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Biomedical subjects

G Pinelli

Publications and source records attributed to G Pinelli.

At least 109 records · Page 6Linked to original sources

[Cardiopathy and acute cerebrovascular insufficiency. Prospective study with two-dimensional echocardiography].

Many cardiac disorders can cause acute cerebrovascular insufficiency. The spectrum of potentially embolic cardiac conditions is wide; early recognition may determine a definite change in the management and prognosis of patients. In recent years the relevance of echocardiography in the screening of patients with cerebral ischemia has been emphasized. In order to identify potentially embolic cardiac conditions, 180 consecutive non selected patients with cerebrovascular insufficiency, underwent a clinical cardiological evaluation and an echocardiogram. The study population included 132 men and 48 women; the mean age was 51.7 years (range 19 to 72 years). A technically adequate echocardiogram was obtained in 153 patients. In 131 patients echocardiography was negative; cardiac lesions were detected in 22 patients (14.4%): mitral stenosis in 2, calcified aortic stenosis in 1, valvular endocarditis vegetations in 3, dilatative cardiomyopathy in 2, hypertrophic cardiomyopathy in 4, mitral valve prolapse in 4, regional left ventricular diskynesia in 5, mitral anulus calcification in 1. Patients were divided into 3 groups according to the results of cerebral angiography: 68 patients with normal angiography (Group I), 54 patients with atheromasic lesions on cerebral angiography (Group II), 31 patients in whom cerebral angiography was not performed (Group III). A higher incidence of cardiac diseases was found in the patients of Group I. The lack of lesions on cerebral angiography and the presence of embolic high-risk cardiac conditions strengthened a causal relationship of the cardiac disorder with cerebrovascular insufficiency in 10 of the 23 patients. In the mean follow-up period of 18 months of these 10 patients who underwent cardiac surgery or anticoagulation, no further attacks of cerebrovascular insufficiency were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Toxins in hepatic encephalopathy: the role of the synergistic effect of ammonia, mercaptans and short chain fatty acids.

Evidence has been recently produced that neurological changes which characterize hepatic encephalopathy due to fulminant hepatic failure in rats are linked with a pathology of GABA receptors. In the search for the peripheral toxins responsible for the CNS impairment present in hepatic encephalopathy it has been shown that the administration of ammonia and mercaptans and octanoic acid in normal rats reproduced behavioural and electrophysiological changes similar to those seen in galactosamine induced encephalopathy. The present report shows that a subacute administration of the above toxins induced a marked alteration of the GABA receptor complex which may account for the CNS derangement of hepatic encephalopathy.

Ammonia↗

Comparative efficacy of nicardipine, a new calcium antagonist, versus nifedipine in stable effort angina.

The relative efficacy of nicardipine and nifedipine was examined in a double-blind placebo-controlled randomized crossover trial. We studied 12 patients with chronic effort angina involving reproducible angina and greater than or equal to 1.5 mm of ST-segment depression on exercise treadmill test performed before and after a 1-week control period of single-blind placebo administration. Subsequently, indistinguishably prepared nicardipine 20 mg, nifedipine 10 mg, or placebo, four times a day, was administered in a randomized double-blind crossover fashion for 3 weeks (total study period 9 weeks). Exercise treadmill test was performed at the end of each 3-week period. Both nicardipine and nifedipine significantly reduced the frequency of anginal attacks and nitroglycerin consumption. Compared with placebo both drugs caused a comparable increase of the duration of exercise, of the time to angina and to the appearance of 1.5 mm ST-segment depression (P less than 0.05 placebo versus nicardipine; P less than 0.01 placebo versus nifedipine respectively). No significant side effects were observed with either drug. We conclude that nicardipine and nifedipine produce similar hemodynamic and clinical effects in patients with stable effort angina.

Aged↗

Supersensitivity of benzodiazepine receptors in hepatic encephalopathy due to fulminant hepatic failure in the rat: reversal by a benzodiazepine antagonist.

