[Implantable cardioverter-defibrillator: prevention of sudden cardiac death and impact on survival in patients with malignant ventricular arrhythmias].
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Biomedical subjects
Publications and source records attributed to E Occhetta.
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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)
His bundle (HB) recording does not allow the recognition of third degree intrahisian block in patients with complete atrio-ventricular block (AVB) associated with idioventricular rhythm, due to the absence of pacemaker activation in the distal HB region. We have observed fixed retrograde distal HB activation in the standard HB recording of a patient with complete AVB and ventricular rhythm at a rate of 28/min. Retrograde distal HB activation (h'r) did not disappear during apical right ventricular pacing, in association with the complete absence of retrograde nodal conduction: concealed retroconduction into the proximal HB did not allow the recording of anterograde hisian deflection when the interval between h'r deflection and the subsequent sinus atriogram was shorter than 200 msec. Distal HB bipolar pacing using low energy stimulus resulted in 1:1 ventricular response and normal QRS duration in the absence of nodal retroconduction, thus proving the localization of bidirectional block within the HB. The unmasking of retrograde V-h' conduction during idioventricular rhythm was likely related to phase 4 retrograde delay in the branch ipsilateral to the site of the emergency ventricular focus and to the subsequent trans-septal activation of the other side of His-Purkinje system. Referring to arrhythmic problems after DDD pace-marker implantation the localization of complete AV blocks and retrograde conduction patterns are discussed.
Dual chamber DDD pacing is fully physiologic when chronotropic response of sinus node to exercise is normal and when retrograde ventriculo-atrial conduction is absent. Comparison of results from exercise test with increasing work load showed that atrial-triggered ventricular pacing provides a significant functional benefit (delta VO2 15%) P less than 0.01, if compared with fixed rate ventricular pacing. The benefit is closely related with the amount of sinus rate increase during exercise. In patients with sinus node syndrome the atrial triggered ventricular pacing rate did not show significant increase during exercise and exercise capability was similar to that observed with fixed ventricular pacing. Retrograde ventriculo-atrial conduction was observed in 56% of patients with sick sinus syndrome and 28% of patients with complete AV block and was the reason for endless loop tachycardias (ELTs). ELTs can be eliminated by lengthening atrial refractory period (ARP). In patients with ARP greater than or equal to 250 ms (47%), mild (8:7, 4:3) or important (2:1) AV block appeared during exercise test, with sudden drop of pacing rate and cardiac output at highest work load. Among other "physiologic" pacing modes, respiration traced ventricular stimulation showed high physiologic sensitivity (90%) and haemodynamic benefit comparable to that obtained during dual chamber pacing and without the related disadvantages.
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Dual chamber pacemakers, with coordinate atrial and ventricular sensing and stimulation (DDD), even if allowing "physiological" pacing, exhibited new and complicated arrhythmic manifestations, whose real frequency is still unascertained. In 65 patients (mean age 68 +/- 12 years), implanted with a DDD multiprogrammable device (15 pts. Medtronic Versatrax 7000 A, 50 pts. Pacesetter AFP 283), we carried out a 24 hours Holter monitoring while pacemaker was programmed with standard parameters. In a subset of 15 patients Holter monitoring was performed before and after pacemaker implantation. We evidenced: a) atrial sensing and/or pacing malfunction in 3 patients (4.5%); b) pacer-unrelated arrhythmias in 49 patients (75%): atrial extra beats 35 patients (54%), ventricular extra beats 23 patients (35%), non-sustained ventricular tachycardias 10 patients (15%), atrial tachyarrhythmias 8 patients (12%); c) supraventricular arrhythmias with PM-mediated high rate ventricular pacing in 12 patients (18%); d) PM induced and sustained endless loop tachycardias in 31 patients (47%); e) arrhythmias depending on over-sensing in 11 patients (17%): myopotential interferences 9 patients (14%), cross-talk ventricular pacing inhibition 2 patients (3%). The prevalence of ventricular arrhythmias was not different before and after the pacemaker implantation. The prevalence of atrial extrasystoles (53% versus 40%) and atrial tachyarrhythmias (26% versus 6%) decreased after the pacemaker implantation. Aimed reprogramming with progressive extension of atrial refractory period (from 250 to 400 msec and DDX) achieved disappearance of PM-endless loop tachycardias in 95%. Use of multi-programmability lowered the incidence and symptoms of most PM-related arrhythmias. Drug therapy was of choice in clinical arrhythmias unrelated to pacer.
