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Biomedical subjects

G Finardi

Publications and source records attributed to G Finardi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Determinants of heart rate variability in heart transplanted subjects during physical exercise.

Respiratory sinus arrhythmia has been described in heart transplanted subjects. In order to investigate the mechanisms involved in the generation of this condition in the transplanted heart and its evolution after surgery, graded exercise was performed (0-75 W in 25 W steps) on a cycle ergometer by 41 subjects (mean age 44 years) who had undergone heart transplantation 28 months (range 3-60) earlier and by six age matched-control subjects. R-R interval, respiratory signal, O2 consumption (VO2) and CO2 production (VCO2) were measured. Respiratory sinus arrhythmia was assessed by the autoregressive power spectrum of the R-R interval and respiration. All subjects reached the anaerobic threshold (heart transplants: 60% at 50 W, 40% at 75 W Controls: 150 W). In control subjects, the respiratory sinus arrhythmia was higher than in heart transplanted subjects (5.80 +/- 0.30 vs 1.45 +/- 0.16 1n ms2) and it decreased significantly (4.66 +/- 0.30 1n ms2, P < 0.05) during exercise, despite the increase in breathing rate and depth. When, the group of heart transplanted subjects was considered as a whole, respiratory sinus arrhythmia was found to be present in all conditions. It significantly increased at 25 W (from 1.45 +/- 0.16 to 2.00 +/- 0.17 1n ms2, P < 0.01), then significantly fell below baseline during recovery (to 0.97 +/- 0.23 1n ms2, P < 0.01). Multiple regression analysis showed that a linear combination of heart rate (inverse correlation) and VO2 (direct correlation) together with months having passed since transplantation surgery, could explain the observed changes in heart rate during exercise (multiple regression: r = 0.658, P < 0.0001). In five long-term transplanted subjects, non respiratory-related low frequency (0.1 Hz) waves were present on the R-R spectrum, but respiratory sinus arrhythmia is also present in the recently transplanted heart and depends on the opposing effects of ventilation and heart rate. In a few cases, sympathetic modulation (re-innervation) could not be excluded.

Adult↗
PubMed1996

Lipoprotein(a) plasma concentrations, apolipoprotein (a) polymorphism and family history of coronary heart disease in patients with essential hypertension.

AIM: The purpose of the study was to investigate lipoprotein (a) (Lp(a)) levels and apolipoprotein (a) (apo(a)) phenotypes, and their relationship with a family history of coronary heart disease (CHD) in patients with essential hypertension (EH). METHODS: One hundred and eight newly diagnosed patients with mild to moderate EH and 159 controls were studied. Lp(a) levels were determined with an ELISA method. Apo(a) isoforms were identified by a capillary immunoblotting technique. RESULTS: Lp(a) levels and frequency distribution of apo(a) isoforms did not show significant differences between patients and controls. Lp(a) levels in hypertensives with a family history of CHD were significantly higher than in those without a family history of CHD (P < 0.01). Hypertensives with a family history of CHD showed significantly different frequencies of apo(a) isoforms to those without a family history of CHD (P < 0.05). In EH patients with a family history of CHD, apo(a) isoforms of low molecular weight (MW) had a higher prevalence (62.6%), while in hypertensives without a family history of CHD, apo(a) isoforms of high MW were prevalent (81.6%); the difference between the two subgroups was significant (P < 0.001). Multivariate analysis showed that both Lp(a) levels and apo(a) isoforms of low MW are significant variables in distinguishing between the subgroups. CONCLUSIONS: Lp(a) levels and apo(a) phenotypes do not differ between hypertensives and controls. High Lp(a) levels and apo(a) isoforms of low MW are strongly associated with a family history of CHD in hypertensives. The quantification of Lp(a) levels and the characterization of apo(a) phenotypes may be used for assessment of familial predisposition to CHD in hypertensives.

Apolipoproteins↗
PubMed1996

Effect of sublingual nifedipine on left ventricular diastolic dysfunction in hypertensives: echo-Doppler study at rest and during handgrip.

