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Biomedical subjects

M P Calabrò

Publications and source records attributed to M P Calabrò.

18 recordsLinked to original sources
PubMed2001

Atrial electroanatomic remodeling after circumferential radiofrequency pulmonary vein ablation: efficacy of an anatomic approach in a large cohort of patients with atrial fibrillation.

BACKGROUND: Circumferential radiofrequency ablation around pulmonary vein (PV) ostia has recently been described as a new anatomic approach for atrial fibrillation (AF). METHODS AND RESULTS: We treated 251 consecutive patients with paroxysmal (n=179) or permanent (n=72) AF. Circular PV lesions were deployed transseptally during sinus rhythm (n=124) or AF (n=127) using 3D electroanatomic guidance. Procedures lasted 148+/-26 minutes. Among 980 lesions surrounding individual PVs (n=956) or 2 ipsilateral veins with close openings or common ostium (n=24), 75% were defined as complete by a bipolar electrogram amplitude <0.1 mV inside the lesion and a delay >30 ms across the line. The amount of low-voltage encircled area was 3594+/-449 mm(2), which accounted for 23+/-9% of the total left atrial (LA) map surface. Major complications (cardiac tamponade) occurred in 2 patients (0.8%). No PV stenoses were detected by transesophageal echocardiography. After 10.4+/-4.5 months, 152 patients with paroxysmal AF (85%) and 49 with permanent AF (68%) were AF-free. Patients with and without AF recurrence did not differ in age, AF duration, prevalence of heart disease, or ejection fraction, but the LA diameter was significantly higher (P<0.001) in permanent AF patients with recurrence. The proportion of PVs with complete lesions was similar between patients with and without recurrence, but the latter had larger low-voltage encircled areas after radiofrequency (expressed as percent of LA surface area; P<0.001). CONCLUSIONS: Circumferential PV ablation is a safe and effective treatment for AF. Its success is likely due to both PV trigger isolation and electroanatomic remodeling of the area encompassing the PV ostia.

Atrial Fibrillation↗
PubMed2001

QRS complex voltage changes associated with supraventricular tachycardia.

INTRODUCTION: The aim of this study was to evaluate the changes in ventricular complex voltage associated with narrow QRS supraventricular tachycardia (SVT). METHODS AND RESULTS: One hundred forty-five patients undergoing catheter ablation for SVT, 85 with AV nodal reentrant tachycardia (AVNRT) and 60 with AV reentrant tachycardia (AVRT) due to a concealed accessory pathway, were studied. Four consecutive tachycardia beats and four consecutive sinus beats were analyzed, excluding the last tachycardia complex and the first sinus one. For each of the 12 leads, the QRS complex voltage was measured, and the results of four beats were averaged both in SVT and in sinus rhythm (SR). The sum (sigma) of the QRS voltages measured in the 12 leads during SVT (sigmaSVT) and SR (sigmaSR) were calculated, as well as the QRS axis during SVT and SR. QRS complex voltage was significantly increased during SVT, with respect to SR, in leads II, III, aVR, aVF, and V2 to V6. In addition, sigmaSVT was significantly greater than sigmaSR. Only lead V1 showed a significant voltage decrease during SVT. These voltage changes were almost identical in patients with AVNRT and patients with AVRT. No relationship was found between tachycardia rate and QRS voltage variation. The QRS axis showed a significant shift during SVT, from 55.8 degrees to 64.5 degrees. CONCLUSION: QRS voltage increase occurs in reentrant SVT, independent of the underlying reentrant circuit. The phenomenon likely depends on tachycardia-related reduced ventricular filling. This could result in displacement of the heart in such a way that the left ventricle becomes closer to the precordial electrodes (proximity effect). Alternatively, decreased intracavitary blood mass could diminish the intracardiac short-circuiting of potentials, resulting in augmented transmission of cardiac vectors to the body surface.

Adolescent↗
PubMed1999

Catheter ablation of paroxysmal atrial fibrillation using a 3D mapping system.

