Biomedical subjects
Publications and source records attributed to E Occhetta.
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The aim of our study was to consider cellular telephone interference using different cellular telephones and implantable cardioverter defibrillator (ICD) models. Thirty (26 men, 4 women) patients with ICDs were considered during follow-up. The ICD models were: Telectronics (7), CPI (7), Medtronic (7), Ventritex (5), and Ela Medical (4). All patients were monitored with surface ECG; permanent telemetric endo-ECG monitoring was activated. Then, the effect of two different European telephone systems were tested: TACS system (Sony CM-R111, 2W power) and GSM system (Motorola MG1-4A11, 2 W power). For both systems, the effect during call, reception, active conversation (dialogue), and passive conversation (listening) were observed. Cellular telephones were located first in contact with the programming head, then near the leads system, and lastly, in the hands of the patient. At the end of the evaluations, memories were interrogated again to check for false arrhythmia detections. In five of these patients during arrhythmia induction at device implant (first implant or ICD replacement), we also evaluated possible interference between cellular telephones in the reception phase and the ventricular fibrillation detection phase of the ICD. All evaluated models showed significant noise in the telemetric transmission when the cellular telephone (both TACS and GSM) was located near the ICD and the programming head; noise was particularly significant during call and reception, in most cases leading to loss of telemetry. No false arrhythmia detections have been observed during tests with cellular telephones located on the ICDs. During tests performed with cellular telephones located near the leads or in the hands of patients, no telemetric noises orfalse arrhythmia detections were observed. During induced ventricularfibrillation and cellular telephones in reception mode near the device, the arrhythmia recognition was always correct and not delayed. In conclusion, present ICD models seem to be well protected from electromagnetic interference caused by European cellular telephones (TACS and GSM), without under-/oversensing of ventricular arrhythmias. However, cellular telephones disturb telemetry when located near the programming head. ICD patients should not be advised against the use of cellular telephones, but it has to be avoided during ICD interrogation and programming.
We describe the prolonged follow-up of a 64-year-old female patient, with an ectopic intracardiac thyroid gland. The mass was first detected 14 years ago, during a routine echocardiographic examination. The patient suffered from episodes of palpitation and cardiac auscultation revealed a systolic murmur. At cardiac surgery a right ventricular mass penetrating most of the interventricular septum was found. The mass was also prolapsing into the pulmonary infundibulum and could not be removed. On histopathology examination, the presence of a normal tissue was demonstrated. Two main clinical events characterized the prolonged follow-up: the gradual development of a massive tricuspid insufficiency, probably due to the strict anatomic relationship between the septal tricuspid papillary muscle and the mass itself; frequent supraventricular arrhythmias, partially refractory to different pharmacologic regimens, which could be ascribed to the chronic overload of the right atrium. The mass size has been stable over the years, and no thyroid hormone derangement was ever found.
Two-dimensional echocardiography is the technique of choice for identifying cardiac masses. Unfortunately, adjacent structures compressing the atrial wall may lead to misdiagnosis. Clinicians should promptly recognize this phenomenon and the related diagnostic features. The case of a 90-year-old woman presenting with a history of recent onset effort dyspnea is described. On transthoracic two-dimensional echocardiography a left atrial mass which closely mimicked an atrial myxoma was evident. A tomographic scan revealed a large sliding hiatus hernia, which was confirmed on traditional radiographic examination. The echocardiographic characteristics of the mass are described in detail, as well as a review of the literature for the purpose of a correct differential diagnosis.
