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Background: The evaluation of the vasodepressor (VD) reflex of the carotid sinus syndrome is usually inaccurate, due to the difficulty in blood pressure measurement., Aim: To study the VD reflex with a beat-to-beat not invasive technique., Methods: We investigated 68 patients (49 males, 19 females; mean age 70 +/- 11 years) affected by carotid sinus syndrome: cardioinhibitory (CI) form was present in 47 patients, mixed (M) form in 10 patients and VD form in 11 patients. The control group consisted of 9 patients (6 male, mean age 71 +/- 8 years) affected by third degree atrioventricular block who had received the implant of a permanent pacemaker and were pacemaker-dependent with a prolonged asystole at time of temporary inhibition of the pacemaker itself. The study of the VD reflex was performed in the supine position; beat-to-beat arterial systolic pressure was monitored by a photoplethysmographic method using a finger cuff (Finapres technique)., Results: In all the patients the carotid sinus massage caused a marked fall in systolic blood pressure which was greatest at the end of the massage: from 143 +/- 25 mm Hg to 74 +/- 20 mm Hg in the patients with CI form, from 144 +/- 14 mm Hg to 76 +/- 18 mm Hg in those with M form and from 125 +/- 26 mm Hg to 65 +/- 13 mm Hg in those with VD form. A decrease in systolic blood pressure > or = 50 mm Hg occurred in 84% of cases. Afterwards, the patients with CI form had a progressive increase of systolic blood pressure that reached the initial value after a mean of 27 seconds. In the patients with VD form systolic blood pressure was significantly (p < or = 0.5) lower than that observed in all the other groups, beginning from the third second after the end of the massage; mean systolic blood pressure value remained significantly lower than the initial value for more than 27 seconds. The patients with M form showed an intermediate pattern. Also control group patients showed a fall in systolic blood pressure immediately after pacemaker inhibition (from 152 +/- 29 mm Hg to 87 +/- 25 mm Hg) that was of similar extent than that observed in carotid sinus syndrome patients, but pressure returned to initial value within 9 seconds., Conclusions: An important VD reflex is present in most patients with carotid sinus syndrome. It lasts more than the CI reflex and it persists for several seconds after the end of the massage. The initial fall of systolic blood pressure is of similar extent in all the forms of carotid sinus syndrome, but the patients with the VD form are characterized by a longer duration and greater entity of the decrease. These results point out the importance of the VD reflex in patients with the carotid sinus syndrome.

Background: Patients with bundle branch block and syncope, especially those with abnormal electrophysiologic study, are at high risk of progression to second-or third-degree atrioventricular block and therefore they often receive a permanent back-up pacemaker. The aim of this study was to evaluate of the incidence of bundle branch block progression to second or third-degree atrioventricular block during long-term follow-up., Methods: A retrospective study was performed on 60 patients (49 males, age 77 +/- 9 years) with bundle branch block and permanent back-up pacemaker. The patients were subdivided into 3 groups: 13 patients, at pre-implant electrophysiologic study had HV interval > or = 100 msec and/or second- or third-degree atrioventricular block induced by ajmaline i.v. administration (Group 1); 20 patients with HV interval of 70-100 msec and/or HV > or = 120 msec after ajmaline administration (Group 2); 27 patients who had received a permanent pacemaker because of carotid sinus syndrome or sick sinus syndrome (22 patients) or because of recurrent syncopes and negative electrophysiologic study (5 patients) (Group 3)., Results: During a mean follow-up of 62 +/- 41 months, 17/60 patients (28%) had progression to second- (n = 4) or third-degree (n = 13) atrioventricular block: atrioventricular block occurred in 54% of Group 1 patients in 25% of Group 2 patients and in 19% of Group 3 patients. The actuarial rate of progression to atrioventricular block for the overall population was, at 5 and 10 years, 25% and 58% respectively; in Group 1 it was 46% and 62%; in Group 2 it was 22% and 55% and in Group 3 it was 21% and 59% (p = 0.06). The patients with right bundle branch block and left anterior hemiblock were at higher risk of progression to atrioventricular block than those with right bundle branch block or left bundle branch block (risk 42% vs 14%, p = 0.06). The presence of an abnormal electrophysiologic study did not increase the progression rate either in the patients with right bundle branch block and left anterior hemiblock (risk of 43%), nor did it in those patients with other types of bundle branch block (risk of 18%). Moreover, the induction of second- or third-degree atrioventricular block during ajmaline administration was associated with a higher risk of block during the follow-up (60% vs 25%, p = 0.06)., Conclusions: Patients treated with pacemaker because of symptomatic bundle branch block have a high risk of progression to second- or third-degree atrioventricular block in the long-term follow-up. The results argue against the practical usefulness of electrophysiological study since a risk stratification could be obtained by the simpler surface electrocardiogram; moreover, risk of block was also present in the patients affected by carotid sinus syndrome or sick sinus syndrome, and in those affected by unexplained syncope with negative electrophysiologic study.

