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Aims: The aim of this study was to assess the effect of granulocyte colony-stimulating factor (G-CSF) on left ventricular (LV) function and volumes in patients with anterior ST-elevation myocardial infarction (STEMI) and depressed LV ejection fraction (EF). Methods and Results: Sixty consecutive patients with anterior STEMI, undergoing primary angioplasty percutaneous coronary intervention (PCI), with symptom-to-reperfusion time of 2-12 h and EF ≤45% after PCI, were randomized to G-CSF 5 μg/kg b.i.d. subcutaneously (n = 24) or placebo (n = 25) for 5 days, starting <12 h after PCI. The primary endpoint was an increase from baseline to 6 months of 5% in left ventricular ejection fraction (LVEF), as measured by magnetic resonance imaging (MRI). Co-primary endpoint was a ≥20 mL difference in end-diastolic volume (EDV). Infarct size and perfusion were evaluated with late gadolinium enhancement (LGE) and gated (99m)Technetium Sestamibi single-photon emission computed tomography (SPECT). Left ventricular EDV and end-systolic volume (ESV) increased from baseline to 6 months in the placebo group (81.7 ± 24.4 to 94.4 ± 26.0 mL/m(2), P < 0.00005 and 45.2 ± 20.0 to 53.2 ± 23.8 mL/m(2), P = 0.016) but were unchanged in the G-CSF group (82.2 ± 20.3 to 85.7 ± 23.7 mL/m(2), P = 0.40 and 46.0 ± 18.2 to 48.4 ± 20.8 mL/m(2), P = 0.338). There were no significant differences in EF or perfusion between groups. A significant reduction in transmural LGE segments was seen at 6 months in the G-CSF vs. placebo groups (4.38 ± 2.9 to 3.3 ± 2.6, P = 0.04 and 4.2 ± 2.6 to 3.6 ± 2.7, P = 0.301, respectively). Significantly more placebo patients had a change in left ventricular end-diastolic volume abovethe median (9.3 mL/m(2)) when reperfusion time exceeded 180 min (median time-to-reperfusion) (P = 0.0123). Severe adverse events were similar between groups. Conclusion: Early G-CSF administration attenuates ventricular remodelling in patients with anterior STEMI and EF ≤45% after successful PCI. [ABSTRACT FROM AUTHOR]

Background: Invasive imaging techniques have been applied for lymphedema (LE) assessment; noncontrast MR lymphography (NCMLR) has potential as an alternative, but its performance is not known in secondary lower limb LE., Purpose: To assess the role of NCMRL for the classification and characterization of secondary lower limb LE., Study Type: Retrospective., Population: Fifty adults with clinically diagnosed secondary LE., Field Strength/sequence: 1.5T, 3D T 2 -weighted turbo spin-echo, 3D T 2 -weighted turbo spin-echo short tau inversion recovery., Assessment: Three radiologists assessed the following characteristics on NCMRL: honeycomb pattern, dermal thickening, muscular abnormalities, distal dilated lymphatics, inguinal lymph node number, appearance of iliac lymphatic trunks. An LE grading based on the MR images was assigned. The relationship between imaging findings and clinical staging was evaluated, as well as between dermal backflow at lymphoscintigraphy and MR staging, and between the limb swelling duration and peripheral lymphatics dilatation., Statistical Tests: Pearson's correlation test and Cramer's V coefficient were computed to measure the strength of association. The Mann-Whitney test was used to compare the limb swelling duration between patients with and without dilated distal vessels. Agreement among raters was assessed through Kendall's W coefficient of correlation., Results: Clinical stage and the MR grading were correlated, with Cramer's V coefficient of 1 for reader 1 (P < 0.05), 0.846 for reader 2 (P < 0.05), and 0.912 (P < 0.05) for reader 3; agreement between interraters was very good (W = 0.0.75; P = 0.05). A honeycomb pattern (P < 0.05), dermal thickening (P < 0.001), muscular abnormalities (P < 0.05), iliac lymphatic trunks appearance (P < 0.05), distal dilated vessels (P < 0.05), and lymph nodes number (P < 0.05) were significantly correlated with LE clinical stage. Dermal backflow at lymphoscintigraphy was described in 10 (20%) patients and showed a significant correlation with the MR grading (P < 0.05)., Data Conclusion: These preliminary results suggest that NCMRL may provide information useful for the staging and management of patients affected by secondary lower limb LE. Level of Evidence 4 Technical Efficacy Stage 2 J. MAGN. RESON. IMAGING 2021;53:458-466., (© 2020 International Society for Magnetic Resonance in Medicine.)

