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Biomedical subjects

M Guazzi

Publications and source records attributed to M Guazzi.

171 records · Page 10Linked to original sources
PubMedDate not supplied

A new formula for echo-Doppler estimation of right ventricular systolic pressure.

The Doppler formulas currently used for right ventricular systolic pressure (RVSP) evaluation include right ventricular-right atrial (RV-RA) gradient and RA pressure. The former is expressed by the velocity of the trans-tricuspid regurgitant flow; the latter is generally assumed and is different from one formula to another. In 110 patients with cardiac disease with normal or elevated pulmonary pressure, we tested a new echo-Doppler formula for the evaluation of RVSP based on the estimation of RA pressure by means of the inferior vena cava collapsibility index (IVCCI) and compared this method with two traditional formulas (methods A and B) and with cardiac catheterization values. Patients were classified into three groups on the basis of IVCCI (group 1 > 45%, group 2 between 35% and 45%, and group 3 < 35%). RVSP was evaluated by method A (RV-RA gradient + 10), method B (RV-RA gradient x 1.1 + 14), and our new method, method C, which assigns 6, 9, and 16 mmHg to RA pressure in the presence of normal (> 45%), moderately reduced (between 35% and 45%), or markedly reduced (< 35%) IVCCI, respectively. IVCCI correctly identified RA pressure in the three groups (group 1, 6.8 mmHg; group 2, 10.8 mm Hg; and group 3, 13.1 mmHg); a high correlation existed between Doppler-derived and invasively determined RV-RA gradient (r = 0.99). Method C improved noninvasive estimation of RVSP in groups 1 and 3 compared with the other methods; in group 2, Doppler estimation of RVSP by methods A and C were comparable, whereas method B significantly overestimated the actual values.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Function, Right↗
PubMedDate not supplied

Long-term treatment of hyperkinetic heart syndrome with propranolol.

Twelve men suffering from the primary hyperkinetic heart syndrome (PHHS) displayed palpitation, rapid and forceful heart action, increased pulsations of the large arteries, cardiac systolic murmur, and the following circulatory values (averages): systolic arterial pressure (SAP) =154 mm Hg; heart rate (HR)=91 b/min; cardiac index (Ci) =5494 ml/min/m2; left ventricular mean systolic ejection rate index (SMEJR) =227 ml/min/m2; left ventricular mean pre-ejection delta P/delta t (delta P/delta t) = 1.32 mm Hg/msec. A two-year followup during which propranolol was administered (80-160 mg/day) revealed good subjective improvement and disappearance of signs of circulatory hyperkinesis. At the end of this period the hemodynamic functions were as follows: SAP=134; HR=69; Cl=3489; MSEJR=171; delta P/delta t=0.89. Substitution of placebo for the active drug caused prompt reappearance of symptoms of cardiac overactivity in each patient, and brought the circulatory functions back to these levels: SAP=157; HR=96; Cl=5530; MSEJR=245; delta P/delta t=1.33. These findings lend further credence to the concept that the PHHS is, indeed, a definable disease entity; they also document that propranolol ameliorates the symptoms of the disease but is ineffective for the underlying disorder.

Adolescent↗
PubMedDate not supplied

Cardiac performance and beta-adrenergic blockade in arterial hypertension.

The purpose of the study was to evaluate the functional changes which may occur in the human hypertensive heart following treatment with beta-blocking agents. In 54 primary hypertensive men investigated in the control state and after three weeks of treatment with propranolol (320 mg/day) it was seen that: (a) beta-adrenergic blockade depresses the pre-ejection, and probably the ejection left ventricular function; (b) the former effect is unrelated to changes in peripheral circulation, while the latter result may be either potentiated or overcome, depending on the direction to which treatment shifts the vascular resistance; (c) variations of impedance, rather than of blood pressure, influence the ejection left ventricular function; and (d) withdrawal of the adrenergic support to the heart, due to beta-blockade, is probably the primary factor responsible for the abnormal ventricular adaptation to an augmented impedance.

Blood Pressure↗
PubMedDate not supplied

Hypoxia-induced pulmonary hypertension: nifedipine only temporarily reduces pulmonary artery pressure and vascular tone.

