[Disturbances of AV and/or IV conduction in sick sinus syndrome. Prevalence, evolution and clinical significance].
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Biomedical subjects
Publications and source records attributed to D D'Este.
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The clinical significance of corrected sinus node recovery time (CSNRT) and the natural and unnatural history of sinus node dysfunctions are not completely known. To gain some insight into this problem, 101 patients (pts) (54M, 47F, mean age +/- SD = 62.02 yrs +/- 14.42) with clinical and ECG signs of definite or suspected sick sinus syndrome (SSS) underwent an electrophysiologic study and then were prospectively followed for a mean period of 44.36 months +/- 18.96 (range: 2-78 months). The pts were divided into two groups: 1) Group A: 68 pts with prolonged CSNRT (greater than 500 msec); 2) Group B: 33 pts with normal CSNRT. Thirty-three pts of Group A (48.5%) and 2 pts of Group B (6.1%) received VVI pacemaker implantation (PM) immediately after the electrophysiologic study. The following results were obtained: 1) Pts of Group A showed a higher prevalence of organic heart disease and of ECG signs of definite SSS than pts of Group B. (p less than 0.05). Moreover, the higher the CSNRT in Group A pts, the more severe the ECG abnormalities of SSS. 2) Pts without PM, both of Group A and Group B, noted during the follow-up period a disappearance of neurological symptoms (syncopes and/or dizziness) and of ECG abnormalities of SSS in more than 50% of the cases. However, this was less evident in Group A pts compared with Group B pts (53.8% vs 78.6% regarding neurological symptoms and 54.3% vs 74.1% regarding ECG abnormalities of SSS) as well as in pts with organic heart disease in comparison with those with primitive SSS. Moreover, the number of pts who needed PM implantation during the follow-up period due to the worsening of clinical and ECG signs of SSS were higher in Group A than in Group B (20% vs 6.5%). The occurrence of cardiac death among the pts without PM was similar in pts of Group A (8.5%) and in those of Group B (9.7%). One pt of Group A without PM died suddenly (less than 1 hour). 3) Pts who required PM implantation were older (p less than 0.01) and showed a prevalence of organic heart disease higher (p less than 0.05) than those who did not require PM implantation. Pts with PM, both of Group A and Group B, showed a complete disappearance of syncopes and a clear-cut reduction of dizziness after implantation of it. On the contrary, dyspnea nearly always persisted and sometimes appeared when initially absent. Sudden and non-sudden cardiac death in PM pts (13.6%) was somewhat more frequent than in those without PM. 4) The incidence of stable atrial fibrillation was 12.1% in pts without PM and 27.2% in pts with PM. The occurrence of stable atrial fibrillation in pts without PM was generally not followed by clinical improvement. 5) The incidence of cerebrovascular accidents was approximately 8%. The accidents always occurred in pts with organic heart disease and often in the older pts (mean age: 75.1 yrs +/- 5.7) particularly in those with PM. A bradycardia-tachycardia syndrome was observed only in 3 pts who had a stroke...
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To investigate the right ventricular activation, filtered bipolar recordings (1 cm interelectrode distance) of Apex (RVA), Inflow tract (RVIT) and Outflow tract (RVOT) of the right ventricle were obtained in 4 groups of subjects. 1st group: 25 cases with normal QRS; 2nd group: 7 cases with left ventricular conduction disturbances (4 LBBB and 3 LAH patterns); 3rd group: 20 cases with chronic coronary heart disease (CCHD) and RBBB alone (5 cases) or combined with LAH (15 cases); 4th group: 9 young subjects without heart disease (7 cases) or ostium secundum atrial septal defect (2 cases) and RBBB pattern. The activation times were calculated from the beginning of the QRS in the first endocavitary rapid deflection. The data obtained (average +/- s.d.) for QRS duration (QRSd), RVA, RVIT and RVOT were respectively: 1st group: 97 +/- 9, 23 +/- 9, 36 +/- 9, 39 +/- 8; 2nd group: 133 +/- 43, 20 +/- 14, 25 +/- 9, 42 +/- 6; 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. Activation times as expected were similar in 1st and 2nd groups. Significant differences were noted between 1st and 3rd groups (p less than 0.001) in activation times of RVA, RVIT and RVOT. Between 1st and 4th group significant differences were noted in activation times of RVA and RVIT (p less than 0.001) while no significant differences were observed for RVOT (p greater than 0.05). In 2 cases of the third group (CCHD) and in the 2 cases of atrial septal defect the activation time of RVA was within the normal range suggesting a peripheral block. In the cases of the 3rd group with troncular RBBB activation times of RVIT and RVOT were significantly related to the QRSd (r = 0.79 and 0.65, p less than 0.001 and less than 0.01 respectively), while there was no significant correlation between the activation time of RVA and the QRSd. In accordance with other Authors our study demonstrates that: 1) the RBBB pattern in ASD has a peripheral electrogenesis; 2) the RBBB pattern in CCHD is generally due to a troncular block but our study also suggests the possibility of a distal block in these patients. In contrast with some Authors the RBBB pattern in young people without heart disease was due to a troncular and not to a peripheral block. Finally, the absence of correlation observed in the cases with troncular block of the 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. QRSd and RVIT and RVOT activation times might be explained as follows: 1) in high degree troncular block the RVA activation time is due to the time employed byt the wave front to cross the septum which is probably similar in all the cases; 2) the QRSd depends on the activation time of the peripheral areas which depends on the variable spread of activation of the right ventricle probably due to a variable participation of the specialized conduction system.
