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Biomedical subjects

A Cherchi

Publications and source records attributed to A Cherchi.

At least 55 records · Page 3Linked to original sources
PubMed1990

Propionyl carnitine in stable effort angina.

The aim of this study was to investigate the anti-ischemic activity of propionyl carnitine (PC) in 18 informed, volunteer male patients, aged 37-70, suffering from a typical stable effort angina. The study design was randomized, balanced, crossover, and double blinded. The study lasted 75 days. In the first 15 days of washout the patients performed two maximal symptom-limited bicycle tests to verify the repeatability of the parameters examined. Then one group received PC for 30 days 500 mg three times a day, and the other group received placebo (PL) three times a day. At the end of 30 days the groups exchanged treatments. At the end of each period, 2 hours after the last oral administration, the patients performed a maximal symptom-limited bicycle exercise test with increased loads of 10 watts/min. No significant differences were observed between the two tests performed during the wash-out period, for a 1 mm ST-segment depression time, for the time to the end of exercise, and for the rate x pressure product at the same experimental time. The oral administration of PC in coronary patients increased both the 1 mm ST-segment depression time and the time to the end of exercise. Furthermore, the drug reduced the ischemic depression of ST at maximal common work and at maximal work. After PC, the rate x pressure product was not significantly different in relation to placebo at submaximal and maximal exercise. Thus PC seems to have an antiischemiclike effect, probably related to its metabolic activity.

Administration, Oral↗
PubMed1990

Different patterns of left ventricular filling in arterial hypertension.

To determine whether left ventricular (LV) filling dynamics may be influenced by the type of LV morphological adaptation to arterial hypertension, pulsed Doppler mitral flow velocity recordings were performed in 30 hypertensive patients and in 18 normotensive subjects matched for age, body surface and heart rate. Peak early (E) and late (A) mitral flow velocity, A/E ratio (A/E), time to peak E (TP), acceleration (AHT) and deceleration half-time (DHT) of early mitral flow and isovolumic relaxation time (IRT) were measured. Compared with the control group, hypertensive patients showed prolonged IRT and DHT, increased A and A/E, whereas TP, AHT and E were unchanged. Hypertensive patients were classified into two subgroups on the basis of h/r ratio (h/r). Subgroup 1: 16 patients with normal h/r, less than 0.42, (five patients with increased LV mass index, greater than 129.2 g m-2, and 11 patients with normal LV mass index, less than 129.2 g m-2). Subgroup 2: 14 patients with increased h/r, greater than 0.42, (nine patients with increased LV mass index, greater than 129.2 g m-2 and five patients with normal LV mass index, less than 129.2 g m-2). In Subgroup 1 the cardiac output (CO) was increased and the total peripheral resistance (TPR) was unchanged in comparison with the control group. In Subgroup 2 the opposite haemodynamic profile was detected: normal CO and increased TPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of enalapril in normotensive patients with stable effort angina: a double blind, placebo controlled study.

To assess the anti-anginal and anti-ischaemic efficacy of the ACE-inhibitor enalapril in normotensive coronary patients, a double-blind, cross-over, placebo-controlled study was performed. Eight male patients, aged 45-68 years, with stable effort angina were given enalapril (10 mg) once a day or placebo for 7 days. Maximal exercise stress tests 10w/min in the upright position were performed at the end of each period. In comparison to placebo, enalapril increased significantly 1 mm of ST depression time and decreased significantly ST depression at maximal common work. Moreover, enalapril increased significantly the angina threshold and exercise duration. Three of the eight patients ended the exercise without pain. The rate-pressure product was not significantly modified at any time. Thus, the anti-ischaemic and anti-anginal activity may be due to an increase of coronary blood flow, rather than a reduction of MVO2 consumption.

Aged↗
PubMed1990

[Cardiovascular response to dynamic physical exercise in adolescents with casual raised values of arterial blood pressure].