Using digitized M-mode echocardiography, we evaluated the acute effect of nifedipine on left ventricular (LV) diastolic dysfunction in 30 untreated hypertensives, evaluated at rest and during handgrip, both before and 30' after nifedipine (20 mg sublingually). At rest, after nifedipine blood pressure and end-systolic wall stress significantly decreased and peak lengthening rate of LV diameter, peak thinning rate of LV posterior wall and Doppler E/A ratio increased. Before and after nifedipine handgrip induced significant increases of blood pressure, heart rate and end-systolic wall stress; diastolic parameters significantly decreased during basal handgrip and did not change during handgrip after nifedipine. Nifedipine induced an acute improvement of LV diastolic dysfunction, that persisted when afterload increased during handgrip. Therefore nifedipine seems to improve LV diastolic function not only by reducing afterload, but also through a direct action on the myocardium. Besides, these results demonstrate that LV diastolic abnormalities in hypertension are partly dynamic and reversible.

Administration, Sublingual↗
PubMed1995

[Oxidation of low-density lipoproteins. Correlation between reduced resistance in vitro and increased oxidation in vivo].

OBJECTIVES: The oxidation of low-density lipoproteins has been recently proposed as one of the critical factors in promoting atherogenesis. This process results from the balance between the prooxidant stimuli and the endogenous antioxidants present in LDL and strictly depends on the concentration of oxidizable substrates, namely unsaturated fatty acids. METHODS: Twelve male hypertriglyceridaemic patients were investigated before and after oral supplementation with omega-3 polyunsaturated fatty acids (PUFA) and compared with eighteen untreated healthy matched control subjects. The plasma lipid profile was measured in all patients. LDL oxidation was evaluated as both the susceptibility to in vitro oxidation and the presence of plasma anti-oxidized LDL antibodies (as a marker for in vivo oxidation). RESULTS: Omega-3-fatty acid supplementation caused a significant reduction in plasma triglyceride level (267 +/- 38 vs 375 +/- 33 mg/dl, p < 0.01) and decreased the resistance of LDL to oxidation as revealed by an early and accelerated generation of conjugated dienes following exposure to CuSO4 (105.3 +/- 7 vs 133 +/- 9.3 min, p < 0.01). Moreover, the concentration of the antioxidant vitamin E in LDL was slightly but significantly decreased at the end of the treatment (2.59 +/- 0.19 vs 2.89 +/- 0.17 nmol/mg LDL, p < 0.05), but its efficiency in preventing LDL oxidation was unaltered. Furthermore, a marked increase of the plasma anti-oxidised LDL antibody titre was found in nearly all patients at the end of the treatment (2.08 +/- 0.48 vs 1.37 +/- 0.2 anti-oxidised/anti-native LDL antibody ratio, p < 0.001). CONCLUSION: These results indicate that PUFA supplementation decreases the resistance of LDL to in vitro oxidation and that this decreased resistance is accompanied by an enhanced LDL oxidation in vivo.

Adult↗
PubMed1995

Left ventricular anatomy and function in normotensive young adults with hypertensive parents. Study at rest and during handgrip.

Using digitized M-mode echocardiograms, we evaluated left ventricular (LV) anatomy and function at rest and during handgrip in 24 normotensive young adults with both parents hypertensive (HP+), each matched for age, sex, body weight, and body surface area with one normotensive adult with both parents normotensive (HP-). LV parameters were within the normal range in all HP+ and HP-. At rest, HP+ as compared to HP- had higher systolic and diastolic blood pressure (BP), septal and posterior wall thickness, and LV mass; LV diastolic diameter and end-systolic wall stress were similar in the two groups. Modified midwall fractional shortening, peak shortening rate of LV diameter and peak thickening rate of LV posterior wall, indices of LV systolic function, and peak lengthening rate of LV diameter and peak thinning rate of LV posterior wall, indices of ventricular relaxation, were significantly higher in HP+. Handgrip induced significant (P < .001) and percent-comparable increases of systolic and diastolic BP, heart rate, and cardiac output in HP+ and HP-; peak shortening and lengthening rates of LV diameter and peak thickening and thinning rates of LV posterior wall increased significantly in HP-, whereas in HP+ the value of the four parameters, higher at rest as compared to HP-, did not show any further increase. In conclusion, normotensive young adults with high genetic risk for hypertension have higher BP and thicker and overactive LV as compared to subjects with normotensive parents. Handgrip stimulates LV function in offspring of normotensives, but not the already hyperkinetic LV of hypertensive offspring.

Adult↗
PubMed1995

Determinants of respiratory sinus arrhythmia in the vagotomized rabbit.

