The long-term effect on surgery-free survival of biological compared to conventional therapy in Crohn's disease in real world-data: a retrospective study.

BACKGROUND: The introduction of biological drugs has led to great expectations and growing optimism in the possibility that this new therapeutic strategy could favourably change the natural history of Inflammatory Bowel Disease (IBD) and, in particular, that it could lead to a significant reduction in surgery in the short and long term. This study aims to assess the impact of biological versus conventional therapy on surgery-free survival time (from the diagnosis to the first bowel resection) and on the overall risk of surgery in patients with Crohn's disease (CD) who were never with the surgical option. METHODS: This is a retrospective, double-arm study including CD patients treated with either biological or conventional therapy (mesalamine, immunomodulators, antibiotics, or steroids). All CD patients admitted at the GI Unit of the S. Salvatore Hospital (L'Aquila. Italy) and treated with biological therapy since 1998 were included in the biological arm. Data concerning the CD patients receiving a conventional therapy were retrospectively collected from our database. These patients were divided into a pre-1998 and post-1998 group. Our primary outcome was the evaluation of the surgery-free survival since CD diagnosis to the first bowel resection. Surgery-free time and event incidence rates were calculated and compared among all groups, both in the original population and in the propensity-matched population. RESULTS: Two hundred three CD patients (49 biological, 93 conventional post-1998, 61 conventional pre-1998) were included in the study. Kaplan-Meier survivorship estimate shows that patients in the biological arm had a longer surgery-free survival compared to those in the conventional arm (p = 0.03). However, after propensity matching analysis, conducted on 143 patients, no significant difference was found in surgery-free survival (p = 0.3). A sub-group analysis showed shorter surgery-free survival in patients on conventional therapy in the pre-biologic era only (p = 0.02; Hazard Ratio 2.9; CI 1.01-8.54) while no significant difference was found between the biologic and conventional post-biologic groups (p = 0.15; Hazard Ratio 2.1; CI 0.69-6.44). CONCLUSION: This study shows that the introduction of biological therapy has only a slight impact on the eventual occurrence of surgery in CD patients over a long observation period. Nevertheless, biological therapy appears to delay the first intestinal resection.

A novel gene therapy strategy using secreted multifunctional anti-HIV proteins to confer protection to gene-modified and unmodified target cells.

Current human immunodeficiency virus type I (HIV) gene therapy strategies focus on rendering HIV target cells non-permissive to viral replication. However, gene-modified cells fail to accumulate in patients and the virus continues to replicate in the unmodified target cell population. We have designed lentiviral vectors encoding secreted anti-HIV proteins to protect both gene-modified and unmodified cells from infection. Soluble CD4 (sCD4), a secreted single chain variable fragment (sscFv(17b)) and a secreted fusion inhibitor (sFI(T45)) were used to target receptor binding, co-receptor binding and membrane fusion, respectively. Additionally, we designed bi- and tri-functional fusion proteins to exploit the multistep nature of HIV entry. Of the seven antiviral proteins tested, sCD4, sCD4-scFv(17b), sCD4-FI(T45) and sCD4-scFv(17b)-FI(T45) efficiently inhibited HIV entry. The neutralization potency of the bi-functional fusion proteins sCD4-scFv(17b) and sCD4-FI(T45) was superior to that of sCD4 and the Food and Drug Administration-approved fusion inhibitor T-20. In co-culture experiments, sCD4, sCD4-scFv(17b) and sCD4-FI(T45) secreted from gene-modified producer cells conferred substantial protection to unmodified peripheral blood mononuclear cells. In conclusion, continuous delivery of secreted anti-HIV proteins via gene therapy may be a promising strategy to overcome the limitations of the current treatment.

[Transcranial magnetic stimulation for psychogenic tremor - a pilot study]. / Der Einsatz der transkraniellen Magnetstimulation beim psychogenen Tremor - eine Pilotstudie.