In this study, we verified if the induction of atrial fibrillation/flutter, during the electrophysiological study, could be useful for the evaluation of syncope of unknown origin. Of 292 patients who underwent an electrophysiological study for unexplained symptoms, we selected 15 patients (5.1%) affected by syncope and pre-syncope. In these, the induction of atrial fibrillation (14 patients) or flutter (1 patient) just at the onset caused, the reproduction of the spontaneous symptoms. No other cause could be identified. These patients were affected by: 1) syncope or pre-syncope without electrocardiographic documentation of paroxysmal atrial fibrillation/flutter 2) syncope or presyncope and documented asymptomatic episodes of paroxysmal atrial fibrillation/flutter. Palpitations closely preceded or followed the syncope in 11/15 patients. Symptom reproduction was obtained in the supine position in 3 patients (heart rate 180 +/- 82 beat/min, systolic blood pressure 53 +/- 6 mmHg) and in the upright position in 12 patients (heart rate 177 +/- 24, systolic blood pressure 65 +/- 18 mmHg). The arrhythmia was induced by incremental atrial pacing or premature atrial beats in 3 cases, ramp in 3 cases and burst--mean rate 339 +/- 48 beat/min--in 9 cases. The arrhythmia lasted for a period of time ranging from a minimum of 1 mm to a maximum of 24 hours (median 1 hour). During sinus rhythm, an abnormal vasodepressor reflex (with a systolic blood pressure fall greater than or equal to 50 mmHg) could be induced in 7/9 patients by carotid sinus massage or 60 degrees tilt test.(ABSTRACT TRUNCATED AT 250 WORDS)

Two patients with isolated atrial septum aneurysm and ventricular tachycardia are reported. In both patients ventricular tachycardia showed left bundle branch block pattern with right axis deviation. The ventricular origin of the arrhythmia was confirmed by electrophysiological study. The aneurysm of the interatrial septum was the only detectable cardiac abnormality. The possible relationship between the atrial abnormality and ventricular tachycardia is discussed.

Unlabelled: At present, patients affected by carotid sinus syndrome and, more general by speaking, by vasovagal syncopes, are being considered more and more for pacemaker implant. However, neither the real incidence of the carotid sinus syndrome or its relation with the sick sinus syndrome with which it is often associated or even confused is precisely known. Of a total of 298 consecutive pacemaker implants, 36 (12%) were executed for carotid sinus syndrome, 33 (11%) for sick sinus syndrome and 24 (8%) for both. The annual incidence was respectively of 40, 37 and 26 implants per year/million of inhabitants. Patients affected by carotid sinus syndrome, when compared with those affected by sick sinus syndrome, showed: a higher prevalence of syncopes (97 vs 42%) more syncopal episodes per patient (2.9 +/- 2 vs 1.8 +/- 0.9), a lower prevalence of associated cardiac diseases (53 vs 100%), cardiac enlargement (36 vs 88%), heart failure (6 vs 36%) and paroxysmal atrial fibrillation (0 vs 97%), a more frequent indication to VVI pacing (75 vs 3%). Generally, when both syndromes were present, the patients showed intermediate characteristics., In Conclusion: carotid sinus syndrome is a frequent indication of cardiac pacing as sick sinus syndrome; even if an association is present in about one third of patients, a distinction between carotid sinus syndrome and sick sinus syndrome is justified by theoretical and practical considerations.

The aim of the study was to evaluate the importance of atrial synchronism for pacing therapy of patients with mixed carotid sinus syndrome. On 23 patients (21 m, 2 f; mean age 69 +/- 8 years) affected by symptomatic mixed carotid sinus syndrome we performed: 1) the study of ventriculo-atrial conduction, 2) the evaluation of pacemaker effect and 3) the carotid sinus massage in standing position during VVI and DVI temporary pacing. All patients received a permanent DVI pacemaker and then underwent a two-month period single-blind, randomized, cross-over study on DVI vs VVI mode. During DVI period, no syncope occurred in any patients, minor symptoms persisted in 11 (48%) of them; during VVI period syncopes recurred in 3 patients, symptoms requiring the withdrawal of VVI pacing and premature DVI reprogramming in 8, minor symptoms were observed in 17 (74%). A comparison between 14 patients who preferred DVI period (Group A) and the remaining 9 patients who had no preference for DVI and VVI period (Group B) revealed that Group A patients had a greater pacemaker effect (-34 +/- 16 mmHg vs -16 +/- 14 mmHg; p less than 0.02) and a higher prevalence of ventriculo-atrial conduction (78% vs 44%; p = 0.1), while the entity of the systolic pressure fall caused by carotid sinus massage was similar in the two groups both during VVI mode (Group A -51 +/- 16 mmHg vs Group B -56 +/- 27 mmHg) and DVI mode (Group A -38 +/- 17 mmHg vs Group B -45 +/- 17 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

