Biomedical subjects

A Cittadini

Publications and source records attributed to A Cittadini.

At least 91 records · Page 5Linked to original sources

PubMed1995

Diastolic dysfunction in patients on thyroid-stimulating hormone suppressive therapy with levothyroxine: beneficial effect of beta-blockade.

Thyroid-stimulating hormone (TSH) suppressive therapy with levothyroxine (L-T4) may cause adverse cardiac effects such as rhythm disturbances and ventricular hypertrophy. The latter is a predisposing condition to diastolic dysfunction. Thus, this study was designed to assess the effect of long-term TSH suppressive therapy on cardiac diastolic function. Because beta-blockade is known to reduce ventricular hypertrophy in patients on L-T4 therapy, we also tried to determine whether the addition of a beta-blocker to L-T4 improved diastolic function. Twenty-five patients (21 female and 4 male; mean age 41 +/- 10 yr) on TSH suppressive therapy for 3-9 yr (9 for differentiated carcinoma and 16 for nontoxic goiter) and 20 control subjects were studied. A subgroup of 10 patients, selected for the presence of symptoms and signs of adrenergic overactivity, was treated for 4 months with the beta-blocker bisoprolol (4.25 +/- 1.2 mg/day), and their maintaining L-T4 therapy was unchanged. In the patient group, left ventricular mass was significantly increased (P < 0.001), isovolumic relaxation time was prolonged (P < 0.001), and early diastolic filling velocity was markedly reduced (P < 0.001), whereas late diastolic filling was increased (P < 0.005). Consequently, the early-to-late diastolic flow velocity ratio was markedly decreased (P < 0.001). These alterations were more pronounced in the subgroup of patients with evidence of adrenergic overactivity. In these patients, beta-blockade induced a significant regression of cardiac hypertrophy and improved diastolic dysfunction. In particular, isovolumic relaxation time decreased (P < 0.01) and the early-to-late flow velocity ratio increased significantly (P < 0.01). Both indices reached values after beta-blockade that were no longer different from those of asymptomatic patients. It is concluded that long-term L-T4 therapy increases myocardial mass and causes relevant diastolic dysfunction, particularly in those patients with evidence of mild hyperthyroidism and adrenergic overactivity. Both myocardial hypertrophy and diastolic dysfunction are significantly improved by adrenergic beta-blockade.

Adult↗

PubMed1995

Impaired left ventricular diastolic filling in patients with acromegaly: assessment with radionuclide angiography.

UNLABELLED: Acromegaly is associated with increased cardiac morbidity and mortality, but it is not clear whether this is the result of a specific disease of heart muscle or of increased incidence of hypertension. METHODS: Twenty-six patients with acromegaly (11 male and 15 female, mean age 45 +/- 13 yr) and 15 and 12 age- and sex-matched normal controls underwent high temporal resolution radionuclide angiography and two-dimensional echocardiography at rest. RESULTS: Normal controls and patients with acromegaly did not differ with respect to heart rate, ejection fraction, time to end systole, peak ejection rate (PER) and time to PER. In contrast, peak filling rate (PFR), normalized to end diastolic volume (EDV), or stroke volume (SV), or expressed as the ratio of PFR-to-PER was reduced (p < 0.01), time to PFR (TPFR) was prolonged (p < 0.01), and echocardiographic left ventricular mass index was higher (p < 0.001) in patients with acromegaly compared to normals. Patients with acromegaly were divided in normotensives (group 1, n = 17) and hypertensives (group 2, n = 9). Although left ventricular mass index was significantly (p < 0.01) higher in group 2 compared to group 1, PFR and time to PFR were not different between the two groups of acromegalic patients. In the entire group of patients with acromegaly significant relationships between left ventricular mass index and EDV/s (r = -0.56, p < 0.01), SV/s (r = -0.73, p < 0.001), and PFR/PER (r = -0.61, p < 0.001) were observed. CONCLUSION: Patients with acromegaly have impaired left ventricular diastolic filling at rest related to greater left ventricular mass index even in the absence of systemic hypertension.

