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Biomedical subjects

A Branzi

Publications and source records attributed to A Branzi.

At least 55 records · Page 3Linked to original sources
PubMed2000

Predictors of atrial defibrillation threshold in internal cardioversion.

This study examined the clinical, echocardiographic, and electrophysiological factors influencing the atrial defibrillation threshold (ADFT) in patients with chronic, persistent AF undergoing transvenous, low energy, atrial cardioversion. Twenty-two patients (age 57 +/- 15 years) with a mean AF duration of 7.8 +/- 7.1 months (range 2-32 months) underwent internal cardioversion with catheters placed in the right atrium and coronary sinus. Biphasic shocks (3/3 ms) were delivered in a step-up protocol. ADFT was defined as the lowest energy shock that converted AF to sinus rhythm. All patients were successfully cardioverted at a mean ADFT of 5.62 +/- 2.82 J (range 2.6-12.9 J). Fifteen variables, including clinical characteristics (age, body mass index, AF duration, etiology), echocardiographic measurements (atrial diameter and volumes, indexes of ventricular performance), hemodynamic measurements, and mean atrial cycle during AF were analyzed as possible predictors of ADFT. In univariate regression analysis, AF duration, mean RR interval, and cardiac index correlated with ADFT. In multivariate regression analysis, AF duration remained as the only significant predictor of ADFT (B coefficient 0.311, P < 0.001; 95% confidence interval [CI] 0.194-0.427). AF duration was the most powerful predictor of ADFT. It should be considered when planning internal CV of AF to limit the number of shocks delivered. Furthermore, long intervals between AF onset and CV should be avoided.

Atrial Fibrillation↗
PubMed2000

Repolarization changes in a double-blind crossover study of dofetilide versus sotalol in the treatment of ventricular tachycardia.

UNLABELLED: The aim of this study was to determine whether a therapeutic response to Class III antiarrhythmic drugs is related to predictable changes in repolarization on the electrocardiogram (ECG). A group of 57 patients with ischemic heart disease and inducible ventricular tachycardia (VT) at electrophysiological study (EPS) were selected from a population enrolled in a randomized double-blind crossover study of dofetilide (500 micrograms bid) versus sotalol (160 mg bid). ECGs were analyzed blindly, and RR, QT (maximum value/12 leads), QTc (Bazett's formula), QT dispersion (QTmax-QTmin over 12 leads) and QTc dispersion, were calculated at baseline and on the third day of treatment (4 hours after dosing), when patients underwent EPS to test the effects of study drugs on VT inducibility. RESULTS: At EPS 21 patients were responders to dofetilide and 22 to sotalol. On day 3, a significant increase in QT and QTc and decrease in QT and QTc dispersion, compared to baseline, was measured in responders and nonresponders, with both dofetilide and sotalol. No significant difference in QTc or QT dispersion between responders and nonresponders was observed in either treatment group. In conclusion, treatment with dofetilide and sotalol was associated with an increase in QT and QTc, and a decrease in QT and QTc dispersion. In contrast with previous reports, a differential effect on QT or QTc dispersion was not observed in drug responders versus nonresponders.

Anti-Arrhythmia Agents↗
PubMed2000

Evaluation of myocardial injury following repeated internal atrial shocks by monitoring serum cardiac troponin I levels.

