Iterative Atrial Tachycardia Originating from the Coronary Sinus Musculature

A case of iterative atrial tachycardia leading to dilated cardiomyopathy is reported. During electrophysiologic study, the tachycardia showed a markedly irregular cycle length associated with changes in atrial activation breakthrough as demonstrated by coronary sinus (CS) recordings and frequently degenerated into self-terminating atrial fibrillation. Left atrial transseptal mapping demonstrated the earliest endocardial atrial activation close to the posterolateral mitral annulus, but this was invariably later than that recorded within the CS, where low-energy radiofrequency applications eliminated the tachycardia. No acute vessel damage was observed at postablation CS angiography. In accordance with previously published experimental data, we hypothesized that the muscular sleeves surrounding the CS might be involved in the genesis of this tachycardia. During 6-month follow-up, the patient remained asymptomatic without tachycardia recurrences and with complete recovery of left ventricular function, confirming the reversible nature of the tachycardia-induced cardiomyopathy.     

Epidural Spinal Electrostimulatory System (ESES) in the Management of Diabetic Foot and Peripheral Arteriopathies

Epidural spinal electrostimulatory system (ESES) or dorsal column stimulation (DCS) may be used for the treatment of peripheral vascular diseases of the lower extremities. ESES has been used in our metabolic and surgical department as a way to ameliorate inadequate blood supply in patients suffering from diabetic foot (seven patients), painful chronic arterial narrowing, or inoperable occlusions (25 patients). The continuous stimulation by an implantable apparatus (Medtronic model Itrel, Medtronic, Inc., Minneapolis, MN, USA) led to a reduction or disappearance of pain, an improvement in plethysmographic curves, functional performance, and trophic lesions in about 75% of the patients. The system is safe and well-tolerated by patients.     

INTERACTION OF CLONIDINE AND GHRH ON GH SECRETION IN VIVO AND IN VITRO

To investigate the mechanism by which clonidine stimulates GH-secretion in vivo and in vitro, we studied its interaction with GHRH. In vivo: eight or six normal male subjects were submitted to five protocols: (1) 150 micrograms clonidine orally followed by 50 micrograms GHRH 1-44 i.v. 2 h later, (2) 50 micrograms GHRH 1-44 i.v. followed by 150 micrograms clonidine orally 2 h later, (3) 150 micrograms clonidine orally followed by GHRH i.v. 30 min later, (4) 300 micrograms clonidine orally followed by 50 micrograms GHRH i.v. 3 h later and (5) 50 micrograms GHRH i.v. followed by 300 micrograms clonidine orally 90 min later. In vitro: Rat anterior pituitary cells were coincubated with clonidine (10(-11), 10(-9), 10(-7) and 10(-5) M) and GHRH (0.005, 0.05, 10 nM) for 4 h. Results: 150 micrograms clonidine alone does not stimulate GH-secretion. Furthermore, the GH-increase was not significantly different when GHRH bolus was given before, after or together with clonidine. When 300 micrograms clonidine was given before GHRH GH-levels were significantly higher (max 28.6 +/- 8.0 mU/l) at 90 min, compared to when clonidine was given after GHRH (max 7.8 +/- 3.6 mU/l). The GHRH bolus after clonidine led to a significantly lower GH-increase (max 31.6 +/- 17.0 mU/l) compared to the GHRH-induced GH-increase (max 47.2 +/- 13.0 mU/l) before clonidine. In vitro, clonidine had no stimulatory effect on GHRH-stimulated GH secretion. These findings are compatible with clonidine leading to stimulation of GH by inducing endogenous GHRH release.     

Surgical Technique for Artificial Mitral Chordae Implantation

Failure of reconstructive procedures of the mitral valve is often ascribed to diffuse alteration of the subvalvular apparatus, which prevents the utilization of well-established techniques such as chordal transposition or shortening. For this reason, in 1986 after 2 years of animal experiments, we started the clinical use of expanded-polytetrafluoroethylene mitral chordae. Details of the surgical procedure are presented. Our experience is based on 51 patients with a mean follow-up of about 20 months (range 3-57). Four patients had the valve replaced during the same operation: one patient died later of cardiac failure and two underwent reoperation, 8 and 18 months after operation. Forty-one patients are in New York Heart Association Functional Class I and three in Class II. We suggest this technique in association with other traditional procedures to increase the number of mitral valves repaired, mostly because of degenerative etiology.     

Influence of Variable Loading Conditions on Pulsed Doppler Indices of Left Ventricular Ejection Dynamics

To investigate the influence of changes in loading conditions on Doppler echocardiography determination of left ventricular ejection dynamics (peak aortic flow velocity and mean acceleration), pulsed Doppler was performed on 20 patients from apical 5-chamber view. Doppler aortic flow velocity curves and hemodynamic values (left ventricular pressure, wedge pressure, and cardiac output) and the first derivative of ventricular pressure (dPIdt) by tip-transducer catheter were simultaneously recorded at baseline and during intravenous infusion of nitroglycerin as well as at baseline and immediately following left ventriculography. During nitroglycerin infusion, the hemodynamic values were reduced and peakdPIdt remained constant, Doppler aortic peak velocity and mean acceleration decreased significantly compared with baseline (0.87 ± 0.11 mlsec vs 1.01 ± 0.14 mlsec and 8.86 ± 1.68 ml sec² vs 10.17 ± 1.88 mlsec² respectively; bothP < 0.001). After ventriculography, the hemodynamic values increased and peak dPIdt was still constant, Doppler aortic peak velocity and mean acceleration increased significantly compared with baseline (1.15 ± 0.17 mlsec vs 0.98 ± 0.16 mlsec and 11.44 ± 2.06 mlsec² vs 9.79 ± 1.88 mlsec² respectively;both P < 0.001). In conclusion, left ventricular ejection dynamics, as evaluated by pulsed Doppler echocardiography, is modified by mild changes in loading conditions. Therefore, when serially evaluating the inotropic state of the left ventricle by the Doppler aortic flow velocity pattern, the potential influence of loading conditions should be takeninto account.