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Biomedical subjects

T Guarnieri

Publications and source records attributed to T Guarnieri.

At least 55 records · Page 3Linked to original sources
PubMed1988

Effect of AF64A on the cholinergic systems of the retina and optic tectum of goldfish.

AF64A, a presumed selective cholinergic neurotoxin has been used to study the effect on cholinergic systems of the goldfish retina and optic tectum. Toxin injection in the vitreum and in the optic tectum caused a selective decrease of choline acetyltransferase activity in both areas, while no significant decrease of glutamate decarboxylase and D-3H aspartate uptake were observed at different times after the injections. The effect was particularly dramatic in the retina of long term-injected animals, where choline acetyltransferase dropped to practically zero level. The ultrastructural analysis showed selective degeneration of some neurons in the amacrine and ganglion cell layer of the retina as well as of synaptic terminals and neuronal cell bodies in the optic tectum. The results favour a selective cholinotoxicity of AF64A in fish nerve tissue at doses substantially higher than those found to have additional unselective effects in mammals.

Animals↗
PubMed1988

Impending sudden cardiac death: treatment with myocardial revascularization and the automatic implantable cardioverter defibrillator.

Myocardial revascularization and implantation of the automatic implantable cardioverter defibrillator (AICD) have individually been shown to improve survival in patients after sudden cardiac death. Their combined role has not been well defined. Twenty-three survivors of sudden death underwent revascularization and AICD implantation at an average age of 59 years. The initial arrest was caused by ventricular fibrillation in 15 and ventricular tachycardia in 8. Exercise stress tests, ambulatory ECGs, and electrophysiological monitoring with programmed electrical stimulation were done preoperatively and postoperatively. Follow-up averaged 24 months with a two-year survival of 91%. Eight patients (35%) required AICD resuscitation an average of 8 months postoperatively, and electrophysiological testing did not accurately predict arrhythmia recurrence. The addition of AICD implantation to revascularization substantially improves survival of patients with sudden cardiac death.

Adult↗
PubMed1988

Regional levels of neurotransmitter markers in the pigeon telencephalon: a comparison with possibly homologous areas of the rat telencephalon.

The levels of cholinergic, gamma-aminobutyric acidergic (GABAergic), and excitatory amino acid neurotransmitter markers have been measured in 18 regions of the pigeon telencephalon as well as in supposedly homologous areas of the rat telencephalon. Among the basal telencephalic areas, some similar patterns of regional distribution were observed, with the noticeable exception of the ratio of levels of cholinergic markers between the striatum and globus pallidus, which was much larger in the rat than in the pigeon. In the rat cortical areas, some interesting differences were noticed among the archicortex, the paleocortex, and various parts of the neocortex. In particular, the area identified as prefrontal cortex by previous studies was significantly richer in cholinergic and excitatory amino acid markers and poorer in GABAergic activity than other neocortical regions. In the pigeon, presumedly neocortical equivalent areas--in particular, those constituting the dorsal ventricular ridge--were quite variable in levels of cholinergic markers, and some apparently well-established areas homologous to mammalian neocortex showed exceptionally low levels of cholinergic markers. The higher variability in levels of neurotransmitter-related markers shown by cortically equivalent areas of the avian dorsal ventricular ridge, as compared with the more uniform pattern present in basal telencephalic regions, may be the result of a greater plasticity of these structures during evolution, in response to different selective pressures.

Acetylcholinesterase↗
PubMed1988

Increased pacing threshold after an automatic defibrillator shock in dogs: effects of class I and class II antiarrhythmic drugs.

A high energy shock delivered by an automatic defibrillator may interfere with pacemaker function. To provide insight into the changes that occur in the threshold for ventricular pacing after the shock from an automatic defibrillator, we measured the time to capture during asynchronous ventricular pacing in dogs from endocardial or epicardial sites, after a 30 joule shock was delivered via conventional automatic defibrillator (AICD) patch electrodes. After a 30 joule shock, there was a transient loss of ventricular capture. The duration of capture loss was related to current strength. During endocardial pacing at threshold current, the time to capture was 4.9 +/- 1.2 s, whereas at current values twice threshold the time to capture from endocardial pacing was 2.2 +/- 0.9 s. No difference was found between endocardial and epicardial pacing sites in the time to capture. To ascertain the mechanism of capture loss we: (1) examined the effects of converting the pacing catheter to a current sink (transiently shunting to ground); (2) altered excitability by an infusion of flecainide; (3) blocked sympathetic input (propranolol). No change in time to capture was noted by shunting the pacer to ground. After an infusion of flecainide the time to capture from endocardial pacing was significantly prolonged to 14.9 +/- 2.2 s at the threshold value (P less than .01) and 5.6 +/- 2.1 s at twice threshold (P less than .05). Conversely, intravenous propranolol had no effect on the time to capture after shock from endocardial pacing. These data indicate that there is a transient increase in pacing threshold after the shock from an automatic defibrillator.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Implanted automatic defibrillators: effects of drugs and pacemakers.