Anterior displacement (AD) of the QRS horizontal loop (Frank VCG method) was induced by programmed right atrial stimulation (PRAS) in 15 cases. When AD occurred we noticed changes of the terminal QRS vectors and of the T loop similar to those observed in incomplete right bundle branch block (RBBB). The increasingly anticipated extrastimuli induced progressively the AD and then progressive degrees of RBBB. The anterior shifting of the efferent limb never appeared after the induction of RBBB. A left conduction disturbance never appeared after the AD. In cases of supposed incomplete left bundle branch block (i.e. left ventricular hypertrophy) the QRS duration decreased when the AD was induced. Therefore, the AD induced by PRAS and probably those observed in some clinical cases are due to a right ventricular conduction disturbance.
In the context of a W.H.O. Community Control Program of Hypertension, 15.187 subjects aged 20-64 years were examined in three distinct areas of the Veneto region: Camposampiero (Padua), Valdagno (Vicenza) and Mirano (Venice). The prevalence of hypertension was evaluated according to W.H.O. criteria. The prevalence of the three forms of hypertension "systolic only", "diastolic only" and "systo-diastolic together", the difference according to sex and the correlation with age were also calculated. In particular the correlation with age was evaluated in four arbitrary classes of relative weight. The mean prevalence of hypertension into the three samples was 30.7%. The most common form was "systo-diastolic together" (15.5%). The prevalence of hypertension was higher in males and increased with age in both sexes. A positive association between the prevalence of hypertension and the age was observed in all the three classes of relative weight. This association was more noticeable in the classes of a higher relative weight. The association between weight and prevalence of hypertension is discussed in view of a primary prevention of hypertension. The results obtained clearly show the extent of the effort involved in order to control hypertension in the community.
Three cases of accelerated idioventricular rhythm with isorhythmic A-V dissociation are presented. One case was affected by hypertrophic non obstructive myocardiopathy and two cases were affected by coronary heart disease with previous myocardial infarction. In all the cases of the arrhythmia persisted for days or months. By means of the electrophysiological study we could establish that 1) the focus was not protected by entrance block and 2) it was localized in the main branches of the conduction system. In the first case the focus was localized in the right bundle branch, in the second case, it was localized in the anterior fascicle of the left bundle branch and in the third case in the posterior fascicle of the left bundle branch. These electrophysiological characteristics suggest that the arrhythmia was due to increased firing of normal idioventricular pacemakers. On the basis of this electrogenetic interpretation we outline that in our cases the term of accelerated idioventricular rhythm should be preferred to others used in literature such as slow ventricular tachycardia.
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Various electrocardiographic and vectorcardiographic (ECG-VCG) patterns of ventricular conduction disturbances are inducible by premature right atrial stimulation (PRAS). These patterns are a consequence of different degrees of refractoriness in the specialized ventricular conduction system. We observed that the intermediate phase of left bundle branch block (LBBB) induced by PRAS in 20 subjects with normal basal QRS (complexes) were similar to those of left ventricular hypertrophy (LVH). In 18 patients with basal ECG-VCG signs of LVH, right bundle branch block (RBBB) induced by PRAS produced a progressive disappearance of these signs and the "normalization" of the tracings. The initial maximum QRS vector decreased, disappeared or remained absent in the patients with LBBB induced by PRAS, and appeared (when absent in the basal VCG) and remained unchanged (when present) in patients with RBBB induced by PRAS. In this paper we discuss the electrogenetic implications of these data. The ECG-VCG sings of LVH are probably dependent on a slowed conduction in the left bundle branch system, while anatomical hypertrophy per se probably plays a less important role.
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