Biomedical subjects
Michael Eldar
Publications and source records attributed to Michael Eldar.
Pericarditis following permanent pacemaker insertion.
BACKGROUND: The appearance of pericarditis following insertion of a permanent pacemaker is not widely acknowledged in the literature. OBJECTIVES: To describe our experience with pericarditis following 395 permanent pacemaker implantations over 2 years. METHODS: We retrospectively reviewed the medical records of 395 consecutive patients in whom new pacing systems or pacemaker leads had been implanted over a 2 year period. We searched the records for pericarditis that developed within 1 month after pacemaker implantation according to the ICD-9 code. The incidence, clinical picture, response to treatment, and relationship to lead design and location were studied. RESULTS: Eight cases (2%) of pericarditis following implantation were detected. Clinical manifestations in all patients were similar to those of post-pericardiotomy syndrome and included chest pain (n = 7), friction rub (n = 1), fever (n = 2), fatigue (n = 2), pleural effusion (n = 2), new atrial fibrillation (n = 2), elevated erythrocyte sedimentation rate (n = 4), and echcardiographic evidence of pericardial effusion (n = 8). All affected patients had undergone active fixation (screw-in) lead implantation in the atrial position. The incidence of pericarditis with screw-in atrial leads was 3% compared to 0% in other cases (P < 0.05). CONCLUSIONS: Pericarditis is not uncommon following pacemaker implantation with active fixation atrial leads. Special attention should be paid to identifying pericardial complications following pacemaker implantation, especially when anticoagulant therapy is resumed or initiated. The use of passive fixation leads is likely to reduce the incidence of pericarditis but this issue should be further investigated.
Association of elevated homocysteine levels with a higher risk of recurrent coronary events and mortality in patients with acute myocardial infarction.
BACKGROUND: Despite the prothrombotic and proinflammatory effects associated with elevated homocysteine levels, only limited data exist regarding the effect of homocysteine levels on outcome of patients with acute myocardial infarction. METHODS: Homocysteine levels were determined within 24 hours of presentation in 157 consecutive patients with acute myocardial infarction. Patients were allocated to 2 groups: those with homocysteine levels of 2.7 mg/L (20 micro mol/L) or more (n = 22 [14%]) and those with homocysteine levels of less than 2.7 mg/L (n = 135 [86%]). RESULTS: Female and diabetic patients had significantly lower homocysteine levels than males (P<.01) and nondiabetic patients (P =.005), respectively, with no significant correlation with age (r = 0.07, P =.42) or other risk factors. Patients with homocysteine levels greater than or equal to 2.7 mg/L and less than 2.7 mg/L did not differ significantly regarding extent of coronary artery disease as reflected by prevalence of multivessel disease (54% vs 61%; P =.87), and their in-hospital course. However, in a mean +/-SD follow-up of 30 +/- 10 months, patients with homocysteine levels greater than or equal to 2.7 mg/L had a higher incidence of recurrent coronary events (36% vs 17%; P =.04) and death (18% vs 5%; P<.05). Homocysteine levels greater than or equal to 2.7 mg/L remain a significant determinant of recurrent coronary event and/or death after controlling for potential cofounders by multivariate analysis (odds ratio, 3.8; 95% confidence interval, 1.3-11.0). CONCLUSIONS: In patients with acute myocardial infarction, elevated homocysteine levels are associated with a higher risk of recurrent coronary events and death, independent of other risk factors and the extent of coronary artery disease.
Prevalence, etiology, and outcome of patients with restrictive left ventricular filling and relatively preserved systolic function.
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RYR2 and CASQ2 mutations in patients suffering from catecholaminergic polymorphic ventricular tachycardia.
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Incidence of dual AV node physiology following termination of AV nodal reentrant tachycardia by adenosine-5'-triphosphate: a comparison with drug administration in sinus rhythm.