The automatic implantable cardioverter defibrillator is an effective device for prevention of sudden cardiac death. Patients who require the implantation of the device often require permanent pacing for symptomatic bradyarrhythmias and may require antiarrhythmic drug therapy. Antiarrhythmic drugs may alter the defibrillation thresholds, arrhythmia cycle length and frequency, pacing thresholds and postshock excitability. Interactions between the defibrillator and the pacemaker may result in sensing problems, leading to multiple counting and inappropriate shocks, or ventricular fibrillation nondetection, sensing or capture failure post defibrillation and pacemaker reprogramming induced by defibrillator discharge. The potential for interactions will increase as the new generation of programmable defibrillators become clinically available, combining features of permanent pacemakers, antitachycardia pacemakers and defibrillators.

Anti-Arrhythmia Agents↗
PubMed1988

The automatic implantable cardioverter defibrillator: T wave sensing in the newest generation.

The AICD uses an automatic gain control amplifier for detecting the small electrograms during ventricular fibrillation. The latest generation of the AICD appears to have a more sensitive lock on gain amplifier, as 6 of 76 patients implanted with the new AICD had double counting of the QRS-T wave complex resulting in asymptomatic discharges. Solutions to the problem of limiting these asymptomatic discharges are difficult and include slowing of the heart rate with beta blockers, changing the lead system, or replacement of the device. One of the six patients was treated with beta blockers. Three patients had their device changed, two patients requested the inactivation of their device until a rate programmable unit was available. The potential for T wave sensing in a lock on gain amplifier represents the unique dilemma between detecting small electrograms of ventricular fibrillation, and detecting diastolic events which occur shortly after the QRS complex.

Adult↗
PubMed1988

Implantation of the automatic implantable cardioverter defibrillator.

Since February 1980 the automatic implantable cardioverter defibrillator has been implanted in over 1,500 patients. Sudden death rates have been reduced to 2%-4% annually. This report reviews the implantation techniques, their indications, and our clinical experience in 200 patients.

Arrhythmias, Cardiac↗
PubMed1988

Changes in myocardial repolarization in patients undergoing balloon valvuloplasty for congenital pulmonary stenosis: evidence for contraction-excitation feedback in humans.

Alterations in ventricular loading conditions lead to changes in action potential duration and arrhythmias via contraction-excitation feedback; a decrease in load leads to prolongation of repolarization. To determine whether changes in right ventricular load alter ventricular repolarization in man, the corrected QT interval, a measure of overall ventricular repolarization, was measured in 32 patients before and after valvuloplasty for pulmonary stenosis. Right ventricular systolic pressure decreased (82.5 +/- 30.7 to 40.5 +/- 9.5 mm Hg, p less than .001) and the QTc increased concurrently (409.1 +/- 24.3 to 440.7 +/- 28.0 msec, p less than .001) after successful valvuloplasty. The increase in QTc was most marked for those patients with a greater than 30 mm Hg decrease in right ventricular pressure (40.0 +/- 23.3 vs 16.3 +/- 21.3 msec, p = .006). In a subset of seven patients in whom monophasic action potentials were recorded, monophasic action potential duration, a measure of local repolarization, was prolonged (230.0 +/- 24.3 vs 216.9 +/- 21.9, p less than .001) after successful valvuloplasty, confirming that the QTc prolongation reflected changes in local ventricular repolarization. In addition, during nine acute right ventricular outflow tract occlusions in a subset of six patients, monophasic action potential duration shortened (206.6 +/- 17.6 vs 221.7 +/- 20.9 msec, p less than .01) and early afterdepolarizations developed consistent with contraction-excitation feedback. These data suggest that, in humans, changes in mechanical load are associated with changes in ventricular repolarization consistent with contraction-excitation feedback.

Action Potentials↗
PubMed1988

Decrease in the transmembrane sodium activity gradient in ferret papillary muscle as a prerequisite to the calcium paradox.

Sodium-dependent calcium exchange may be an important mediator of calcium reperfusion damage during the calcium paradox phenomenon. We measured intracellular sodium activity with ion-selective electrodes during a 15-min period of calcium reperfusion in isolated ferret papillary muscles. During the calcium-free period, alpha Nai increased from 9.0 +/- 0.9 to 18.9 +/- 4.3 mM. With reinstitution of calcium there was a significant contracture. The amount of contracture after calcium reinstitution was related to sodium loading during the calcium-free period. We were unable to block sodium entry during the calcium-free period with either nitrendipine, tetrodotoxin, or low concentrations of amiloride. 10(-3) M amiloride or lithium for sodium substitution in the calcium-free period, however, obliterated the increase in alpha Nai activity and the subsequent paradox. These data suggest that sodium loading is a necessary prerequisite for the calcium paradox and that one mechanism of sodium entry is through Na+/Ca2+ exchange. Under these conditions, no increase in the rest force is seen without previous sodium gains, suggesting that sodium-dependent calcium exchange is an important trigger for the calcium reflow, the calcium paradox.