The blood pressure response to dynamic exercise was studied in 90 adolescents (45 males and 45 females) mean age 15 years (range 13-16 years) with casual systolic and/or diastolic hypertension (H) and in 50 matched for age adolescents (26 males and 24 females) with casual blood pressure about the fiftieth percentile for age and sex (N). During the third blood pressure control they underwent a maximal bicycle exercise test in sitting position (10 W/min). During exercise and recovery ECG was recorded every 30 s and blood pressure, with a mercury sphygmomanometer, every 3 min. Adolescents with casual hypertension at rest showed, in comparison to normotensives, an increase in blood pressure (H: 176.1 +/- 18.8 mmHg; N: 167.4 +/- 14.2 mmHg, p less than 0.01 at peak of exercise) and in rate-pressure product (H: 326.8 +/- 40.9 X 10(-2); N: 308.7 +/- 29.4 X 10(-2); p less than 0.01 at peak of exercise) during exercise and recovery. Heart rate was greater at rest in hypertensive adolescents, but there was no difference between the 2 groups during exercise. Exercise tolerance was similar in the 2 groups. Casual transient hypertension at rest and excessive increase of systolic blood pressure during exercise could be expression of early cardiovascular changes preceding sustained hypertension.

Adolescent↗
PubMed1990

Catecholamine injections in canine paravertebral ganglia produce hypotension by neurogenic vasodilatation.

In the present study the alpha 1 selective agonist phenylephrine (PE), the alpha 2 selective agonist clonidine (CLO) and the non-selective endogenous catecholamine norepinephrine (NE) and dopamine (DA) were injected directly into the blood supply of the paravertebral sympathetic ganglia (PSG) of anesthetized open-chest dogs. Intra-arterial injection of all agonists produced dose-dependent decreases in mean arterial pressure (MAP) and femoral vascular resistance (FVR) but had no effect on heart rate. Their potency order was CLO greater than NE greater than PE greater than DA. Intravenous injections of the medium dose for NE and PE produced significant increases in MAP, while the medium dose of CLO injected iv produced a small decrease in MAP. The ganglionic blocking agent, hexamethonium (10 mg/kg iv) completely eliminated the hypotensive response to all agonists. Intra-arterial administration of the alpha 1 selective antagonist terazosin (0.5 mg) significantly reduced the decrease in MAP produced by the ganglionic actions of PE, but had no significant effect on the response to CLO. In contrast, the alpha 2 selective antagonist rauwolscine (100 micrograms) significantly reduced the decreases in MAP produced by ia CLO, but not that produced by ia PE. However, both antagonists inhibited the hypotensive effect of NE and DA. These findings suggest that both subtypes of alpha-adrenoceptors, alpha 1 and alpha 2, are present in the PSG and that both subtypes are inhibitory since their activation results in reduced transmission of impulses through the ganglia.

Animals↗
PubMed1990

[Electrocardiographic and echocardiographic changes during antihypertensive therapy].

To investigate the changes of electrocardiographic and echocardiographic indexes of left ventricular hypertrophy (LVH) during antihypertensive therapy, 100 hypertensive patients, mean age 46 years, were studied in pretreatment condition and during 12 months of antihypertensive therapy. In pretreatment condition, 83 patients showed LVH by echocardiography (echo; left ventricular mass index greater than 130 g/m2) and 30 patients had LVH by electrocardiography (ECG) (Sokolow index greater than 35 mm). In comparison to echo index of LVH, Sokolow index showed a sensibility of 34% and a specificity of 88%. Both LV mass echo index and ECG index significantly decreased after 3 months but in different way. LV mass index mainly decreased after 12 months, whereas Sokolow index particularly decreased after 6 months, with no further changes in the subsequent months. After 12 months of therapy, the LV mass echo index normalized in 19% of the patients (16/83) and Sokolow index normalized in 57% (17/30). ECG sensibility and specificity, in comparison to LV mass echo, was 20% and 100%, respectively. Thus, ECG appears less sensitive than echo in the detection of LVH. During antihypertensive therapy ECG index of LVH normalized more precociously and to a greater extent than the echo index. However, the normalization of LVH by ECG does not necessarily mean that a complete anatomic regression of LVH has occurred.

