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M Pepi

Publications and source records attributed to M Pepi.

At least 73 records · Page 4Linked to original sources
PubMed1993

[The improvement of the Doppler echocardiographic method for the estimation of pulmonary systolic pressure].

The formulas currently utilized for noninvasive evaluation of right ventricular systolic pressure (RVSP) include right ventricular-right atrial pressure gradient (RV-RAG) and right atrial pressure (RAP). The former is expressed by trans-tricuspid systolic flow velocity, the latter is generally assumed. We recently observed that ultrasound estimation of RAP through inferior vena cava collapsibility index (CI) may help in the choice of the more appropriate formula for the evaluation of RVSP. However, these traditional methods (method A:RV-RAG + 10; method B:RV-RAG x 1.1 + 14) have limitations, particularly when RAP is low. The present study was undertaken to improve noninvasive estimation of RVSP through new formulas based on CI prediction of RAP. One hundred and four patients, in whom tricuspid regurgitation was adequately documented with CW-Doppler, were included in this study. They were classified into 3 groups: Group 1 with CI > 45%, Group 2 with CI < or = 35%, Group 3 with CI 35-45%. RVSP was evaluated by 3 different methods: A, B, and C. Method C was based on CI, assigning 6, 16, or 9 mmHg to RAP (respectively, the mean values in the 3 groups of our previous study). Results indicate that method C improves noninvasive estimation of RVSP in Group 1 and Group 2, with respect to other methods, with reduction of the SEE and of the mean difference of the t-test between hemodynamic and echographic values. In Group 3, Doppler estimation by method A and C, and catheter measurements are comparable, whereas method B significantly overestimates the actual value.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Modulation of chromium(VI) toxicity by organic and inorganic sulfur species in yeasts from industrial wastes.

Two chromium(VI) resistant yeast strains (Candida sp. and Rhodosporidium sp.) were isolated from industrial wastes. Four different yeasts, three from the Industrial Yeast Collection and one of pharmaceutical origin, were also studied in relation to chromate toxicity and its alleviation by sulfur species. The growth of yeasts from industrial wastes was inhibited by 50% by high concentrations of Cr(VI): Candida sp. by 4 mM Cr(VI) and Rhodosporidium sp. by 10 mM Cr(VI) in Sabouraud Broth medium. The other Cr(VI)-sensitive yeasts were inhibited by 0.1 mM Cr(VI). The general mechanism of chromium resistance in Candida sp. and Rhodosporidium sp. was due to reduced uptake of chromium, but not to biological reduction from Cr(VI) to Cr(III). In Cr(VI)-sensitive yeasts, chromium was accumulated as much as 10-fold, as in Saccharomyces cerevisiae. Cr(VI) toxicity in Candida sp. was modulated from Cr(VI)-resistance to Cr(VI)-hypersensitivity depending on the addition of methionine, cysteine, sulfate and djenkolic acid. If Candida sp. was grown in the presence of S-amino acids, especially methionine, it was more resistant than if the sulfur source was sulfate. When sulfate transport was enhanced by addition of djenkolic acid, Candida sp. became hypersensitive. Rhosporidium sp. was always resistant to Cr(VI) because sulfate transport was inefficient and it assimilated sulfur as S-amino acids. Cr(VI)-sensitive yeasts required larger amounts of S-amino acids, especially methionine, to tolerate Cr(VI) toxicity. Cysteine was toxic for C.famata 6016 above 50 microM.

Amino Acids, Sulfur↗
PubMed1991

[The noninvasive estimation of right atrial pressure improves the Doppler evaluation of the pulmonary systolic pressure].

The right ventricular systolic pressure can be evaluated with the Doppler method through the right ventricular-atrial gradient (RV-RA gradient) and the right atrial pressure. The former is expressed by the transtricuspid velocity of flow, the latter is generally assumed. In 50 patients with elevated pulmonary pressure we tested whether ultrasounds may be utilized for the evaluation of the right atrial pressure, and whether the derived values contribute to improve the accuracy of the method. We estimated the right ventricular systolic pressure with method A: RV-RA gradient + 10; and method B: RV-RA gradient x 1.1 + 14, where 10 and 14 are the assumed right atrial pressure (mmHg). Through the collapsibility index of the inferior vena cava, taken as an ultrasound-derived index of right atrial pressure, we were able to identify 3 groups of patients with normal (Group 1, 14 cases), elevated (Group 2, 21 cases) and moderately elevated (Group 3, 15 cases) right atrial pressure, respectively. In them the right ventricular systolic pressures obtained with both method A and method B were compared to those derived with catheter. In Group 1 the non-invasive values were significantly closer to the invasive ones when calculated with method A; the same was true of method B in Group 2. In Group 3 the accuracy of the 2 methods was similar. We conclude that ultrasound assists in the non-invasive approximation of the right atrial pressure as well as in the choice of the appropriate formula, so that Doppler estimation of the right ventricular systolic pressure is improved.

Adult↗
PubMed1990

Cardiac tamponade produced by a loculated pericardial hematoma simulating a right atrial mass.

