Transesophageal echocardiographic evaluation of the morphologic and hemodynamic cardiac changes during ventricular fibrillation.

To analyze cardiac motion during ventricular fibrillation (VF), we used transesophageal echocardiography to study nine male subjects, aged 44 +/- 7 years, affected by heart disease who have poor left ventricular function, during implantation of an Implantable Cardioverter Defibrillator, when VF is induced several times to determine the defibrillation threshold. Wall and valvular motion, transmitral and transaortic blood flow, and blood echoreflectivity were evaluated in all patients. Moreover, in basal conditions, during VF, 1 and 5 minutes after restoration of basal rhythm, we calculated the left ventricular end-diastolic volume (EDLVV) and area (EDLVA), the left ventricular end-systolic volume and area, the ejection fraction, and the fractional area change with a four-chamber echocardiographic view. At the onset of VF, the myocardium and valves exhibited a chaotic motion. About 10 seconds later the oscillatory movement of the heart walls became more ample and regular; the mitral valve showed a cyclic closure and opening with a forward flow, and the aortic valve exhibited similar behavior, although at a lower intensity. A spontaneous echo contrast appeared inside the atrial and ventricular cavities, gradually becoming an incrt homogeneous mass that was completely flushed away with the restoration of the basal rhythm. When VF started, EDLVV (286 +/- 98 ml) and EDLVA (50 +/- 16.5 cm2) decreased abruptly (EDLVV = 182 +/- 65 ml, p < 0.02; EDLVA = 38 +/- 9.2 cm2,p < 0.05); so did ejection fraction (31.8% +/- 15% versus 11% +/- 5%; p < 0.003) and fractional area change (25.8% +/- 6.5% versus 7% +/- 3.4%; p < 0.001). When the basal rhythm was restored, the heart extended again and EDLVV, EDLVA, ejection fraction, and fractional area change after 1 and 5 minutes were similar to those calculated before induction of VF. This behavior was observed during both the first and last induced VF. Thus during VF, great variations of heart morphology and dynamics, as well as blood echoreflectivity, occur; the heart seems to make attempts to organize its dynamics during the arrhythmia. Repeated episodes of VF and defibrillation with low energies do not seem to worsen left ventricular dynamics even in impaired hearts.

[Acute and chronic cardiac decompensation: is vasodilator therapy useful?]. / Scompenso cardiaco acuto e cronico: è utile la terapia con vasodilatatori?

Systemic vasodilators represent a new approach in the treatment of the acute and chronic heart failure, as they reduce the afterload acting on the aortic impedance and/or the venous return to the heart. Vasodilators have been classified as venodilators (nitrates), which reduce left ventricular filling pressure and relieve pulmonary congestion; arteriolar dilators (hydralazine, phentolamine) which enhance cardiac output; and balanced vasodilator (nitroprusside, prazosin), which dilate both resistance and capacitance vessels. While nitroprusside and phentolamine are used in the treatment of the acute myocardial infarction, nitrates, hydralazine and prazosin are used in the long term treatment of the chronic congestive heart failure. Presumably, the renin-angiotensin system plays an important role in increasing peripheric vascular resistance in congestive heart failure. For this reason the inhibitors of the angiotensin-converting enzyme, such as captopril and teprotide, are also used. The treatment with vasodilators, recommended to patients with severe heart failure, is not an alternative to that with digitalis and diuretics: such a combination may in fact result as a very useful one.

[Changes in plasma ionized calcium levels during fluorescein angiography]. / Variation du calcium ionisé plasmatique au cours de l'angiographie en fluorescence.

The authors have demonstrated a significant decrease of the plasmatic ionized calcium level in 84 patients during retinal fluorangiography likely due to a chemical bond between calcium and fluorescein. The side effects noticed during the procedure were similar to that quoted in the literature; their frequency, however, was not correlated with the decrease of the plasmatic ionized calcium level, even though the magnitude of the decrease was twice as great in the patients who experienced some trouble as in those who did not. This lack of correlation may be related to the too small patients sample. A greater frequency of side effects has been noticed in patients treated by calcium inhibitors.