Acromegaly↗

PubMed1994

cAMP activates magnesium efflux via the Na/Mg antiporter in ascites cells.

In intact ascites cells magnesium efflux is substantially stimulated by cAMP analogues and by low concentrations of prostaglandins (PGE1 and PGE2) which increases the synthesis of cAMP. cAMP stimulates magnesium efflux by directly stimulating the Na-Mg antiporter rather than determining a magnesium release from mitochondria as reported for other cell types. Protein kinase inhibitors abolish the cAMP stimulated magnesium efflux suggesting that the stimulation is mediated by the phosphorylation of the carrier protein, increasing its affinity for intracellular magnesium. These data provide evidence that receptor-mediated stimuli eventually leading to cell activation are directly connected to the regulation of intracellular magnesium.

Animals↗

PubMed1994

Characterization of magnesium efflux from Ehrlich ascites tumor cells.

Magnesium efflux from intact Ehrlich ascites tumor cells (EATC) has been characterized under 0-trans conditions. It is shown that a magnesium-extruding mechanism operates in these cells which brings about magnesium efflux up to 20% of the cell total content. EATC magnesium efflux is independent from extracellular Ca2+ and its apparent velocity is not affected by [Mg2+]o up to 160 microM. This extrusion, however, is strictly dependent on extracellular Na+ and it is inhibited by ouabain (1 mM), amiloride (1 mM), imipramine (0.5 mM) and quinidine (1 mM). It is not affected by HMA (5-N,N-hexamethylene) amiloride) (0.5 microM) and vanadate (0.1 mM). Bumetanide (0.5 mM) enhances magnesium extrusion in these cells. EATC magnesium extrusion can be significantly stimulated by db cAMP, forskolin, and IBX (3-isobutyl-1-methyl-xanthine). The intracellular magnesium distribution, studied also by means of the ionophore A23187, is regulated by energy metabolism and cell ATP content. Altogether our data demonstrate that EATC exhibit a magnesium extrusion sustained by Na+ gradient across the plasma membrane and carried out by a Na+/Mg2+ antiport. In these cells magnesium homoeostasis results, regulated efficiently by cell ATP and cAMP content.

1-Methyl-3-isobutylxanthine↗

PubMed1994

Impaired cardiac performance in GH-deficient adults and its improvement after GH replacement.

Cardiac performance was investigated by radionuclide angiography in 11 patients with childhood-onset growth hormone (GH) deficiency and in 12 control subjects. Both at rest and during maximal physical exercise, systolic function was markedly depressed in GH-deficient patients. Ejection fraction rose from 66 +/- 6 to 76 +/- 7% during exercise in control subjects, whereas in GH-deficient patients it remained unchanged or even decreased (55 +/- 6 and 54 +/- 9% at rest and after exercise, respectively; P < 0.01 vs. controls). Cardiac index was significantly lower in GH-deficient patients than in controls, both at rest (2.7 +/- 0.6 vs. 3.7 +/- 0.5 l.min-1.m-2; P < 0.001) and during exercise (8 +/- 1.2 vs. 10 +/- 1.5 l.min-1.m-2; P < 0.01). Five GH-deficient patients were treated with recombinant human (rh) GH for 6 mo at a dose of 0.05 IU.kg-1.day-1. Cardiac index at rest improved from 2.8 +/- 0.6 to 3.3 +/- 0.8 l.min-1.m-2 (P < 0.01) after rhGH. Also, cardiac index response to exercise improved markedly and became similar to that of controls (7.5 +/- 1.2 and 10.1 +/- 1.1 l.min-1.m-2 before and after rhGH, respectively; P < 0.005). Exercise tolerance was impaired in GH-deficient patients and was restored by rhGH treatment. The data support the hypothesis that GH plays an important role in the maintenance of a normal cardiac performance in humans.

Adult↗

PubMed1994

Growth hormone and the heart.