INTRODUCTION: Electrical shocks delivered for atrial cardioversion (CV) may cause myocardial damage. The aim of this study was to assess the extent of myocardial injury caused by repeated intracardiac shocks delivered for low-energy internal atrial CV. METHODS AND RESULTS: Thirty-five patients with chronic persistent atrial fibrillation (AF) of different etiologies underwent CV with delivery of synchronized biphasic shocks (3.0/3.0 ms) between two catheters positioned in the right atrium and the coronary sinus. Shocks were delivered according to a step-up protocol (50 V, 180 V, then steps of 40 to 56 V up to 500 V, if necessary). In 23 patients, AF was reinduced after baseline CV, and CV was repeated. Myocardial injury was monitored by measuring cardiac troponin I (cTnI) serum concentrations in blood samples taken at baseline and at 2, 4, 8, 12, and 24 h after the procedure, by means of an immunoenzymologic assay (normal values, < or =0.6 ng/mL). A mean (+/- SD) of 6.9 +/- 3.4 shocks per patient were delivered (range, 2 to 17). Shocks delivered in each patient had a maximal energy of 7.3 +/- 4.0 J (range, 1.7 to 15.7). In 20 patients (57%), no evidence of myocardial injury (cTnI level, < or = 0.6 ng/mL) was found. In 13 patients (37%), mildly elevated cTnI levels (range, 0.7 to 1.4 ng/mL) in samples taken 4 to 12 h after CV suggested minor myocardial injury. In two patients (6%), higher cTnI levels were found in samples taken 4 to 8 h after CV (peak, 1.7 and 2.4 ng/mL), indicating a necrotic damage. Patients with no cTnI elevation, with mild cTnI elevation, or with cTnI levels >or =1.5 ng/mL did not differ significantly with respect to the total number of shocks delivered, the mean amount of energy delivered, and the cumulative amount of energy delivered. No clinical complications were observed. CONCLUSIONS: Following internal CV with the delivery of repeated shocks, minor elevations of cTnI serum levels could be detected in a significant proportion of patients, and this suggests subtle asymptomatic minor myocardial injury. The elevations of cTnI levels do not appear to be related to the number of shocks or to the amount of energy delivered.

Adult↗
PubMed2000

Increasing plasma homocysteine during follow-up in heart transplant recipients: effects of folate and renal function.

BACKGROUND: Hyperhomocysteinemia is a common finding in heart transplant recipients and may represent a risk factor for graft failure. However, the time-course, determinants and effects of medical therapy on total homocysteine plasma levels after heart transplantation remain undetermined. The aim of this study was to prospectively analyze 1) the time-course of total homocysteine in heart transplant recipients; 2) the effects of folate supplements and cyclosporine A on total homocysteine; 3) the relation among renal function, serum vitamin levels, and total homocysteine. METHODS: Fifty-two heart transplant recipients consecutively evaluated for routine follow-up during 1998 were included in the study (mean age 54 +/- 12 years; 28% female). Among the 52 patients, 10 patients were treated with folate for the entire period of the study (Group F), while 26 patients never received folate (Group NF). The remaining 16 patients who did not take folate on a regular basis were excluded from subgroup analysis. Total homocysteine and creatinine plasma levels were assayed at entry into the study (time 0) and at the end of the study, 12 months later (time 12). RESULTS: Homocysteinemia increased significantly from time 0 to time 12 (p < 0.001), regardless of creatinine plasma levels (p = 0.03) and folate intake (p < 0.01). However, total homocysteine levels were lower in Group F compared to Group NF at time 0 and time 12 (p < 0.02). On multivariate analysis, time of follow-up, serum creatinine and lack of folate intake were positive independent predictors of total homocysteine. CONCLUSIONS: Homocysteinemia increased over time in heart transplant recipients, regardless of renal function and folate administration. Lower total homocysteine levels were associated with folate intake, suggesting that folate supplements may play a role in the prevention of vascular allograft disease.

Creatinine↗
PubMed2000

[Interventional or conservative approaches in acute coronary syndromes].

The past decade has witnessed a dramatic expansion in the scope of both mechanical and pharmacologic methods for treating patients with acute coronary syndromes. New device technologies, such as intracoronary stenting, more potent and more fibrin-specific thrombolytic agents, and new antithrombotic and antiplatelet drugs are now available. What is the best strategy to treat patients with acute coronary syndromes still remains a matter of debate. This article briefly reviews this topic.

Acute Disease↗
PubMed2000

[Critical analysis of beta blockers in heart failure: certainty and incompleteness].