We report a case of cardiac tamponade due to thrombosis of a loculated pericardial effusion which occurred after open heart surgery. The loculated hematoma was highly echogenic and mimicked a right atrial mass. Cross-sectional echocardiography, in association with color Doppler flow imaging, was extremely useful in identifying this rare complication of cardiac surgery and, therefore, in determining the subsequent surgical approach.

Cardiac Surgical Procedures↗
PubMed1989

Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure.

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.

Adult↗
PubMed1989

[Anomalies of diastolic filling common to both ventricular cavities in hypertension].

In a population of 43 primary hypertensive patients we investigated the mitral and tricuspid valve flow in order to test whether: a) hypertension, as compared to normotension (Group 0, 10 normotensive subjects), alters the ventricular filling; b) changes are shared by the left and the right side of the heart; c) the structural characteristics (ultrasounds) of the left ventricle (LV) correlate with these changes. Hypertensives were divided into: Group 1, 11 patients in whom thickness (th) of both the ventricular septum (VS) and LV posterior wall (PW) was within a normal range (mean +/- 1 SD of values derived from 145 normal subjects); Group 2, 8 patients whose VSth exceeded normal values by more than 1 SD; Group 3, 24 patients in whom both VSth and PWth exceeded normal values by more than 1 SD. Groups 0, 1, 2 and 3 were homogeneous regarding gender, age, heart rate, LV cavity dimensions and systolic function. Blood pressure was slightly increased from Group 1 to Group 2 to Group 3. Mitral peak flow velocity in early diastole (PFVE) was similar in the 4 groups; in late diastole peak flow velocity (PFVA) through the same valve in each of the 3 hypertensive groups was significantly higher than in Group 0; as a consequence, PFVE/PFVA and E'/A' areas in hypertensives were significantly smaller than in normotensives. The flow pattern through the tricuspid valve was quite similar to this in each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Electrocardiographic alterations suggestive of myocardial injury elicited by rapid pressure lowering in hypertension.

In hypertensive cardiac hypertrophy, the elevated coronary perfusion pressure compensates importantly for the raised coronary resistance. An imbalance between perfusion and left ventricular (LV) mass, such as that occurring with rapid or excessive blood pressure lowering, may result in an inadequate oxygen supply. In 28 primary hypertensives (Group A) with LV mass index within the mean + 1 SD (96 + 19 g m-2) of 145 controls, and in 26 patients whose LV mass exceeded these values (Group B), we lowered the diastolic blood pressure rapidly to 85-90 mmHg, using both s.l. nifedipine and i.v. nitroprusside. During each test, eight patients in Group B had inversion of T waves in lead I, aVL, V3-V6, which waxed and waned in parallel with the pressure fall and recovery, and was independent of conduction disturbances, variations or group differences in the QRS axis, QTc interval, heart rate, LV fractional shortening and wall stress. A 'coronary steal phenomenon' or passive collapse in compliant lesions consequent to vasodilatation may trigger acute myocardial ischaemia in the presence of severe coronary disease. Patients developing the ECG alterations, however, were free from angina and four, who were subjected to coronary angiography, had normal arteriograms. Patients with the myocardial injury pattern showed greater LV mass indices and larger falls in diastolic pressure for it to reach normal levels. The supply of energy to the hypertrophied hypertensive heart seems to depend importantly on the coronary perfusion pressure, suggesting the cautious use of rapid acting drugs.

Adult↗
PubMed1988

Cardiac hypertrophy in hypertension. Repolarization abnormalities elicited by rapid lowering of pressure.

In hypertension, coronary flow is augmented and oxygen balance is adequate despite an increase in coronary resistance. For the maintenance of flow in the presence of and after regression of ventricular hypertrophy, the ratio of pressure and ventricular mass must remain normal. Coronary reserve would be altered if treatment normalized pressure but not ventricular mass or if pressure were lowered too fast. We investigated 42 patients with primary hypertension. In 28 (Group I) left ventricular mass index (by ultrasound) was within the mean value +2 SD (96 + 38 g/m2) of 145 controls and exceeded these values in the remaining 14 patients (Group 2). The diastolic pressure was lowered rapidly to between 85 and 90 mm Hg with two potent vasodilators, nifedipine (sublingually) and nitroprusside, while a 12-lead electrocardiogram was recorded continuously. During both tests, seven patients in Group 2 (responders) showed inversion of normal T waves, in lead I, aVL, and V3-6. These changes waxed and waned in parallel with the pressure fall and recovery and were not attributable to alterations in adrenergic tone, conduction disturbances, variations, or group differences in the QRS axis, QTc interval, heart rate, left ventricular fractional shortening, wall stress, rate of dimension increase in early diastole, or isovolumic relaxation. A ""steal phenomenon'' or passive collapse in compliant coronary lesions during vasodilatation seems unlikely; in fact, patients were free from coronary symptoms, and the electrocardiographic alterations occurred only in seven patients in Group 2, who had a greater left ventricular mass index and required a larger pressure drop to return the diastolic pressure to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Anterior uveitis in ankylosing spondylitis. A retrospective study].