GH exerts direct effects on myocardial growth and function. Evidence from laboratory models shows that GH (or IGF-I) induces mRNA expression for specific contractile proteins and myocyte hypertrophy. Furthermore, GH increases the force of contraction and determines myosin phenoconversion toward the low ATPase activity V3 isoform. These data provide plausible explanations for the cardiac abnormalities observed in clinical settings of excessive or defective GH production. In acromegaly, the functional consequences of GH excess initially prevail (hyperkinetic syndrome), followed by alterations of cardiac function when myocardial hypertrophy develops. This involves both ventricles and is purposeless because it occurs without increased wall stress. Hypertrophy also entails proliferation of the myocardial fibrous tissue that leads to interstitial remodeling. The functional consequence is an impaired ventricular relaxation that causes a diastolic dysfunction, followed by impairment of systolic function. In untreated disease, cardiac performance slowly but inexorably deteriorates and heart failure eventually develops. Several lines of evidence support the specificity of heart disease in acromegaly. Particularly demonstrative are the recent studies in which GH production was suppressed by octreotide, with a consequent significant regression of hypertrophy and improvement of cardiac dysfunction. It is not yet established whether full recovery of normal cardiac morphology and function is possible after correction of GH excess. The point is not a minor one since the possibility to revert, albeit partially, myocardial fibrosis is of great relevance to the control of cardiac hypertrophy in general. GHD leads to a reduced mass of both ventricles and to impaired cardiac performance with low heart rate (hypokinetic syndrome). These alterations are particularly evident during physical exercise and might provide an important contribution to the reduced exercise capacity of GHD patients, in addition to the reduced muscle mass and strength. The data also support a role of GH in the maintenance of a normal cardiac structure and performance. The hypokinetic syndrome is well documented in young patients in whom GHD began very early in their childhood. In contrast, the data in adult-onset GHD are less consistent. This suggests that the consequences of GHD are more relevant if the disorder starts during early heart development. As observed with other abnormalities associated with GHD, cardiac dysfunction is also susceptible to marked improvement by hrGH. This observation lends further support to the proposal to treat these patients with replacement therapy.

Acromegaly↗

PubMed1994

Control of adrenergic overactivity by beta-blockade improves the quality of life in patients receiving long term suppressive therapy with levothyroxine.

Several symptoms and signs of hyperthyroidism are frequently shared by patients receiving L-T4 suppressive therapy. The aim of this study was to evaluate whether a beta-adrenergic blocking drug could reduce the severity of these symptoms and signs in these patients, as previously reported in patients with hyperthyroidism. Eleven patients (mean age, 42 +/- 11 yr; 10 females and one male) affected with differentiated thyroid carcinoma or nontoxic goiter were selected from a more numerous group of patients receiving suppressive therapy based on the presence of palpitations, increased heart rate, left ventricular systolic function, and other symptoms mimicking exaggerated beta-adrenergic activity. In these patients the cardioselective beta-blocking drug bisoprolol was added to the L-T4 suppressive therapy at a dose of 2.5-5 mg/day. Blood samples were collected for the determination of thyroid hormones and TSH concentration during L-T4 therapy and after 3 and 6 months of associated L-T4 plus bisoprolol therapy. Cardiac function was assessed by clinical evaluation, standard and Holter electrocardiogram, as well as one- and two-dimensional echocardiography. Furthermore, we applied the symptom-rating scale previously used by Klein et al. in hyperthyroid patients to assess the quality of life in our group of patients. Our findings show that the addition of bisoprolol to L-T4 suppressive therapy produces a normalization of heart rate, which was significantly increased during TSH suppressive therapy, and the disappearance of atrial arrhythmias with considerable reduction of palpitations. Furthermore, bisoprolol produced an effective improvement in measures of the hyperthyroid symptom scale, with significant reduction of the mean score. The echocardiographic data showed an increased left ventricular mass index with significantly enhanced systolic function at the basal evaluation. After 6 months of combined L-T4 plus bisoprolol therapy, left ventricular mass index normalized, and the indices of left ventricular systolic function were reduced, with a tendency to normalize. Further studies conducted on a larger series of patients are required to verify the long term implications of cardiac parameter variations on cardiovascular morbidity and mortality. Our results, however, show that the addition of bisoprolol to L-T4 suppressive therapy improves the quality of life in those patients with clinical features of enhanced adrenergic activity.