Heart failure is one of the commonest debilitating conditions of industrialized society, with mortality and morbidity comparable with that of the common neoplastic diseases. The role of beta-blockers in heart failure has been the subject of debate for many years. The results of recent prospective, placebo-controlled studies of the addition of beta-blockers to standard therapy in patients with chronic heart failure have confirmed a significant beneficial effect on ventricular function, clinical status, morbidity and mortality. The importance of these trials suggests that beta-adrenergic blocker therapy can save one life out of every 35 patients treated with mild-to-moderate heart failure. These major trials have used one of four beta-blockers (metoprolol, bisoprolol, carvedilol, or bucindolol) in varying study designs with different patient populations. Beta-blockers improve function of the failing left ventricle, prevent or reverse progressive left ventricular dilation, chamber sphericity, and hypertrophy, and consequently have a positive impact on cardiac remodeling. Beta-blockers also reduce heart rate and left ventricular wall stress, leading to reduced myocardial oxygen consumption, a clear benefit to the failing heart. Moreover, beta-blockers can improve the intrinsic contractile function of cardiomyocytes and have been shown to improve myocardial energetics in heart failure, possibly through desirable changes in substrate utilization. Many important clinical questions still remain unanswered. These questions include whether beta-blockers are of benefit in patients with severe NYHA functional class (IIIB-IV), in patients with asymptomatic left ventricular dysfunction, in the extreme elderly, in patients with diabetes mellitus and renal impairment. Furthermore, it is not clear whether beta-blockade by itself is the real mechanism of clinical benefit. Although certain effects of beta-blockers may be considered class effects, it is not yet clear whether there are differences between beta 1-selective antagonists and nonselective agents. Major studies are currently being undertaken to address the above questions.

Adrenergic beta-Antagonists↗
PubMed1999

Transvenous internal cardioversion for atrial fibrillation: a randomized study on defibrillation threshold and tolerability of asymmetrical compared with symmetrical shocks.

UNLABELLED: The aim of the study was to compare, according to a randomized cross-over design, two different biphasic waveforms (6.5/2.5 ms and 3.0/3.0 ms phases duration, respectively) for low energy internal atrial cardioversion with regard to energy requirements for cardioversion and shock induced discomfort. METHODS: Nineteen patients with chronic persistent atrial fibrillation (AF)(mean duration 16+/-20 months) were submitted to internal atrial cardioversion (shock delivery between catheters in right atrium and coronary sinus, respectively) and were randomly allocated to baseline cardioversion with an asymmetrical biphasic shock (6.5/2.5 ms) or with a symmetrical biphasic shock (3.0/3.0 ms), according to a step up protocol. After baseline cardioversion, a sustained AF was reinduced and the patients crossed to the alternative waveform. The procedure was performed without routine administration of sedatives and shock induced discomfort was monitored by a subjective score (1 to 5). Sedatives or anesthetics were administered at patient's request. RESULTS: The procedure was effective in all the patients and was performed without need for sedatives/anesthetics in 17/19 patients (89%). Leading edge voltage of effective shocks resulted lower for asymmetrical shocks compared to symmetrical shocks (290+/-76 vs. 337+/-104 V, P<0.001) with no statistically significant differences in delivered energy (7.74+/-4.25 vs. 8.65+/-5.94 J). Moreover shock induced discomfort resulted lower for asymmetrical shocks compared to symmetrical (pain score=4.18+/-0.73 vs. 4.59+/-0.62, P<0.02). Shock impedence of effective shocks was 59+/-10 ohms for both waveforms. No significant complications occurred during the procedure and no ventricular arrhythmia was observed after atrial cardioversion. Transient bradycardia requiring support ventricular pacing was observed in one patient. CONCLUSIONS: Delivery of biphasic asymmetrical shocks (6.5/2.5 ms) results in lower leading edge voltage of effective shocks and better patients tolerability compared with conventional biphasic symmetrical shocks (3.0/3.0 ms). These findings are of interest both for transvenous internal cardioversion of chronic persistent AF and for implantable atrial defibrillators.

Adult↗
PubMed1999

Long-term arterial patency after coronary reperfusion.

Coronary reocclusion is a frequent event after reperfusion and may be responsible for the deterioration of left ventricular function. It may occur early as well as in the chronic phase after hospital discharge. Current, evidence based, strategies to prevent reocclusion include antiplatelet and anticoagulant agents as well as the use of intracoronary stenting in those patients who are treated by PTCA. The combination of aspirin and ticlopidine adds on the results of stenting. Further treatments are currently investigated and may significantly improve the long-term coronary patency.