Amiloride↗
PubMed1987

Success of chronic defibrillation and the role of antiarrhythmic drugs with the automatic implantable cardioverter/defibrillator.

Because the automatic internal cardioverter defibrillator's long-term ability to reduce arrhythmic mortality in patients with ventricular tachycardia/fibrillation is unknown, it is important to determine whether the threshold for defibrillation changes over time. Serial defibrillation thresholds were measured in 23 patients over a mean replacement time of 24.8 +/- 7.5 months. In all cases the lead system was a superior vena cava coil to a left ventricular epicardial patch. The defibrillation threshold for the entire group increased from 12.3 +/- 4.7 J to 16.9 +/- 5.9 J (p less than 0.05). Striking increases in the defibrillation threshold were seen in the subgroup of patients taking amiodarone (from 10.9 +/- 4.3 J at implantation to 20.0 +/- 4.7 J at replacement, p less than 0.05). Defibrillation threshold decreased in patients taking no antiarrhythmic drugs or taking class I agents. Thus, the increase in mean defibrillation threshold was the result of an increase in the patients taking amiodarone. These data suggest that at initial implantation lead systems associated with the lowest defibrillation threshold should be used and the defibrillation threshold should be measured at generator change to guarantee an adequate margin of safety.

Aged↗
PubMed1987

Refractory symptomatic ventricular tachycardia and ventricular fibrillation in elderly patients.

The problem of refractory life-threatening ventricular tachyarrhythmias in elderly patients has not been previously studied. To determine if clinical, anatomic, or electrophysiologic variables and prognosis are significantly different in elderly subjects, 49 elderly (68 to 84 years) and 44 younger (44 to 53 years) survivors of refractory symptomatic ventricular tachycardia and/or ventricular fibrillation secondary to coronary artery disease were studied. Elderly patients displayed more extensive anatomic coronary artery disease, with 80 percent having three-vessel disease in comparison with 30 percent of the younger patients (p less than 0.001). Prior myocardial infarction, heart failure, and cardiomegaly were more common in the elderly group (p less than 0.01, p less than 0.001, and p less than 0.034, respectively), whereas angina was more common in the younger group (p less than 0.001). In 55 percent of the elderly patients and 58 percent of the younger patients, electrophysiologic testing demonstrated inducible sustained ventricular tachycardia that required treatment with an investigative antiarrhythmic drug and/or cardiac surgery, including implantation of an automatic defibrillator. Elderly patients tolerated aggressive evaluation as well as did younger patients, and despite the difference in clinical and anatomic findings, long-term survival curves were similar, although the probability of survival at 20 months was 62 percent in the elderly and 80 percent in the younger patients. This difference in early survival is explained by eight surgical deaths in the elderly group, compared with two in the younger group.

Age Factors↗
PubMed1987

Pathologic findings related to the lead system and repeated defibrillations in patients with the automatic implantable cardioverter-defibrillator.

The purpose of the present study was to examine at autopsy the effect of multiple defibrillations on the myocardium and the pathologic consequences of short- and long-term placement of the intravascular and interpericardial leads of the automatic implantable cardioverter-defibrillator. Twenty-five patients were examined at autopsy; 8 of them underwent lead implantation only and 17 received both leads and the automatic implantable cardioverter-defibrillator. Twelve patients (48%) died of ventricular tachycardia or ventricular fibrillation; seven (28%) died of other causes. Acute pericarditis occurred in all patients, resulting in a localized, progressive fibrosis around the apical patch lead without giving rise to pericardial restriction. Thrombus formation was associated with the superior vena cava spring electrode in four patients (17%) and the right ventricular rate-sensing electrode in one patient (4%). Asymptomatic pulmonary emboli occurred in two patients (8%). In one patient who underwent defibrillation 59 times, superior vena cava changes consisted of vein wall destruction, fibrosis and thrombus formation. Pathologic changes under the apical patch related to defibrillation were observed in seven patients; two of these had fewer than 5 defibrillations, one had 8 defibrillations and four had 21 to 74 defibrillations. These changes consisted of contraction band necrosis in four patients, vacuolar cytoplasmic clearing and loss of myocytes confined to the myocardium under the patch electrode in five patients who had multiple defibrillations. The observed pathologic changes were estimated to affect less than 2% of the total myocardial mass. Thus, the automatic implantable cardioverter-defibrillator lead system and multiple defibrillations result in localized myocardial injury confined to the tissue under the patch electrode.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

The long R-P' tachycardias.