Administration of adenosine triphosphate (ATP) in sinus rhythm identifies dual atrioventricular node physiology (DAVNP) in 75% of patients with inducible slow/fast AV nodal reentrant tachycardia (AVNRT). The incidence of DAVNP following termination of AVNRT with ATP is unknown. Incremental doses of ATP (10-60 mg) were administered, first in sinus rhythm and then during tachycardia induced at electrophysiologic study, to 84 patients with inducible AVNRT and to 18 control patients with inducible AV reentrant tachycardia (AVRT) and no electrophysiologic evidence of DAVNP. Study end-points were the occurrence of DAVNP or > or = 2nd degree AV block following administration of ATP in sinus rhythm and tachycardia termination following administration of ATP during tachycardia. Of the 82 patients with AVNRT who completed the study, 62 (75.6%) exhibited DAVNP following administration of 17.1 +/- 9.4 mg ATP in sinus rhythm, while 30 (36.5%) exhibited DAVNP at the termination of AVNRT following administration of 10.6 +/- 2.4 mg ATP. The occurrence of DAVNP following the administration of 10 mg ATP in sinus rhythm.was a good predictor (62%) of its occurrence after termination of AVNRT with ATP. The dose of ATP had a strong correlation between the presence of DAVNP following AVNRT termination and the ATP doses needed for tachycardia termination. Of the 18 control patients, none had DAVNP at ATP test during sinus rhythm but 1 (5.5%) showed slight (60 msec) PR jump after termination of AVRT with ATP. In conclusion, DAVNP is present in a relatively high proportion (36.5%) of patients following termination of AVNRT with ATP but is much less frequent (5.5%) in control patients. Thus, findings at termination of tachycardia by ATP may be useful in the noninvasive diagnosis of the mechanism of a paroxysmal supraventricular tachycardia.
Characterization of arterial stenosis and elasticity by analysis of high-frequency pressure wave components.
We describe a novel method for assessing stenosis severity based on pressure wave measurements. Pressure waves for several degrees of stenosis at different distances proximal to the stenosis were recorded from in vitro and in vivo models. Signal analysis was performed using power spectral density, and radial compliance was also measured. Pressure wave components at the acoustic frequency band (400-2500Hz) changed gradually and were dependent upon the distance from the stenosis and its severity. The shift of the pressure components could also demonstrate the elastic properties of tubes and arteries and explain the effect of a bifurcation in the system.
A missense mutation in the CASQ2 gene is associated with autosomal-recessive catecholamine-induced polymorphic ventricular tachycardia.
Catecholamine-induced polymorphic ventricular tachycardia (CPVT), a rare disease that occurs in subjects without obvious organic heart disease, is characterized by episodes of syncope, seizures, or sudden death in response to physiologic or emotional stress. This report reviews evidence that a missense mutation in the CASQ2 gene is associated with autosomal-recessive CPVT.
Refractoriness and conduction interaction during modulation of non-ischemic ventricular fibrillation by flecainide.
PURPOSE: To study refractoriness and conduction interaction during modulation of non-ischemic ventricular fibrillation (VF) by flecainide. METHODS: Isolated feline and rabbit hearts were used. (a) In the feline hearts (n = 8), electrophysiological parameters were measured before and after flecainide administration (0.6, 1.2 x 10(-6) M). During pacing the parameters were: epicardial conduction time, refractoriness and 1:1 pacing/response capture. During 8 min of electrically-induced tachyarrhythmias they included heart rate and normalized entropy reflecting the degree of organization. (b) In rabbit hearts (n = 4), three-dimensional mapping was performed before and after flecainide administration (2 x 10(-6) M). To follow changes in organization, local RR-intervals and differences in activation time between adjacent epicardial electrodes were measured immediately and 80 sec after VF induction. RESULTS: In feline hearts with flecainide, fibrillation was more difficult to induce, more frequently terminated spontaneously and was slower and more organized; conduction time was markedly lengthened, and refractoriness less than 1:1 capture, was moderately prolonged. An inverse correlation was observed between arrhythmia properties, rate and organization, and changes in refractoriness and conduction time. In rabbit, the number of wave fronts was reduced, RR-intervals were prolonged but at the same time activation time differences between adjacent electrodes were smaller following flecainide administration. CONCLUSIONS: It is suggested that flecainide modulation of VF properties is associated with conduction suppression and refractoriness prolongation, which act in a synergistic, additive way.