Angioplasty, Balloon, Coronary↗
PubMed1999

Effects of wave reflection timing on left ventricular mechanics.

UNLABELLED: The aim of this study was to evaluate how the timing of the pressure pulse produced by peripheral reflection affects the left ventricle (stroke volume, ventricular work, coronary driving pressure). Ten isolated perfused rabbit hearts were attached to rubber tubes of different lengths (0.5, 0.8 and 1 m) connected to a hydraulic resistance. The different lengths produced reflections at different times and the reflected pulse returned to the ventricle in early (at 84 ms), middle (at 134 ms) and late systole (at 168 ms) for the three tubes, respectively. The loading parameters (ventricular filling pressure and hydraulic resistance) were not changed during the procedure. Ventricular and aortic pressure and aortic flow were monitored continuously and recorded; cardiac cycle was fixed at 800 ms. An operator-independent procedure was used to calculate instantaneous and total systolic external work, mean diastolic aorto-ventricular pressure difference and ventricular stroke volume. RESULTS: The mean value of stroke volume for the three different length rubber tubes was 320 +/- 71, 348 +/- 77 and 368 +/- 87 microliters, respectively. The mean value of total external work was 20.3 +/- 8.3, 22.5 +/- 8.8 and 24.2 +/- 9.6 mJ, respectively. The mean aortoventricular pressure difference was 40 +/- 12, 46 +/- 13, 50 +/- 14 mmHg, respectively (1 mmHg = 133 Pa). The differences between the parameters measured in the three conditions were statistically significant (p < 0.05). A reduction of reflection timing, reduces, on a pure mechanical basis, cardiac output and external ventricular work and has a negative effect on coronary driving pressure.

Animals↗
PubMed1999

Favorable effects of flecainide in transvenous internal cardioversion of atrial fibrillation.

OBJECTIVES: The aim of the study was to evaluate the effects of intravenous (IV) flecainide on defibrillation energy requirements in patients treated with low-energy internal atrial cardioversion. BACKGROUND: Internal cardioversion of atrial fibrillation is becoming a more widely accepted therapy for acute episode termination and for implantable atrial defibrillators. METHODS: Twenty-four patients with atrial fibrillation (19 persistent, 5 paroxysmal) underwent elective transvenous cardioversion according to a step-up protocol. After successful conversion in a drug-free state, atrial fibrillation was induced by atrial pacing; IV flecainide (2 mg/kg) was administered and a second threshold was determined. In patients in whom cardioversion in a drug-free state failed notwithstanding a 400- to 550-V shock, a threshold determination was attempted after flecainide. RESULTS: Chronic persistent atrial fibrillation was converted in 13/19 (68%) patients at baseline and in 16/19 (84%) patients after flecainide. Paroxysmal atrial fibrillation was successfully cardioverted in all the patients. A favorable effect of flecainide was observed either in chronic persistent atrial fibrillation (13 patients) or in paroxysmal atrial fibrillation (5 patients) with significant reductions in energy requirements for effective defibrillation (persistent atrial fibrillation: 4.42+/-1.37 to 3.50+/-1.51 J, p < 0.005; paroxysmal atrial fibrillation: 1.68+/-0.29 to 0.84+/-0.26 J, p < 0.01). In 14 patients not requiring sedation, the favorable effects of flecainide on defibrillation threshold resulted in a significant reduction in the scores of shock-induced discomfort (3.71+/-0.83 vs. 4.29+/-0.61, p < 0.005). No ventricular proarrhythmia was observed for any shock. CONCLUSIONS: Intravenous flecainide reduces atrial defibrillation threshold in patients treated with low-energy internal atrial cardioversion. This reduction in threshold results in lower shock-induced discomfort. Additionally, flecainide may increase the procedure success rate in patients with chronic persistent atrial fibrillation.

Adult↗
PubMed1999

Evaluation of atrial refractoriness and atrial fibrillation inducibility immediately after internal cardioversion in patients with chronic persistent atrial fibrillation.

