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Biomedical subjects

T Guarnieri

Publications and source records attributed to T Guarnieri.

At least 73 records · Page 4Linked to original sources
PubMed1986

Reversal of dysfunction in postischemic stunned myocardium by epinephrine and postextrasystolic potentiation.

After brief coronary occlusions, myocardium may become "stunned," exhibiting prolonged depression of function despite the absence of necrosis. Because of the accompanying decline in adenosine triphosphate and adenine nucleotide precursors, a deficiency of energy supply has been proposed as the basis for postischemic dysfunction. This study examined whether sufficient functional and metabolic reserve exists in stunned myocardium to sustain a prolonged, maximal inotropic response to epinephrine and postextrasystolic potentiation. In 11 open chest dogs, the left anterior descending coronary artery was occluded for 5 minutes, followed by 10 minutes of reflow, repeated 12 times, with a final 1 hour recovery period. Regional myocardial function was measured using pairs of ultrasonic dimension crystals implanted in ischemic and nonischemic zones. During repetitive reflows a progressive decrease in mean systolic segment shortening occurred: baseline 21.8%, 1st reflow 15.2%, 12th reflow 4.3%, 1 hour recovery 7.9%. Intravenous epinephrine, titrated to produce a maximal inotropic response, caused segment shortening to increase to 21.6% after 10 minutes and to 24.8% after 1 hour of infusion, despite a 20 mm Hg increase in systolic pressure. The same dose of epinephrine given before ischemia increased segment shortening to 30.5%. In six of the dogs, postextrasystolic potentiation before ischemia increased segment shortening from 21.8 to 31.1%, and after 1 hour of recovery from ischemia, from 7.9 to 24.8%. Lesser increases in segment shortening were also seen in nonischemic segments. The results indicate that stunned myocardium possesses considerable functional reserve. Deficient energy stores are therefore not likely to be the basis for depressed function seen at rest in stunned myocardium.

Animals↗
PubMed1986

The characterization of human transmyocardial impedance during implantation of the automatic internal cardioverter defibrillator.

We set out to determine in a prospective fashion the characteristics of energy delivery related to defibrillation in a population of patients receiving the AICD. Specifically, we examined the characteristics of the delivered current, transmyocardial voltage, and transmyocardial impedance. Secondly, we determined the relationship between the energy delivered, the impedance encountered and the defibrillation threshold. Since the AICD will deliver a succession of shocks if the initial shock does not cardiovert, the effects of consecutive shocks at different energy levels on the transmyocardial impedance were also assessed.

Cardiac Surgical Procedures↗
PubMed1986

The use of ambulatory monitoring in the prognostic evaluation of patients with sustained ventricular tachycardia treated with amiodarone.

We recently reported a retrospective experience with serial Holter monitoring as a guide to therapy in patients with sustained ventricular tachycardia treated with amiodarone. To confirm and substantiate these findings, a prospective study was designed that included baseline 24 hr Holter monitoring and serial Holter monitoring after 1 week of therapy with amiodarone. Fifty-two patients with documented sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring were treated with amiodarone. Thirty-four patients (group I) had nonsustained ventricular tachycardia completely suppressed and 18 patients (group II) had continued nonsustained ventricular tachycardia on serial Holter monitoring performed on days 8, 9, and 10 of therapy. At 11.6 +/- 1.0 (mean +/- SE) months follow-up, three (9%) group I patients and 12 (67%) group II patients had recurrent sustained ventricular tachycardia or sudden cardiac death (p less than .01). The sensitivity, specificity, positive and negative predictive value, and predictive accuracy of ventricular tachycardia on 24, 48, and 72 hr Holter monitoring over days 8, 9, and 10 for predicting recurrent sustained ventricular tachycardia or sudden cardiac death were analyzed. The positive and negative predictive values were 89% and 84%, 69% and 89%, and 67% and 91% for 24, 48, and 72 hr Holter monitoring, respectively. Overall predictive accuracy was 85%, 83%, and 83%, respectively. We conclude that early Holter monitoring is useful in assessing the clinical efficacy of amiodarone in patients with sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring.