Aortic valve disease is known to be the most frequent valvular disease in the elderly and aortic valve replacement is often the best therapeutic strategy. Hemodynamic performance of prostheses is critical in this subset of patients to ensure an optimal quality of life. Moreover, old patients with small aortic ostia are getting more and more common in clinical practice, making often necessary to implant small prostheses. If a significant pressure drop is not achieved, hypertrophy persists and left ventricular function may not improve. Such conditions have not yet been extensively studied in the elderly. The aim of this study was firstly to assess echocardiographically the performance of aortic prosthetic heart valves in old patients (> or = 70 years) and compare the results obtained in patients with prostheses of different type and size, and secondly to evaluate the postoperative changes in left ventricular hypertrophy and function in a subset of patients with isolated or prevalent aortic stenosis. One hundred fifty-one patients were initially considered; global mortality was 9.3% at 20 +/- 12 months from intervention. In the 75 patients with a postoperative echocardiogram, transprosthetic gradient was 27 +/- 12 (max) and 15.1 +/- 6.6 (mean) mmHg. Mean functional prosthetic area (FPA) was 1.5 +/- 0.5 cm2. No statistically significant differences could be demonstrated between mechanical and biological prostheses. Three groups were identified, according to prosthetic size (Group 1: diameter < 23 mm, Group 2: diameter 23 mm, Group 3: diameter > 23 mm). Among groups, max and mean gradients as well as FPA were found to be significantly different. Respectively max gradient was 33.2 +/- 13, 26 +/- 11, 20.2 +/- 7.2 mmHg (p < 0.05), mean gradient was 17.2 +/- 6.1, 15.4 +/- 7.6, 11.7 +/- 4.3 mmHg (p < 0.01) and FPA was 1.2 +/- 0.3, 1.5 +/- 0.3, 1.8 +/- 0.7 cm2 (p < 0.05 between Group 1 and Group 3). In a subgroup of 31 patients with isolated or prevalent aortic stenosis, a significant interventricular septal thickness reduction was found postoperatively (14.3 +/- 2.3 vs 12.6 +/- 8.0 mm, p < 0.001). Posterior wall thickness decreased similarly, but to a lesser extent; left ventricular diameters and myocardial mass also significantly decreased (left ventricular mass: 186 +/- 45 vs 146 +/- 38 g/m2, p < 0.001). When prosthetic size was considered, septal thickness reduction was more evident in Group 1 and Group 2 (p < 0.05 and p < 0.01). On the contrary, a significant improvement in left ventricular diameters was observed only in Group 3 (p < 0.05). Left ventricular mass decreased significantly in Group 2 and Group 3 (p < 0.01 and p < 0.05). Such improvements could be demonstrated only in those patients (79%) who showed at least a 50% reduction in the transvalvular gradient. In this subset, left ventricular function also significantly improved (fractional shortening: 29 +/- 0.7 vs 33 +/- 0.7%, p < 0.02). In conclusion, aortic valve replacement in the elderly is a safe and effective therapeutic strategy. In patients with small aortic prostheses, the transvalvular gradient was found to be slightly but significantly higher as compared to that of larger prostheses. However, left ventricular function was good and similar in all subgroups. No significant differences were found between mechanical and biological prostheses. In old patients with isolated or prevalent aortic stenosis a significant reduction in left ventricular hypertrophy and mass is observed within 2 years from intervention. An increase in myocardial contractility can also be expected, if at least a 50% reduction in transvalvular gradient is obtained.
Effectiveness of dual-chamber pacing in patients with dilated cardiomyopathy is still controversial. Our study was performed: to select the most favorable individual atrioventricular (AV) delay; to compare hemodynamic short-term effects in each patient after 2 periods of DDD pacing and sinus rhythm (AV spontaneous); to assess hemodynamic long-term (1 year) effects after DDD pacing at optimum AV delay. In 1996, 9 patients (7 men, 2 women; mean age 69 +/- 5 years) with dilated cardiomyopathy (5 idiopathic, 4 ischemic), NYHA functional class III-IV, ejection fraction < 30%, end-diastolic volume > 60 ml/m2, mitral regurgitation +2/+3, PR interval > or = 200 ms, were enrolled. All patients were implanted with DDD pacemakers and monitored for: ejection fraction and end-diastolic volume (measured by echocardiography and radionuclide angiography); clinical conditions; exercise tolerance and maximum oxygen consumption (by Weber exercise protocol); neurohormonal activity (plasma renin, aldosterone, atrial natriuretic factor). Data were recorded: before DDD implantation; after 2 randomized, single-blind periods of 3 months in VVI mode (at ventricular "sentinel" rate of 50 b/min) and in DDD mode with the optimum AV delay, corresponding for each patient to the minimum end-diastolic volume measured by radionuclide angiography and to the highest cardiac output recorded by echocardiography; after 6 months of DDD pacing with most favorable AV delay. Three more patients died 6 months after (between sixth and twelfth month of follow-up), due to refractory heart failure; 1 patient dropped out because his pacemaker was programmed in VVI mode at low rate, due to intolerance of DDD pacing. Among the other 4 patients no clinical and laboratory parameters were significantly different after 1 year of follow-up. In conclusion, DDD pacing in selected patients with dilated cardiomyopathy showed disappointing results, despite a strict and laboratory monitoring; DDD pacing could be of major benefit in larger populations, according to Doppler mitral flow pattern: those patients with a larger A-wave amplitude could be more sensitive to DDD pacing than those with evidence of poor atrial systole. Moreover, biatral and/or biventricular pacing could also play a significant role.