OBJECTIVE: To prospectively evaluate right atrial refractoriness and sustained atrial fibrillation (AF) inducibility at programmed electrical stimulation in two groups of patient: a series of patients with chronic persistent AF, studied immediately after successful low energy internal atrial cardioversion, and a group of control patients without history of supraventricular arrhythmias. PATIENTS: Nineteen patients with chronic persistent AF (mean AF duration 11 +/- 10 months, range 2-61 months) submitted to successful internal low energy atrial cardioversion in fully conscious state and 11 control patients without history of supraventricular arrhythmias. METHODS: An electrophysiological evaluation was performed to measure atrial refractoriness and AF inducibility, by delivering single atrial extrastimuli in high right atrium, at decremental coupling, during spontaneous sinus rhythm and after 8 beats at 600, 500, 400 and 330 ms cycle length. If sustained AF was induced the protocol was terminated. RESULTS: During programmed atrial stimulation sustained AF was induced in 8 out of 19 (42%) of the AF patients but in none of the control group. Atrial effective refractory period was significantly shorter in AF patients compared to controls both at basic cycle length, at 600 ms, 500 ms and 400 ms cycle length, meanwhile no statistically significant differences were found at 330 ms cycle length. An altered relationship between atrial effective refractory period and cycle length was found in AF patients compared to controls: the slope of linear correlation slope was significantly lower in AF group than in controls (0.04 +/- 0.07 vs 0.17 +/- 0.10, p < 0.002). CONCLUSIONS: Marked abnormalities of atrial refractoriness and of its heart rate relationship are observed after internal cardioversion of chronic persistent AF in humans and these abnormalities are associated with an high vulnerability to AF. These observations may explain the high risk of AF recurrences in the early phases following successful cardioversion. In this scenario antiarrhythmic drug therapy seems to be mandatory for reducing arrhythmia relapses.

Adult↗
PubMed1999

A randomized placebo-controlled trial of fluvastatin for prevention of restenosis after successful coronary balloon angioplasty; final results of the fluvastatin angiographic restenosis (FLARE) trial.

BACKGROUND: The 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors competitively inhibit biosynthesis of mevalonate, a precursor of non-sterol compounds involved in cell proliferation. Experimental evidence suggests that fluvastatin may, independent of any lipid lowering action, exert a greater direct inhibitory effect on proliferating vascular myocytes than other statins. The FLARE (Fluvastatin Angioplasty Restenosis) Trial was conceived to evaluate the ability of fluvastatin 40 mg twice daily to reduce restenosis after successful coronary balloon angioplasty (PTCA). METHODS: Patients were randomized to either placebo or fluvastatin 40 mg twice daily beginning 2-4 weeks prior to planned PTCA and continuing after a successful PTCA (without the use of a stent), to follow-up angiography at 26+/-2 weeks. Clinical follow-up was completed at 40 weeks. The primary end-point was angiographic restenosis, measured by quantitative coronary angiography at a core laboratory, as the loss in minimal luminal diameter during follow-up. Clinical end-points were death, myocardial infarction, coronary artery bypass graft surgery or re-intervention, up to 40 weeks after PTCA. RESULTS: Of 1054 patients randomized, 526 were allocated to fluvastatin and 528 to placebo. Among these, 409 in the fluvastatin group and 427 in the placebo group were included in the intention-to-treat analysis, having undergone a successful PTCA after a minimum of 2 weeks of pre-treatment. At the time of PTCA, fluvastatin had reduced LDL cholesterol by 37% and this was maintained at 33% at 26 weeks. There was no difference in the primary end-point between the treatment groups (fluvastatin 0.23+/-0.49 mm vs placebo 0.23+/-0.52 mm, P=0.95) or in the angiographic restenosis rate (fluvastatin 28%, placebo 31%, chi-square P=0.42), or in the incidence of the composite clinical end-point at 40 weeks (22.4% vs 23.3%; logrank P=0.74). However, a significantly lower incidence of total death and myocardial infarction was observed in six patients (1.4%) in the fluvastatin group and 17 (4.0%) in the placebo group (log rank P=0.025). CONCLUSION: Treatment with fluvastatin 80 mg daily did not affect the process of restenosis and is therefore not indicated for this purpose. However, the observed reduction in mortality and myocardial infarction 40 weeks after PTCA in the fluvastatin treated group has not been previously reported with statin therapy. Accordingly, a priori investigation of this finding is indicated and a new clinical trial with this intention is already underway.