Acebutolol↗
PubMed1990

[Effects of indenolol on left ventricular mass in patients with essential arterial hypertension].

This study evaluated the effect of long-term antihypertensive therapy with indenolol, a beta blocking agent with beta 2 stimulating activity, its antihypertensive hemodynamic mechanism and its effect on hypertensive left ventricular (LV) hypertrophy. Fourteen hypertensive patients, mean age of 48 years, were serially studied during 12- month therapy with indenolol (60-120 mg daily), by recording blood pressure, electrocardiogram and echocardiogram. Blood pressure, heart rate and cardiac output significantly decreased after 1 months of therapy, LV posterior wall thickness decreased after 6 months, interventricular septum thickness and LV mass decreased after 12 months. LV fractional shortening did not change throughout the study. Blood pressure normalized (less than or equal to 140/90 mmHg) in 50% of the patients; LV mass normalized in 40% of the patients. In conclusion, indenolol was an effective antihypertensive agent, also in the long-term treatment. Its antihypertensive hemodynamic effect seems to be due mainly to a reduction in cardiac output. Indenolol caused a regression of LV hypertensive hypertrophy without impairment of LV systolic function.

Adult↗
PubMed1989

[Echocardiographic study at rest and during effort in adult asymptomatic thalassemic patients].

An echocardiographic study was performed in 21 young patients with thalassemia major (TM, age 16-22 years), with no cardiac symptoms, and in 24 age-matched normals (N) at rest and during sitting bicycle exercise (EX). All TM were receiving blood transfusions regularly to maintain hemoglobin level above 11 g/dl and subcutaneous infusion of desferrioxamine (40 mg/Kg/day) to reduce hemosiderosis. At rest, in comparison to N, TM showed a significant increase in LV end-diastolic dimension (EDD), septal, posterior wall thickness and mass, whereas wall thickness to EDD ratio and LV fractional shortening (FS) were not different. Stress echocardiography was recorded with success in 90% of TM and 83% of N. During EX, FS increased progressively with increase of heart rate in both groups, though the increase of FS was lower in TM. Thus, asymptomatic young patients with thalassemia major, under well transfusion-chelation therapy, showed cardiac changes from volume overload. LV systolic function, normal at rest, was moderately impaired during exercise test.

Adolescent↗
PubMed1988

Anti-ischaemic and anti-anginal activity of atenolol, nifedipine and their combination in stable, chronic effort angina.

To assess the anti-anginal and anti-ischaemic activity of the beta-blocker atenolol (ATN) and the calcium antagonist nifedipine (NIFE) and their combination in coronary patients, a double-blind, cross-over, placebo-controlled study was performed. Ten male patients (mean age: 58 +/- 2.9 years) suffering from a stable effort angina were studied. The study lasted 14 weeks: after 2 weeks of wash-out, patients were randomly assigned to ATN (100 mg/day) and placebo-NIFE, or placebo-ATN and NIFE (10 mg three times/day), or ATN (100 mg) plus NIFE (10 mg three times/day) for 4 weeks. Maximal symptom-limited stress tests on a bicycle (10 watt/min) during the wash-out period (on days 10 and 14) and at the end of each treatment period were performed. All treatments significantly increased the work load at 1 mm ST depression, the angina threshold and the total work, and reduced ST depression at the maximal common work and at the maximal work. Also the atenolol-nifedipine combination significantly reduced ST depression at maximal common work and maximal work as compared to ATN and NIFE alone. In conclusion, this study confirms the anti-ischaemic and anti-anginal activity of both atenolol and nifedipine in stable effort angina and shows that their combination is able to increase anti-ischaemic activity.

