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Animal experiments suggest that an important component of the antihypertensive effects of ACE inhibitors might derive from an inhibition of the sympathetic vasomotor tone. We addressed this problem on 22 mildly hypertensive subjects (48 +/- 2 years; arterial pressure 151 +/- 3/95 +/- 1 mmHg), in whom sympathetic vasomotor tone was non invasively inferred by the power of the low frequency component (0.1 Hz) of the spontaneous oscillations of systolic arterial pressure (LFSAP), during placebo and after 4 weeks of treatment with a new ACE inhibitor, cilazapril, 5 mg per os oid. LFSAP was computed at rest and during physical (active orthostatism) and mental (computerized attentional test and mental arithmetic) stimuli capable of enhancing sympathetic drive. Cilazapril treatment reduced resting arterial pressure to 128 +/- 3/80 +/- 2 mmHg, without affecting heart rate (78 +/- 2 and 74 +/- 2 b/min, respectively). The increases in LFSAP produced by standing were significantly greater during placebo than during active treatment (delta LFSAP = 10 +/- 3 and 5 +/- 2 mmHg2, respectively). These data suggest that an important reduction of sympathetic vasomotor tone accompanies the antihypertensive effects of chronic ACE-inhibitor treatment.

Using digitized M-mode ecocardiography, 26 young subjects with type I diabetes mellitus of at least three years duration, without any clinical evidence of heart disease have been studied, searching for subclinical impairment of left ventricular function. Patients have been divided in two groups according to the presence (Group I, N degrees 7 patients) or absence (Group II, N degrees 19 patients) of retinopathy. The time interval from the shortest left ventricular diameter to the onset of mitral valve opening was significantly increased as compared with the control Group (10.20 +/- 8.88 control Group; 29.21 +/- 12.99 Group II, p less than 0.001; 41.00 +/- 12.29 Group I, p less than 0.001). Furthermore, a close correlation between the above named time interval and the duration of diabetes was found (r = 0.496, p less than 0.01). Finally, the change of left ventricular dimension during the time interval from the shortest left ventricular diameter to the onset of mitral valve opening, expressed as a percentage of left ventricular end-diastolic diameter, was increased (3.20 +/- 3.43 control Group; 8.21 +/- 5.51 Group II, p less than 0.02; 12.43 +/- 5.56 Group I, p less than 0.001). Our results suggest an impairment of ventricular relaxation due to increased wall stiffness. We conclude that there are often subclinical cardiac abnormalities in young diabetics resulting in impairment of diastolic function that is correlate with the duration of diabetes and with the presence of clinical complications such as retinopathy.

Thirty eight acromegalic patients (A) and a control group (C) of subjects without heart disease, were studied with echocardiography. Acromegalies were divided in two groups, A1 and A2, who had increase or normal serum growth hormone (GH) levels respectively after treatment (pituitary adenectomy and/or bromocriptine), at the time of the study. In acromegalic patients (A) mean left ventricular (LV) dimensions were normal while LV wall and septal thickness, LV mass and left atrial (LA) dimension were increased compared to control subjects. LVH was present in 79% of acromegalic patients. Asymmetric septal hypertrophy (ASH) was found in 10,5% of our patients. In group A1, IVS, LVPW, LVMM/m2 were significantly increased as compared to group A2. Fractional shortening (FS), ejection fraction (EF), mean velocity of circumferential fibre shortening (Vcf), frequency-normalized Vcf (Vcfn), posterior left ventricular wall velocity (PWV), and normalized PWV (PWVn) were normal in both groups. In patients with active acromegaly (Al) IVS and LVMM/m2 correlated well with the total duration of the disease (r=0.550 p less than 0.01 for IVS; r=0.624 p less than 0.01 for LVMM/m2) and with the duration of acromegaly before treatment (r=0.568, p less than 0.01 for IVS; r=0.500 p less than 0.01 for LVMM/m2). Furthermore a positive correlation was found between IVS and GH levels (r=0,550 p less than 0.01). Concomitant coronary artery disease and or hypertension did not seem to play any role in causing the above mentioned echocardiographic changes. Echocardiography is useful in assessing the cardiac involvement in patients with acromegaly.

The purpose of this study is to evaluate four methods of determining left ventricular stroke volume (SV) from aortic valve (AV) and aortic root (AR) M-mode echocardiogram (Table I, formulas 1-4); secondly, to study relations between echocardiographic aortic variables and SV. We studied 20 patients (Pts) in our Coronary Unit, 14 men and 6 women; their ages ranged from 38 to 76 (mean 53.4) years. Seventeen Pts had acute myocardial infarction; two Pts had previous myocardial infarction and heart failure; one Pt had dilated cardiomyopathy and heart failure. Three out of the twenty Pts, had mitral insufficiency (Table II, clinical and hemodynamic data). Patients were studied with high quality M-mode echocardiography. Immediately after the examination repeated measurements of cardiac output by thermodilution technique (TD) were carried out, and values of SV calculated (SV-TD). Twenty-five complete procedures were accomplished. The formulas were applied to every patient's echocardiographic data, and results (SV-ECHO) compared with SV-TD (Table III). Echocardiographic variables, whether single or multiple (terms), were also studied with regard to their relation with SV-TD (Table IV). Mean +/- SD value of SV-TD of the study group was 60.3 +/- 24.7 ml; range 22.7 to 108 ml. Mean +/- SD values of SV-ECHO were as follows: Yeh's formula, based on squared mean AV opening and LVET, 56 +/- 22.6 (ml), r = 0.8278, SEE 12.98; Jacobs' formula, based on aortic box planimetry, 68 +/- 32.5 (ml), r = 0.7129, SEE 23.31.(ABSTRACT TRUNCATED AT 250 WORDS)

In 11 subjects with mild hypertension (sitting arterial pressure of 146 +/- 5/97 +/- 2 mm Hg), the effects of chronic angiotensin-converting enzyme (ACE) inhibition (cilazapril, 5 mg p.o. once daily for 4 weeks) were studied at rest and during active standing by means of spectral analysis. Sympathetic vascular control was inferred from the power of the low-frequency (LF) component of the systolic arterial pressure (SAP) variability, assessed noninvasively with a plethysmographic technique. Simultaneously, quantitative indices of neural control of the sinoatrial (SA) node were obtained with the power of the LF and of the high-frequency (respiration linked) component of R-R variability. Before treatment, active standing produced a clear increase in the LF components of R-R and SAP variabilities. At the end of the 4 weeks of cilazapril treatment, the LF component of SAP variability during standing was significantly lower than prior to treatment, while the increase in the LF component of R-R variability was left unchanged. These findings suggest an inhibitory effect of chronic ACE inhibition upon vasomotor sympathetic control, as assessed non-invasively by this technique.