Psychogenic tremor is the most common psychogenic movement disorder. Its prognosis is widely held to be poor and strongly depends on the patient's insight into the psychogenicity of the syndrome. The clinical value of transcranial magnetic stimulation (TMS) for (i) establishing the diagnosis with a high level of certainty, (ii) modulating symptom severity and (iii) facilitating patients' insight into psychogenicity was tested in 11 patients with psychogenic tremor of the upper limb. After explaining the psychogenic origin of the syndrome and providing a neurobiological model, 30 TMS pulses were applied over the hand area of the primary motor cortex contralateral to the affected hand(s) at a rate of 0.2 Hz. 15 pulses were administered at intensities of 120 % and 140 % of the resting motor threshold, respectively. Kinematic motion analysis was used to document the effectiveness of the TMS procedure. All patients met the diagnostic criteria of conversion disorder. Time elapsed since symptom onset was on average 48 to 57 months. Tremor affected both hands in 8 patients, one patient had additional head tremor. The TMS procedure caused a significant reduction of tremor frequency and thus established the diagnosis of documented psychogenic tremor according to the criteria proposed by Fahn and Williams (1988) in each patient. The duration of symptom relief was transient in 7 patients, 4 patients had lasting symptom relief. The present pilot study demonstrates that TMS is a helpful tool to (i) establish the diagnosis of psychogenic hand tremor with a high level of certainty, (ii) reduce tremor intensity and (iii) facilitate the patient's insight into the psychogenic origin of the syndrome as a prerequisite to obtain adherence to psychotherapy.

Electrical somatosensory stimulation improves movement kinematics of the affected hand following stroke.

AIM: The effect of electrical somatosensory stimulation on motor performance of the affected hand was investigated in 12 chronic subcortical stroke subjects. METHODS: Subjects performed index finger and hand tapping movements as well as reach-to-grasp movements with both the affected and unaffected hand prior to (baseline conditions) and following (1) 2 h of electrical somatosensory stimulation (trains of five pulses at 10 Hz with 1 ms duration delivered at 1 Hz with an intensity on average 60% above the individual somatosensory threshold) of the median nerve of the affected hand or (2) 2 h of idle time on separate occasions at least 1 week apart. The order of sessions was counterbalanced across subjects. RESULTS: Somatosensory stimulation of the median nerve of the affected hand, but not a period of idle time, enhanced the frequency of index finger and hand tapping movements and improved the kinematics of reach-to-grasp movements performed with the affected hand, compared with baseline. Somatosensory stimulation did not impact on motor performance of the unaffected hand. DISCUSSION: The data suggest that electrical somatosensory stimulation may improve motor function of the affected hand after stroke; however, further studies are needed to test if the implementation of somatosensory stimulation in rehabilitation of hand function also impacts on manual activities of daily life after stroke.

Frequency of inter- and intraventricular dyssynchrony in patients with heart failure according to QRS width.

AIMS: Cardiac resynchronization therapy (CRT) is an effective treatment for heart failure patients with prolongation of QRS duration. Despite careful patient selection, some do not respond to CRT based on QRS complex duration. We sought to evaluate the presence of left ventricular dyssynchrony using tissue Doppler imaging (TDI) according to QRS duration in heart failure patients. METHODS AND RESULTS: Ninety-nine patients (mean age 52.6 +/- 15.3 years) with severe heart failure [left ventricular (LV) ejection fraction, <35%] were prospectively evaluated. On the basis of QRS width, the patients were divided into two groups. Forty-eight patients (48.5%) had a normal QRS duration (<120 ms), Group I, and 51 (51.5%) had a prolonged QRS duration, Group II. All patients underwent echocardiography coupled with TDI. Spectral displays of six basal and six middle LV segments with pulsed-wave TDI were obtained to assess the time to peak systolic point from R-wave on electrocardiogram (Ts). The standard deviation of Ts (Ts-SD) and the maximal temporal difference of Ts (Ts-diff) were measured. Interventricular dyssynchrony [defined as the presence of an interventricular mechanical delay (IVMD) >40 ms] and intra-LV mechanical delays (defined as Ts-SD >33.4 ms and Ts-diff >100 ms) were correlated with the QRS width and morphology. We found a greater IVMD in Group II patients, compared with patients in Group I (42.5 +/- 22.3 vs. 26.8 +/- 21, respectively, P < 0.001). Intraventricular dyssynchrony defined as Ts-SD > or =33.4 ms was found in 45.1% of patients in Group II compared with 23% of patients in Group I (P = 0.03). Similarly, the Ts-diff was prolonged in Group II patients compared with Group I (P = 0.02). By linear regression analysis, a weak relation was found between Ts-SD and QRS duration (P = 0.055). A substantial portion of patients with prolonged QRS did not exhibit ventricular dyssynchrony defined either as total asynchrony index > or =33.4 ms or as IVMD >40 ms. CONCLUSION: A substantial proportion of patients with prolonged QRS (32.1%) did not exhibit inter- or intraventricular dyssynchrony, which may represent a limitation in identifying the ideal QRS interval for the selection of patients for CRT.

