[Diagnosis of total block in the bundle of His with rhythm of idioventricular substitution]. / Diagnosi di blocco totale intra-hissiano con ritmo di sostituzione idioventricolare.

His bundle (HB) recording does not allow the recognition of third degree intrahisian block in patients with complete atrio-ventricular block (AVB) associated with idioventricular rhythm, due to the absence of pacemaker activation in the distal HB region. We have observed fixed retrograde distal HB activation in the standard HB recording of a patient with complete AVB and ventricular rhythm at a rate of 28/min. Retrograde distal HB activation (h'r) did not disappear during apical right ventricular pacing, in association with the complete absence of retrograde nodal conduction: concealed retroconduction into the proximal HB did not allow the recording of anterograde hisian deflection when the interval between h'r deflection and the subsequent sinus atriogram was shorter than 200 msec. Distal HB bipolar pacing using low energy stimulus resulted in 1:1 ventricular response and normal QRS duration in the absence of nodal retroconduction, thus proving the localization of bidirectional block within the HB. The unmasking of retrograde V-h' conduction during idioventricular rhythm was likely related to phase 4 retrograde delay in the branch ipsilateral to the site of the emergency ventricular focus and to the subsequent trans-septal activation of the other side of His-Purkinje system. Referring to arrhythmic problems after DDD pace-marker implantation the localization of complete AV blocks and retrograde conduction patterns are discussed.

[Late potentials, myocardial kinetics and ventricular vulnerability as markers of sudden death after myocardial infarct]. / Potenziali "tardivi", cinetica miocardica e vulnerabilità ventricolare come "markers" di morte improvvisa dopo infarto miocardico.

The 1st myocardial infarction requires the identification of patients who are at high risk of malignant ventricular arrhythmias. Our study group included 55 consecutive patients (age less than 70): all had non-invasive "signal averaging" recording and 24 hour dynamic electrocardiogram at the post-acute phase of their 1st myocardial infarction (MI) and 3 months later. Wall motion abnormalities were evaluated in each patient but two. 24 randomized patients (without documented sustained ventricular tachycardia) underwent right programmed ventricular stimulation at the 3rd month after MI and pathological repetitive responses were evaluated (Table III); they were hemodynamically stable and without persistent ischemia. Late potentials have been compared to spontaneous and induced ventricular arrhythmias, wall motion abnormalities (Table II) and two-year follow-up (Table VI), in order to identify predictive markers of sudden death or malignant arrhythmias. Ventricular late potentials were identified in 28 patients (51%) 4-8 days after MI: mean duration was equal to 75 +/- 33 msec; they did not show any relationship to the site (Table I) and to the extension of necrosis (Table II). Ventricular late potentials had no significant association with myocardial dyskinesia (Table II) while their association with complex ventricular arrhythmias, detected on Holter monitoring within 8 days after MI, and with the induction of repetitive ventricular responses (greater than or equal to 2 complexes) showed significant correlations (respectively p = 0.02; p = 0.01). In regard of the recognition of spontaneous ventricular tachycardia (greater than or equal to 3 complexes) in the follow-up, the detection of late potentials showed 75% sensibility with predictive value equal to 32% (Table V); the combination of late potentials and ventricular dyskinesia exhibited the highest specificity (88%) and predictive value (54%). By the end of follow-up there had been 6 cardiac deaths (2 sudden, 4 from left ventricular failure): late potentials longer than 75 msec were recorded in all patients who had cardiac death; in the post acute phase of MI repetitive ventricular arrhythmias were detected in only 1 of the 2 case of sudden cardiac death and in none of the patients who developed sustained ventricular tachycardia in the follow-up (Table VI). Myocardial dyskinesia was present in each patient who developed non sudden cardiac death (Table VI).(ABSTRACT TRUNCATED AT 400 WORDS)

Electrophysiological study of atrio-ventricular block and ventricular conduction defects. Prognostic and therapeutical implications.