Modulation of ventricular fibrillation in isolated perfused heart by dofetilide.
The authors studied the involvement of IKr potassium current in ventricular fibrillation during perfusion. Electrophysiologic parameters were measured before and after dofetilide administration (2.5, 7.5, and 12.5 x 10-7 M, n = 8) in isolated perfused feline hearts. During pacing, these parameters included epicardial conduction time, refractoriness, and the fastest rate for 1:1 pacing/response capture. During 8 minutes of electrically induced tachyarrhythmias, they included heart rate and normalized entropy reflecting the degree of organization. In all groups, arrhythmia rate was slower in the right ventricle than in the left ventricle. Dofetilide decreased the arrhythmia rate more than it increased organization, reduced its maintenance, or increased difficulty in initiation. Refractoriness was prolonged in a reverse use-dependent way which was less than 1:1 pacing/response capture. Unexpectedly, a moderate prolongation of conduction time was observed. Inverse correlation was found between the arrhythmia rate and changes in refractoriness and conduction time and between the degree of organization and refractoriness (both ventricles) and conduction time (right ventricle). Dofetilide, which intensively blocks IKr current and unexpectedly suppressed conduction, has different quantitative effects on fibrillation features. These changes in fibrillation suggest that these effects are mainly associated with refractoriness prolongation and do not seem to be attenuated by conduction suppression.
Managing pacemaker safety alerts: experience with three successive models of a single manufacturer.
This report describes the experience of a large pacemaker center during three successive replacement operations due to safety alerts involving three models from the same manufacturer. Between March 1993 and May 1999, 210 patients were implanted with three DDD pacemaker models (Sorin Biomedica, Saluggia, Italy) that were subsequently subject to safety alerts. Pacemaker records were reviewed for complications related to device malfunction, and those secondary to the replacement procedure. Pacemaker malfunction was observed in 16.4% of units despite much lower estimates from the company (range 1-4%). With the exception of one, all units were replaced. Malfunctions were discovered in 7 of 20 pacemakers following an urgent call for follow-up issued as a result of the alert. Twenty units implanted as substitutes for those replaced following the first alert turned out to be subject to the third alert. Significant clinical consequences of malfunction occurred in 5.3% of patients including a near fatal event in one case, while complications related to the replacement procedure occurred in 8.3% of patients, including one fatality. On the issuance of a safety alert, failure rates in a particular center may be higher than published by the manufacturer, and should prompt action by the center to weigh local incidence of device failure against complications of replacement procedures. When device failure mechanism is not entirely clear, particularly in cases of successive model failures, replacement devices from a different manufacturer should be considered.
Wavelet analysis of instantaneous heart rate: a study of autonomic control during thrombolysis.
Myocardial infarction (MI) is known to elicit activation of the autonomic nervous system. Reperfusion, induced by thrombolysis, is thus expected to bring about a shift in the balance between the sympathetic and vagal systems, according to the infarct location. In this study, we explored the correlation between reperfusion and the spectral components of heart rate (HR) variability (HRV), which are associated with autonomic cardiac control. We analyzed the HR of patients during thrombolysis: nine anterior wall MI (AW-MI) and eight inferoposterior wall MI (IW-MI). Reperfusion was determined from changes in ST levels and reported pain. Reocclusion was detected in four patients. HRV was analyzed using a modified continuous wavelet transform, which provided time-dependent versions of the typically used low-frequency (LF) and high-frequency (HF) peaks and of their ratio, LF/HF. Marked alterations in at least one of the HRV parameters was found in all 18 reperfusion events. Patterns of HRV, compatible with a shift toward relative sympathetic enhancement, were found in all of the nine reperfusion events in IW-MI patients and in three AW-MI patients. Patterns of HRV compatible with relative vagal enhancement were found in six AW-MI patients (P < 0.001). Significant changes in HRV parameters were also found after reocclusion. Time-dependent spectral analysis of HRV using the wavelet transform was found to be valuable for explaining the patterns of cardiac rate control during reperfusion. In addition, examination of the entire record revealed epochs of markedly diminished HRV in two patients, which we attribute to vagal saturation.
