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Biomedical subjects

A Mammarella

Publications and source records attributed to A Mammarella.

At least 55 records · Page 3Linked to original sources
PubMed1983

[The effects of Levissima oligomineral water on diuresis and water exchange].

Research on healthy and diseased subjects and laboratory animals have shown that Levissima oligomineral water: a) has no unpleasant or harmful subjective and/or objective side-effects even when taken at high doses for long periods. b) Encourages diuresis. Comparison with saline solution of the same osmolality showed: 1) mean increase in diuresis: 16%; 2) more rapid elimination of water; 3) significant increase in free water clearance; 4) no change in the stock of electrolytes during protracted administration. c) Influences purine exchange: 1) by increasing uric acid clearance (same comparison); 2) by reducing the hyperuricaemising effect of a rapid i.v. fructose load; 3) by opposing hyperuricaemia due to depression of mechanisms responsible for the increase of uric acid owing to enhancement of serum lactic acid after the administration of alcohol. d) Results in a characteristic change in certain coagulation parameters when compared with saline solution and tap water. It is suggested that this method be used to recognise the persistence over time of the biological activities of bottled mineral waters.

Blood Coagulation↗
PubMed1979

Creatinol O-phosphate therapy in patients with inadequate coronary circulation. Double-blind clinical trial.

N-Methyl-N-(beta-hydroxyethyl) guanidine O-phosphate (creatinol O-phosphate, COP) was checked on patients suffering from inadequate coronary circulation (12 patients had a recent myocardial infarction and 13 were suffering from angina pectoris) versus a reference substance (solvent of COP) in a double blind study. COP improved rhythm disturbances, chest pains and symptoms of contractility failure to a statistically significant degree.

Adult↗
PubMedDate not supplied

Morphologic left ventricular patterns and prevalence of high-grade ventricular arrhythmias in the normotensive and hypertensive elderly.

In the elderly, systemic hypertension is the main risk factor for cardiovascular diseases. Left ventricular hypertrophy, the most common adaptation to chronic pressure overload, has been recognized as an independent risk factor for an increased incidence of sudden death and arrhythmic disturbances. This study compared the prevalence of serious ventricular arrhythmias in elderly individuals with uncomplicated hypertension and in normotensive age-matched controls, using left ventricular mass index (LVMI) to differentiate patterns of anatomic adaptation to systolic, diastolic, or systolic-diastolic hypertension. The study enrolled 378 consecutive untreated elderly subjects (> or = 65 years of age), without clinical evidence of heart failure; 203 were hypertensive and 175 were normotensive. Each participant underwent standard 12-lead electrocardiography, M-mode and B-mode echocardiography, and 24-hour ambulatory electrocardiographic monitoring. Serious, statistically significant arrhythmias (Lown classes > or = 3) were present in 6.8% of normal subjects versus 17.1% of individuals with systolic, 31.5% of those with diastolic, and 20.4% of participants with systolic-diastolic hypertension. Arrhythmias did not differ in terms of left ventricular morphologic patterns or LVMI or between subgroups of hypertensive patients. Our data support the hypothesis that the pathogenesis of arrhythmias is related not to the electrophysiologic derangement of hypertrophied muscle but, rather, to the effects of hypertension on the cardiac structure. Cardiac fibrosis, one of the deleterious events accompanying hypertension, may be the main substrate for ventricular arrhythmias.

Aged↗
PubMedDate not supplied

Natural history of cardiac involvement in myotonic dystrophy (Steinert's disease): a 13-year follow-up study.

Myotonic dystrophy (MD) is associated with a wide spectrum of cardiac abnormalities, but only a few longitudinal studies have investigated the natural course of heart disease in MD. To assess whether neuromuscular involvement significantly predicts cardiac disorders in MD, 83 patients with various grades of disease severity were enrolled in a 13-year follow-up study (mean, 60.6 +/- 37.8 months) that included periodic physical and instrumental cardiac examinations (standard and Holter electrocardiography, echocardiography). During follow-up, muscular disease worsened clinically in 9 patients (11%) whose baseline severity grade changed accordingly; only 3 of them demonstrated parallel worsening of cardiac disturbance, however, compared with a large number of patients who showed additional cardiac abnormalities. These included further worsening of pre-existing pathologic features (19/83) and the appearance de novo of serious arrhythmias and/or conduction defects (23/83). Pacemaker implantation was necessary in 11 of 83 patients (13.2%) who had symptomatic bradyarrhythmias, bifascicular block, and P-R prolongation with a His-to-ventricle interval exceeding 55 ms, as documented by electrophysiologic study. Eight (9.6%) patients died: 2 from noncardiac and 1 from unknown causes, 1 from heart failure, and 4 from sudden death closely related to documented ventricular tachycardia. The incidence and seriousness of arrhythmic and conduction disturbances correlated with the severity of the muscular involvement. Nevertheless, cardiac and muscular disease did not show a linear progression. Cardiac involvement generally worsened more rapidly than did skeletal muscle disease.