Objective: To assess whether granulocyte colony-stimulating factor (G-CSF) treatment induces a sustained benefit on adverse remodelling in patients with large anterior ST-elevation myocardial infarction (STEMI) and left ventricular (LV) dysfunction after successful reperfusion., Methods: The STEM-AMI Trial was a prospective, placebo-controlled, multicentre study. Sixty consecutive patients with a first anterior STEMI, who underwent primary percutaneous coronary intervention 2-12 h after symptom onset, with LV ejection fraction (LVEF) ≤45% measured by echocardiography within 12 h after successful revascularisation (TIMI flow score ≥2), were randomised 1:1 to G-CSF (5 µg/Kg body weight b.i.d.) or placebo. Clinical events and Major Adverse Cardiac and Cerebrovascular Event (MACCE) were monitored, and LVEF, LV end-diastolic (LVEDV) and end-systolic (LVESV) volumes, and infarct size were evaluated by MRI at the final 3-year follow-up., Results: Fifty-four patients completed the study, of whom 35 with MRI. No significant differences were found in mortality and MACCE between G-CSF and placebo-treated groups. The 3-year infarct size was not different between groups, whereas LVEDV was significantly lower in G-CSF (n=20) than in placebo (n=15) patients (170.1±8.1 vs 197.2±8.9 mL, respectively; p=0.033 at analysis of covariance). A significant inverse correlation was detected in G-CSF patients between the number of circulating CD34 cells at 30 days after reperfusion and the 3-year absolute and indexed LVEDV (ρ=-0.71, 95% CI -0.90 to -0.30, and ρ=-0.62, -0.86 to -0.14, respectively), or their change over time (r=-0.59, -0.85 to -0.11, and r=-0.55, -0.83 to -0.06, respectively)., Conclusions: G-CSF therapy may be beneficial in attenuating ventricular remodelling subsequent to a large anterior STEMI in the long term. No differences have been detected in clinical outcome.

A 40-year-old man was found to have hypertrophic cardiomyopathy (HCM) with severe mid ventricular obstruction. The obstruction produced two distinct left ventricular chambers with an estimated 60 mmHg continuous wave (CW) Doppler intraventricular gradient. Pulsed wave (PW) Doppler showed high velocity systodiastolic flow from apex to base and flow from base to apex confined mostly to the second half of diastole. Cardiac magnetic resonance (CMR) showed midventricular obstruction, due to septal, parietal, and to an hypertrophic, double posteromedial papillary muscle; an apical aneurysm was detected. Aneurysm is underdiagnosed by echocardiography in HCM and an accurate anatomic definition is needed if surgery is planned; thus, a CMR should always be obtained in these patients., Competing Interests: Conflict of Interest: None declared.

A 56-years-old man with previous myopericarditis (10 months earlier, coronary angiography not performed) was admitted because of pericarditis pain and ST segment elevation, together with myocardial necrosis markers rise. Electrocardiogram (EKG) showed negative T waves in lateral and inferior leads; echocardiogram showed mild pericardial effusion and inferior and lateral basal hypokinesis. Cardiac magnetic resonance imaging (CMRI) on day 7 post-admission showed increased T2-short tau inversion recovery (T2-STIR) signal of inferior wall and two different noncontiguous late gadolinium enhancement (LGE) areas: Ischemic-like with about 75% transmural extension (inferior wall) and subepicardial (inferolateral wall) along with pericardial LGE (inferior and inferolateral wall). Coronary angiography showed three vessel disease. Pathogenetic hypothesis of these unexpected findings are discussed. This case shows again the ability of CMRI to unreveal unusual and unexpected pathologic patterns., Competing Interests: Conflict of Interest: None declared.