[Effects of nifedipine in patients with chronic obstructive bronchitis and pulmonary hypertension undergoing artificial respiration]. / Effets de la nifédipine chez les bronchitiques chroniques obstructifs avec hypertension pulmonaire soumis à la ventilation artificielle.

During an acute decompensation of chronic obstructive pulmonary disease (COPD) associated with pulmonary arterial hypertension (PAHP), the right cardiac ventricle is unable to tolerate the increased workload required to overcome the increase in pulmonary arterial pressure (Ppa). As a result, the cardiac (CI) and systolic (SI) indices decrease much more than in those patients without PAHP. This study aimed to evaluate the effects of nifedipine on haemodynamic parameters and oxygen availability (QO2) when given to mechanically ventilated COPD patients with PAHP during an acute decompensation. The series included 14 patients aged 68 +/- 8 yr, admitted to an intensive care ward for an acute decompensation of COPD, with Ppa greater than 20 mmHg. They remained haemodynamically stable throughout the study period. The measurements were made 20 min after the Swan-Ganz and radial artery catheters were set up (t0), and one hour after administration of 10 mg sublingual nifedipine (t1). Thereafter this agent was given three times a day. A further set of measurements were carried out in seven patients, 24 h after the first dose of nifedipine (t2). At t1, there was a significant increase in CI (+12.3%) and QO2 (+14.1%), whereas Ppa, indexed pulmonary vascular resistances, indexed systemic vascular resistances (SVRI) and PaO2 decreased significantly (-9.2%; -20%; -12.8% and -6.4% respectively). At t2, QO2 was significantly higher (+18.4%), whereas Ppa and SVRI were significantly lower, than at t0. PaO2 and the shunt fraction (Qs/Qt) returned to basal values, with a significant decrease in Qs/Qt when compared with t1.(ABSTRACT TRUNCATED AT 250 WORDS)

[Case report of a stage IV S neuroblastoma regressing without any aggressive treatment]. / Un caso di neuroblastoma stadio IV S regredito senza trattamenti aggressivi.

The authors describe a case of stage IV-S neuroblastoma in a boy forty days old with impressive enlargement of the liver whose left lobe was initially mistaken for splenomegaly. Regression was obtained without active treatment. Factors affecting the prognosis and treatment are briefly discussed. Is reported the association with persistent elevation of serum acid phosphatase.

Endothelin-1 and endothelin-3 stimulate insulin release by isolated rat pancreatic islets.

Endothelins (ETs) are potent vasoconstrictive peptides released from the endothelium and other tissues, which act on target cells by receptorial calcium-mediated mechanisms. ET-1 levels are increased in diabetes, and observations suggest the involvement of ETs in the pathogenesis of diabetic angiopathy. However, it is not possible to exclude that ETs might also influence insulin secretion or function. In vivo infusion of ET-1 in rats induces hypoglycaemia and hyperinsulinemia and in vitro incubation with ET-1 stimulates insulin release by mouse islets. Therefore, ETs might be involved in a circulus vitiosus, resulting in hyperinsulinemia and diabetic angiopathy. The purpose of our study was to verify the effect of ET-1 on rat islets, in both the presence and absence of physiological glucose concentration. Moreover, we tested the effect of another isoform of endothelins, ET-3, and verified the involvement of extracellular calcium in such events. Islets were incubated with increasing ET-1 or ET-3, with or without glucose 5.6 mM. Other samples were prepared using calcium-free medium. Incubation in medium containing ET-1 and ET-3, in the presence of glucose and calcium, induced an increase in insulin release. When ET-1 and ET-3 were incubated without glucose and calcium, insulin release was not modified. Our studies demonstrate that: 1) ET-3, like ET-1, stimulates insulin release by rat isolated islets; 2) direct insulin stimulating effect on islets of both ET-1 and ET-3 is evident with physiological glucose concentrations and is calcium mediated. These results support the hypothesis of ET involvement in the regulation of insulin secretion.