The rapid and sustained cardiac improvement seen in our patients shows that octreotide therapy for patients with acromegaly may be highly beneficial, even in those patients with advanced cardiac failure.

In 30 patients, simultaneous measurements of ascending aortic pressure and diameter were performed, allowing one to evaluate: (1) the influence of age, the aortic diastolic pressure, and the radius on the aortic elasticity; (2) the correlations between characteristics impedance of the aorta (Zo), systemic arterial resistance, age and diastolic aortic pressure; and (3) the importance of Zo when comparing two indices of left ventricle performance; one during isovolumic phase ([dP/dt]/Pt)max and the other during the outflow phase (maximum acceleration of aortic blood flow).

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An eighteen-year-old woman with pseudoxanthoma elasticum (PXE) suffered from mild angina pectoris over a ten-year period. Severe triple-vessel disease with mild left ventricular dysfunction was demonstrated on angiography. No revascularization was feasible. Despite a reported high frequency of angina pectoris among patients with PXE, only 10 convincing reports have appeared in the literature. Careful coronary artery evaluation is required in young patients with PXE, even though asymptomatic, because coronary artery disease (CAD) seems to be frequent and because no precise feature can be distinguished between types with or without severe vascular disease. Through very rare reports, surgical revascularization appears feasible and beneficial in a less severe form of CAD in patients with PXE. The risk of premature and severe diffuse CAD in PXE does not seem to be explained only by the combination of increased Lp [a] (or any other risk factor) and PXE.

Pretreatment with the low-molecular-weight heparin nadroparin continued for 3 months after balloon angioplasty had no beneficial effect on angiographic restenosis or on adverse clinical outcomes.

18 patients without valvular pathology, coronary artery disease, or idiopathic hypertrophic subaortic stenosis were haemodynamically and angiographically investigated in order to analyse the effects of a ventricular extrasystolic beat upon the post-extrasystolic left ventricular peak pressure. In eight normal patients (group I), the post-extrasystolic peak pressure (P.ES.P.P.) was lower than that of the pre-extrasystolic beat; in 10 patients with symptoms of left ventricular failure (group II) the P.ES.P.P. significantly increased. The reasons are: 1) cardiac origin: stroke volume increased more in group II; 2) arterial origin. a) aortic compliance was lower in group II (this is probably related to the older age of patients in group II), and by decrease in end-diastolic aortic pressure was smaller in group II. Part of this arterial effect (2b) may probably be explained from the fact that post-extrasystolic compensatory pauses are equal in both groups, but the decay time of arterial pressure during diastole (assuming an exponential decay) is larger in group II. At the same age and with the identical aortic compliance only the two factors 1 and 2b play a part in the changes in P.ES.P.P.

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