Introduction: A 71 year old asymptomatic woman came for an echocardiogram because of a left bundle branch block. A much dilated coronary sinus (CS) with an entering large vessel was found along with a mild left ventricular systolic dysfunction. Cardiac Magnetic Resonance (CMR) showed a persistent left superior vena cava (PLSVC), and an absent right superior vena cava (ARSVC). PLSVC drained into the dilated CS. No other cardiac abnormalities were found. Any late Gadolinium enhancement was also not seen. PLSVC and ARSVC are associated with sinus node and conduction tissue maldevelopment and atrial arrhythmias, and thus clinical follow up is indicated., Conclusion: CMR is a useful addition to echocardiogram to search for further cardiac abnormalities, and outline the anatomy with precision in doubtful cases., Competing Interests: Conflict of Interest: The authors have no conflict of interest to disclose.

A case of a young man with myocarditis simulating acute coronary syndrome is reported. The possibility of vasospasm is discussed. The use of cardiac magnetic resonance imaging (MRI) is highlighted.

Telemedicine is extremely useful when distance could hinder diagnostic procedures, disease management, or when severe side-effects may occur in patients not within easy reach of medical care and requiring prompt action and specific therapies. Telemedicine has been successfully adopted in the management of chronic patients, particularly in those with cardiologic or oncologic diseases. In the treatment of differentiated thyroid cancer, requiring long-term check-ups and visits as well as administration of high doses of levothyroxine (TSH - thyroid-stimulating hormone - suppression), also in elderly patients, telemedicine seems particularly indicated. Moreover, these distant monitoring techniques could not only reduce long-term management costs but also considerably decrease cardiovascular risks associated with these patients. The present review aims to provide some general information on telemedicine and its possible fields of action with regard to distant monitoring of patients with differentiated thyroid carcinoma.

Background: Altitude-induced sympathetic hyperactivity can elicit rhythm disturbances in healthy subjects, in particular during exercise., Aim: To asses the real susceptibility of healthy myocardium to malignant ventricular arrhythmias during exercise at high altitude using microvolt T-wave alternans (MTWA)., Methods: We evaluated eight healthy trained participants (one female, 42 +/- 9 years) during a mountain climbing expedition on Gashembrum II (Pakistan, 8,150 m). MTWA and heart rate variability (HRV) were measured in each subject at sea level and at high altitude, both under rest conditions and during exercise. MTWA was determined with the modified moving average method. HRV was expressed as root mean square of successive differences., Results: Rest HRV at high altitude was significantly lower compared to rest HRV at sea level (36 +/- 5 vs 56 +/- 9 ms, P = 0.003). HRV during exercise was significantly lower with respect to rest condition both in normoxia (46 +/- 7 vs 56 +/- 9 ms, P = 0.0001) and hypoxia (27 +/- 4 vs 36 +/- 5 ms, P = 0.005). Moreover, HRV was significantly lower during exercise at high altitude compared to exercise at sea level (27 +/- 4 vs 46 +/- 7 ms, P = 0.0002) and arrhythmias were more frequent during exercise in hypoxia. Nevertheless, MTWA was absent under rest conditions both at sea level and at high altitude and minimally evoked during exercise in both conditions (22 +/- 3 microV and 23 +/- 3 microV, respectively, P = 0.2)., Conclusions: In spite of an enhanced sympathetic activity, MTWA testing during exercise at high altitude was negative in all participants. Healthy trained subjects during exercise under hypoxia seem to be at low risk for dangerous arrhythmias.