Effective discrimination of retrogradely conducted P waves would allow distinguishing sinus tachycardia from supraventricular tachycardias due to AV or nodal reentry, and would prevent pacemaker-mediated tachycardia in AV sequential pacing. This might be especially relevant in VDD implants, where retroconduction could be induced by escape ventricular stimulation. In order to analyze the respective waveform properties, anterograde and retrograde atrial signals were recorded by a wide floating electrode dipole, on the implantation of a permanent single-pass lead for VDD pacing. Generally, bipolar recording did not allow reliable discrimination, while the signal nature could be readily diagnosed from the main features of the unipolar atrial electrograms. The unipolar waveform recorded under sinus rhythm in high right atrium, close to the superior vena cava opening (proximal EGM), started with a negative deflection in 88% of the patients. In 7% of the patients, the first deflection of the signal was positive in some cardiac cycles only, and, on the average, the amplitude of the positive phase was not higher than 5% of the signal peak-to-peak amplitude. Conversely, under retroconduction, the starting deflection attained higher positive values in 98% of the patients, being stably over 15% of the peak-to-peak amplitude in 86% of the Furthermore, in 69% of the cases, the lag time between the onset of the negative deflection of proximal and distal (mid-low atrium) unipolar EGM changed unambiguously when retroconduction occurred, exceeding the range of variation observed in each patient during sinus activity. The combined evaluation of unipolar EGM shape and lag time allowed specific retroconduction recognition in 95% of the patients. We suggest that this approach may yield useful information for the discrimination of retrograde atrial signals, provided that the recording dipole is sufficiently long and the proximal electrode is properly positioned in the high right atrium.
In sick sinus syndrome with chronotropic incompetence, dual-demand rate responsive pacing (DDDR) may be better than ventricular-inhibited rate responsive pacing (VVIR) and dual-demand pacing without rate responsive function (DDD). In order to compare exercise performance during different activity-driven pacing modes, 15 patients (9 males, 6 females; mean age 59 +/- 13 years), implanted with Synchrony 2020T pacemaker (Siemens-Pacesetter Inc, USA, activity sensor) for sick sinus syndrome, randomly performed 3 treadmill tests (modified Bruce protocol) during DDD, VVIR and DDDR pacing, with pacing heart rate, oxygen consumption (Q-Plex 5000, Quinton), work time, anaerobic threshold and human atrial natriuretic peptide level monitoring. Four patients were excluded from the data results (3 for normalization of chronotropic incompetence, 1 for angina pectoris during rate responsive pacing). Heart rate at the end of exercise was significantly higher during VVIR pacing mode (131 +/- 21 b/min) and DDDR (136 +/- 14 b/min) than during DDD pacing mode (105 +/- 21 b/min), p < 0.05. During DDDR we obtained a significantly higher work tolerance (652 +/- 161 s) and a higher oxygen uptake (22.7 +/- 7.1 ml/kg/min) than during DDD (565 +/- 106 s; 20.1 +/- 6.5 ml/kg/min) and VVIR (599 +/- 155 s; 18.8 +/- 6.5 ml/kg/min), p < 0.05. Also the work time and the oxygen uptake at anaerobic threshold were better during DDDR stimulation (350 +/- 119 s; 14.2 +/- 4.9 ml/kg/min) than during DDD (280 +/- 101 s; 12.2 +/- 4.6 ml/kg/min) and VVIR pacing mode (306 +/- 122 s; 11.6 +/- 4.60 ml/kg/min), p < 0.05. On the contrary, human atrial natriuretic factor values at the maximum exercise were lower during DDD (139 +/- 100 pg/ml) than VVIR (256 +/- 182 pg/ml) and DDDR (209 +/- 195 pg/ml) pacing mode, p < 0.05. In conclusion, DDDR pacing proved to be better than VVIR and DDD in patients with sick sinus disease and chronotropic incompetence.