The systolic blood pressure was measured during clinostatism and 15'', 1', 5' after standing in 101 patients with carotid sinus syndrome and in 101 controls matched for age, sex, and prevalence of organic heart disease. In the carotid sinus syndrome group we observed a greater systolic blood pressure reduction from the supine to standing position (20 +/- 19 vs 14 +/- 11 mmHg), a lower orthostatic pressure (111 +/- 23 vs 120 +/- 21 mmHg) and a greater incidence of orthostatic hypotension (defined as a blood pressure reduction greater than or equal to 50 mmHg or greater than or equal to 20 mmHg when orthostatic pressure was lower than 100 mmHg) (35% vs 17%). Twenty-three carotid sinus syndrome patients received a VVI pacemaker for control of their symptoms; after a mean follow-up of 12.2 +/- 7.7 months, unchanged or reduced symptoms persisted in 6 out 9 (67%) patients with previous orthostatic hypotension while only in 1 out of 14 (7%) patients without this feature. In conclusion, orthostatic hypotension is frequently associated with a carotid sinus syndrome and may account for relapses in some patients treated with VVI pacing.

We studied the unnatural history of sinus node function in severe sick sinus syndrome treated with AAI or DDD pacemakers. In 19 patients (10 m; 9 f; mean age +/- 1 SD 69 +/- 7 years) we executed serial bicycle exercise tests and electrophysiological studies before, 7 days and 3 months after pacemaker implant. Sinus heart rate at maximum effort was: 118 +/- 23 beats/min and 117 +/- 23 beats/min (two different evaluations) before pacemaker implant, 125 +/- 21 beats/min after 7 days (p less than 0.05) and 133 +/- 20 beats/min after 3 months (p less than 0.001) with an average increment of 12.7%. A positive correlation (y = 50.4 + 0.7 X beats/min; p less than 0.001) between the first basal test and the third month one was found. In analogy exercise test lasted 8.7 +/- 3, 8.6 +/- 2.8, 9.5 +/- 2.5, 9.7 +/- 2.5 minutes respectively, with an average increment of 11.5% between the first basal test and the third month one. Sinus heart rate at maximum effort in 14 age matched normal subjects was 138 +/- 15 beats/min. The difference with sick sinus syndrome patients was statistical (p less than 0.05) when compared with the basal test but not with 3rd month test. Parameters determined during electrophysiological studies were: spontaneous heart rate, corrected sinus node recovery time, sino-atrial conduction time evaluated before and after autonomic blockade (propranolol 0.2 mg/kg i.v. plus atropine 0.04 mg/kg i.v.). All these parameters, excepting basal corrected sinus node recovery time, improved significantly after pacemaker implant.(ABSTRACT TRUNCATED AT 250 WORDS)

Three patients with 1:1 atrio-ventricular conduction at rest developed fixed 2nd or 3rd degree atrio-ventricular block during exercise testing. In all patients electrophysiologic study documented block distal to the atrioventricular node. The exercise induced block probably occurred because of increased atrial rate and abnormal refractoriness of the His-Purkinje conduction system. These findings suggest that high degree atrioventricular block appearing during exercise reflects conduction disease of the His-Purkinje system rather than of the atrio-ventricular node, even in absence of bundle branch block. These patients should be considered for permanent cardiac pacing.