The aim of the present functional study was to assess the role of beta3-adrenoceptors in the light of recent findings suggesting the existence of a putative fourth beta-adrenoceptor in adipose and heart tissue. The effect of the non-conventional beta3-adrenoceptor partial agonist CGP12177A is resistant to the effect of the beta3-adrenoceptor antagonist SR59230A. Under isotonic conditions in circular muscle strips of human distal colon, the concentration-effect relationship of CGP12177A and SR59104A (beta3-adrenoceptor agonists), alone and in the presence of CGP20712A (beta1-adrenoceptor antagonist) ICI118551 (beta2-adrenoceptor antagonist) and SR59230A, all 0.1 microm was studied. CGP12177A concentration-dependently relaxed circular muscle strips (pEC50=6.16+/-0.05). This effect was left unchanged by beta1-/beta2-adrenoceptor blockade, but antagonised by SR59230A (pA2=8.12+/-0.02). SR59104A concentration-dependently relaxed circular muscle strips (pEC50=5.43+/-0.01), an effect that was not significantly affected by pretreatment with CGP20712A and ICI118551, but competitively antagonised by SR59230A (p KB=7.89). Isoprenaline-induced relaxations were antagonised by propranolol with a low pA2value (7.76+/-0.16). These results provide further evidence for the presence of functional beta3-adrenoceptors in the human colon, but do not support a role for an atypical beta-adrenoceptor distinct from the beta3-subtype., (Copyright 1999 The Italian Pharmacological Society.)

The motor effect of erythromycin was characterized in conscious rabbits chronically fitted with electrodes and strain-guage force transducers implanted along the proximal and distal colon. Fecal pellet output was also evaluated as an index of propulsive activity. In order to get an insight into the pathways involved in mediating the effect of erythromycin, the macrolide was also administered after pretreatment with atropine, nifedipine or ondansetron. Furthermore, in vitro experiments with erythromycin alone and in the presence of atropine, nifedipine, tetrodotoxin or ondansetron were carried out with circular muscle strips taken from rabbit distal colon. In vivo, erythromycin (0.087-5.6 mg/kg i.v. bolus) dose-dependently stimulated spike and mechanical activities at both colonic levels, with a more marked effect on the distal colon. Erythromycin also dose-dependently increased the number of aborally migrating long spike bursts and fecal pellet output. The reproducibility of the response to erythromycin was confirmed by experiments with the dose of 2.8 mg/kg i.v. bolus, repeated in five consecutive experiments at 48-hour intervals. Nifedipine, but not atropine or ondansetron, significantly reduced the colonic motor response to erythromycin. In vitro experiments gave results in line with the in vivo data: the concentration-dependent contractile effect of erythromycin was almost suppressed by nifedipine, but resistant to atropine, tetrodotoxin or ondansetron. In conclusion, this study provides evidence that: (1) erythromycin is a prokinetic drug at the colonic level in rabbits, and (2) both in vivo and in vitro, the effects of erythromycin are exerted at the smooth muscle level by mechanisms depending on influx of extracellular calcium, while muscarinic and 5-HT3 receptors are not involved, at least in this model.

The role of beta 3-adrenoceptors in human colonic circular smooth muscle was assessed in vitro by use of the beta 3-selective antagonist SR 59230A. Isoprenaline, in the presence of the selective beta-adrenoceptor antagonists CGP 20712A (beta 1) and ICI 118551 (beta 2), both at 0.1 microM, concentration-dependently relaxed the preparation (pEC50 = 5.22). This effect was potently and competitively antagonized by SR 59230A with a pA2 of 8.31, while its R,R enantiomer SR 59483A gave an apparent pKB of 6.21. Relaxation was likewise produced by CGP 12177A (pEC50 = 6.05), but not by BRL 37344. Although only one of these beta 3-selective agonists was effective, the remarkably high potency of SR 59230A as a stereospecific antagonist of non-beta 1 non-beta 2 relaxation of human colonic muscle by isoprenaline provides strong functional evidence of beta 3-adrenoceptors in that tissue.