Adult↗

PubMed1994

Impaired cardiac performance is a distinct feature of uncomplicated acromegaly.

This study was designed to assess right and left ventricular function in patients with active acromegaly. To this end, 26 acromegalic patients (9 of whom had arterial hypertension) and 15 normal subjects of comparable age and sex distribution were studied by radionuclide angiography at rest and during supine bicycle-ergometer exercise and echocardiography. At rest, the filling rates of left (-19%; P < 0.005) and right ventricle (-32%; P < 0.001) were significantly reduced in acromegalic patients, whereas right and left ventricle ejection fractions (EFs) were normal. During physical exercise, EF was considerably lower in the acromegalic patients than in controls. This was true for both left (61 +/- 11% vs. 75 +/- 8%; P < 0.001) and right ventricle (45 +/- 13 vs. 58 +/- 11%; P < 0.002). In as many as 73% of patients, EF increased less than 5%, thus fulfilling the criteria for impaired cardiac performance. Left ventricular mass index was 60% greater in acromegalics than in controls (P < 0.001). A significant difference in left ventricular mass index was also present when normotensive acromegalic patients were compared with controls (P < 0.001). No significant difference in the indices of systolic and diastolic function was observed between the subgroups of normotensive and hypertensive acromegalics, either at rest or during exercise. The data demonstrate that in uncomplicated acromegaly, besides cardiac hypertrophy, there are also important alterations of systolic and diastolic function of both ventricles, leading to a significant impairment of cardiac performance.

Acromegaly↗

PubMed1994

Mg deficiency induces mineral content changes and oxidative stress in rats.

We have studied the effect of Mg deficiency on both tissue mineral content and liver oxidative status. Male Wistar rats kept for eight weeks on a Mg-deficient diet (Mg 152ppm) quickly developed a severe plasma Mg deficiency (73% decrease). The content of Cu and Fe significantly increased in different tissues following the treatment. Liver glutathione, CuZn-superoxide dismutase, and vitamin E were significantly reduced (by about 16%, 18% and 30% respectively). Lipid peroxidation, induced in vitro by NADPH/ADP-Fe3+ and measured as MDA formation, increased by about 100% after 20 min incubation in liver microsomes isolated from Mg-deprived rats. The alterations found in the content of transition metals and in the level of both cytosolic and membrane antioxidants, as well as the higher sensitivity of liver microsomes to lipid peroxidation in vitro, are consistent with an oxidative stress occurring in vivo in the tissues of Mg-deficient animals.

Adenosine Diphosphate↗

PubMed1993

Evidence for biventricular involvement in acromegaly: a Doppler echocardiographic study.

To investigate left and right ventricular involvement in acromegaly, 20 patients were studied by Doppler echocardiography. Nine of them had systemic hypertension. Right ventricular free wall thickness was significantly increased in acromegalic patients (8 +/- 2 vs 4 +/- 1 mm; P < 0.001). Left ventricular mass index was augmented both in the whole group and in the subgroup of normotensive acromegalics, as compared with normals (134 +/- 33 and 115 +/- 20 vs 80 +/- 18 g.m-2; P < 0.01). Ejection phase indices were normal in the patient group, while impaired left and right ventricular diastolic filling was found. In fact isovolumic relaxation time was prolonged (118 +/- 21 vs 78 +/- 12 ms; P < 0.001), ratio of early to late mitral (0.9 +/- 0.3 vs 1.8 +/- 0.5; P < 0.001) and tricuspid (1.0 +/- 0.2 vs 1.4 +/- 0.3; P < 0.001) flow velocities were significantly decreased as compared with controls. Superior vena cava flowmetry was also abnormal showing a marked decrease of diastolic filling wave and, consequently, of the ratio between peak diastolic and peak systolic flow velocity. No significant differences were observed between normotensive and hypertensive acromegalics, except for left ventricular mass index (115 +/- 20 vs 156 +/- 31 g.m-2; P < 0.01). These findings indicate that abnormal diastolic filling patterns of transmitral, transtricuspid, and superior vena cava flowmetry suggesting 'impaired relaxation' associated with increased left and right ventricular mass, frequently occur in acromegaly.