His bundle study with long term follow-up (mean 42 months) was performed in 155 patients (107 with previous syncope, 48 without or with few symptoms). The electrocardiogram showed various conduction abnormalities, but in some cases it was normal. Patients were excluded at the beginning of the study, if they showed sick sinus syndrome, recorded 3rd degree atrioventricular block, angina pectoris, recent myocardial infarction, congenital or surgical cardiac block. In previous studies the diagnostic sensibility and specificity of ajmaline (1 mg/kg/1' i.v.) and overdriving tests have been evaluated. In this study the prognostic meaning of these tests has been evaluated. During a mean 42 months follow-up, 17 patients (10.9%) developed advanced atrioventricular block. A higher risk of developing advanced atrioventricular block below the AV node was detected in patients who showed: basal HV greater than or equal to 65 ms (33% developed advanced atrioventricular block vs 4.7% of patients with basal HV less than 65 ms; p less than 0.001); HV value greater than or equal to 120 ms or 2nd-3rd degree atrioventricular block during ajmaline test (40% progressed to advanced atrio-ventricular block vs 0.85%; p less than 0.001); HV prolonged greater than 10 ms or 2nd-3rd degree atrioventricular block during atrial pacing (40% progressed to a atrioventricular block vs 3.4%; p less than 0.001) regardless of previous syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

[Non-invasive recording of the His bundle electrogram: choice of leads and reliability of the "averaging" technic]. / Riconoscimento non invasivo dell'elettrogramma hisiano: scelta delle derivazioni e attendibilità della tecnica di "averaging".

An improvement in detecting His bundle activity using a Marquette high resolution Mac unit, without pharmacologic depression of AV node conduction, was obtained with two surface lead systems, which were selected on the basis of the His bundle anatomical position and its electrostimulation axis. In 8 patients the direction of the His bundle bipolar stimulation vector was evaluated in the frontal plane, on the orthogonal leads and with map of the chest potential. In 39 patients the surface recording, using high-gain amplification, filtering between 50-300 Hz and an averaging of 256-512 cycles, was obtained by positioning the electrodes in the following sites: manubrium sterni-xiphisternum-V4. When this lead system failed, it was replaced by another one, which included V4-right sternal and right vertebral border at the level of the 3rd intercostal space. In 24 patients (PR less than 0.16" in 4 cases) intracavitary and surface H-V recording were compared. The surface interval was measured between the apex of the surface "blip" and onset of the QRS. Sensitivity was 86% with a good correlation (r = 0.94) between invasive and non-invasive measurements. The surface leads, in which the His bundle activity was best detected, were the manubrium-xiphisternum (on the midsternal line) and V4-right vertebral border at the 3rd intercostal space level. Our external measurement technique avoids subjective misinterpretations; the surface H-V interval was on an average 6 msec. shorter than the invasive one. The upper normal value of non-invasive H-V interval is therefore 50 msec in our measurement method.

[Damages of malfunction of the electrostimulating system (author's transl)]. / Guasti o malfunzioni del sistema elettrostimolante.

In this study we describe the damages, or the ill-functioning of the electrostimulating system due to failure or bad functioning of the catheter electrode, of the electronic circuits and of the energy sources. Complications due to iatrogen causes or to clinical pathology have not been dealt with. Defects of electrostimulation are described in their clinical, electrocardiographic, oscilloscopic and electrophysiologic aspects, and in the operative report, through the study of 1455 cases. In the differential diagnosis of the defects of electrostimulation we point out their biological causes. The sheath interruption, observed in 31 cases, causes defects in electrostimulation, depending on the extension and on the position of the unsheathing. The circuit variations can be compared with the effect produced by a shunt capacitor. The sheath interruption causes a current reduction which reaches stimulating surface and the differential diagnosis concerns the electronic failure of the generator, the battery discharge, the organic liquid infiltration in the insertion point, the position of the catheter, and the tip perforation of it. The breaking of the spiral (in 6 cases) can be partial or total, and may be compared to the forming of a series capacitor between the electrodes which may sham the increase of the myocardic threshold. The stimulating surface, too wide respecting the intensity supplied by the electrostimulator, brings about a low current density and failures in electrostimulation; the difference between such condition and the one caused by a high myocardiac threshold is shown by determining the safety factor. A very small stimulating surface increases the electrode impedance and may cause a defect of the perception function, if the generator input impedance (4 cases) is reduced. The fall of the output voltage may be caused by a battery discharge, and is the most frequent cause of electrostimulation disturbances; it has been observed in 432 cases. Other causes of the fall of the output voltage (30 cases) are the outflow of mercury from the cells, or mycotic formations. The ill-functionning or the loss of perception (9 cases) caused by defects of the electrostimulator must be distinguished from the ones caused by the endocavitarian potential reduction (myocardiac infarction, conduction disturbances: 2 cases). Variations of the stimulating cycle can be caused by ageing, humidity on resistances and on oscillator condensers (9 cases). Accelerated stimulating was observed in 1 case, plate corrosion in 3 cases, high density of anodic current in 9 cases, generator turnover in 3 cases. Finally we give the chief points of electrical stimulating disturbances due to interferences of electromagnetic radiation.