Exercise stress test in patients with sick sinus syndrome helps to evaluate the heart rate response to the increased sympathetic and to the decreased parasympathetic discharge. Aim of our study was the assessment of the diagnostic accuracy of exercise stress test in this condition. To do so, we measured the heart rate at peak stress in 18 patients with sick sinus syndrome (16 men and 2 women aged 51-78 years, mean 68). Two control groups were chosen: one of 14 healthy subjects of the same age and sex and a second one of 19 patients of the same age and sex, with comparable heart disease as the patients under study, but without sinus dysfunction. Heart rate at peak stress was expressed as percent of the expected maximal sex--and age--corrected heart rate (% max HR). The sick sinus syndrome group was characterized by the presence of: syncope and/or near-syncope in 10 patients; slight (2), moderate (9), severe (7) sinus bradycardia; corrected sinus node recovery time longer than 500 msec in 7 out of 15 patients, detected during an electrophysiological study; abnormal intrinsic heart rate in 5 out of 11 patients, obtained by means of drug-induced autonomic blockade (metoprolol 0,2 mg/Kg i.v. and atropine 0,04 mg/Kg i.v.), and evaluated according to Jose's equation; abnormal intrinsic corrected recovery time (greater than 450 msec) in 8 out of 11 patients; increase in heart rate after atropine infusion (0,02 mg/Kg i.v.) of less than 90 beats/min in 15 out of 18 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to evaluate the relative role of the automatic nervus system and of the intrinsic electrophysiologic properties on the sinus node function, we measured the corrected sinus node recovery time before and after autonomic nervous system blockade in 24 patients. Fourteen had a sick sinus syndrome, five had a carotid sinus syncope, two had syncope of unknown origin associated with bradycardia. Beta blockade was obtained by infusing metoprolol intravenously at a dosage of 0.2 mg/kg; complete automatic blockade was achieved by further i.v. administration of atropine at a dosage of 0.04 mg/kg. After beta blockade, the corrected sinus node recovery time increased in patients with sick sinus syndrome and intrinsic slow heart rate, whereas it decreased in patients with carotid sinus syncope or with syncope and bradycardia. In patients with sick sinus syndrome and normal intrinsic heart rate the response was variable. A positive direct correlation was found between the changes of the corrected sinus node recovery time induced by beta blockade and those induced by autonomic blockade; that is, both either prolonged or shortened the corrected sinus node recovery time. The changes of the corrected sinus node recovery time after beta blockade alone were inversely correlated with the intrinsic heart rate. We conclude that patients with intrinsic depression of the sinus node have an increased sympathetic tone.

A patient died suddenly during Holter monitoring 19 days after admission for myocardial infarction. Death occurred while the patient was straining at stools. Cardiac arrest, preceded by a short lasting sinus tachycardia, was brought about by some late ectopic ventricular beats, which triggered a fast ventricular tachycardia promptly into ventricular fibrillation.

The effect of body position during carotid sinus massage (CSM) for diagnosis of carotid sinus syndrome (CSS) of the cardioinhibitory type (CI) is not yet defined in the literature. The diagnosis of CSS-CI was made in 17 patients, the age range was 54 to 87 years (mean 74,7) on the basis of the following criteria: --history of recurrent syncope; --reproduction of symptoms during CSM repeated in different days in the presence of ventricular asystole that lasted more than 3 seconds; --absence of a vasodepressor reflex capable of producing symptoms, after a CI reflex was abolished by intravenous atropine; the blood pressure drop never exceeded 40 mmHg; --exclusion of other causes of syncope. In every patient the CSM was made in the supine position. If the test results were normal or left diagnostic doubts, the CSM was performed again in the standing position. Three different groups of patients were identified: a) normal result in the supine position, abnormal result in the standing position (cases 1 through 6); b) abnormal response both in the supine and in the standing position (7 and 8); c) abnormal response in the supine position, normal result in the standing position (9 and 10). In the cases 11 through 17 the CSM was not performed in the standing position because it was sufficiently diagnostic in the supine position. It is concluded that in the 35% of cases (6 of 17) the diagnosis of CSS-CI was obtained only after CSM was performed on the standing patient. In 53% of cases (9 of 17) the diagnosis was defined by CSM in supine position.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to evaluate the influence of an arterio-venous fistula on cardiac function, a non-invasive study was conducted in thirty-three patients before and during compression of the fistula. Significant changes of PEP/LVET ratio and ITD were observed by means of such a technique only in patients with proximal (forearm) fistula; on the contrary no significant change were noted in those with distal (radiocephalic) a-v fistula. A systolic apical or precordial murmur, that was present in the control state in ten patients, was abolished or reduced in intensity in seven of them. Therefore suppression of blood flow through the shunt appears to affect the systolic time intervals in patients with proximal forearm fistula.