After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, beta-adrenergic blockade, and phasic and steady changes in right atrial pressure (RAP) induced by changes in tidal volume (VT, 20, 40, 60 ml), respiratory frequency (RF, 10, 20, 30 cycles/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of variations of the rate of change due to respiration. RSA was assessed by combined autoregressive power spectral analysis of R-R interval and respiration on sequences of 256 heart-beats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P < 0.025 and P < 0.001, respectively) and correlated with dRAP (P < 0.001) and arterial PO2 (P < 0.001). beta-Adrenergic blockade did not change the amplitude of this residual RSA or its dependence on ventilatory mechanics. Dextran-induced increase in mean RAP from 2.9 to 11.9 mmHg did not modify RSA or dRAP. During 100% O2 inhalation, RSA changes were no longer significantly linked to RF and VT, and also the correlation of RSA with dRAP was reduced (P < 0.05). Changing the arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1995

Autoantibodies against oxidatively modified low-density lipoproteins in NIDDM.

Diabetes is an independent risk factor in the development of atherosclerosis, although the pathophysiological processes underlying this association are poorly understood. The oxidation of low-density lipoprotein (LDL) is considered a key event in the development and progression of atherosclerosis because it generates molecular epitopes that are more atherogenic than parent LDL. A total of 138 patients suffering from non-insulin-dependent diabetes mellitus (NIDDM) and 80 matched control subjects were investigated. LDL oxidation was evaluated as the presence of autoantibodies against oxidatively modified LDL, since they mirror the in vivo occurrence of oxidative processes. NIDDM patients had an antibody ratio (calculated as the ratio of antibodies against modified versus native LDL) significantly higher than control subjects for Cu(2+)-oxidized LDL (1.88 +/- 0.6 vs. 1.05 +/- 0.3, P < 0.01, for IgG), malondialdehyde-modified LDL (2.54 +/- 0.73 vs. 2.04 +/- 0.11, P < 0.01, for IgG and 3.96 +/- 1.51 vs. 2.90 +/- 0.15, P < 0.01, for IgM), and malondialdehyde-modified human serum albumin (1.79 +/- 0.54 vs. 1.46 +/- 0.1, P < 0.05 for IgG). The possible role played by glycation in sensitizing LDL to oxidation was investigated by measuring autoantibodies against both glycated LDL (glycLDL) and glycoxydated LDL (glycoxLDL). NIDDM patients had an antibody ratio significantly higher than control subjects for anti-glycLDL and anti-glycoxLDL IgG (1.79 +/- 0.38 vs. 1.12 +/- 0.23, P < 0.01 and 2.55 +/- 1.03 vs. 1.39 +/- 0.44, P < 0.01, respectively) but not anti-glycLDL and anti-glycox-LDL IgM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

[Heart failure at the end of the 2nd millennium].

After a historical overview of heart failure, the author points out the most recent findings concerning the pathophysiology, the molecular and cellular biology of this clinical syndrome. Bearing in mind the extensive research and studies that have been made in the domain of heart failure, the author emphasizes the importance of the relationship between the physician and the patient and of the human aspect in the practice of clinical medicine.

Heart↗
PubMed1995

Presence of autoantibodies against oxidatively modified low-density lipoprotein in essential hypertension: a biochemical signature of an enhanced in vivo low-density lipoprotein oxidation.

OBJECTIVE: We have previously reported that low-density lipoproteins (LDL) isolated from patients with essential hypertension are more susceptible to in vitro oxidation than lipoproteins isolated from normotensive control subjects. In the present study we investigated the occurrence of in vivo LDL oxidation in hypertensive patients. DESIGN: The presence of antioxidatively modified LDL autoantibodies was taken as a suitable index of in vivo LDL oxidation because, after oxidative modifications, LDL express antigenic epitopes that elicit an immune response. The antibody titres were measured in plasma from untreated patients with newly diagnosed essential hypertension. METHODS: An enzyme-linked immunosorbent assay method was employed, using native LDL, Cu(2+)-oxidized LDL and malondialdehyde-derivatized LDL (MDA-LDL) as antigens. Human serum albumin and MDA human serum albumin were also used to monitor cross-reactivity with other oxidized molecules. The antibody titre was expressed as the ratio between anti-modified and anti-native antigen absolute values. RESULTS: The patients with essential hypertension had an antibody ratio significantly higher than control subjects with respect to anti-Cu(2+)-oxidized LDL immunoglobulins G and M, and with respect to anti-MDA-LDL immunoglobulins G and M. A significant positive correlation was found between anti-MDA-LDL and anti-Cu(2+)-oxidized LDL antibody titres. The anti-MDA human serum albumin antibody titre was not different in the two groups of patients. An inverse correlation was detected between the anti-MDA-LDL immunoglobulin M titre and the age of the patients. CONCLUSIONS: The results obtained are consistent with the view that, during the early phases of hypertension development, LDL undergo in vivo oxidation that is mirrored by the generation of autoantibodies against epitopes of oxidized LDL. The oxidation process appears specific for LDL and might be relevant both for the progression of hypertension and for the development of the atherosclerosis that often complicates hypertension itself.