Mechanism of mitral regurgitation in inferior wall acute myocardial infarction.
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Transcutaneous detection of aortic arch atheromas by suprasternal harmonic imaging.
OBJECTIVES: The goal of the present study was to examine whether suprasternal harmonic imaging (SHI) (i.e., harmonic imaging from the suprasternal windows) can visualize protruding arch atheromas (PAAs) and reliably predict the presence or absence of significant lesions. BACKGROUND: Protruding arch atheromas are a major source of cerebral and peripheral embolism and probably the most frequent cause of stroke during cardiac catheterization and open-heart surgery. Preprocedural screening by transesophageal echocardiography (TEE) would be desirable but is limited by the nature of the examination. METHODS: Of 354 patients who underwent a TEE study in our laboratory during the study period, 106 were referred for detection of a source of embolism. Findings were classified based on the French Aortic Plaque study criteria as: 1) no or minimal atherosclerotic changes; 2) PAAs < 4 mm; 3) PAAs > or =4 mm or presence of a mobile component. RESULTS: Adequate transcutaneous image quality could be achieved in 89 patients (84%). Protruding arch atheromas were present in 42 patients (47%) and absent in 47 (53%). Positive and negative predictive values for large PAAs on TEE were 91% and 98%, respectively. In one case, SHI detected a complex PAA inaccessible for TEE due to interposition of the left bronchus as demonstrated by dual helical computed tomography. Inter-observer agreement for SHI was 91%. CONCLUSIONS: Suprasternal harmonic imaging reliably predicted or excluded the presence of PAAs in a sizable, consecutive group of patients referred to TEE for detection of a source of embolism. It represents an excellent screening test and provides complimentary views of regions, which may be blind spots for TEE.
Effects of adrenaline on electrophysiological parameters during short exposure to global ischemia. A ventricular fibrillation study in isolated heart.
BACKGROUND: The mechanisms by which adrenaline may enhance defibrillation success rate, is poorly understood. OBJECTIVES: To study electrophysiological effects of adrenaline during short exposure to global ischemia. METHODS: In isolated perfused feline hearts, coronary perfusion was eliminated repeatedly for 1 min with 10 min reperfusion intervals. Treatment included: (1) continuous perfusion alone-control, (2) global ischemia alone, (3) adrenaline (10(-7) M) during perfusion, (4) adrenaline (10(-7) M) during global ischemia (n = 10), in separate hearts, (5) control and higher adrenaline concentration (1 x 10(-6) M), (6) during perfusion, (7) during global ischemia (n = 9). Measurements during pacing included: (1) diastolic threshold of excitability; (2) refractoriness; (3) epicardial conduction time; and (4) all tissue resistivity to indirectly detect changes in passive properties of conduction. Measurements during 1 min (or 90 sec) of electrically induced ventricular fibrillation included-all tissue resistivity and, based on maximal entropy spectral analysis and normalized entropy, rate of arrhythmia and degree of arrhythmia organization. RESULTS: Adrenaline (10(-7) M) during global ischemia vs control caused spontaneous arrhythmia termination, increased threshold significantly but reduced conduction time. Higher adrenaline concentration (1 x 10(-6) M) during global ischemia improved the passive properties of conduction and arrhythmia organization and reduced arrhythmia rate. Global ischemia alone increased conduction time but had a deleterious effect on passive properties. Adrenaline (10(-7) M) during perfusion improved conduction, but did so less than during global ischemia. Higher adrenaline concentration during perfusion (10(-6) M) improved arrhythmia organization and caused spontaneous arrhythmia termination but again less than during global ischemia. CONCLUSIONS: During short periods of global ischemia adrenaline improved the passive properties of conduction and arrhythmia organization, reduced arrhythmia rate and increased its spontaneous termination. Such changes may be operative in improving defibrillation success.
Dalteparin sodium (fragmin) administration following acute infarction does not affect myocardial perfusion and function in swine.