Acromegaly↗

PubMed1993

Platelet aggregability in patients with a VVI pacemaker.

Several studies have suggested an increased incidence of thromboembolic events in patients with VVI pacemaker (VVI patients); furthermore, other authors have demonstrated that a treatment with anticoagulants or antiplatelet drugs may be effective in reducing thromboembolic events, thus suggesting an increased formation of platelet thrombi in these patients. In this respect, platelet aggregability was investigated in ten VVI patients and ten age- and sex-matched subjects. beta-thromboglobulin (beta-Tg) and platelet factor 4 (PF4) plasma levels were determined as well as platelet aggregation induced by ADP, collagen, epinephrine, and arachidonic acid. Plasma beta-Tg levels were increased in the patient group (86 +/- 24 vs 24 +/- 13 ng/mL; P < 0.001) in presence of normal PF4 values (14 +/- 11 vs 13 +/- 6 ng/mL; NS). Aggregation curves showed abnormal values of maximal amplitude, slope, and lag time. In particular, maximal amplitude was significantly higher in VVI patients as compared with controls (ADP P < 0.01, collagen P < 0.001, adrenaline P < 0.01, arachidonic acid P < 0.05). These findings strongly suggest an increase of platelet activity in VVI patients.

Adenosine Diphosphate↗

PubMed1993

Cardiac effects of long term thyrotropin-suppressive therapy with levothyroxine.

To investigate the effects of long term thyroid hormone suppressive therapy on the heart, 20 patients were evaluated by noninvasive techniques. Of them, 10 were athyreotic after surgery for differentiated thyroid cancer, and 10 had diffuse or nodular goiter. The mean age of the group was 39 +/- 11 yr. Twenty age- and sex-matched subjects served as controls. The mean dose of levothyroxine was 163 +/- 34 micrograms daily. Plasma TSH was undetectable in all patients. Mean serum T4, free T4, and sex hormone-binding globulin were significantly higher (P < 0.001), whereas mean serum T3, free T3, and osteocalcin did not differ from control levels. Cardiac evaluation consisted of a standard 12-lead electrocardiogram, an ambulatory electrocardiographic monitoring (Holter), and an echocardiographic study. Two patients showed abnormal electrocardiograms for left ventricular hypertrophy. Holter demonstrated an increase in average heart rate (84 +/- 7 vs. 70 +/- 6 beats/min; P < 0.01). Prevalence of atrial premature beats was higher in the patient group than in the control group (100% vs. 60%; P < 0.006). The echocardiogram showed an increased left ventricular mass index in the patient group (97 +/- 24 vs. 80 +/- 18 g/m2; P < 0.02). Furthermore, left ventricular systolic function was enhanced, with higher values of fractional shortening (38 +/- 7% vs. 34 +/- 4%; P < 0.05) and rate-adjusted velocity of shortening (1.2 +/- 0.13 vs. 1.05 +/- 0.14 circumferences/sec; P < 0.01). These findings indicate that long term levothyroxine therapy at suppressive doses markedly affects cardiac function.

Adult↗

PubMed1993

Chronic treatment with the somatostatin analog octreotide improves cardiac abnormalities in acromegaly.

