[Criteria for the production of clinical guidelines (CGL). ANMCO--the Committee for Clinical Research. Assoziazione Nazionale Medici Cardiologi Ospedalieri].
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Biomedical subjects
Publications and source records attributed to M Disertori.
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The spontaneous beat-to-beat variation of atrioventricular (AV) interval was analyzed in time and frequency domains and compared with atrial cycle length (A-A) variability. The analysis was applied in humans at rest and tilt position during sinus rhythm and atrial pacing. The AV intervals showed spontaneous oscillations of small amplitude with a relative standard deviation of 1.8%. Spectral analysis of AV interval series showed the existence of two main oscillatory components at low frequency (LF; 0.04-0.13 Hz) and at high frequency (HF; 0.17-0.4 Hz), synchronous with those of A-A interval series. The same LF and HF fluctuations were found in AV interval variability during atrial pacing. Tilt maneuver inducing a sympathetic stimulation and vagal withdrawal increased LF power and decreased HF power of A-A interval spectra (P < 0.05). On the contrary, tilt decreased the LF (46%, P < 0.05) and HF power (29%, P = NS) of AV conduction spectra. In parallel, tilt decreased (P < 0.0001) the mean A-A interval, leaving the mean AV interval unchanged. When heart rate was held constant by atrial pacing, tilt reduced the mean AV interval, the LF power (65%, P < 0.05), and HF power (10%, P = NS). These results indicate a direct influence of the autonomic nervous system on the LF and HF oscillations of AV conduction. The decrease of AV interval oscillations during tilt demonstrates a marked reduction of autonomic modulation of AV conduction mainly attributable to parasympathetic withdrawal.
BACKGROUND: Slight variation in cycle lengths of common and rapid atrial flutter in humans is an established phenomenon, but its mechanisms have not been completely clarified. In a previous study, we demonstrated that in common atrial flutter the variations in atrial cycle length were due to atrial stretch affecting the revolution time of a reentrant circuit. In the present study, we investigate the nature of atrial cycle length variations in the rapid type of human atrial flutter. METHODS AND RESULTS: Atrial interval variations of 17 episodes of rapid atrial flutter in 14 patients were investigated by measuring the sequence of atrial intervals from intraesophageal or intra-atrial leads and the onset of QRS complexes from a surface lead (V1). To study whether interval variation in flutter cycle was related to ventricular activity, a phase plot was constructed in which the flutter cycle length was plotted against the time after the previous QRS complex. This showed that the interval fluctuations were strictly coupled to the moment of ventricular activation. After the onset of the QRS complex, the rapid atrial flutter interval gradually decreased by an average of 4.1% (P < .001) and reached a minimum value after 300 to 600 milliseconds. Thereafter, the intervals increased again until the next ventricular beat occurred. In 10 patients developing both common and rapid atrial flutter, two different phase relations were found. Whereas during common atrial flutter the atrial interval increased after the QRS complex, it decreased during rapid atrial flutter. In three patients, intra-atrial pressure was recorded together with the electrical activity during both common and rapid atrial flutter episodes. This showed that variations in atrial flutter cycle length were associated with the rise of atrial pressure during ventricular contraction. CONCLUSIONS: These findings indicate a role of contraction-excitation feedback caused by atrial stretch after a ventricular activation. The shortening of the atrial interval after the onset of the QRS complex as found in patients during rapid atrial flutter can be explained by stretch-induced shortening of atrial refractoriness and consequent shortening of the revolution time of a functionally determined intra-atrial circuit.
Acute myocardial infarction is a rare complication of ascending aortic dissection; it is usually due to the coronary ostium involvement. The authors describe an unusual case with anomalous left coronary origin too; they suggest that, due to this combination, the aneurysmatic area pushes the anomalous coronary artery, causing acute myocardial infarction.