Benzodiazepine receptors were studied in rats with hepatic encephalopathy due to fulminant hepatic failure induced by galactosamine. [3H]-Diazepam binding studies on brain synaptic membranes of rats with mild and severe encephalopathy show a significant increase in the number of receptors in both stages of coma. [3H]Diazepam binding to synaptic membrane preparations from rats in the mild or severe stage of encephalopathy hyper-responded to the stimulatory effect of gamma-aminobutyric acid (GABA) applied in vitro at doses which for control rat preparations were in a subthreshold range. The effect of GABA was shown to be specific, since it was blocked by bicuculline methiodide. The sensitivity of benzodiazepine receptors in hepatic encephalopathy to nanomolar concentrations of GABA, which induced a significant increase in their affinity, seems to indicate a functional supersensitivity of benzodiazepine receptors in vivo in both mild and severe stages of encephalopathy. The phenomena described may be attributed to a partial degeneration of nerve terminals in hepatic encephalopathy, leading to a supersensitivity of benzodiazepine receptors, which parallels the previously described denervation supersensitivity of GABA receptors present in this animal model of fulminant hepatic failure. These findings may account for the brain hypersensitivity to sedatives administered to patients with liver diseases. The administration in vivo of a benzodiazepine antagonist, 2-phenylpyrazolo[4,3-c]-quinolin-3(5H)-one, counteracted the hypersensitivity of benzodiazepine receptors in the mild stage of encephalopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Visual evoked potential: a diagnostic tool for the assessment of hepatic encephalopathy.

Visual evoked potential recordings were examined in 45 liver cirrhosis patients with (n = 29) and without (n = 16) encephalopathy, in 15 normal volunteers, and in one patient with an opioid induced stupor state. Visual evoked potential parameters were classified on the basis of EEG recordings. Plasma concentrations of amino acids, octopamine, and ammonia were assayed in order to document the metabolic change of hepatic encephalopathy. Latencies and wave patterns recorded after flash stimulation differentiated the four degrees of the coma one from another according to EEG classification in the 29 patients with encephalopathy. In the group of 16 patients without clinical and EEG evidence of encephalopathy the visual potential recordings discriminated a group of patients (n = 10) in a preclinical stage of encephalopathy. Biochemical parameters and subsequent clinical observation of patients confirmed our judgement of a preclinical stage of encephalopathy. These results suggest that visual evoked potentials are a simple, suitable and objective method for differentiating the degrees of encephalopathy and for identifying the preclinical stage of encephalopathy.

Adult↗

[Cardiac arrhythmias associated with subarachnoid hemorrhage. Prospective study with dynamic electrocardiography].

Electrocardiographic abnormalities associated with intracranial diseases, especially subarachnoid hemorrhage, are well known, while there is hardly mention of cardiac arrhythmias in the neurological and cardiological literature. In order to assess the incidence of arrhythmias 52 consecutive patients with subarachnoid hemorrhage secondary to ruptured aneurysm were investigated with 24-hour Holter recordings. Bradyarrhythmias and tachyarrhythmias were found in 46 patients (88%); premature ventricular beats in 25 pts (12 of these in 3rd-5th Lown classes), ventricular tachycardia in 2, premature supraventricular beats in 14, paroxysmal atrial fibrillation in 1, sinoatrial blocks and arrests in 18, atrioventricular dissociation in 2 and idioventricular rythm in 2. Moreover in 5 pts ST segment changes were found, suggestive of transitory acute myocardial ischemia. The presence and severity of arrhythmias were correlated with the time elapsed from the episode of bleeding, with the QT interval, and with the hemorrhage extent. Our results indicate an high incidence of arrhythmias in subarachnoid hemorrhage, sometimes serious mainly in early stage. Continuous electrocardiographic monitoring is therefore extremely useful and provides data for therapeutic consideration.

Adult↗

Comparative efficacy of nicardipine, a new calcium antagonist, versus nifedipine in effort stable angina.