Mid-term follow-up of patients with Brugada syndrome following a cardioverter defibrillator implantation: a single center experience.

BACKGROUND: Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increase risk of sudden cardiac death. Risk stratification for the life-threatening arrhythmic events in Brugada syndrome is not yet established. In the present study, we report our experience in patients with Brugada syndrome, following an ICD implantation. METHODS AND RESULTS: A total of 12 patients (11 men, 1 woman) with a mean age of 46.5+/-11.8 were studied. At diagnosis, 7 patients had syncope of unknown origin, 2 patients were asymptomatic, 2 patients were survivors of cardiac arrest, and 1 had documented clinical VT requiring direct cardioversion for termination. Age was similar between the symptomatic and asymptomatic patients (46.6+/-13 vs. 46+/-2.8, respectively). Two patients reported a family history of sudden cardiac death. In 3 patients, spontaneous coved-type ECG was found at baseline. In 9 patients, a class I antiarrhythmic drug administration unmasked the characteristic type I ECG. In 4 patients (2 symptomatic with syncope at presentation and 2 asymptomatic), who underwent PES, sustained polymorphic VT or VF was induced. VF was induced by single extrastimuli in 2 symptomatic patients (1 from RV apex and 1 from RVOT). In 2 asymptomatic patients, VF was induced by two and triple ventricular extrastimli (1 from RV apex and 1 from RVOT). None of them experienced an event during follow-up. No significant difference was found between symptomatic and asymptomatic patients (p=NS). The mean follow-up period for the entire study population was 27.83+/-11.25 months. During follow-up, 2 patients (one with prior cardiac arrest and another with syncope) had VF. Both of them had a type I ECG after provocation with a class I antiarrhythmic drug. None of them had undergone programmed ventricular stimulation. Five patients (41.7 %) had inappropriate ICD interventions during follow-up. The cause of inappropriate therapy was sinus tachycardia in 2 patients, AF in 2 patients and T wave oversensing in 1 patient. CONCLUSION: Knowledge about Brugada syndrome is steadily progressing but there are still unanswered issues dealing with the risk stratification and the management of patients.

The rotation of the alpha subunit of F1 relative to minor subunits is not involved in ATP synthesis. Evidence given by using an anti-alpha subunit monoclonal antibody.

To test whether ATP synthesis could occur via a mechanism of rotational catalysis in which the alpha and beta subunits of F1 would rotate with respect to the minor subunits, we have measured the rate of ATp synthesis after binding various masses of antibodies to F1. If the rotation was an essential feature of the mechanism, the rate of ATP synthesis should be inhibited either completely or proportionately to the load carried by F1. Bivalent immunoglobulins (IgG) or monovalent Fab fragments of an anti-alpha monoclonal antibody (7B3) were bound to F1 present in electron-transport particles in a ratio of 2 Fab or 2 IgG per F1. This binding similarly inhibited the rate of ATP synthesis by a maximum of about 50%. When anti-mouse immunoglobulins were added to the F1-7B3 (IgG) complex, no significant change in the rate of inhibition was observed. In conclusion, the rate of ATP synthesis was the same when F1 was loaded with 100 kDa (2 Fab), 300 kDa (2 IgG, 7B3) or 900 kDa (2 IgG + 4 ant-mouse IgG). It is concluded that the rotation of the alpha subunits is extremely unlikely to play an essential role in the mechanism of ATP synthesis.