BACKGROUND: We treated paroxysmal recurrent atrial fibrillation (AF) with radiofrequency (RF) catheter ablation by creating long linear lesions in the atria. To achieve line continuity, a 3D electroanatomic nonfluoroscopic mapping system was used. METHODS AND RESULTS: In 27 patients with recurrent AF, a catheter incorporating a passive magnetic field sensor was navigated in both atria to construct a 3D activation map. RF energy was delivered to create continuous linear lesions: 3 lines (intercaval, isthmic, and anteroseptal) in the right atrium and a long line encircling the pulmonary veins in the left atrium. After RF application, the atria were remapped to validate completeness of the block lines, demonstrated by late activation of the areas circumscribed by the lines. The mean procedure duration was 312+/-103 minutes (range, 187 to 495), with mean fluoroscopy time of 107+/-44 minutes (range, 32 to 185 minutes). No acute complications occurred, but 1 patient experienced early prolonged sinus pauses and received a pacemaker. During the first day, 17 patients (63%) had AF episodes, but at discharge, 25 patients were in sinus rhythm. After a follow-up of 6. 0 to 15.3 months (average, 10.5+/-3.0 months), 16 patients are asymptomatic, 3 have an almost complete disappearance of symptoms, 1 patient is improved, and 7 patients have their AF attacks unchanged. CONCLUSIONS: Paroxysmal recurrent drug-refractory AF can be treated by RF catheter ablation. Creation of long continuous linear lesions necessary to compartmentalize the atria is facilitated by a nonfluoroscopic electroanatomic mapping system.

Adult↗
PubMed1999

Myocardial ischaemia in neonates with perinatal asphyxia. Electrocardiographic, echocardiographic and enzymatic correlations.

In asphyxiated neonates, hypoxia is often responsible for myocardial ischaemia. To evaluate cardiac involvement in neonates with respiratory distress, ECG and echocardiographic recordings were performed, and cardiac enzymes determined. These data were related to clinical presentation and patient outcome. Three groups of neonates were studied: 22 healthy newborn infants (group I) with 5 min Apgar scores > 9 and pH > 7.3; 15 neonates with moderate respiratory distress (group II) which had Apgar scores ranging between 7 and 9, and pH between 7.2 and 7.3; and 13 neonates with severe asphyxia, Apgar scores < 7, and pH < 7.2 (group III). The ECGs were evaluated according to the 4-grade classification proposed by Jedeikin et al. [8]. On the echocardiograms, fractional shortening and aortic flow curve parameters were taken into account. Serum creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and lactate dehydrogenase were determined. All of groups I and II survived, but 5 out of 13 in group III died within the 1st week. Grade 3 or 4 ECG changes were observed only in group III patients, while all group II and 3 patients of group I showed grade 2 ECG changes. Fractional shortening, peak aortic velocity and mean acceleration were significantly reduced in group III, whereas the only abnormality found in group II was a reduced fractional shortening. CK, CK-MB, CK-MB/CK ratio and lactate dehydrogenase were all increased in group III, while in group II only CK-MB and the CK-MB/CK ratio were abnormal. Severely asphyxiated newborn infants reflect relevant ischaemic electrocardiographic changes, depressed left ventricular function and marked cardiac enzyme increase. These alterations are far less pronounced in neonates with mild respiratory distress.

Asphyxia Neonatorum↗
PubMed1998

Post-ventricular tachycardia P wave change simulating atrial enlargement.

An abnormal P wave was observed in a child affected by prolonged idiopathic ventricular tachycardia (fascicular tachycardia). After sinus rhythm restoration, the P wave was very tall and peaked (0.5 mV in lead II), suggesting a diagnosis of atrial enlargement. No cardiac abnormality, however, was detected by clinical and echocardiographic examination. The P wave abnormality lasted for about 1 month, with progressive voltage and shape normalization. These P wave changes were probably dependent on tachycardia; since the arrhythmia was long-lasting and characterized by atrioventricular dissociation, repetitive atrial contraction against closed atrioventricular valves caused stretching of atrial fibers, resulting in P wave abnormality. This observation suggests that very prolonged ventricular tachycardia may be associated with an electrocardiographic pattern of pseudoatrial enlargement.

Bundle-Branch Block↗
PubMed1992

Electrocardiographic changes associated with haematocrit variations.

The electrical resistivity of intracardiac blood is less than the resistivity of the surrounding tissues. This affects the transmission of cardiac forces to the body surface: the radial forces are enhanced, whereas the transmission of tangential forces is diminished (the Brody effect). Blood resistivity is directly related to haematocrit, hence, haematocrit changes are expected to affect the transmission of cardiac forces, resulting in changes in QRS complex voltage. To assess this hypothesis, a 12-lead electrocardiogram was recorded in 40 patients affected by thalassaemia before and after a transfusion of concentrated red cells. The voltage of each QRS component was carefully measured in every lead, and the sum of all R wave amplitudes (sigma R) was calculated. The post-transfusional electrocardiogram reflected a significant decrease in the R wave amplitude in every lead. sigma R also decreased, whereas S wave amplitude in lead V6 increased. A negative correlation between the ratio of haematocrit pre/post transfusion and that of the corresponding sigma R values was also observed (r = -0.434; P less than 0.01). An increase in haematocrit is therefore associated with a decrease in R wave amplitude. These findings explain why several patients with high haematocrit manifest relatively low voltage QRS complexes.