In ankylosing spondylarthritis (AS), there is sometimes an anterior uveitis (AUV) or a previous history of AUV. The authors have reviewed the medical files of 338 hospitalised AS and 30 AS seen in consultation. They found an AUV in 28 hospitalised AS, or 8.3 p. cent of all cases (7.7 p. cent in men and 14.8 p. cent in women). In 3 cases (0.9 p. cent), the AUV was the first manifestation of the disease, preceding joint involvement. AUV was never found in patients seen in consultation. The findings of this investigation agree, but only partially, with those from the literature which, usually, acknowledge a greater frequency of AUV. Comparison with other previous investigations conducted in Italy enables to confirm that among Italian AS, AUV is less frequent than in other European and out of Europe series. It is possible that in a certain number of cases the AUV is not diagnosed clinically. However, it seems that the reduced incidence of the AUV discovered by a few Italian authors is not fortuitous (genetic factors?).

Adult↗
PubMed1986

Hypersensitivity of lung vessels to catecholamines in systemic hypertension.

Among patients with primary systemic hypertension pressure and arteriolar resistance in the pulmonary circulation exceed normal values and are hyper-reactive to sympathetic stimulation. A study was therefore carried out in 16 patients with uncomplicated essential hypertension and nine healthy subjects to compare the pulmonary vascular reactivity to exogenous catecholamines. In the normotensive group the dose response relation to adrenaline (microgram: dyn) was 1 = -4, 2 = -9, 3 = -9, and 4 = -10 and to noradrenaline 2 = +3, 4 = /8, 6 = +4, and 8 = +3. The relations in the hypertensive subjects were 1 = +18, 2 = +42, 3 = +59, and 4 = +77 and 2 = +39, 4 = +54, 6 = +76, and 8 = +100, respectively. Group differences were highly significant. Cardiac output (blood flow through the lungs) was raised by adrenaline and reduced by noradrenaline. In either case the driving pressure across the lungs was significantly augmented in the hypertensive patients but not in the normotensive group. Both catecholamines had a vasoconstrictor effect on the pulmonary circulation as a result of vascular over-reactivity. The opposite changes in resistance between normal and hypertensive subjects produced by adrenaline suggest that a constrictor vascular hypersensitivity occurs in the pulmonary circulation with the development of systemic high blood pressure.

Adult↗
PubMed1986

Pulmonary vascular supersensitivity to catecholamines in systemic high blood pressure.

Pulmonary pressure and arteriolar resistance are elevated in uncomplicated primary systemic hypertension. This study was carried out in 16 men with this form of hypertension and in 9 healthy men to compare 1) their pulmonary vascular reactivity to endogenous catecholamines released during mental arithmetic and cold pressor tests, and 2) the dose-response relation to exogenous epinephrine and norepinephrine. Arithmetic and cold pressor tests were associated, respectively, with a predominant increase in plasma epinephrine and norepinephrine concentration; changes were significantly greater in hypertensive men. During the two tests, pulmonary arteriolar resistance in the normotensive group was reduced by 13% and augmented by 7% of baseline, respectively, whereas it was raised by 31 and 70%, respectively, in the hypertensive group. In normal subjects, the dose (microgram)-response (delta dynes) relation to epinephrine was 1 = -4, 2 = -9, 3 = -9 and 4 = -10; to norepinephrine it was 2 = +3, 4 = +6, 6 = +7 and 8 = +7. In hypertensive patients, the respective relations were 1 = +18, 2 = +44, 3 = +59 and 4 = +77; and 2 = +39, 4 = +54, 6 = +76 and 8 = +98. Group differences were highly significant. In each of these circumstances, the driving pressure across the lungs was significantly augmented in the hypertensive but not the normotensive group. Both epinephrine and norepinephrine have a vasoconstrictor influence on the lesser circulation as a consequence of vascular overreactivity. The opposite changes in resistance between normotensive and hypertensive subjects produced by epinephrine suggest that a constrictor vascular supersensitivity becomes active in the pulmonary circuit with the development of systemic high blood pressure.

Blood Pressure↗
PubMed1985

Hemodynamic response to oral prenalterol in dilated decompensated cardiomyopathy as a result of cardiac and vascular effects.

The initial antifailure efficacy of beta-adrenergic agonists is generally lost during prolonged treatment. The reasons are not fully understood. In 11 patients with advanced cardiac decompensation due to dilated cardiomyopathy, prenalterol, a selective beta 1 adrenergic agonist, improved the left ventricular contractility after acute intravenous and during prolonged oral administration. However, after periods of treatment ranging from 2 to 18 weeks, blood pressure and systemic vascular resistance were raised in each patient. These changes resulted in an increase of the left ventricular afterload which was such as to overwhelm the effects of the enhanced contractility, and to extinguish the initial improvement of the cardiac function and of the clinical condition. Stimulation of the presynaptical beta-receptors facilitating norepinephrine release or of the renin secretion by this beta 1 agonist, may be the causes of the systemic vasoconstriction and of the loss of effectiveness in the long run.

Administration, Oral↗