Amiodarone↗
PubMed1986

The monophasic action potential upstroke: a means of characterizing local conduction.

The upstrokes of monophasic action potentials (MAPs) recorded with an extracellular pressure electrode were characterized in isolated canine tissue preparations in vitro. The characteristics of the MAP upstroke were compared with those of the local action potential foot as well as with the characteristics of approaching electrical activation during uniform and asynchronous conduction. The upstroke of the MAP was exponential during uniform conduction. The time constant of rise of the MAP upstroke (TMAP) correlated with that of the action potential foot (Tfoot): TMAP + 1.01 Tfoot + 0.50; r2 = .80. Furthermore, changes in Tfoot with alterations in cycle length were associated with similar changes in TMAP: Tfoot = 1.06 TMAP - 0.11; r2 = .78. In addition, TMAP and Tfoot both deviated from exponential during asynchronous activation; the inflections that developed in the MAP upstroke correlated in time with intracellular action potential upstrokes that were asynchronous in onset in these tissues. Finally, the field of view of the MAP was determined and was found to be dependent in part on tissue architecture and the space constant. Specifically, the field of view of the MAP was found to be greater parallel compared with transverse to fiber orientation (6.02 +/- 1.74 vs 3.03 +/- 1.10 mm; p less than .01). These data suggest that the MAP upstroke may be used to define and characterize local electrical activation. The relatively large field of view of the MAP suggests that this technique may be a sensitive means to record focal membrane phenomena in vivo.

Action Potentials↗
PubMed1985

Multifocal atrial tachycardia: a toxic effect of theophylline.

Sixteen patients with multifocal atrial tachycardia (MAT) who were taking theophylline were identified over 6 months. After theophylline was discontinued the atrial rate fell and MAT resolved in all sixteen patients. Five patients were challenged with intravenous aminophylline to investigate the role of theophylline in the genesis of MAT. MAT with a rapid ventricular response occurred in all five even though metabolic and respiratory variables did not change. MAT returned on challenge in three patients in whom serum theophylline levels were within the generally accepted therapeutic range (10-20 mg/l). In individual patients, theophylline had a dose-related effect on the atrial rate and the amount of ectopic atrial activity. Thus, theophylline may commonly precipitate MAT and treatment with the drug should be carefully considered in patients with respiratory insufficiency and MAT.

Aged↗
PubMed1985

Cesium chloride-induced long QT syndrome: demonstration of afterdepolarizations and triggered activity in vivo.

The identification of afterdepolarizations and their relationship to arrhythmias in vivo is not available. Experiments were undertaken to determine whether afterdepolarizations could be detected in monophasic action potentials (MAPs) recorded in vivo and whether they were related to arrhythmias in an intact canine preparation of the long QT syndrome. Isolated cardiac tissues from six dogs were studied to validate the technique. In simultaneous MAP and transmembrane recordings, afterdepolarizations induced with barium (early) or acetylstrophanthidin (delayed) were detected in MAPs when present in microelectrode recordings. MAPs were then recorded in situ in eight dogs with cesium chloride-induced long QT syndrome associated with ventricular arrhythmias. Afterdepolarizations were identified in each of the dogs and were similar to early afterdepolarizations identified in vitro; they occurred during phase 3 and were attenuated during overdrive pacing. The afterdepolarizations were closely related to arrhythmias: (1) afterdepolarizations always preceded ventricular arrhythmias, (2) the coupling intervals (CI) of the afterdepolarizations (AD) and the ventricular premature beats (VPB) were nearly identical (VPB CI = 1.06 AD CI -10.24; r2 = .87), (3) the take-off potentials of the ventricular premature beats were nearly identical to the amplitude of the afterdepolarizations (take-off potential = 0.98 afterdepolarization amplitude +0.46, r2 = .87), and (4) afterdepolarizations and ventricular arrhythmias resolved concurrently during overdrive pacing and with time. Thus, a new catheter technique has been validated and has been used to directly identify afterdepolarizations and triggered activity in vivo.