BACKGROUND: Heparin and low molecular weight heparin (LMWH) derivatives are considered angiogenic factors in ischemic and infarcted myocardium. However, the effect of dalteparin sodium (fragmin, a LMWH derivative) on angiogenesis post infarction has not yet been investigated.Purpose. To assess the effect of systemically-administered dalteparin sodium on left ventricular perfusion and function during remodeling in swine subjected to acute microembolization infarction (MI).Methods. MI was induced in 12 anesthetized female pigs which randomly received dalteparin sodium (12,500U) or placebo through intra-peritoneal osmotic pump, for one week, beginning immediately after the MI. Myocardial perfusion and function were measured using radionuclear scan and echocardiography, respectively, at baseline, immediately post MI, and at 2 and 4 weeks post MI. Dobutamine stress echocardiography was performed 4 weeks post MI. Serum level of basic fibroblast growth factor (bFGF) was analyzed using a commercially available ELISA kit.Results. No differences were observed in myocardial perfusion at all time points following MI. No significant changes were observed in myocardial function and wall motion during the 4 weeks follow-up period, or after dobutamine administration. Serum bFGF did not change throughout the study period.Conclusion. Under the setting of the current experiment, one week of dalteparin sodium administration does not affect myocardial perfusion and function following acute infarction in swine, either at rest or following pharmacological stress.
Human experience with transvenous biventricular defibrillation using an electrode in a left ventricular vein.
This study investigated the safety and feasibility of transvenous biventricular defibrillation in ICD patients. Some patients may have high DFTs due to weak shock field intensity on the LV. Animal studies showed a LV shocking electrode dramatically lowered DFTs. This approach might benefit heart failure patients already receiving a LV lead or conventional ICD patients with high DFTs. A modified guidewire was used as a temporary left venous access defibrillation electrode (LVA lead). In 24 patients receiving an ICD, the LVA lead was advanced through a guide catheter in the coronary sinus (CS) and into a randomized LV vein (anterior or posterior) using a venogram for guidance. Paired DFT testing compared a standard right ventricular defibrillation system to a biventricular defibrillation system. There were no complications or adverse events. As randomized, LVA lead insertion success was 87% and 71% for anterior and posterior veins, respectively, and 100% after crossover. Total insertion process time included venogram time (32.5 +/- 26.9 minutes, range 5-115, mode 15 minutes) and LVA lead insertion time (15 +/- 14 minutes, range 1-51, mode 7 minutes). An apical LVA lead position was achieved in 11 (45%) of 24 patients and 7 (64 %) of these 11 displayed a DFT reduction; however, mean DFTs were not statistically different. Transvenous biventricular defibrillation is feasible and was safe under the conditions tested. Additional clinical studies are justified to determine if optimized LV lead designs, lead placement, and shock configurations can yield the same large DFT reductions as observed in animals.
ST-segment deviation following implantable cardioverter defibrillator shocks: incidence, timing, and clinical significance.
ST-segment analysis is frequently used during surgical procedures, while ST deviation is considered a sign of myocardial injury. ST deviations were reported following transthoracic and epicardial electrical shocks. The prevalence, timing, and clinical significance of ST-segment deviation following endocardial ICD shocks are discussed in this article. Twenty-eight patients undergoing 125 shock episodes during ICD implantation or testing were included. A 12-lead ECG was recorded at baseline, continuously during the first 3-10 seconds, 1 minute after test shocks, 3-10 seconds and 1 and 5 minutes after each shock given to terminate VF. ST deviation was diagnosed when the ST-segment was displaced > or = 1 mm in at least one lead compared to baseline. ST-segment deviations were observed after 49 (39%) of all shock episodes in 17 (61%) of patients. ST elevation was observed after 30 (24%) of all shock episodes, and ST depression after 31 (25%). Following 13 shock episodes in seven patients, ST-elevation and depression were observed. ST depressions occurred more frequently after shocks given to terminate VF than after lower energy test shocks (28% vs 18% respectively, P = 0.045). However, there was no significant difference in the prevalence of ST elevations between the lower or higher energy shocks. No adverse clinical events were observed in patients with or without postshock ST-segment deviation. ST-segment deviation following endocardial ICD shocks is a frequent phenomenon, occurring acutely and resolving during the first few minutes postshock. It mayhave no prognostic implications.