Availability to monoclonal antibodies of antigenic sites of the alpha and beta subunits in active, denatured or membrane-bound mitochondrial F1-ATPase.

The binding of five monoclonal antibodies to mitochondrial F1-ATPase has been studied. Competition experiments between monoclonal antibodies demonstrate that these antibodies recognize four different antigenic sites and provide information on the proximity of these sites. The accessibility of the epitopes has been compared for F1 integrated in the mitochondrial membrane, for purified beta-subunit and for purified F1 maintained in its active form by the presence of nucleotides or inactivated either by dilution in the absence of ATP or by urea treatment. The three anti-beta monoclonal antibodies bound more easily to the beta-subunit than to active F1, and recognized equally active F1 and F1 integrated in the membrane, indicating that their antigenic sites are partly buried similarly in purified or membrane-bound F1 and better exposed in the isolated beta-subunit. In addition, unfolding F1 by urea strongly increased the binding of one anti-beta monoclonal antibody (14 D5) indicating that this domain is at least partly shielded inside the beta-subunit. One anti-alpha monoclonal antibody (20 D6) bound poorly to F1 integrated in the membrane, while the other (7 B3) had a higher affinity for F1 integrated in the membrane than for soluble F1. Therefore, 20 D6 recognizes an epitope of the alpha-subunit buried inside F1 integrated in the membrane, while 7 B3 binds to a domain of the alpha-subunit well exposed at the surface of the inner face of the mitochondrial membrane.

Stoichiometry of the oligomycin-sensitivity-conferring protein (OSCP) in the mitochondrial F0F1-ATPase determined by an immunoelectrotransfer blot technique.

The ratio between the amount of oligomycin-sensitivity-conferring protein (OSCP) and the amount of the alpha and beta subunits of F1-ATPase in the mitochondria has been determined by a method combining electrophoresis, electrotransfer and immunotitration with monoclonal antibodies. The peptides separated in SDS-polyacrylamide gel electrophoresis were blotted to nitrocellulose sheets by electrotransfer. The nitrocellulose sheets were incubated with 125I-labelled purified monoclonal antibodies specific to various peptides. The 125I-labelled immune complexes were located by immunodecoration using peroxidase-conjugated second antibodies and the blotted peptides were revealed with H2O2 and alpha-naphthol. The amount of immune complex present on the nitrocellulose was determined by counting the radioactivity present on the spots. The amount of peptide blotted is directly proportional to the amount of protein loaded on the electrophoresis. By comparing standard curves made with the isolated proteins to the values obtained in the presence of various amounts of the membrane-protein complex, one can calculate the content of this peptide in the membrane. It was found that the mitochondrial membrane contains 2 mol of OSCP per mol of F1.

Heart rate variability: does it change after RF ablation of reentrant supraventricular tachycardia?

BACKGROUND: Following RF ablation of reentrant supraventricular tachycardia, inappropriate sinus tachycardia may occur. Local parasympathetic denervation is a possible mechanism for these rhythm disturbances. The purpose of this study was to determine the incidence of sinus tachycardia and to determine the relation between endocardial lesions at different ablation sites and alterations in autonomic tone in several different groups of patients with supraventricular tachycardia, using techniques of heart rate variability analysis. METHODS: The subjects of this study were 75 patients (48 women, 27 men) with a mean age of 39.99 (SD = 13.39). They underwent RF ablation of AV nodal slow pathways (40 cases), posteroseptal APs (23 cases), left lateral and right free wall APs (12 cases) because of symptomatic tachycardias. The mean sinus rate and time domain (standard deviation of RR intervals and root mean square of differences of adjacent RR intervals) and frequency domain (low frequency, high frequency and low frequency/high frequency ratio) analyses of heart rate variability were obtained by use of 24 hour Holter monitoring before and 1 month after ablation compared with pre-ablation values. RESULTS: Analysis of 24 hour ambulatory Holter-monitors, performed 1 month after RF ablation, showed no significant changes in time and frequency domain parameters of heart rate variability in different groups. A significant increase in mean heart rate was noted after RF ablation at AV nodal slow pathway group and left freewall/right free wall accessory pathways group. Patients undergoing RF ablation of right or left posteroseptal accessory pathways had no significant increase in the mean heart rate. CONCLUSION: In summary, an increase in sinus tachycardia may be initiated by RF ablation of atrioventricular reentrant tachycardia (AVNRT) and right free wall or left free wall accessory pathways. This finding shows that the modifications of heart rate are not directly related to the posteroseptal region or to the accessory pathways.