[Hyperglycemia in acute myocardial infarction (author's transl)]. / Sull'iperglicemia della fase acuta dell'infarto miocardico.

50 non-diabetic patients, less then 70 y.o. and with fasting blood sugar (FBS) subsequently proved to be normal, consecutively admitted to the Coronary Care Unit by the 10th hour of acute myocardial infarction (AMI), have been studied. Blood sugar (BS) and white blood cell count (WBC) on admission and serum CPK every four hour until the 36th hour, have been determined. Oral glucose tolerance test (OGTT) has been performed at least one week later, when FBS has been determined. In 16 patients with normal OGTT the test has been repeated twice, 4 to 15 months later, before and after a cortisone load. Data have been statistically computed. Mean blood sugar on admission was significantly higher then mean FBS. No correlation was found between BS and WBC neither between BS and maximal CPK. No significant difference has been found between the mean BS on admission among 25 patients with normal OGTT and the one among the remaining 25 patients with abnormal OGTT. The OGTT was confirmed to be normal in the 16 patients belonging to the former group, who had the test repeated, with a single exception as far as the cortisone-OGTT is concerned. The above results are consistent with the opinion that the hyperglycemia usually observed during the first hours of AMI, is related to the acute medical stress and in no way indicates subclinical and/or latent diabetes.

[Echocardiographic study of the Björk-Shiley disc prosthesis (author's transl)]. / Studio ecocardiografico delle protesi a disco di Björk-Shiley

The echocardiography of 25 patients with Björk-Shiley disc prosthesis (16 aortic, 7 mitralic, 1 both mitralic and aortic and 1 both mitralic and tricuspidal) was studied. Mitralic prosthesis were placed with the shortest disc segment looking forward; aortic prosthesis faced the shortest disk segment looking towards the coronaric sinus. The echo's morphology is related to the multiple relationships among position and direction of the prosthesis and the probe. In the aortic echocardiogram, it is possible to recognize echoes from the ring dissociated by anterior and posterior aortic walls. Between them echoes corresponding to the open disc appear, making a quadrangular figure. The values of the internal diameter of the ring obtained were very similar to the real value (difference 0-1 mm). Mitralic echocardiogram is characterized by the valvular disc movement tracing the typical quadrangular pattern, which is due to its opening and closure. Echoes of the supporting apparatus can be recorded directing the probe toward the heart base. In aortic and mitralic prosthesis, disc movements can be estimated. Opening and closure speed rate and their correlation vary on a large scale, both within different patients and in the same patient. Maximum disc excursion appears to be a more homogeneous and constant data in long-term controls and can be used to estimate valvular functionality: in aortic prosthesis valve the obtained value (mean = 17.46 +/- 0.53 "ES") is similar to the real diameter of the disc, in mitral prosthesis valve the value obtained (mean = 17.50 +/- 0.74 "ES") is shorter than the real value.

Influence of "Polarizing" infusions on anthiarrhythmic effects of beta-blockers.

The antiarrhythmic effect of practolol (0.30 mg/kg) was studied in 25 patients pretreated with infusion of glucose-insulin (GI) solution. GI solution showed an antiarrhythmic effect either after or before the beta-blocker with pH in normal range or compensated metabolic acidosis. GI infusion produced a metabolic acidosis and an arrhythmogenic effect in some cases. Practolol had no antiarrhythmic effect in patients with VPB and GI infusion raised metabolic acidosis.