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Late potentials (LPs) detected on the signal-averaged (SA) electrocardiogram (ECG) predict arrhythmic events after acute myocardial infarction (AMI). The effect of thrombolysis on the incidence of LPs after AMI is controversial and its impact on subsequent arrhythmic events is not known. Moreover, the effects of beta blockers on the SAECG have not been studied. Six hundred eighteen patients with AMI were studied; thrombolysis was given to 228 (37%). In comparison with patients treated conventionally, those receiving thrombolysis were significantly younger and more frequently male, had higher peak values of creatine kinase, a lower prevalence of non-Q-wave AMI, and a higher incidence of ventricular fibrillation in the acute phase, and more frequently received beta blockers. An SAECG obtained 6 to 8 days after AMI showed LPs in 24% of patients receiving and in 25% not receiving thrombolysis (p = NS). On admission, intravenous beta blockers were administered to 110 patients (18%); those receiving beta blockers were younger, had lower peak values of creatine kinase and more frequently received thrombolysis. LPs were less frequently found in patients treated than in those not treated with beta blockers (15 vs 27%; p = 0.007); however, this effect was found only in those with an ejection fraction > or = 40%. Independent predictors of LPs by multivariate analysis were an ejection fraction < 40% (p = 0.007), ventricular fibrillation in the acute phase (p = 0.02), and absence of beta-blocking therapy (p = 0.03). During a mean follow-up of 12 +/- 7 months, there were 39 cardiac deaths (6%), 13 of which were sudden (2%), and 9 sustained ventricular tachycardias.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: In order to assess possible functional and hemodynamic benefits of different programming of atrioventricular (AV) delay--156 ms fixed vs 156 to 63 adaptive--two maximal exercise tests (cyclette) were performed in 8 patients (6 males, 2 females; 69 +/- 6 years) implanted with Chorus 6003 (Ela Medical, France) DDD pacemakers for complete AV block with normal sinus node function. METHODS: The measured parameters were: pacing rate, cardiac output (thermodilution method), oxygen consumption (2001 gas-exchange analyser), arterial-venous difference (derived from pulmonary oxygen saturation, through an optical-fibers Swan-Ganz catheter coupled to an Oximetric3-Abbott oximeter), human atrial natriuretic factor and lactate plasmatic levels, anaerobic threshold. RESULTS: A better cardiac output (11.4 +/- 1.7 vs 10.1 +/- 1.8 l/min) and oxygen consumption (1521 +/- 425 vs 1408 +/- 465 ml/min) were observed at maximal exercise with adaptive rather than with fixed AV delay programming (p < 0.05); moreover anaerobic threshold point was reached later during exercise test with adaptive AV delay (242 +/- 92 vs 216 +/- 109 sec, p = 0.05). On the contrary, with adaptive and fixed AV delay, there were not statistically different values of maximal heart rate (139 +/- 9 vs 139 +/- 9), levels at maximal exercise of arterial-venous difference (12.5 +/- 2 vs 12.8 +/- 1.4 Vol%O2), human atrial natriuretic factor (63 +/- 17 vs 78 +/- 48 pg/ml), lactate (29 +/- 15 vs 29 +/- 18 mg/dl), and oxygen consumption at anaerobic threshold point (772 +/- 164 vs 786 +/- 229 ml/min). CONCLUSIONS: In DDD pacing adaptive AV delay causes aerobic and hemodynamic benefits.