To determine the existence of beta 3-adrenoceptors in functional assays in isolated preparations for which data are lacking, we compared the effects of SR 58611A, a selective beta 3-adrenoceptor agonist, and isoprenaline in the guinea pig common bile duct, distal colon and urinary bladder. SR 58611A and isoprenaline relaxed the common bile duct (EC50: 6.85 and 0.41 mumol/l, respectively). The effect of SR 58611A was resistant to CGP 20712A, ICI 118551, propranolol and tetrodotoxin, but was antagonized by alprenolol (pA2 = 6.86), while the effect of isoprenaline was antagonized by CGP 20712A, ICI 118551, propranolol and alprenolol (pA2 = 7.04, in the presence of propranolol to saturate beta 1- and beta 2-adrenoceptors). In colonic preparations, SR 58611A and isoprenaline relaxed circular muscle strips (EC50: 5.48 and 0.49 mumol/l, respectively). The effect of SR 58611A was resistant to CGP 20712A, ICI 118551, propranolol and tetrodotoxin, but was antagonized by alprenolol (pA2 = 7.01). The effect of isoprenaline was resistant to CGP 20712A, but was antagonized by ICI 118551, propranolol and alprenolol (pA2 = 6.88, in the presence of propranolol). In urinary bladder strips, SR 58611A had no effect, whereas isoprenaline reduced resting tone (EC50:0.87 mumol/l), an effect antagonized by alprenolol (pA2 = 8.14). These data provide functional evidence for the presence of beta 3-adrenoceptors in the guinea pig common bile duct and colon, but not in the urinary bladder. At the concentrations used, the effect of SR 58611A was probably mediated solely by activation of beta 3-adrenoceptors located on smooth muscle cells, whereas the effects of isoprenaline were due to beta 3- and also to beta 1-and/or beta 2-adrenoceptor activation.

1. In order to clarify whether atypical or beta 3-adrenoceptors can modulate canine colonic motility in vivo, we studied the effects of SR 58611A (a selective agonist for atypical beta-adrenoceptors) alone and after pretreatment with beta-adrenoceptor antagonists on colonic motility in the conscious dog. The gastrocolonic response (postprandial increase in motility) was monitored by means of electrodes and strain-gauge force transducers chronically implanted along the distal colon. In some experiments, heart rate was also measured. The possible role of beta 3-adrenoceptors in mediating the effects of SR 58611A was also tested in vitro in circular muscle strips taken from the canine distal colon. 2. Intravenous infusion of SR 58611A, ritodrine or isoprenaline at doses inducing the same degree of tachycardia inhibited the gastrocolonic response to a different extent, with SR 58611A and ritodrine being more effective than isoprenaline. 3. In a dose-response study, SR 58611A was more potent in inhibiting colonic motility than in inducing tachycardia: the ED35 values for inhibition of colonic motility and induction of tachycardia were 23 and 156 micrograms kg-1, i.v., respectively. 4. The inhibitory effect of SR 58611A 100 micrograms kg-1, i.v., on the gastrocolonic response was reversed by alprenolol (non-selective beta-adrenoceptor antagonist), but resistant to CGP 20712A (beta 1-adrenoceptor antagonist) or ICI 118551 (beta 2-adrenoceptor antagonist). 5. In vitro, SR 58611A concentration-dependently relaxed circular muscle strips, an effect that was competitively antagonized by alprenolol with a pA2 value of 7.1, but resistant to CGP 20712A (100 nM), ICI 118551 (100 nM) or tetrodotoxin (1 microM). 6. The present study provides strong functional evidence for a role of atypical or beta 3-adrenoceptors in the modulation of canine colonic motility both in vivo and in vitro by an inhibitory effect most likely at the smooth muscle level.