Angioplasty, Balloon, Coronary↗
PubMed1999

Low energy internal atrial cardioversion in atrial fibrillation lasting more than a year.

UNLABELLED: The aim of this study was to evaluate the efficacy of low energy internal atrial cardioversion in restoring sinus rhythm (SR) in patients with chronic atrial fibrillation (AF) persisting > 1 year. Fifteen patients with chronic AF lasting > 1 year (from 13-48 months, mean 24 +/- 13 months) were studied. R wave synchronized 3/3 ms biphasic shocks were delivered between right atrial and coronary sinus (left pulmonary artery in five patients) electrodes. Sedatives or anesthetics were administered only at the patient's request. RESULTS: Stable SR was restored in 14 (93%) of 15 patients after shocks with a mean leading edge voltage of 377 +/- 77 V (range 260-500) and a mean delivered energy of 7.3 +/- 3.4 J (range 2.6-12.9). The procedure was performed without anesthesia in 6 (40%) patients. All successfully cardioverted patients were treated with flecainide, sotalol, or amiodarone. During a follow up of 7.7 +/- 7.9 months (range 1-24) AF recurred in five (36%) patients. Three of five AF recurrences occurred within 3 days after conversion to SR. CONCLUSION: Internal low energy atrial cardioversion is highly effective in restoring SR even in patients with AF lasting > 1 year. The long-term results from the standpoint of freedom from AF recurrences, are satisfactory, although additional antiarrhythmic treatment is required, particularly in the first days after conversion.

Anti-Arrhythmia Agents↗
PubMed1999

Electrophysiological effects of flecainide and propafenone on atrial fibrillation cycle and relation with arrhythmia termination.

OBJECTIVES: (1) To investigate the electrophysiological effects of flecainide and propafenone during atrial fibrillation, and their relation to arrhythmia termination; (2) to investigate the effects of isoprenaline on atrial fibrillation in basal conditions and during treatment with class 1C drugs to evaluate the role of adrenergic stimulation on proarrhythmic events occurring during this treatment. DESIGN: Prospective, single centre study. SETTING: University hospital. METHODS: 10 patients with lone paroxysmal atrial fibrillation underwent an electrophysiological study. The dynamic behaviour of MFF (the mean of 100 consecutive atrial fibrillation intervals) was evaluated at two atrial sites after induction of atrial fibrillation either at baseline or after class 1C drug administration (flecainide or propafenone 2 mg/kg). The effects of isoprenaline on MFF and RR interval were also investigated both under basal conditions and during class 1C drug treatment. RESULTS: After induction of atrial fibrillation, mean (SD) MFF shortened with time, and was further shortened by isoprenaline infusion (177 (22) v 162 (16) v 144 (11) ms, p < 0.05). The administration of class 1C drugs reversed this trend and significantly increased the MFF to an average of 295 (49) ms, leading to conversion to sinus rhythm within 10 minutes in all patients. Atrial fibrillation was then reinduced on class 1C drugs: isoprenaline shortened the MFF and RR interval with a trend to AV synchronisation (223 (43) v 269 (49) ms for the MFF, 347 (55) v 509 (92) ms for the RR, p < 0.05); 1:1 sustained AV conduction occurred in two patients, at 187 and 222 beats/min respectively. One of these patients underwent electrical cardioversion because of haemodynamic collapse. CONCLUSIONS: Class 1C drugs are effective at restoring sinus rhythm by increasing the MFF to a much greater extent than observed in self terminating atrial fibrillation episodes, and reversing the spontaneous atrial fibrillation behaviour (progressive shortening of MFF and self perpetuation of atrial fibrillation). MFF prolongation with 1:1 conduction at fast ventricular rates may lead to synchronisation during adrenergic stimulation, with a very short ventricular cycle; hence it is advisable to keep the patients at rest after acute class 1C drug loading or to consider pharmacological modulation of AV conduction for patients who are prone to a fast ventricular response.

Adrenergic beta-Agonists↗