Effect of autonomic nervous system modulation on retrograde atrioventricular nodal conduction in the human heart.

Although the influence of the autonomic nervous system on anterograde atrioventricular nodal conduction is well established, its effect on retrograde atrioventricular nodal conduction has not been examined systematically. Since retrograde atrioventricular nodal conduction in subjects with normal anterograde conduction may vary from intact retrograde conduction to complete retrograde block when assessed during ventricular pacing, in this study patients with (a) intact retrograde atrioventricular nodal conduction (group 1) were studied during parasympathetic (vagal) stimulation by carotid sinus pressure and during sympathetic inhibition (propranolol 0.2 mg.kg-1 intravenously) and (b) retrograde atrioventricular nodal block (group 2) were studied during vagal blockade (atropine 0.04 mg.kg-1 intravenously) and during sympathetic stimulation (isoproterenol 1-4 micrograms.min-1 infusion). In both groups changes in sinus cycle length and anterograde atrioventricular nodal conduction were measured. In group 1 vagal stimulation by carotid sinus pressure in 20 patients caused the cycle length at which retrograde atrioventricular nodal block was induced to be significantly lengthened from a mean(SD) of 375(59) to 451(51) ms in six patients; caused complete retrograde block in 10 patients; and had no effect in four patients. Sympathetic inhibition by propranolol in another 15 patients delayed the onset of pacing induced retrograde atrioventricular nodal block from a mean(SD) of 340(60) to 418(80) ms in 11 patients; caused complete retrograde atrioventricular nodal block in three patients; and had no effect in one patient. In group 2 vagal blockade by atropine caused a 1:1 retrograde response during ventricular pacing up to a mean(SD) cycle length of 470(135) ms in six out of eight patients. The infusion of isoproterenol caused the retrograde atrioventricular nodal block to be abolished and 1:1 conduction to be resumed up to a ventricular pacing mean(SD) cycle length of 364(57) ms in six out of eight patients. It is concluded that (a) the autonomic nervous system modulates retrograde atrioventricular nodal conduction in a similar manner to its anterograde counterpart and (b) that since retrograde atrioventricular nodal conduction was reversible after the administration of either atropine or isoproterenol retrograde atrioventricular nodal block may be dynamic (physiological) rather than fixed (anatomical) in nature.

Common topology within a non-collagenous domain of several different collagen types.

The secondary structure of a conserved non-collagenous module in alpha 1(V), alpha 1(XI), alpha 1(IX), alpha 1(XII), alpha 1(XIV) and alpha 1(XVI) collagen chains and in proline- and arginine-rich protein was analyzed using different algorithms. The results predict that a common anti-parallel beta-sheet structure composed of nine consensus beta-strands is present in these non-collagenous modules. A model for the packing of these beta-sheets is proposed which suggests that the predicted beta-sheet structure may be involved in molecular recognition functions.

Different splice variants of cartilage alpha1(XI) collagen chain undergo uniform amino-terminal processing.

Collagen XI is found mainly as a component of cartilage fibrils. Among the different transcripts identified by RT-PCR for the alpha1 (XI) chain, the major tissue form has been reported to be the splicing product of exons I, III and V. In this study, two other splice isoforms of the alpha1(XI) chain were identified using N-terminal sequencing. Like the major alpha1(XI) chain, the fully processed isoforms begin at Gln254 within the N-terminal domain encoded by exon I. This sequence is followed by sequences encoded by exon IIA or III. An anti-peptide antibody allowed the identification of the exon IV encoded sequence within both isoforms. Therefore, these isoforms of the alpha1(XI) chain correspond to the splicing of exons I, IIA, III, IV and V or of exons I, III, IV and V, thus presenting larger acidic sequences than the major form. They could mediate strong ionic interactions within the cartilage matrix.