Adolescent↗
PubMed1992

[Left ventricular false tendon: the most frequent cause of "innocent" murmur in childhood?].

BACKGROUND: The left ventricular false tendon (FT) is an anomalous fibrous or fibromuscular band stretching across the left ventricle. The false tendons extend from the septum to the left ventricular free wall or, more rarely, from the septum to a papillary muscle. The association between FT and innocent cardiac murmur has been pointed out. The aim of the present study was to assess the incidence of FTs in children with a murmur classified as innocent. METHODS: Two groups of subjects were selected. Group A consisted of 253 children with: 1) systolic ejection murmur; 2) normal electrocardiogram and 3) absence of clinical data suggesting cardiac disease. Group B consisted of 240 children clinically free of cardiac disease, and without any cardiac murmur. A FT was diagnosed by means of 2D echocardiogram whenever a linear band stretching across the left ventricular chamber was evident in at least two sections. RESULTS: One hundred and sixty-one children of group A (63.6%) reflected a left ventricular FT; only in 3 patients out of 161 the FT was associated with a small ventricular septal defect, whereas in 158 children the FT was the only abnormal finding. A normal echocardiogram was observed in 71 children (28.1%) of group A; whereas in 21 patients (8.3%) a congenital heart disease was diagnosed. In group B, only 33 subjects (13.8%) had a FT. The different incidence of FT in the two groups (63.6% versus 13.8%) was statistically significant (p less than 0.01). CONCLUSIONS: The study shows that about two thirds of children with innocent heart murmur reflect a left ventricular FT. Furthermore, FT is far more common in subjects with innocent cardiac murmur than in normal subjects. The relationship between FT and murmur thus appears very likely, although not definitely proven.

Adolescent↗
PubMed1991

Ventricular extrasystoles masquerading as aberrantly conducted atrial extrasystoles because of postectopic T wave change.

This presentation reflects a case where broad and bizarre premature QRS complexes are preceded by sinus beats whose T wave is "abnormal," and seems to contain a premature P wave. A diagnosis of atrial extrasystoles with aberrancy thus could be entertained. The extrasystoles, however, are ventricular in origin. The pattern is explained on the basis of postectopic T wave change, that is, the change in configuration of the T wave that occurs in the sinus beat after an extrasystole.

Cardiac Complexes, Premature↗
PubMed1991

[A-V conduction in atrial fibrillation and flutter].

The assessment of A-V conduction in the presence of atrial fibrillation is based upon analysis of the R-R intervals. This is because in atrial fibrillation it is impossible both to identify the impulse that has been conducted to the ventricles, and to measure the A-V conduction time. The first step is, therefore, to evaluate whether the QRS complexes are the expression of conducted atrial impulses, or they are A-V junctional or ventricular in origin. In other words, it is necessary to distinguish between A-V conduction and A-V dissociation. Conduction in atrial fibrillation commonly results in irregular R-R cycles, whereas in the presence of dissociation the R-R cycles are mainly regular. This differentiation can be difficult in the presence of: aberrant conduction; A-V conduction disturbances; or A-V junctional tachycardia with anterograde 2nd degree exit block. The problem occurs both with tachycardia-dependent (or phase 3), and with bradycardia-dependent (or phase 4) aberrant conduction. Distinction between aberration and ectopy is helped by: the sequence long cycle-short cycle; the pause that follows the wide QRS complex; the configuration of the wide QRS complex. Since aberrant conduction may be sustained, due to the linking phenomenon, the pattern may mimick ventricular tachycardia. In atrial flutter the atrial electrical activity is far less chaotic than in atrial fibrillation, so that assessment of A-V conduction is less difficult. Nevertheless, it is impossible to determine exactly which out of the atrial impulses has been conducted, due to the extremely fast atrial rate: the conducted impulse, indeed, is not always the one that immediately precedes the QRS complex. Furthermore, it is also difficult to measure the A-V conduction time, because the F waves follow to each other without any interruption, so that it is impossible to define exactly the beginning of atrial activation. In atrial flutter, thus, as well as in atrial fibrillation, A-V conduction may be assessed by analysis of the R-R intervals, apart from measurement of F-R intervals. In the absence of drugs, atrial flutter is usually associated with 2:1 (or, less frequently, 4:1) conduction ratio, being the odd ratios (3:1, 5:1) far more rare. Due to concealed penetration of non-conducted impulses, A-V conduction intervals are often variable, so that the R-R cycles are irregular even in the presence of a constant A-V conduction ratio. The most common mechanisms leading to irregularity are the alternation of A-V conduction times, and the alternating Wenckebach phenomenon.(ABSTRACT TRUNCATED AT 400 WORDS)