A case of severe tricuspid insufficiency with ruptured chordae tendineae due to nonpenetrating major chest trauma caused by a car accident is described. Electrocardiographic signs of complete right bundle branch block and olosystolic murmur were present and not observed before. Transthoracic echocardiography showed a significant prolapse of the septal tricuspid leaflet with severe tricuspid regurgitation and severe right heart overload, which progressively worsened. Transesophageal echocardiography confirmed the transthoracic echocardiographic findings. It also demonstrated the presence of ruptured chordae tendineae and the coexistence of a severe prolapse of the tricuspid anterior leaflet with flail movement. Although the patient remained asymptomatic, these findings prompted us to refer the case to the surgeon. The patient underwent valvuloplasty with excellent late result. In presence of traumatic tricuspid insufficiency the use of transesophageal echocardiography can be helpful to optimize the anatomic evaluation of the valvular apparatus allowing adequate therapeutic decision.
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A family is described in which two brothers (44 and 48 years old) had aortic dissecting aneurysms (the first one died, the other one underwent surgical treatment and is still living) in the absence of clinical features of Marfan syndrome and of systemic hypertension. Two of the six living siblings have aortic dilation on echocardiography. Histologic examination of the aortic wall at autopsy or surgery revealed a loss of elastic fibers, deposition of mucopolysaccaride-like material and medionecrosis. We can postulate a genetically-determined disease of connective tissue usually described as "Marfan's forme fruste".
Here we report on a study of 181 episodes of spontaneous atrial flutter (AF) (mean atrial cycle length 250 +/- 32 msec) treated by transesophageal atrial pacing (TAP) in 138 patients (92 men and 46 women; mean age 59.5 +/- 12.6 years). TAP was effective in 163 episodes (90%); sinus rhythm resumption was immediate in 36 (19.9%) and followed a short period of atrial fibrillation in 64 (35.3%); in 63 episodes (34.8%) a stable atrial fibrillation was obtained. TAP was unsuccessful in 18 cases (10%). All the patients tolerated the procedure well. A statistical elaboration with the Fisher exact test did not evidence a correlation between efficacy and age, sex, atrial cycle length, or underlying heart disease but showed a significant correlation between efficacy and AF duration of less than 1 day (p less than 0.05) and absence of antiarrhythmic pharmacologic pretreatment (p less than 0.01). These data strongly support the immediate first-choice use of TAP in AF therapy.
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Even today there is controversy as regards the best approach to asymptomatic or slightly symptomatic athletes with the WPW syndrome as regards fitness for sports activity, especially in some countries where the doctor is responsible for certifying sports fitness. This study concerns 84 asymptomatic or slightly symptomatic athletes (66 males, 18 females, mean age 21.7 years, range 12-44 years) who underwent a stimulation protocol the end-point of which was the induction of atrial fibrillation (or, if not possible, atrial tachyarrhythmia) in the basal state and during bicycle stress test with transesophageal atrial pacing. The 81 athletes in whom the end-point was reached were divided into two groups: Group I includes the 32 athletes with the shortest R-R interval between pre-excited beats less than or equal to 240 ms in the basal state and/or less than or equal to 210 ms during bicycle ergometer test, Group II includes the other 49 patients. The evaluation during exercise was not carried out in four athletes because of serious haemodynamic compromise due to the arrhythmia induced in the basal state. Only 21/32 athletes would have been included in Group I if only evaluated in the basal state. In 30/81 athletes (37%), there was discrepancy between the result of stimulation and the result of the usual non-invasive evaluation (Holter monitoring, ergometric stress test, ajmaline test). On average, 40 min are required for the performance of the study protocol except when the induced arrhythmia lasts more than 5 min.(ABSTRACT TRUNCATED AT 250 WORDS)
A microprocessor-based timer has been developed for routine and research use in cardiac electrophysiologic studies. The cycle length (A-A) and the conduction times through the right atrium (A(HRA)-A(HIS], the AV node (A-H) and the His-Purkinje system (H-V) can be automatically measured beat-to-beat in real-time both during sinus rhythm and during atrial pacing. The design has been refined during three years of use in over 80 clinical studies. A comparison between manual and automatic measurements has been executed for randomly chosen portions of 10 studies. With the manual measurements as reference procedures the sensitivities of the automatic measurements of the A, H and V waves were 0.98, 0.88 and 0.92, respectively, while the specificities were 0.93, 0.92 and 0.93, respectively. For the true positive measurements the correlation coefficients of the intervals were r(A-A) = 0.9998, r(A-H) = 0.987 and r(H-V) = 0.988. The statistical analysis of the differences between manual and automatic readings for the intervals A-A, A-H and H-V yielded mean values of -1 ms, -0.8 ms and 0.6 ms and standard deviations of 3 ms, 4 ms and 4 ms which are smaller than the accuracy of the common manual measurements.