Late results of balloon pulmonary valvuloplasty in adults.

This study shows late results of adult patients with pulmonary stenosis after successful balloon pulmonary valvuloplasty. Late results of this procedure are as good as early results.

Efficacy and safety of intravenous and oral diltiazem for Wolff-Parkinson-White syndrome.

The electrophysiologic effects and safety of diltiazem administered either intravenously or orally were studied in 14 patients with Wolff-Parkinson-White syndrome during orthodromic reentrant tachycardia and atrial fibrillation (AF). Anterograde and retrograde effective refractory periods of the accessory pathway did not change significantly from baseline during either i.v. or oral administration. Administration by either route prevented induction of sustained reentrant tachycardia in 8 patients. In 6 patients, the reentrant tachycardia was either nonsustained (2 patients) or sustained at much slower rates than the baseline rates (mean +/- standard deviation, baseline, 290 +/- 41 ms; i.v., 355 +/- 40 ms [p less than 0.001]; and oral, 377 +/- 33 ms [p less than 0.001]). In these patients anterograde atrioventricular conduction was prolonged significantly from the mean baseline value of 163 +/- 36 ms to 212 +/- 35 ms with i.v. administration (p less than 0.005) and 225 +/- 33 ms with oral administration (p less than 0.005). Retrograde conduction via the accessory pathway did not change significantly after administration of diltiazem. The shortest preexcited RR intervals during AF were significantly reduced during i.v. but not during oral administration: control, 327 +/- 47 ms; i.v., 270 +/- 28 ms (p less than 0.001); and oral, 323 +/- 44 ms (difference not significant). In 5 patients AF was sustained for a mean of 20 minutes after i.v. and for 12 minutes after oral administration (p less than 0.20), compared with a baseline mean value of 0.83 minute.(ABSTRACT TRUNCATED AT 250 WORDS)

Microfibrillar composition of umbilical cord matrix: characterization of fibrillin, collagen VI and intact collagen V.

Ultrastructural studies made on human umbilical cord revealed that the striated collagen fibrils of the Wharton's jelly matrix are mixed with many microfibrillar structures. Microfibrils were found with a tubular cross-section of 10-12 nm diameter and were organized as beaded filaments characteristic of fibrillin-rich microfibrils. Beads had an average diameter of 25 nm and were spaced at about 50-80 nm. This ultrastructural observation was confirmed by indirect immunofluorescent staining of the jelly matrix using monoclonal antibody to fibrillin. Another constituent of the microfibrillar network was present as typical 100-nm periodic filaments of type VI collagen. Indirect immunofluorescent staining using antibodies to collagen VI showed for the first time that this collagen appeared to be distributed largely in the jelly matrix. In addition, other microfibrils with no specific banding pattern were observed. These microfibrils may constitute an organization of type V collagen different from the one which is generally assembled in heterotypic fibrils with collagen I. Among the latter heterotypic fibrils, type V collagen was studied using an anti-peptide antibody to the most N-terminal non-collagenous region of its alpha 2(V) chain. This antibody recognized a filamentous mesh decorating the bundles of collagen fibrils by immunofluorescent staining. This indicates that at least this part of alpha 2(V) chain may be accessible to the antibody at the surface of the fibrils.

Surgical treatment of hydatid cysts of the heart: report of six cases.

Six patients with hydatid cysts of the heart have undergone successful enucleation of the cysts with the aid of cardiopulmonary bypass. Various locations of the cysts and their consequences are discussed in detail. The findings have been confirmed by clinical, radiologic, electrocardiographic, echocardiographic, cardiac catheterization, cardioangiographic, and coronary angiographic studies. All patients are in good condition. Length of follow-up is reported.

Tachycardia cycle length and maximum capacity of anterograde and retrograde atrioventricular conduction in paroxysmal supraventricular tachycardia.