The relative efficacy of nicardipine and nifedipine was examined in a double-blind randomized trial. We studied 12 patients with chronic effort angina who had reproducible chest pain and greater than or equal to 1.5 mm of ST-segment depression on treadmill exercise testing performed before and after 1-week control period of single-blind placebo administration. Subsequently over a 9-week period, nicardipine 20 mg or nifedipine 10 mg or an identical placebo four times a day, was administered in a randomized double-blind crossover fashion. Treadmill exercise testing was performed at the end of each 3-week period. Both nicardipine and nifedipine reduced the frequency of anginal attacks and trinitrate consumption. Compared with placebo both drugs caused a comparable increase of the total duration of exercise (p less than 0.05 placebo versus nicardipine; p less than 0.01 placebo versus nifedipine) and of the time to the onset of angina (p less than 0.05 placebo versus nicardipine; p less than 0.01 placebo versus nifedipine) and to the appearance of 1.5 mm ST depression (p less than 0.05 placebo versus nicardipine; p less than 0.01 placebo versus nifedipine). Moreover 4 patients no longer had angina with either drug and only 1 patient with placebo. Both drugs increased resting heart rate and reduced systolic blood pressure at resting (p less than 0.01) and submaximal exercise (p less than 0.01). Peak heart rate, systolic blood pressure and rate-pressure product were similar with placebo, nicardipine and nifedipine. No important side effects were observed with either drug. We conclude that nicardipine and nifedipine produce similar haemodynamic and clinical effects in patients with stable angina.

Aged↗

[Evaluation of the effects of a new calcium antagonist, diltiazem, in patients with stable effort angina and a therapeutic comparison with nifedipine].

The comparative efficacy of diltiazem, a new calcium-antagonist drug, and nifedipine were evaluated with computerized treadmill exercise test in 12 patients with stable effort angina. The drugs were administered in a random single-blind fashion in divided doses (diltiazem 60 mg three times daily and nifedipine 10 mg four times daily) over 3 weeks. Maximal exercise tests were performed before and at the end of each 3-week treatment period. Both diltiazem and nifedipine increased the total duration of exercise (p less than 0.001) and the time to appearance of 1.5 mm of ST depression (p less than 0.001). Both drugs reduced resting systolic and diastolic blood pressure; however the effect was greater with nifedipine. Nifedipine, but not diltiazem, caused a significant increase of resting heart rate (p less than 0.05). Both drugs blunted the blood pressure and heart rate response to exercise: nifedipine had a greater effect on the former (p less than 0.001), diltiazem on the latter (p less than 0.05). The rate-pressure product was significantly reduced at rest (p less than 0.01) and submaximal (p less than 0.001), but not maximal exercise with both drugs. The reduction of rate-pressure product is possible as the mechanism by which calcium-antagonist drugs enhance the duration of exercise in the coronary patients. Our results documented a comparable therapeutic efficacy of the two drugs, but side effects were more common with nifedipine.

Aged↗

[Syncopal episodes in healthy young athletes. Report of 3 cases in the course of ergometric evaluation].

We report the occurrence of syncope in three healthy athletes during exercise stress testing. In two subjects the syncope occurred in the late recovery stage and was due to inhibition of sinus activity. In the third case a Mobitz type II A-V block developed during hyperventilation, which was followed by a complete A-V block with ventricular asystole and subsequent sinoatrial arrest. We discuss the probable pathophysiological mechanisms of these arrhythmias and their implications in sports practice.

Adult↗

[Non-invasive evaluation of left ventricular function in chronic alcoholics. Histo-morphological and echo-polygraphic correlations].

Alcohol decreases myocardial contractility through direct, toxic effect. Ingestion of more than 150 g per day for more than 10 years carries a high risk of developing alcoholic cardiomyopathy. The discontinuance of alcohol intake--if put into effect early in the natural history of patients with alcoholic cardiomyopathy--commonly but not invariably results in remission of heart failure. In order to evaluate the left ventricular (LV) function and to find out a possible correlation between the degree of cardiac dysfunction and the severity of the morpho-functional aspects of alcoholic liver disease, 20 chronic alcoholic patients without clinical evidence of heart disease were examined. Echocardiography, systolic time intervals, mechanical polygraphic recordings and liver biopsy were obtained. According to the morphological alterations showed by the needle biopsy of the liver, we separated 12 patients with liver steatosis (Group I) from 8 subjects with alcoholic hepatitis and fibrosis. In Group I LVET, ICT, PEP/LVET indices and LV fractional shortening (delta %) were not statistically different from control subjects. Patients of Group II showed marked impairment of myocardial function, as revealed by significant ICT, PEP, PEP/LVET prolongation and by an equally significant reduction of fractional shortening of the LV. The noninvasive method has proved to be quite useful in detecting early LV dysfunction in asymptomatic chronic alcoholics and has revealed a correlation between the severity of the morphological involvement of the liver and the impairment of cardiac performance.

Adult↗