Atrial Fibrillation↗
PubMed1989

[A-V conduction in atrial flutter. Electrocardiographic study].

One hundred and twenty-nine cases of atrial flutter were analyzed to assess the A-V conduction. The R-R intervals, the A-V conduction ratio, and the F-R intervals were measured in each case. Conduction in atrial flutter was defined either as constant or as variable depending on whether the A-V conduction ratio was fixed or variable. Furthermore, atrial flutter was defined as regular whenever the R-R intervals were mathematically related to each other, any interval being a multiple of the F-F cycle. On the other hand, atrial flutter was defined as irregular when the R-R cycles did not reflect a precise mathematical relationship. The R-R intervals in irregular atrial flutter were not exactly multiples of the F-F cycle. This was because the F-R intervals were variable. Sixty-five cases of atrial flutter had constant A-V conduction, whereas 64 cases were associated with variable A-V conduction. Eighty-eight per cent of cases with constant conduction were regular. On the contrary, 91% of cases with variable A-V conduction were irregular. These data reflect a relationship between the constancy of the A-V conduction ratio and the regularity of the R-R intervals. Several mechanisms were identified as being responsible for atrial flutter irregularity. Alternation of the F-R intervals was the most frequent mechanism leading to irregularity of atrial flutter with constant A-V conduction. Alternating Wenckebach periodicity was the most common cause of irregularity in atrial flutter with variable conduction ratio. Concealed conduction of blocked impulses was also frequently involved in determining atrial flutter irregularity.

Atrial Flutter↗
PubMed1984

[Ventricular extrasystole of re-entry originating in the myocardium surrounding a parasystolic focus: a mechanism responsible for the irregularity of the interectopic intervals during parasystole].

We have observed a case of ventricular parasystole in which the ectopic beats occurred often in couplets. The analysis of the interectopic intervals suggests that the first beat of the couplet is parasystolic in origin, whereas the second one is due to a re-entry which takes place in the myocardium surrounding the parasystolic focus. Moreover, our observations lead us to speculate that an occasional supraventricular beat could cause an exit block of the parasystolic focus through a concealed re-entry.

Aged↗
PubMedDate not supplied

[Arrhythmia in thalassemia major: evaluation of iron chelating therapy by dynamic ECG].

Arrhythmias and sudden death represent striking features in the natural history of thalassemia major. Antiarrhythmic treatment, however, does not appear to change the clinical course. During recent years the disease's therapeutics approach has undergone a substantial evolution, being more adequate the transfusional regimens as well as more effective the iron chelation therapy through subcutaneous infusion of deferoxamine. The aim of the present study was to determine possible influences exerted by the current treatment upon disease's arrhythmic disorders. Thirty patients of both sexes were enrolled in the study. The age ranged from 9 to 24 years. No congenital or acquired heart diseases were present. Each patient underwent concentrated red cell transfusions (in order to obtain pretransfusional hemoglobin levels of 10-11 g%), and iron-binding therapy through continuous subcutaneous microinjection of deferoxamine 40-50 mg/kg/day (6-8 hours/day, 6 days/week). Patients were divided in 2 groups: the first group (group A) comprising the 16 patients with good therapeutic compliance and regular pharmacological regimen; the second group (Group B) including the remaining poorly compliant 14 patients. The following parameters were analyzed: age, average hemoglobin levels during the last year, total amount of red cell transfusions, ferritin levels, starting age of iron-binding therapy. Moreover, each patient underwent 24-hour ECG Holter monitoring. Age (Group A: 18 +/- 4.6; Group B: 14 +/- 2.7; p < 0.02), total amount of transfusions (Group A: 272 +/- 73; Group B: 211 +/- 44; p < 0.03), and ferritin levels (Group A: 1697 +/- 860; Group B: 2908 +/- 730; p < 0.002) proved to be significantly different in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