The 1st myocardial infarction requires the identification of patients who are at high risk of malignant ventricular arrhythmias. Our study group included 55 consecutive patients (age less than 70): all had non-invasive "signal averaging" recording and 24 hour dynamic electrocardiogram at the post-acute phase of their 1st myocardial infarction (MI) and 3 months later. Wall motion abnormalities were evaluated in each patient but two. 24 randomized patients (without documented sustained ventricular tachycardia) underwent right programmed ventricular stimulation at the 3rd month after MI and pathological repetitive responses were evaluated (Table III); they were hemodynamically stable and without persistent ischemia. Late potentials have been compared to spontaneous and induced ventricular arrhythmias, wall motion abnormalities (Table II) and two-year follow-up (Table VI), in order to identify predictive markers of sudden death or malignant arrhythmias. Ventricular late potentials were identified in 28 patients (51%) 4-8 days after MI: mean duration was equal to 75 +/- 33 msec; they did not show any relationship to the site (Table I) and to the extension of necrosis (Table II). Ventricular late potentials had no significant association with myocardial dyskinesia (Table II) while their association with complex ventricular arrhythmias, detected on Holter monitoring within 8 days after MI, and with the induction of repetitive ventricular responses (greater than or equal to 2 complexes) showed significant correlations (respectively p = 0.02; p = 0.01). In regard of the recognition of spontaneous ventricular tachycardia (greater than or equal to 3 complexes) in the follow-up, the detection of late potentials showed 75% sensibility with predictive value equal to 32% (Table V); the combination of late potentials and ventricular dyskinesia exhibited the highest specificity (88%) and predictive value (54%). By the end of follow-up there had been 6 cardiac deaths (2 sudden, 4 from left ventricular failure): late potentials longer than 75 msec were recorded in all patients who had cardiac death; in the post acute phase of MI repetitive ventricular arrhythmias were detected in only 1 of the 2 case of sudden cardiac death and in none of the patients who developed sustained ventricular tachycardia in the follow-up (Table VI). Myocardial dyskinesia was present in each patient who developed non sudden cardiac death (Table VI).(ABSTRACT TRUNCATED AT 400 WORDS)
Clinical and prognostic significance of ventricular repolarization anomalies in sportsmen is still uncertain, even if they are most commonly regarded as benign. We studied a patient in whom those manifestations didn't show any progression within 30 years even after interruption of athletics and were related to idiopathic hypertrophic cardiomyopathy. Anatomical findings were combined with cardiac rhythm and conduction disturbances (paroxysmal atrial flutter, premature contractions, 2nd degree AV block). In our patient ventricular repolarization anomalies, even though without a negative prognosis, can't be related to "athlete's heart" but rather to organic cardiomyopathy.
A pacemaker that adapts heart rate in response to the patient's metabolic requirements has been developed. The pacemaker uses breathing frequency and tidal volume as the indicators of physiologic demand. Maximal physical work capacity, anaerobic threshold, oxygen uptake (16 patients) and hemodynamic variables (9 patients) were assessed with fixed rate (VVI), atrial synchronous (VDT/I) and respiration-dependent ventricular (VVI-RD) pacing. All subjects attained their anaerobic threshold in stress tests with VVI pacing. The maximal physical capacity (p less than 0.001), work time to attain the anaerobic threshold (p less than 0.01) and oxygen uptake (p less than 0.001) were significantly greater with VVI-RD than with VVI pacing. The transition from the supine to the standing position was characterized by a significant increase of cardiac index at rest with both VDT/I and VVI-RD pacing as compared with VVI pacing. Progressive increments in the cardiac index and average left ventricular stroke work index were significantly different at submaximal and maximal exercise when VVI and VVI-RD were compared. At maximal exercise, mean cardiac output was also significantly different: 10.21 +/- 2.5 (SD) liters/min with VVI, 11.2 +/- 0.8 liters/min with VDT/I (p less than 0.05) and 12.65 +/- 3.1 liters/min with VVI-RD (p less than 0.05) pacing. Maximal oxygen extraction values were greater with VVI and VVI-RD pacing than with VDT/I pacing. Pulmonary artery end-diastolic pressures at maximal exercise were within the normal range with the three different modes of pacing. In conclusion, there is a significant (25%) improvement in exercise performance with VVI-RD pacing as compared with VVI pacing.(ABSTRACT TRUNCATED AT 250 WORDS)
The rate responsive pacemaker using respiratory rate as a sensor was implanted in 22 patients, 19 patients for ventricular pacing and three for atrial pacing. The level of exercise achieved with this system was consistently higher than with a fixed ventricular pacing rate. In addition, no special chemical or mechanical sensors are required; the sensor itself is simple, long-lasting, and energy efficient. Thus, this system adapts easily to the individual patient.
Time and costs involved in electrophysiologic study for sino-atrial and/or atrio-ventricular blocks were evaluated in 42 patients. Analysis of charge for staff, specific electrophysiologic equipment and disposable items reveals an operating cost of 540.000 lire per study. An electrophysiologic study is the only method of diagnosing with certainty the level of A-V block and of assessing the prognosis of patients with infranodal conduction disease. It also allows a careful choice of permanent pacing mode. The potential risk, although small involved in this procedure, its cost and the need of a high operating standard suggest however that the number of electrophysiology laboratories should not indiscriminately increase.