Fifteen patients affected by hypoxia-induced pulmonary hypertension were studied before and during (1st and 8th week) nifedipine (180 mg/die) treatment. Nifedipine reduced pulmonary pressure (33 +/- 4 vs 26 +/- 3 mmHg, p less than 0.02) after 1 week of treatment; this pulmonary hypotensive effect was due to a reduction of pulmonary vascular tone as assessed by a reduction of Y-intercept on the pulmonary pressure/flow plot drawn from invasive recordings of pulmonary pressure/cardiac output obtained during exercise. Oxygen breathing effects on pulmonary pressure were also measured with and without nifedipine. Oxygen significantly reduced pulmonary pressure only in the absence of nifedipine regardless of the severity of pulmonary hypertension. Therefore nifedipine is not suitable for long-term treatment of hypoxia-induced pulmonary hypertension and inhibits O2 capability to reduce pulmonary pressure.

Adult↗
PubMedDate not supplied

Elliptic Fourier analysis of mandibular shape.

Craniofacial growth and development involve both size and shape variations. Shape variations can be assessed independently from size using mathematical methods such as the elliptic Fourier analysis, which allows a global evaluation of the shape of organs identified by their outlines independently from size, spatial orientation, and relation to reference planes. The mandibular outlines were digitized from the tracings of the Bolton standards (lateral view) from 1 to 18 years of age, and the age differences in shape independently from size were quantified using the elliptic Fourier series. A "morphologic distance" MD (i.e., a measurement of differences in shape) between each younger mandible and the oldest one was computed using the relevant Fourier coefficients like the cartesian coordinates in standard metric measurements. MD equals 0 when the profiles are identical. MD (Y) between the Bolton standard at 18 years of age and all the other Bolton tracings were significantly correlated (correlation coefficient r = 0.987, P < or = 0.001) with age (X) (semi-logarithmic interpolation Y = -3.87.log(e) X + 13.593). Differences between the size-independent shape of the Bolton standard at 18 years and the relevant plot at 1 year were located at the chin, gonion, coronoid process, anterior border of the ramus. Size differences were measured from the areas enclosed by the mandibular outlines. Mandibular area (Y) increased about 2.58 times from 1 to 18 years of age (X) (Y = -0.071.X2 + 4.917.X + 35.904, r = 0.997, P < or = 0.001). The shape effect was largely overwhelmed by the very evident size increments, and it could be measured only using the proper mathematical methods. The method developed could also be applied to the comparison between healthy and diseased individuals.

Adolescent↗
PubMedDate not supplied

[Effectiveness of long-term ACE-inhibition on pulmonary diffusion and ventilation-perfusion ratio in chronic heart failure: correlation with physical performance].

Pulmonary dysfunction contributes to exercise intolerance in patients with chronic heart failure, and ACE-inhibition improves the functional capacity of these subjects. In this study, we investigated whether and how ACE-inhibitors affect pulmonary function and ventilatory response during exercise in chronic heart failure. Twenty patients with idiopathic dilated cardiomyopathy and left ventricular ejection fraction < 35% underwent pulmonary function tests and exercise evaluation with analysis of expired gases before and after 1 year of treatment with enalapril (10 mg bid). To explore whether or not the respiratory influence of ACE-inhibitors is peculiar to the syndrome of cardiac failure, we also studied 19 subjects with mild, untreated primary hypertension who followed the same protocol. In this group, enalapril exerted a neutral effect on pulmonary function. In chronic heart failure patients, lung volumes were abnormal and did not improve after enalapril treatment; on the contrary, alveolar diffusing capacity for carbon monoxide increased towards normal values. Exercise tolerance time, peak exercise oxygen consumption, ventilation, and tidal volume also improved and the dead space to tidal volume ratio was reduced at the peak exercise and intermediate exercise phases (20, 60 W). Changes in carbon monoxide diffusion were positively correlated to those occurring during peak exercise oxygen consumption. A negative correlation was found between the variations in oxygen consumption and those in dead space to tidal volume ratio at peak exercise. We conclude that in patients with chronic heart failure, ACE-inhibition restores diffusing lung properties and improves ventilation-perfusion matching during exercise. In this syndrome, sustained reduction in gas exchange resistance is a fundamental therapeutic property of this class of drugs.

Adult↗