The aim of this study was to investigate the effects of a 6-month octreotide treatment on cardiac mass and function by means of Doppler echocardiography in 11 normotensive patients affected with active acromegaly. The GH and insulin-like growth factor-I levels were normalized during octreotide therapy from 34 +/- 6.5 and 767.4 +/- 72.4 micrograms/L to 4.6 +/- 0.9 and 235 +/- 10.3 micrograms/L, respectively (P < 0.001; mean +/- SEM). After the 6-month treatment, we observed a significant decrease in the left ventricular mass index from 138 +/- 11 to 116 +/- 13 g/m2 (P < 0.001) and in the mean wall thickness/internal end-diastolic radius ratio from 0.47 +/- 0.1 to 0.44 +/- 0.1 (P < 0.001). No significant differences were found in systolic function indices, whereas diastolic filling indices improved over the course of the therapy; the isovolumic relaxation time decreased from 115 +/- 6 to 100 +/- 6 ms (P < 0.05), tricuspid late diastolic filling velocities decreased from 41 +/- 3 to 36 +/- 2 cm/s (P < 0.03), and tricuspid deceleration time decreased from 280 +/- 28 to 198 +/- 15 ms (P < 0.005); the ratio of early to late peak velocity of the right ventricular filling significantly increased from 1 +/- 0.01 to 1.3 +/- 0.1 (P < 0.03). A significant correlation was detected between left ventricular mass regression and increase in the early to late peak velocity ratio of the left ventricular filling (r = 0.62; P < 0.05). The results of this study show an improvement in cardiac structural and functional abnormalities during chronic treatment with octreotide, thus supporting the hypothesis of a specific heart disease secondary to high circulating GH levels.

Acromegaly↗

PubMed1993

Cardiac structural and functional abnormalities in adult patients with growth hormone deficiency.

Little information is available on cardiac involvement in GH-deficient adults. Thus, we evaluated cardiac structure and function by means of one- and two-dimensional echocardiography in 11 adult patients [3 women and 8 men; mean age, 27.2 +/- 3.8 (+/- SD) yr] affected with GH deficiency. Twelve age- and sex-matched normal subjects served as the control group. All patients had been treated with extractive GH over 9 yr, and therapy withdrawal had been performed at least 3 yr before entering the study. GH-deficient patients had significantly lower values of interventricular septum (7.1 +/- 1 vs. 9 +/- 0.4 mm; P < 0.01) and left ventricular posterior wall thickness (6.1 +/- 1 vs. 9 +/- 0.4 mm; P < 0.01), which resulted in a significantly smaller left ventricular mass index (54 +/- 11 vs. 85 +/- 15 g/m2; P < 0.001). The left ventricular end-diastolic and end-systolic diameters did not differ significantly after correction for body area surface, whereas ejection phase indices showed lower values, with a fractional shortening of 34 +/- 4% vs. 38 +/- 5% (P < 0.05) and an ejection fraction of 59 +/- 9% vs. 69 +/- 10% (P < 0.05). In conclusion, the results of this study demonstrate the involvement of cardiac muscle in patients affected with GH deficiency.

Adult↗

PubMed1993

Body composition, bone metabolism, and heart structure and function in growth hormone (GH)-deficient adults before and after GH replacement therapy at low doses.

The effects of recombinant GH doses (10 micrograms/kg.day, 3 times a week for 6 months) lower than those previously used in the treatment of GH-deficient adults (GHDA) on body composition, bone mineral content, and heart structure and function were investigated in seven (six males and one female, aged 25-27 yr) GHDA. They were studied before treatment, after treatment, and 6 months after stopping therapy, and findings were compared with those for 20 sex-, age-, and body mass index-matched healthy controls. Before treatment, GHDA showed a significant reduction in insulin-like growth factor-I levels, an increase in bioimpedance and fat mass percentage, a reduction of bone density at both distal and proximal sites, a decrease in bone Gla-protein and procollagen III levels, and significant cardiac impairment supported by a reduction of left ventricular mass index and left ventricular systolic function with decreased fractional shortening and rate-adjusted mean velocity of circumferential fiber shortening. GH treatment normalized insulin-like growth factor-I levels, body composition and echocardiographic findings, but not bone density. Six months after stopping therapy, all parameters investigated returned to the pretreatment conditions. Our results suggest that prolonged GH deficiency induces alterations in body composition and bone metabolism and density, and impairment of cardiac structure and function in adult life. GH replacement therapy for 6 months, despite the low doses used by us, is able to improve all previously impaired biochemical and clinical features, except for bone density. This improvement disappears 6 months after the withdrawal of therapy.

Adult↗

PubMed1993

[Cardiac effects of GH].