The family of tachycardias that are called long R-P' tachycardias represent a unique group of tachycardias which have been notably refractory to pharmacologic therapy in the past. On the surface electrocardiogram, the rhythms may be indistinguishable. It is only with careful electrophysiological evaluation in many cases that these rhythms can be sorted out. The differential diagnosis in these rhythms is important because with incessant tachycardia, ventricular dysfunction may be produced. In many of the instances of long R-P' tachycardias definitive and directed ablation of the tachycardia can be accomplished. New techniques involving catheter ablation and super-selective surgical dissection are now present which makes ablation of these tachycardias possible.

Atrioventricular Node↗
PubMed1987

Automatic implantable cardioverter defibrillator/permanent pacemaker interaction: loss of pacemaker capture following AICD discharge.

A 78-year-old man treated with amiodarone for recurrent ventricular tachycardia, had sequential placement of a bipolar VVI pacemaker and an automatic implantable cardioverter defibrillator (AICD). During defibrillation threshold testing, there was failure to capture of the pacer in the post-shock period. The time of failure to capture appeared energy-related: the greater the energy delivered, the longer the failure to capture. Careful attention will be necessary in constructing combined AICD/pacemaker units.

Aged↗
PubMed1987

Intracellular sodium-calcium dissociation in early contractile failure in hypoxic ferret papillary muscles.

1. Intracellular sodium activity (aNai) and intracellular calcium activity (aCai) were measured in isolated quiescent right-ventricular ferret muscle: aNai = 9.8 +/- 2.2 mM and aCai = 71 +/- 19 nM. 2. When the muscles were exposed to 10(-5) M-ouabain, aNai increased to 20.4 +/- 3.1 mM while aCai increased to 260 +/- 99 nM. Twitch tension approximately doubled. 3. During prolonged hypoxia with glucose in the perfusate, aNai and twitch tension were unchanged. 4. During prolonged hypoxia with sucrose (substrate free) in the perfusate aNai increased to 18.9 +/- 3.1 mM, but aCai did not change. Twitch tension declined by 50%. 5. The addition of 10(-5) M-ouabain to the substrate-free hypoxic perfusate caused aNai to increase to 31.6 +/- 2.8 mM and aCai to increase to 150 +/- 35 nM. Twitch tension was unchanged. 6. These data indicate that only during prolonged substrate-free hypoxia does aNai increase. Despite the increase in aNai, no change in aCai is seen, unless the sodium-potassium pump is concomitantly inhibited. The lack of rise of aCai is consistent with inhibition of the sodium-calcium exchange, although other avenues of calcium exchange cannot be excluded.

Action Potentials↗
PubMed1987

The cellular electrophysiologic changes induced by ablation: comparison between argon laser photoablation and high-energy electrical ablation.

The cellular electrophysiologic effects of myocardial ablation performed in vitro with argon laser energy were compared with those of high-energy electrical shocks. A border zone of injured but nonnecrotic tissue surrounding the site of energy delivery was present after tissue ablation by both energy modalities. A decrease in resting membrane potential, action potential amplitude, and maximum rate of upstroke velocity was noted in each tissue sample, was greatest nearest the site of energy delivery, and was of graded severity at increasing distances from the crater edge. The extent of injury, as indexed by changes in action potential variables and necrosis, histologically determined, was greater for tissues exposed to high-energy shocks. The relatively focal injury after argon laser photoablation may explain the lower incidence of arrhythmias and hemodynamic dysfunction noted with the use of this method of ablation in vivo.

Action Potentials↗
PubMed1986

Treatment of malignant ventricular arrhythmias with endocardial resection and implantation of the automatic cardioverter-defibrillator.

Although ventricular resection guided by endocardial mapping has been a successful treatment for drug-refractory ventricular arrhythmias, 20 to 30 percent of patients still have postoperative sustained ventricular tachycardia or sudden death. To improve the outcome of the procedure, we implanted an automatic cardioverter-defibrillator in conjunction with endocardial resection in 28 patients, all of whom had had previous myocardial infarctions and between one and five cardiac arrests. There were three perioperative deaths. During follow-up of 8 to 51 months (mean, 25), 4 of the 25 survivors had recurrences of hypotensive ventricular tachycardia, which in all instances were automatically terminated by the implanted device. One patient, whose automatic cardioverter-defibrillator was not functional, died suddenly. We conclude that patients undergoing mapping-directed endocardial resection can be provided with additional protection against recurrent ventricular tachyarrhythmias or sudden death by implantation of an automatic cardioverter-defibrillator.

Adult↗