Angina Pectoris↗
PubMed1987

Diagnosis of amiodarone-iodine-induced thyrotoxicosis(AIIT) associated with severe nonthyroidal illness.

A rare case of amiodarone-iodine-induced thyrotoxicosis (AIIT) associated with nonthyroidal illness is reported. Serum total thyroxine (TT4) and free T4 (FT4) concentrations were elevated and serum TSH was undetectable as frequently observed also in euthyroid amiodarone-treated patients. At variance with common forms of AIIT, serum total triiodothyronine (TT3) was reduced due to low-T3 syndrome. The laboratory diagnosis was made on the basis of elevated free T3 (FT3) levels. Thus, in patients with severe nonthyroidal illness submitted to chronic amiodarone treatment, thyroid status can only be determined by free hormone measurement, particularly FT3 in the case of thyrotoxicosis.

Aged↗
PubMed1987

Peripheral dopamine receptors in the antihypertensive action of dihydroergotoxine in humans.

The effect of the intravenous administration of dihydroergotoxine (6 micrograms/kg) on arterial blood pressure, heart rate, and plasma concentrations of norepinephrine and 3,4-dihydroxyphenylacetic acid (the deaminated dopamine metabolite) was studied in 20 subjects with essential hypertension (8 men and 12 women aged 32-68 years old, World Health Organization Class I-II). In supine resting subjects, dihydroergotoxine significantly decreased systolic blood pressure (from 175 +/- 5 to 156 +/- 4 mm Hg; p less than 0.001), diastolic blood pressure (from 109 +/- 4 to 95 +/- 3 mm Hg; p less than 0.001), and heart rate (from 71 +/- 2 to 63 +/- 2 beats/min; p less than 0.001) as compared with the results of placebo treatment. Moreover, dihydroergotoxine reduced plasma levels of norepinephrine (from 368 +/- 39 to 238 +/- 33 pg/ml; p less than 0.001) and 3,4-dihydroxyphenylacetic acid (from 1.57 +/- 0.21 to 1.22 +/- 0.13 ng/ml; p less than 0.01). The time course of the blood pressure decrease paralleled that of plasma norepinephrine concentration. Dihydroergotoxine did not suppress the cardiovascular and plasma norepinephrine concentration. Dihydroergotoxine did not suppress the cardiovascular and plasma norepinephrine response to standing. The effect of domperidone, a peripheral presynaptic dopamine receptor antagonist, on dihydroergotoxine response was studied in six of the 20 subjects (3 men and 3 women 48-64 years old). The intravenous administration of domperidone (0.3 mg/kg) prevented the dihydroergotoxine-induced reduction in blood pressure and heart rate and the fall in plasma norepinephrine and 3,4-dihydroxyphenylacetic acid levels. Domperidone administered alone failed to significantly modify any measured variables.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Possible regression of left ventricular hypertrophy during antihypertensive treatment with diuretics and/or beta blockers.

The possible regression of left ventricular hypertrophy (LVH) during treatment with diuretics and/or beta blockers was assessed in 78 hypertensive patients by echocardiography. Five groups of patients were treated, respectively, with diuretics alone, chlorthalidone plus SR oxprenolol, acebutolol followed by atenolol, timolol alone, or atenolol alone. All patients, except those receiving acebutolol had a significantly reduced LV mass within 12 months. Acebutolol did not modify LV mass even after 24 months, in spite of its antihypertensive efficacy. The reduction of LV mass was due to a decrease in wall thickness after administration of beta blockers and a decrease in LV dimension after chlorthalidone. Normalization of LV mass (less than 130 g/m2) occurred only in 31% of patients. LV mass was not significantly modified in patients with normal mass in pretreatment condition. The decrease of LV mass correlated with a decrease in cardiac output but not with the reduction in blood pressure. In conclusion, LV systolic function showed a tendency toward improvement after long-term antihypertensive therapy.

Adrenergic beta-Antagonists↗