To investigate cardiac effects of excess and deficiency of growth hormone (GH) we studied twenty acromegalic subjects and eleven adult patients with GH deficiency by means of a non invasive method, the Doppler echocardiography. The results obtained in the group of patients were compared with those of two groups of twenty and eleven normal subjects, respectively, age and sex matched. The age of the acromegalic patients ranged from 20 to 62 years. Nineteen patients were considered to have active acromegaly at the time of the study. Mean duration of disease since treatment was 12 +/- 5 years (range 5 to 24 years). The age of GH deficient adults ranged from 21 to 33 years. All these patients have been treated with extractive GH over nine years and the therapy withdrawal was performed at least three years before entering the study. In the group of acromegalic patients, a subgroup including nine patients with mild to moderate hypertension was considered. All subjects gave informed consent and the study protocol was approved by the Ethical Committee of the Medical School of Naples. Right ventricular free wall thickness resulted significantly increased in acromegalic patients (8 +/- 2 vs 4 +/- 1 mm; p < 0.001). Left ventricular mass index was augmented both in the whole group and in the subgroups of normotensive and hypertensive acromegalics as compared with normals (134 +/- 33 p < 0.001, 115 +/- 20 p < 0.01 and 156 +/- 31 p < 0.001 vs 80 +/- 18 g.m-2). Ejection phase indices were normal in patient group, while impaired left and right ventricular diastolic filling was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

PubMed1993

[Growth hormone and the heart].

To investigate cardiac effects of excess and deficiency of growth hormone (GH) 20 acromegalic subjects and 11 adult patients with GH deficiency were studied by means of a non invasive method, the Doppler echocardiography. The results obtained in the group of patients were compared with those of 2 groups of 20 and 12 normal subjects, respectively, age and sex matched. The age of the acromegalic patients ranged from 20 to 62 years. Nineteen patients were considered to have active acromegaly at the time of the study. Mean duration of disease since treatment was 12 +/- 5 years (range 5 to 24 years). The age of GH deficient adults ranged from 21 to 33 years. All these patients have been treated with extractive GH over 9 years and the therapy withdrawal was performed at least 3 years before entering the study. In the acromegalic patient group, a subgroup including 9 patients with mild to moderate hypertension was considered. All subjects gave informed consent and the study protocol was approved by the Ethical Committee of the Medical School of Naples. Right ventricular free wall thickness resulted significantly increased in acromegalic patients (8 +/- 2 versus 4 +/- 1 mm; p < 0.001). Left ventricular mass index was augmented both in the whole group and in the subgroup of normotensive acromegalics as compared with normals (134 +/- 33 and 115 +/- 20 versus 80 +/- 18 g.m-2; p < 0.01). Ejection phase indices were normal in patient group, while impaired left and right ventricular diastolic filling was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

PubMed1993

[The regression of left ventricular hypertrophy and improvement in diastolic filling during antihypertensive therapy with cilazapril].

In order to evaluate the effects of cilazapril on left structure and function in essential hypertension, we evaluated 10 patients (4 females and 6 males) affected with mild-to-moderate systemic hypertension. All patients were treated with cilazapril 5 mg/day over a 6-months period and underwent a 24 hours ambulatory blood pressure monitoring and a complete Doppler echocardiographic examination at study entry, after 3 and 6-months of therapy. After therapy, mean systolic and diastolic arterial pressure decreased significantly from 153 +/- 16/102 +/- 8 mmHg to 135 +/- 13/83 +/- 6 mmHg respectively (p < 0.005/0.001 respectively). Moreover there was a significant decrease of left ventricular mass from 109 +/- 27 to 87 +/- 23 g/m2 (p < 0.005). Ejection phase indices did not change significantly, whereas left ventricular diastolic filling improved after therapy with a significant increase of M1/M2 ratio from 0.9 +/- 0.2 to 1.1 +/- 0.3 (p < 0.02). In conclusion, these data demonstrate that cilazapril 5 mg/day is effective in reducing blood pressure in mild-to-moderate essential hypertension. This normalization of blood pressure measurements is paralleled by a significant decrease of left ventricular mass index and by an improvement of left ventricular diastolic filling.

Adult↗