Adolescent↗
PubMedDate not supplied

Doppler echocardiographic assessment of left ventricular diastolic function in myotonic dystrophy.

We utilized Doppler echocardiography to characterize left ventricular diastolic function in 42 patients with myotonic dystrophy (mean age 37 +/- 12 years, 64% male) who had no symptoms of heart failure and had normal left ventricular systolic function. Data were compared with those in 41 normal control subjects of similar age and gender. Heart rate, systemic blood pressure, and cardiac dimensions (wall thickness, left atrial and left ventricular cavity dimensions) were similar and not significantly different in patients and controls. As a group, patients showed significantly increased deceleration time and decreased rate of decline of flow velocity in early diastole (p < 0.0001 and p < 0.01, respectively) when compared to controls. Individual patient analysis showed that 10 (24%) of the 42 patients with myotonic dystrophy had 2 or more abnormal Doppler indexes of diastolic function consistent with a pattern of impaired left ventricular relaxation. The most common abnormalities were increased deceleration time (> 224 ms; 9 patients), prolonged isovolumic relaxation time (> 103 ms; 8 patients) and reduced rate of decline of flow velocity in early diastole (< 2.1 m/s2; 5 patients). In addition, peak early diastolic flow velocity was reduced (< 43 cm/s) in 3 patients and early to atrial peak flow velocity ratio was reduced (< 1) in 2 patients. Comparison of subgroups of patients with and without abnormal Doppler indexes showed no significant differences with regard to age, gender, heart rate, systemic blood pressure, severity of neuromuscular disease, and cardiac dimensions. After study, patients were clinically followed up for a mean period of 20 +/- 7 months (range 12-35). During observation no patients died and none experienced symptoms of heart failure. This Doppler echocardiographic analysis demonstrates that diastolic abnormalities may be present in patients with myotonic dystrophy, even in the absence of symptoms of cardiac failure or left ventricular systolic dysfunction. These diastolic abnormalities suggest an intrinsic myocardial abnormality in patients with myotonic dystrophy; however, whether they represent a preclinical phase of myocardial involvement or an intrinsic feature of the primary myocardial disease process in myotonic dystrophy remains to be elucidated.

Adolescent↗
PubMedDate not supplied

[Rationale for the use of renin-angiotensin inhibitors in the treatment of arterial hypertension and correlated organ damage].

The treatment of hypertension has evolved in recent years. Blood pressure lowering per se is no longer a sufficient parameter to evaluate its beneficial effects on end-organ damage. Drugs must be considered on the basis of their effects on cellular level and structural alterations that occur in the vasculature, heart and kidney. Angiotensin converting enzyme inhibitors and angiotensin II receptor blockers, two classes of drugs that inhibit angiotensin II effects, may protect target organs from damage and thereby improve outcomes. The mechanisms of action are different even if both counteract all noxious effects of angiotensin II. Angiotensin II receptor blockers selectively inhibit AT1 receptors whose stimulation mediates the hypertensive and proliferative effects of angiotensin II while do not interfere with AT2 receptors. These last ones have a role not well established but it has been postulated that they have antihypertensive and antiproliferative effects. A review will be made on the cellular mechanisms of angiotensin II activity and the effects of AT receptor antagonists.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

[Efficacy-safety relationship of AT1 angiotensin II receptor antagonists: current data].

In evolution of hypertension's treatment it may no be sufficient to lower blood pressure to achieve beneficial effects in long term outcomes. Several goals of antihypertensive treatment remain unrealized. There is so great interest for new drugs that may protect target organs and improve outcomes. The angiotensin II, the major effector of the renin-angiotensin-aldosterone system, causes a variety of potentially noxious cardiovascular effects which are specially mediated by AT1 subtype receptors. AT1 receptor blockers (losartan, candesartan, irbesartan, valsartan) are available drugs in the angiotensin-II-antagonist class. This paper examine the peculiar features of this new class of drugs.

Angiotensin Receptor Antagonists↗