The effectiveness of amiodarone and quinidine in converting atrial fibrillation of recent onset (less than three weeks) to sinus rhythm was compared in a randomized, open-label study. Patients with signs of heart failure determining a NYHA class 3 or 4, acute myocardial infarction, unstable angina pectoris, sick sinus syndrome, Wolff-Parkinson-White syndrome, conduction disturbances, dysthyroidism, or undergoing concomitant therapy with antiarrhythmic drugs, were excluded from the study. Sixty-eight consecutive patients were randomized to receive amiodarone (group A) or quinidine (group B). Group A was treated with amiodarone intravenously as a bolus of 5 mg/Kg over a 20 min period followed by a 15 mg/Kg infusion during the first 24 hours and then orally at a dose of 0.4 g every 6 hours. Group B was treated with quinidine sulphate orally at a dose of 0.2 g every 6 hours during the first day; 0.4 g every 6 hours the second day and 0.6 g every 6 hours during the third day of therapy. Quinidine was preceded by rapid intravenous digitalization depending on the patient's clinical status so as to obtain a ventricular rate of about 100 beats/min, with subsequent oral digitalis administration in maintenance doses. Both treatments were continued until conversion or for a maximum of three days. If the sinus rhythm was not restored, patients underwent electrical cardioversion. Drug efficacy was assessed on the basis of conversion to sinus rhythm. Six patients converted to sinus rhythm with intravenous digitalization alone and were excluded from the comparison between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The incidence of ventricular arrhythmias during muscular work in 400 patients hospitalized for clear or suspected coronary artery disease who underwent coronaroangiography and exercise test was studied. The correlations between the arrhythmias and some hemodynamic parameters and the coronaroangiogrphy patterns and left ventricle cineangiography were investigated. None of the factors that were supposed to be significant in the mechanism of the ventricular arrhythmias, such as high left ventricular end dyastolic pressure, modified myocardial contractility, previous myocardial infarct, or higher lesions of coronary arteries, gave significant correlations. In the present study, the ventricular arrhythmias during muscular work do not seem to be of diagnostic significance.

--123 atrial pacings (AP) performed as diagnostic investigations in patients with chest pains were re-examined. By using floating catheter without fluoroscopic control, this technique is very simple to perform and free from relevant risks. The diagnostic sensibility and specificity of AP were examined in 93 patients in which a coronary arteriography was performed; these figures were compared with the corresponding values observed in 65 patients in which an adequate diagnostic exercise test (ET) was also available. The diagnostic sensibility of AP examined in 63 patients with significant coronary artery disease was 90%; the corresponding value of ET was 79%. In particular, in patients with single vessel disease, the sensibility of AP (90%) was much higher than that observed in ET (40%). The specificity of AP examined in 30 patients free from significant stenosis of the coronary arterial tree was 43%. This value was largely lower than that observed in ET (82%) in the same patients, and appears to be inadequate for validation AP as a diagnostic tool in coronary heart disease. Therefore, AP must be limited to functional, and not diagnostic, evaluation of patients in which the diagnosis of coronary heart disease can be made by other means.

The efficacy of transdermal nitroglycerin patches, releasing 20 mg of active substance over a period of 24 h (TDN 20), was investigated in 10 patients with stable exercise-induced angina pectoris. The study was divided into 3 periods: the first part was an acute, within-patient, crossover, double-blind, placebo-controlled study, in which patients performed a cycloergometric exercise test 4 and 24 h after the application of the patches (TDN 20 or placebo). During the 2nd period, patients were given TDN 20, in single blind conditions, for 4 weeks and another exercise test was performed, on the last day, 4 and 24 h after patch application. Finally, after a one-day placebo wash-out, a second acute study similar to the first was performed. Four h after dosing, exercise duration to 1 mm ST segment depression was 441 s and 314 s (p less than 0.01) for TDN 20 and placebo, respectively (first acute study), 394 s for TDN 20 after chronic treatment (p less than 0.001 vs acute placebo) and 472 and 354 s (p less than 0.001) for TDN 20 and placebo, respectively (second acute study). No difference in exercise duration to 1 mm ST segment depression was found between TDN 20 and placebo, 24 h after administration, in any of the periods. Blood pressure significantly decreased and heart rate significantly increased 4 h after TDN dosing (in comparison with placebo) in both the acute studies, but no difference was observed after chronic TDN treatment. In conclusion, TDN 20 increases exercise tolerance 4 h after the application of both acute and chronic treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Among 173 patients with typical effort angina (159 men and 14 women) which underwent exercise test and coronary angiography, significant stenosis (greater than or equal to 70%) of one or more of important coronary branches were present in 93,1% of the cases (96,3% among the males and 57% among the females). In the same group the exercise test sensitivity was 88,8%; when 3 coronary branches were involved the sensitivity rises to 94,3%. The 96,6% of patients with positive exercise test had coronary lesions too (true positives). We did not find any correspondence between the site of transient subendocardial ischemia occurred during the exercise test and coronary branch involved, when the stenosis was limited only one important coronary branch. Finally the researche of correlation between the entity of coronary disease (number of coronary vessels involved, entity of left ventricular contractility impairment) and behavior of patient during exercise test, evaluated with different parameters measured at the moment of stopping of exercise (heart rate and threshold work load, rate-pressure product, maximal downsloping of ST segment, different positivity criteria for exercise test) allowed us to show a good correlation only between the extent of coronary involvement and rate-pressure product or maximal downsloping of ST segment.