Action Potentials↗
PubMed1985

Clinical experience with the automatic implantable defibrillator.

Since February 1980, worldwide, over 400 survivors of sudden arrhythmic death have been treated with the automatic implantable defibrillator. Recently, the device has been further improved; it is now a cardioverter-defibrillator (AICD), able to treat ventricular tachycardias as well as ventricular fibrillation. There are two defibrillating electrodes which are used also for waveform analysis; one is located in the superior vena cava, the other is placed over the cardia apex. A third bipolar right ventricular electrode serves for rate counting and R-wave synchronization. When ventricular fibrillation occurs, a 25-joule pulse is delivered; when ventricular tachycardia faster than a preset rate is detected, the discharge is R-wave synchronized. Special batteries can deliver over 100 shocks or provide a three-year monitoring life. Implantation of the device can be achieved through a thoracotomy or by a subxiphoid or a subcostal approach. Thus far, the longest follow-up period has been 58 months. Actuarial analysis shows the one-year mortality attributed to arrhythmias reduced to less than 2%. Thus, the automatic cardioverter-defibrillator can reliably identify and correct potentially lethal ventricular tachyarrhythmias, leading to a substantial increase in survival in properly selected high-risk patients.

Death, Sudden↗
PubMed1984

Clinical performance of the implantable cardioverter-defibrillator.

The automatic implantable cardioverter-defibrillator has been implanted in 276 patients with ventricular tachyarrhythmias refractory to therapy with a follow-up period up to 50 months (average 9.75 months). The functional performance of the device has so far been most encouraging. The risks and complications associated with its use are acceptable and quite similar to those observed in patients with implanted pacemakers. Acceleration of ventricular tachycardia to a faster rhythm or to ventricular fibrillation is dealt with successfully through recycling. Actuarial analysis indicates that the device has a significant impact on the survival rate of the implantees, reducing the one-year mortality rate attributed to arrhythmias to only 2%.

Actuarial Analysis↗
PubMed1984

The nonpharmacologic management of the permanent form of junctional reciprocating tachycardia.

The permanent or recurring form of junctional reciprocating tachycardia (PJRT) is an incessant tachycardia that has characteristic clinical and electrophysiologic features of PJRT. Each patient demonstrated near-incessant reciprocating tachycardia with a 1:1 atrioventricular (AV) relationship and with a retrograde P wave (P') occurring closer to the succeeding QRS complexes (i.e., long RP'). With initiation of the tachycardia, there was no prolongation of the PR or AH interval. All patients had evidence of early retrograde atrial activation in their posterior atrial septa and this retrograde limb had properties of decremental conduction. Eight of the nine patients underwent elective surgical ablation of the retrograde limb of tachycardia, and in seven it was successful. Epicardial and endocardial atrial maps recorded during PJRT demonstrated that the site of earliest retrograde activation was in the posterior atrial septum near the coronary sinus orifice. The seven patients in whom surgery was successful left the hospital in sinus rhythm with antegrade conduction, and all are free of tachycardia during the mean follow-up period of 31 months (range 1 to 70 months). In the two remaining patients PJRT was controlled by interruption of the antegrade limb of the tachycardia, the AV node-His bundle. In one patient this was done under direct vision at surgery after an unsuccessful attempt at pathway dissection.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Differentiation of septal from free wall accessory pathway location: observations during bundle branch block in reciprocating tachycardia in the presence of type I antiarrhythmic drugs.