Anterograde and retrograde pathways are the two major components of the reentry circuit in patients with paroxysmal supraventricular reentrant tachycardias. Therefore, the capacity of each pathway to maintain 1:1 conduction would be expected to determine the cycle length (CL) of the tachycardia. In this study, the possible relationship between the CL of reentrant tachycardia and the maximum capacities of anterograde and retrograde conduction in the maintenance of a 1:1 response during atrial and ventricular pacing were examined. This relationship was analyzed in 26 patients with orthodromic reentrant tachycardia due to Wolff-Parkinson-White syndrome (group 1) and compared with that in 26 patients with atrioventricular nodal reentrant tachycardia (group 2). There were no statistically significant differences between the two groups in the shortest tachycardia CLs (mean +/- SD, 325 +/- 44 versus 329 +/- 52 ms); in the shortest ventricular pacing CLs with 1:1 response (314 +/- 63 versus 319 +/- 38 ms); nor in the CLs that produced retrograde atrioventricular block (306 +/- 62 versus 301 +/- 37 ms). In contrast, the longest atrial pacing CL that produced Wenckebach's phenomenon and the shortest atrial pacing CL with 1:1 response were significantly shorter for group 1 than for group 2 patients (290 +/- 38 versus 390 +/- 88 ms, P less than 0.001) and (305 +/- 38 versus 406 +/- 90 ms, P less than 0.001), respectively. It was concluded that the CL of orthodromic tachycardia can best be predicted from the shortest atrial pacing CL that maintains 1:1 anterograde conduction via the normal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Depressant effect on the retrograde atrioventricular nodal conduction of beta-adrenergic blockade by propranolol in humans.

Propranolol is known to have a depressant effect on anterograde atrioventricular (AV) nodal conduction in normal subjects and in those with AV nodal reentrant tachycardia. Using His bundle recording and programmed ventricular stimulation, the effect of propranolol-induced beta-adrenergic blockade (1 mg/kg intravenously) on retrograde AV nodal conduction was studied in 17 patients without (group I) and nine with (group II) AV nodal reentrant tachycardia. During baseline studies the ventricular pacing cycle length that induced ventriculoatrial block was 338 +/- 60 ms (range 260 to 450 ms) in group I and 305 +/- 39 ms (range 260 to 375 ms) in group II patients (not significant). After injection of propranolol, the ventricular pacing cycle length that induced ventriculoatrial block in group I patients was 416 +/- 97 ms (range 300 to 550 ms) (P less than 0.001, compared to baseline state) in 15 patients, and complete block occurred in two patients. In group II patients ventriculoatrial block occurred at a ventricular pacing cycle length of 375 +/- 97 ms (range 260 to 510 ms) (P less than 0.02 compared to baseline value) in eight patients, and complete block occurred in one patient. Retrograde AV nodal conduction expressed as the H2A2 interval was 75 +/- 33 ms (range 35 to 150 ms) in group I and 49 +/- 16 ms (range 20 to 80 ms) in group II patients (P less than 0.05). Following the administration of propranolol, the H2A2 interval was prolonged in group I patients by 10 to 45 ms in 11 patients, no retrograde AV nodal conduction was observed in three patients, and there was no effect in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined vascular and neurogenic claudication.

Eight patients with combined vascular and neurogenic claudication were presented. In the adult with coexistent neurospinal and vascular disease, a careful history and examination often suggested the pathology more productive of symptomatology. Among patients presenting with predominately vascular claudication, six of six patients had calf pain as part of the pain pattern, and in three of six patients the pain was crampy. Five of six patients had a consistent exercise tolerance pain pattern and obtained relief of symptoms by resting the leg. Among patients presenting with mainly neurogenic claudication. Only four of eight patients had associated calf pain, and none experienced crampy pain. Five of eight patients had a variable exercise tolerance pain pattern and obtained complete relief of symptoms only by assuming the recumbent position. Doppler testing was very helpful as the initial step in the evaluation of the significance of an arterial lesion and in the follow-up assessment of these patients after vascular surgery. Lumbosacral-spine, cardiovascular, and neurologic examination was similar in the two groups of patients.