The normal range and the reproducibility of the cardioinhibitory carotid sinus reflex were studied in 288 apparently healthy subjects of different ages (aged from 17 to 84 yrs., 156 males, 132 females). In each subject we chose the longest RR interval as an activation index of the reflex obtained by carotid sinus massage; its mean value increased slightly with advancing age. In the were 1, 5, 2, 5, 3, 3 sec. respectively, with a 99% confidence limit. No sex difference was found. We studied also a group of 105 patients (aged from 39 to 82 yrs., 67 males, 38 females) with various types of cardiovascular disorders, without a previous history of spontaneous syncope. Abnormal maximum RR values were found in 18 of them (17%). This percentage was significantly higher than in normals (2%). In 11 patients (10%) the carotid sinus stimulation evoked a syncopal attack. It seems therefore that a statistically abnormal carotid sinus hypersensitivity can occur in a substantial number of cardiovascular patients without necessarily leading to spontaneous syncopal attacks. Finally the reproducibility of the cardioinhibitory reflex was tested in 42 patients with maximum RR interval values ranging from normal to extremely abnormal. In each subject a significant correlation (r = 0.79) was found between the maximum RR interval values tested in two occasions at intervals ranging from 1 hour to 3 months; besides a concordance in normal or abnormal result was present in 93% of the cases.

Five patients with lymphoma and Vincristine induced myocardial infarction are described in the medical literature. We report two new cases, in whom an anterior myocardial infarction developed few hours after the second administration of the drug. In the reported cases a strict cause-to-effect relationship between the drug and acute myocardial infarction seems indicated by: the striking temporal coincidence between Vincristine administration and onset of chest pain; the additional myocardial infarctions in patients in whom the treatment was continued after the first event; the nearly constant absence of important coronary risk factors and the young age of the patients, making preexisting coronary atherosclerosis unlikely. The mechanism for the described association is still unknown: the possible causes are discussed.

Cardioinhibitory carotid sinus hypersensitivity is present in about one third of patients affected by sinus dysfunction. Aim of the study was to evaluate whether carotid sinus hypersensitivity is related to a well defined (intrinsic or extrinsic) sinus node damage. Fifty-four patients with ecg signs of sinus dysfunction underwent an electrophysiological study and carotid sinus massage. Spontaneous heart rate and corrected sinus node recovery time were measured in basal condition, after adrenergic blockade (propranolol 0.2 mg/Kg i.v.) and after autonomic blockade (propranolol 0.2 mg/Kg i.v. plus atropine 0.04 mg/Kg i.v.). The association between sinus dysfunction and cardioinhibitory carotid sinus hypersensitivity was found in 18/54 pt. (16 men, 2 women; mean age +/- 1 SD 63.6 +/- 14.5 years). The remaining 36 patients (19 men, 17 women; mean age +/- 1 SD 65.8 +/- 9.8 years), affected by sinus dysfunction alone, were used as controls. No electrophysiological differences between the two groups were found; particularly, an abnormal intrinsic heart rate (according to Jose values) or an abnormal intrinsic corrected sinus node recovery time (greater than 385 msec.) were present in 83% of the patients in both groups. Among sinus dysfunction clinical features, heart rate, presence of spontaneous syncope, sino-atrial block or sinus arrest and organic heart disease were similar in the two groups while the percentage of patients with spontaneous atrial tachyarrhythmias (bradi-tachy syndrome) was significantly smaller (11% vs 44%; p less than 0.01) in carotid sinus hypersensitivity group. In conclusion, in sinus dysfunction patients, the presence of carotid sinus hypersensitivity cannot be used as a criterion to differentiate a subgroup with peculiar clinical and electrophysiological sinus node characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

In this prospective study, we evaluated pacing therapy in 60 consecutive patients affected by syncopes or pre-syncopes and cardioinhibitory or mixed carotid sinus hypersensitivity. We preferred DDD/DVI pacing for the 26 patients who had: 1) the cardioinhibitory form and presence of symptomatic pacemaker effect, or 2) the mixed type I form and presence of symptomatic pacemaker effect, ventriculo-atrial conduction, or orthostatic hypotension, or 3) the mixed type II form, or 4) the presence of severe sinus bradycardia. We preferred VVI mode in the other 34 patients. Syncope or pre-syncope persisted in one patient of the VVI group after the pacemaker implant and in one patient of the DDD/DVI group. Therefore, we obtained the suppression of severe symptoms in 97% of cases (58/60 pts). Yet minor symptoms persisted in 35% and 38% of patients of the two groups, respectively. No patient developed clinical signs of cardiac insufficiency or intolerance to pacing therapy. Besides, in DDD/DVI patients, we performed a single-blind, randomized, cross-over study for a comparison between the DDD/DVI and VVI mode: each patient was paced for two months using each mode and for each period symptoms were analyzed. The VVI period, compared to the DDD/DVI, resulted in a significantly higher incidence of symptoms: syncope 8% vs. 0%; pre-syncope 31% vs 0%; minor symptoms 58% vs. 31%; cardiac failure 19% vs. 0%. So the DDD/DVI mode was preferred by 69% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)