In patients with Wolff-Parkinson-White syndrome, observations during bundle branch block (BBB) in reciprocating tachycardia are of value in accessory pathway localization. Most importantly, an increase in the ventriculoatrial (VA) interval of greater than or equal to 35 ms has indicated an ipsilateral free wall location and excluded a septal location. The present study examined whether data collected in the presence of type I antiarrhythmic drugs retained localizing value. Review of retrospective data showed that observations in the drug-free state were precluded by the need to suppress atrial arrhythmia during electrophysiologic study in 20% of patients with Wolff-Parkinson-White syndrome who underwent preoperative workup. Prospectively, in 15 patients with left free wall or posteroseptal pathways, we observed transient left BBB during tachycardia before and after administration of procainamide, disopyramide or quinidine. Serum drug levels ranged from 4.6 to 6.9 mg/liter, except in 1 patient with a serum procainamide level of 18 mg/liter. Drugs increased the VA interval during narrow QRS tachycardia by 17% (p less than 0.01). However, the change in the VA interval with left BBB was not significantly affected. The baseline and drug values averaged 73 ms (range 39 to 94) and 70 ms (range 39 to 90), respectively, for left free wall pathways (n = 8), and 19 ms (range 0 to 28) and 21 ms (range 2 to 35), respectively, for posteroseptal pathways (n = 7). Among the latter, the interval increased less than 30 ms during left BBB except in the patient with the high serum procainamide level, in whom the increase was 35 ms. Thus, the VA interval change that accompanied left BBB remained of localizing value with moderate blood levels of type I drugs, and an increase greater than or equal to 35 ms indicated a left free wall rather than posteroseptal pathway.

Adolescent↗
PubMed1983

Effects of exercise and isoproterenol during atrial fibrillation in patients with Wolff-Parkinson-White syndrome.

The effects of exercise and isoproterenol on atrial fibrillation (AF) were studied in 17 patients with Wolff-Parkinson-White syndrome (WPW) to assess the risk of developing a rapid ventricular response. Mean cycle length (R-R interval) and shortest R-R interval between both preexcited and nonpreexcited QRS complexes were recorded, as well as the percentage of preexcited complexes during control periods, during bicycle exercise, and during isoproterenol infusion. Exercise resulted in significantly shorter mean cycle length and the shortest R-R interval between nonpreexcited complexes. Exercise also resulted in a significantly lower percentage of preexcited complexes during AF, but had no effect on the R-R intervals between preexcited complexes. Isoproterenol had a variable effect on the percentage of preexcited QRS complexes, but resulted in significant shortening of mean cycle length and the shortest R-R interval between both normal and preexcited complexes. With isoproterenol, 12 of 17 patients had shortest preexcited R-R intervals less than or equal to 215 ms, compared with 6 of 17 in the control state. Isoproterenol infusion increased the rate of conduction over the accessory pathway during AF and allowed better assessment of the risk of excessively rapid rates occurring during AF. Exercise is not an adequate test for this purpose.

Atrial Fibrillation↗
PubMed1983

Effects of energy delivery via a His bundle catheter during closed chest ablation of the atrioventricular conduction system.

In this paper we summarize our experience and report the characteristics of energy delivery in 23 patients who have undergone closed chest ablation of the normal atrioventricular (AV) conduction system for the treatment of refractory supraventricular arrhythmias. The induction of AV block was achieved by the synchronous delivery of electrical energy with a damped sinusoidal waveform utilizing a standard direct current defibrillator and a standard tripolar His bundle catheter. The procedure was well tolerated, though one patient experienced ventricular fibrillation, which was uneventfully converted with external paddles. Complete AV block was achieved in 20 of 23 patients and all were rendered arrhythmia free, though two still required antiarrhythmic drugs. A stable escape rhythm was seen in all patients with a cycle length of 1,294 +/- 243 ms. Creatine phosphokinase-MB was positive at low levels in 19 of 23 patients and cleared within 24 h. 99mTc pyrophosphate scans were faintly positive in only 2 of 22 patients. Left ventricular wall motion and ejection fractions were unchanged in 19 of 19 patients, two-dimensional echocardiography with microcavitation technique was unchanged in 12 of 12 patients, and a slight increase in pulmonary artery wedge pressure was seen in only 1 of 11 patients. Current, voltage, and their product (power) waveforms were recorded in 12 patients (12 recordings at a defibrillator setting of 200 J and 5 recordings at a defibrillator setting of 300 J) and revealed a complex voltage-current relationship due to changes occurring at the catheter electrode-tissue interface. At 200 J the peak values were 42.2 +/- 3.3 A, 2.16 +/- 0.11 kV, and 87.9 +/- 4.7 kW, while at 300 J the peak values were 58.2 +/- 2.8 A, 2.40 +/- 0.10 kV, and 134.4 +/- 6.7 kW, respectively. No instance of catheter disruption was seen, though "pitting" of the distal electrode (through which current passed) occurred in all but one catheter.