To obtain information on endocardial activation-sequence, unipolar recordings at seven left ventricular and six right ventricular points were performed in a 37-year-old man suffering from cardiomyopathy and tachycardia-dependent left bundle branch block (LBBB). Results were as follows: 1) the recovery time was longer in anterior than in posterior portion of left bundle branch fibers; 2) an high posterior left ventricular point was directly activated via posterior left bundle branch fibers; 3) the directly activated left ventricular zone was too small and relatively too late excited in respect of the right interventricular septum, from which the stimulus reached the left septum, to mask the LBBB electrocardiographic pattern; 4) in the presence of tachycardia-dependent LBBB the duration of left ventricular endocardial activation was about twice (62 msec) that found in the absence of tachycardia-dependent LBBB (28 msec).

Three patterns of swallowing-induced supraventricular tachycardia in an asymptomatic young man are described. The patient had no esophageal disease. The electrophysiologic mechanism of arrhythmias remains speculative. Vagal stimulation produced by swallowing appears to cause tachcardias because atropine (1,5 mg iv) prevents their occurrrence.

The antianginal efficacy of nitroglycerin (NTG), given in a new transdermal therapeutic system (TTS), was compared with that of nifedipine and verapamil, both in slow-release (SR) formulation, in a randomized, double-blind, placebo-controlled study, carried out in 8 patients with stable exercise-induced angina pectoris. TTS NTG 40 cm2 (releasing 20 mg of NTG over 24 hours), nifedipine 20 mg SR, verapamil 120 mg SR and placebo were given once on 4 consecutive days according to a 4 X 4 latin-square design, twice replicated. A cycloergometric symptom-limited exercise test was performed 4 and 8 hours after the administration of each drug. Four hours post-dosing, mean exercise duration was 407 sec. after placebo and 523 (+28%) and 485 (+ 19%) sec. after TTS NTG and nifedipine SR respectively, while at the 8th hour it was 375 sec. after placebo, and 515 (+ 37%) and 457 (+ 21%) sec. after TTS NTG and nifedipine SR. Exercise duration after verapamil was similar to that after placebo. In comparison with placebo maximal workload and total work performed were significantly higher on TTS NTG and on nifedipine at both times of observation, but no significant differences were seen after verapamil. Peak exercise systolic blood pressure was nearly identical after all the treatments tested. Peak exercise heart rate and pressure rate product were both significantly higher on TTS NTG, as well as on nifedipine, in comparison with placebo, while values after verapamil did not differ from those after placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

To obtain information on normal left ventricular activation, endocardial recordings with an electrode catheter were made a seven left ventricular sites in ten patients undergoing diagnostic heart catheterization. All the patients had: 1) sinus rhythm; 2) normal duration and shape of the QRS complex of left chest leads; 3) normal left ventriculography, i.e. normal volume and contractility of the left ventricle. The earliest left ventricular endocardial activation was recorded at septal and/or posterior level, i.e. at the septum (6 to 16 msec, average 9.7 msec, after the onset of intracardiac QRS complex) in seven patients; at the posterior wall (0 to 4 msec, average 2.6 msec, after the onset of intracardiac QRS complex) in three patients (in one of these, the earliest activation occurred at the posterior wall and apex simulaneously). If the earliest activation occurred at the left interventricular septum, the next excited point was found on the posterior wall or at the apex, and vice versa. The latest part to be activated was on the lateral free wall in seven patients; on the posterior wall in two patients; at the apex in the last one.