Endless loop tachycardia (ELT) is a possible complication in dual chamber pacing; it is usually prevented by programming the atrial refractory period (PVARP) longer than the retrograde ventriculoatrial (VA) conduction interval; this in some patients limits the upper rate. In 15 patients with a DDD (nine patients) or a single-pass lead VDD pacemaker (six patients) and retrograde atrial activation, telemetric recording documented a significant difference in amplitude of antegrade, and retrograde atrial potentials (VDD 1.21 +/- 0.32 mV vs 0.56 +/- 0.23 mV, P = 0.008; DDD 2.7 +/- 1 vs 1.8 +/- 1 mV, P = 0.038; Student's t-test for paired data). In 3/15 patients ELT stopped after programming of atrial sensitivity to a value greater than the retrograde P wave amplitude; in 11/15 patients this occurred at a sensing value lower than or equal to retrograde P wave amplitude with a high pass band filter operating. One patient required PVARP lengthening. Holter monitoring showed no more ELTs. In most patients with a DDD or single-pass lead VDD pacemaker with widely programmable sensing amplitude and Hi/Low bandpass filters, individual programming of atrial channel sensitivity prevents ELT without affecting the PVARP and, consequently, upper rate limit.
Present paper reports on a patient referred for sustained, hemodynamically well tolerated, ventricular tachycardia, terminated by noninvasive temporary pacing. The tachycardia was refractory to chest tump and intravenous standard drugs (lidocaine and propafenone). Demonstration of spontaneous atrioventricular dissociation and ventricular capture during transesophageal atrial pacing allowed rapid and correct diagnosis. Overdrive with external noninvasive ventricular pacing proved effective in terminating ventricular tachycardia and converting it to sinus rhythm. These observations suggest that noninvasive approach to hemodynamically stable ventricular tachycardia can provide a safe and effective alternative to more aggressive medical management.
Dual chamber pacing (DDD) maintains atrioventricular (AV) sequence; AV delay programmability modifies the relationship between atrial and ventricular contraction. To evaluate the hemodynamic effects of such a modification, ten patients with a DDD unit for complete AV block were studied by time-motion (M-mode) and Doppler echocardiography during inhibited ventricular pacing (VVI), atrial-triggered ventricular pacing (VDD) and atrioventricular sequential pacing (DVI) at different AV delay (90, 140, 190, 240 msec). A significant improvement in stroke volume (SV) (15%-20%, P less than 0.05) was seen during DDD versus VVI pacing; no changes, however, were observed in the same patient with different AV delay or during DVI versus VDD pacing. These data suggest that programming of AV delay does not affect systolic performance at rest; longer diastolic filling times recorded during DDD pacing with "short" AV delay (90-140 msec) do not seem to be a hemodynamically relevant epi-phenomenon of PM programming.
Myocardial reperfusion after thrombolytic therapy in acute myocardial infarction can be directly demonstrated with coronary angiography or it can be assessed thanks to indirect markers of reperfusion, such as modifications in the "averaged" QRS complex. We assessed the presence of late potentials in 37 patients within 5 hours of acute myocardial infarction onset and evaluated their disappearance or modification after reperfusion. Signal-averaged electrocardiogram, obtained computerizing QRS complexes filtered through Simson's bidirectional filter (25-250 Hz), was serially recorded in each patient: at admission, as well as 12 hours, 3 and 10 days following urokinase and/or heparin therapy. Other indirect markers of reperfusion (incidence of ventricular arrhythmias, serum CK-MB level, ST elevation) were contemporaneously evaluated. All patients underwent coronary angiography between 6 and 83 days after acute myocardial infarction. Late potentials (Total QRS greater than 115 ms; Under 40 microV greater than 39 ms; RMS Last 40 ms less than 25 microV) were present only in 25% of patients, and they always disappeared after successful thrombolysis. On the contrary if ischemia-related vessel occlusion persisted, late potentials persisted as well or else were first recorded on the 3rd or 10th day following acute myocardial infarction. Quantitative analysis of the "averaged" QRS complex showed a statistically significant reduction in QRS duration (-9.1 +/- 12.7 ms) 3 days after acute myocardial infarction in reperfused patients (group A, n = 24), while no significant reduction in the total QRS (-1 +/- 6.7 ms) was observed in non-reperfused cases (group B, n = 13), (p less than 0.05 group A vs group B). So, 10 ms reduction in total QRS duration was a good marker of reperfusion, with specificity = 92% and sensitivity = 54%; marker sensitivity was even higher (= 79%) when coupled with serum CK-MB peak within 12 hours of therapy (diagnostic accuracy = 84%). In conclusion, even if late potentials have a low prevalence in acute myocardial infarction (25%) their disappearance correlates with myocardial reperfusion. Furthermore, a reduction in total QRS duration greater than or equal to 10 ms can itself be a good marker of successful thrombolysis.