Adult↗
PubMed1982

Intracellular potassium activity in guinea pig papillary muscle during prolonged hypoxia.

During prolonged hypoxia, intracellular potassium concentration, [K](i) has been reported to fall by 70% with a concomitant decrease in the calculated potassium equilibrium potential, E(K). Nevertheless, resting membrane potential, V(m), declined only slightly. Because V(m) depolarized very little in relation to the calculated E(K), it was hypothesized that electrogenic Na-K pumping contributed up to 40 mV to V(m) during prolonged hypoxia. To further test this hypothesis we studied what changes prolonged hypoxia makes in the thermodynamically active fraction of cellular potassium, intracellular potassium activity, alpha(K) (i), and how change in alpha(K) (i) affects the relationship between V(m), E(K) and, by inference, the Na-K pump. Using double-barrel K-selective electrodes, V(m) and alpha(K) (i) were measured in quiescent guinea pig right ventricular papillary muscles superfused for 8 h with hypoxic Tyrode's solution. Over the 8-h period both V(m) and alpha(K) (i) decreased. However, the decline in V(m) was paralleled by a decrease in the E(K) calculated from alpha(K) (i). At no time was there hyperpolarization of V(m) beyond E(K). After 8 h the Na-K pump was inhibited by exposing the muscles to 0.1 mM ouabain. The onset of an increase in extracellular potassium activity, measured with a double-barrel electrode, was used to mark the amount of depolarization of V(m) due solely to pump inhibition. After hypoxia, V(m) depolarized 8.4+/-4.4 mV before extracellular potassium activity (alpha(K) (e)) increased. Thus, the decrease in alpha(K) (i) during hypoxia is much less than that reported for [K](i). The parallel decline in V(m) and E(K) and the small depolarization of V(m) with ouabain suggest that after prolonged hypoxia the Na-K pump continues to contribute to V(m), but the amount of this contribution is substantially less than previously reported.

Action Potentials↗
PubMed1981

Ouabain effects on intracellular potassium activity and contractile force in cat papillary muscle.

The relationship between the positive inotropic and toxic effects of cardiac glycosides and their effects on intracellular ionic composition is incompletely defined. We measured intracellular potassium activity (alpha ik), extracellular potassium activity (alpha ek), resting potential, action potential duration, and contractile force at 32 degrees C in paired papillary muscles from feline right ventricles exposed to ouabain. Muscles used for electrophysiological measurements were quiescent except for isolated stimulation to confirm impalement and record action potential duration. Muscles used for contractile force measurements were quiescent except for 4-min periods when force was measured at a cycle length of 1,400 ms. Muscle length was adjusted to achieve 50% of maximal tension at this cycle length before each experiment. In four experiments, alpha ik and contractile force were measured in the same muscle. Alpha iK was measured with single and double-barrel K-sensitive electrodes. At 10 nM ouabain, action potential duration is prolonged. Among the concentrations tested, the threshold for a clear positive inotropic effect is 0.1 microM ouabain. The threshold for decrease in alpha iK, increase in alpha eK, and decrease in membrane potential is 1 microM, at which concentration toxic signs develop, including arrhythmias, aftercontractions, and alteration in the staircase response of contractile force to repetitive stimulation. Ouabain need not change alpha iK to effect positive inotropy in ventricular muscle, a relationship different from that reported between [K]i (intracellular potassium concentration) and positive inotropy. Higher ouabain concentrations, which others have shown to clearly inhibit active Na and K transport, are shown to upset intracellular potassium activity homeostasis and to consistently produce toxicity.