Flecainide and encainide (class IC) are presently under clinical evaluation in Italy. They prolong the duration of the QRS but not the period of ventricular repolarisation: the prolongation of QT is due solely to the prolongation of the Q-J. Flecainide and encainide are extremely powerful and are suitable for the treatment of reciprocating supraventricular paroxysmal tachycardia and of persistent reciprocating tachycardia, the prophylaxis of WPW atrial fibrillation including cases with a short anterograde refractory period of the anomalous pathway and the treatment of ventricular ectopic beats and ventricular tachycardia. Both drugs are probably effective for the treatment of atrial fibrillation. However, in the case of atrial flutter they are of little effect of sinus rhythm cardioversion; on the other hand they significantly prolong the duration of the A-A interval, with variable results on ventricular rate. Flecainide and encainide have 'parodoxical' arrhythmogenic effects, related to administration dosages, severity of the arrhythmia and seriousness of cardiopathy. Encainide shows peculiar pharmacokinetics due to hepatic oxidating metabolisation and to production of metabolites; among these the O-demethylencainide and the 3-methoxy-O-demethylencainide have an antiarrhythmic activity, which is probably more important than the encainide parent and is longer-lasting. There are 'extensive', 'poor' and 'non-metaboliser' subjects. This results in wide pharmacokinetic inter- and intraindividual variability which must be taken into account during clinical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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The most suitable approach to the athletes with WPW is controversial. Therefore 66 symptom-free athletes with WPW and without heart disease (53 M, 13 F, mean age 21.98 yrs, min 12--max 44) underwent a study protocol whose end-point was the induction of supraventricular tachyarrhythmia, i.e. atrial fibrillation or, if not possible, atrial flutter or atrial tachycardia at rest and during ergometric stress test. The athletes with shortest R-R interval between preexcited beats less than or equal to 240 ms at rest and/or less than or equal to 210 ms during exercise were judged as being at risk i.e. no fit for sport activity. The end-point was reached in 64/66 athletes (in 62 atrial fibrillation). In 4 athletes with life threatening arrhythmia induced at rest the evaluation during exercise was not performed. According to the evaluation at rest we were able to identify only 18 athletes (28.1%) as being at risk, while according to the complete study protocol 26 athletes (40.6%) were judged as such. In 23/64 athletes (36%) this judgement was discordant with the usual non invasive evaluation (i.e. Holter monitoring, ergometric stress test, ajmaline test). During induced atrial fibrillation no significant difference, was found between the percentage of preexcited beats at rest and during exercise. On the average, 40 min. are required for performance of this study protocol (if the induced arrhythmia lasts less than 5 min.). According to our results we conclude: a) the non invasive assessment of the WPW athletes is unsatisfactory; b) the induction of atrial fibrillation during exercise gives a remarkable increase of the diagnostic power with respect to the assessment only at rest; c) since it is simple to perform and not expensive (in time, staff and cost) and because of its high diagnostic yield, we regard this protocol as fundamental for the electrophysiological evaluation of WPW athletes and also suitable for systematic study of WPW patients.
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Here we report on the case of a patient with idiopathic complete AV block and ventricular ectopic beats in basal state. The patient had been asymptomatic until the age of 50 and then suddenly began to suffer from relapsing episodes of syncope, related to "Torsade de Pointe" and Ventricular Fibrillation (hypokalaemia was present at the same time). We deal with the prognostic significance of ventricular ectopic beats and we make the hypothesis that hyperkinetic ventricular arrhythmias play a role in the origin of the symptoms of patients with congenital or idiopathic complete AV block. Finally, we discuss the limits of the therapeutic effectiveness of permanent pacing in these cases.
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