Clinical and physiological data on long-term follow-up of 143 patients with respiratory-dependent pacemakers (RDP3) are reported; 121 patients received ventricular (VVI-RD) and 22 patients atrial (AAI-RD) respiratory-dependent stimulation. Functional evaluation was based on the exercise testing (130 pts) with oxygen uptake VO2, ventilation, ECG and arterial pressure monitoring and the dynamic Holter electrocardiogram (95 pts). In each patient, the stimulation rate curve selected was that which produced the best work tolerance and moved the anaerobic threshold to the right. Respiratory levels were assessed by telemetry verifying proper sensing of tidal volume variations and absence of interference and artefacts. In patients with VVIR or AAIR stimulation, exercise tolerance, oxygen uptake and anaerobic threshold increased significantly in comparison with VVI or AAI pacing respectively. The physiological sensitivity of the stimulation system (i.e., a linear relationship of the pacing rate with metabolic requirements) was excellent (up to exhaustion) in 70%, very good (up to anaerobic threshold) in 20% and erratic (no relationship between pacing rate and VE/VO2) in 10% of patients. In dynamic electrocardiographic monitoring, the automatic pacing rate was always predominant during the night and during rest periods; the pacing rate increased properly with daily activity; myopotential inhibition (none longer than 3,500 ms) was observed in 38 patients, but without subjective complaints. The incidence of the RDP3 malfunction was less than 8%; it may have stemmed from the pacing system itself, or from other clinical conditions. Oversensing of impedance system pulses has not been recorded in the last 3 years. Partial respiration undersensing results from incorrect accessory lead position, pulmonary emphysema, marked obesity or other causes. Respiratory sensing becomes erratic at the anaerobic threshold point in such patients, but functions well at submaximum exercise levels. In patients with left ventricular failure, exercise tolerance was improved by setting a lower ratio between the pacing rate and respiration, which prevented the occurrence of excessive pacing rates.
The effectiveness of respiratory-dependent atrial pacing (AAI-RD) was assessed in 23 patients (11 male, 12 female; 68 +/- 10 years) with symptomatic isolated sinus node disease (SND). Follow-up was performed at 3 month intervals and included history taking, physical examination, ECG recording and 24-hour Holter monitoring. An incremental treadmill exercise test was performed in 21/23 patients before pacemaker implantation, in 23/23 patients after implantation (at least two tests with different programmed settings of respiratory rate/paced rate ratio); 21/23 patients underwent treadmill tests during both fixed rate 70 bpm and AAI-RD pacing. Physiological sensitivity of AAI-RD pacing was found excellent in 34 tests (85%) and fair in six (15%). Spontaneous heart rate was significantly higher after pacemaker implantation (bpm 115 +/- 20 vs 98 +/- 24, P less than 0.001). In 10/21 patients paced rate was significantly higher during AAI-RD vs AAI pacing (131 +/- 9 vs 106 +/- 16, P less than 0.001) with better total work time (min 9.9 +/- 4 AAI-RD vs 6.8 +/- 2.6 AAI, P less than or equal to 0.002), higher oxygen consumption at anaerobic threshold (ml/min 1137 +/- 406 AAI-RD vs 882 +/- 268 AAI-RD vs 5.5 +/- 2.6 AAI, P = 0.001). No significant difference was found in 7/21 patients (overlap between spontaneous and paced rate during both AAI-RD and AAI programming); 4/21 patients did not reach anaerobic threshold owing to osteomuscular limitations. AV block was detected in 1/23 patients, Biorate circuital failure in 1/23, sporadic undersensing in 5/23, short and symptom-free myopotential inhibitions in 10/23.(ABSTRACT TRUNCATED AT 250 WORDS)