Animals↗
PubMed1980

Contractile and biochemical correlates of beta-adrenergic stimulation of the aged heart.

The age dependence of contractile and associated biochemical parameters of basal- and catecholamine-stimulated myocardial contractile performance was investigated using isolated perfused septa from adult and senescent rats. Base-line maximum rate of force development (dF/dt), beta-receptor number and affinity, cAMP levels, and cAMP-dependent protein kinase activity were not different in the two age groups. During maximal isoproterenol stimulation, the increase in dF/dt was 40% less in the senescent hearts, and the cAMP levels and cAMP activation of protein kinase increased two fold but to the same extent in both age groups. The maximum contractile response to dibutyryl cAMP (DBcAMP) in the senescent was half that observed in the adult hearts. However, adult and senescent septa responded equally to an increase in perfusate [Ca2+] to 1.0 mM, which enhanced contractility to the same extent as that obtained with isoproterenol and DBcAMP in adult septa. These data taken together suggest that the factors that limit the contractile response to catecholamines in the senescent heart act subsequent to protein kinase activation but proximal to the Ca2+-troponin interaction.

Adrenergic beta-Agonists↗
PubMed1980

Enhanced contractile response and protein kinase activation to threshold levels of beta-adrenergic stimulation in hyperthyroid rat heart.

The contractile response measured as maximum rate of force development to a near threshold concentration of isoproterenol (1 nM) was enhanced in perfused interventricular septa from hyperthyroid (128+/-4% control) compared with euthyroid rats (105+/-2%, P < 0.01). This enhanced contractile response was accompanied by a significant activation of cyclic (c)AMP-dependent protein kinase (protein kinase activity ratio increased from 0.159+/-0.008 to 0.218+/-0.019, P < 0.005, although no significant changes from base line occurred in euthyroid septa, 0.152+/-0.007-0.179+/-0.012). No difference between hyperthyroid and euthyroid hearts was observed in the contractile response to 0.1 mM dibutyryl cAMP (126.5+/-2.5% and 122.0+/-9.2% in hyperthyroid and euthyroid, respectively), and the magnitude of the response to dibutyryl cAMP was comparable with that observed in the hyperthyroid group with 1 nM isoproterenol. These results suggest that the mechanism for enhanced protein kinase activation and contractile response to low concentrations of isoproterenol in the hyperthyroid heart is at or proximal to cAMP generation. The maximum contractile response to isoproterenol (0.5 muM), however, was decreased in hyperthyroid myocardium (192+/-13%) compared with euthyroid (291+/-37%, P < 0.05). Both protein kinase activity ratio (0.356+/-0.017 and 0.344+/-0.013) and the maximum contractile response to Ca(++) (335+/-15 and 340+/-12% control in hyperthyroid and euthyroid, respectively) were similar, suggesting that the mechanism of the diminished maximum response was distal to protein kinase activation but not a function of an altered Ca(++)-troponin interaction. The diminished maximum rate of force development response in the hyperthyroid hearts was accompanied by significantly less shortening of the contraction duration that was 85.6+/-2.1% control in hyperthyroid vs. 66+/-2.8% control in euthyroid, P < 0.001. Although the basal rate of Ca(++) accumulation was greater in microsomes isolated from hyperthyroid than from euthyroid hearts, there was significantly less additional stimulation of Ca(++) accumulation in response to exogenous cAMP and protein kinase in hyperthyroid compared with euthyroid hearts. This reduction may explain the diminished effect of isoproterenol on the shortening of contraction duration in hyperthyroid compared with the euthyroid myocardium, and may explain, at least in part, the diminished maximum contractile response to isoproterenol.

Adrenergic beta-Agonists↗