disease was associated with systemic platelet activation. MVP itself was not associated with increased platelet activation. The degree of platelet activation was positively correlated with the severity of MR and was independent of the underlying etiology of mitral valve disease, age and left atrial size. The possibility of a higher incidence of thromboembolism and the role of antiplatelet agents in such patients will require further studies to determine.

Objectives. This prospective, multicenter trial was aimed at defining efficacy and safety of low energy shocks during atrial fibrillation in a diverse cohort of patients.Background. Experimental studies in sheep and preliminary data in humans have suggested that low energy internal shocks delivered between right atrial and coronary sinus electrode catheters may terminate atrial fibrillation.Methods. Biphasic 3/3-ms R wave synchronous shocks were delivered between two electrode catheters in the right atrium and coronary sinus. The defibrillation protocol started with a test shock of 20 V, and shocks increased in 40-V steps until restoration of sinus rhythm or a maximum of 400 V. Shock delivery was withheld after short RR intervals. In 141 patients with atrial fibrillation, the protocol was carried out under sedation in case the shock was associated with discomfort. The atrial arrhythmia was paroxysmal (≤7 days) in 50 patients, chronic (>30 days) in 53, intermediate (>7 days, ≤30 days) in 18 and induced in 20. Underlying heart disease was present in 88 patients (62%).Results. Paroxysmal atrial fibrillation was successfully terminated in 46 (92%) of 50 patients, chronic atrial fibrillation in 37 (70%) of 53, intermediate in 16 (89%) of 18 and induced in 16 (80%) of 20. Mean conversion threshold was 1.8 J (213 V) in the induced group, 2.0 J (229 V) in the paroxysmal group, 2.8 J (272 V) in the intermediate group and 3.6 J (311 V) in the chronic group. The conversion voltage was significantly (p < 0.001) higher in the chronic group than in the other groups of atrial fibrillation and increased significantly with the duration of atrial fibrillation and with left atrial size (p < 0.05). Of 1,779 R wave synchronized shocks delivered with a mean (±SD) preceding RR interval of 676 ± 149 ms, no ventricular arrhythmia was induced. The latter may occur after unsynchronized shocks.Conclusions. Low energy transvenous shocks in patients with atrial fibrillation are effective and safe, provided that shocks are properly synchronized to R waves with preceding RR intervals that meet appropriate cycle length criteria. This study provides data that may be useful in the development of an implanted atrial defibrillator.(J Am Coll Cardiol 1997;29:750–5)

To the Editor: Alternate- and multiple-site atrial pacing (AP) have been proposed as methods to prevent atrial fibrillation (AF) ([1,2][1]). However, changes in atrial activation by alternate- or multiple-site(s) AP might adversely affect atrial mechanical function and cardiac performance via