Antibody Specificity↗
PubMed1994

Enhanced LDL oxidation in uremic patients: an additional mechanism for accelerated atherosclerosis?

Since oxidized low-density lipoprotein (LDL) is more atherogenic than native LDL, LDL oxidation was investigated in uremic patients who often develop accelerated atherogenesis. Three groups of uremic patients were studied (10 on predialysis conservative therapy, 11 on repetitive hemodialysis, 13 on peritoneal dialysis) and compared with seventy matched controls. LDL oxidation was evaluated in all patients as: (i) the susceptibility to in vitro oxidation (by measuring the resistance to Cu(++)-induced formation of conjugated dienes), (ii) vitamin E concentration in LDL, and (iii) presence of plasma anti-oxidized LDL antibodies, expressed as the ratio anti-oxLDL/anti-nativeLDL antibodies. The lipid profile was studied in all patients. Vitamin E concentration did not differ between the various groups, although LDL from uremic patients appeared more susceptible to in vitro and in vivo oxidation (as demonstrated by an earlier generation of conjugated dienes and by the presence of an higher antibody ratio) compared to control subjects. Subclass analysis of the different patients revealed that peritoneal dialysis treatment ameliorated the oxidation markers. However, a prolonged dialytic treatment caused a decrease in vitamin E concentration in LDL and increased their susceptibility to oxidation.

Arteriosclerosis↗
PubMed1994

Non-respiratory components of heart rate variability in heart transplant recipients: evidence of autonomic reinnervation?

1. Although the high-frequency fluctuations in R-R interval (respiratory sinus arrhythmia) observed in heart transplant recipients are not a reliable marker of reinnervation because of a previously shown direct mechanical effect of breathing, the presence of a non-respiration-related low-frequency oscillation reflects rhythms generated outside the heart, and thus could be neurally mediated. 2. To evaluate the presence of reinnervation, the spontaneous variability in R-R interval was investigated, supine and after passive tilting, in 23 heart transplant recipients (age 43 years, range 23-64 years) and in 25 normotensive control subjects by autoregressive spectral analysis of low- and high-frequency spontaneous fluctuations in R-R interval and respiration. The response of R-R interval to amyl nitrite inhalation was also evaluated in five heart transplant recipients and eight control subjects. 3. Detectable low-frequency oscillations, unrelated to respiration, were present in 13/23 heart transplant recipients, particularly in those who were transplanted at least 20 months earlier (11/14). The natural logarithm of the power of low-frequency fluctuations was markedly lower than in control subjects (0.75 +/- 0.21 versus 5.62 +/- 0.20 ms2, P < 0.001). The low-frequency but not the high-frequency fluctuations correlated with time since transplantation (r = 0.44, P < 0.05). The subjects with low-frequency fluctuations showed a sudden decrease in R-R interval with amyl nitrite linearly related to the decrease in mean blood pressure (r > or = 0.94). The slopes obtained in these heart transplant recipients were comparable (although of lower values) with those obtained in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

LDL oxidation in patients with severe carotid atherosclerosis. A study of in vitro and in vivo oxidation markers.

Among the various risk factors involved in the development and progression of carotid atherosclerosis, the oxidation of LDL has been proposed to play a relevant role. LDL oxidation has been investigated in 94 patients with severe carotid atherosclerosis undergoing elective carotid artery endarterectomy and in 42 matched control subjects. LDL oxidation was evaluated in all patients as (1) the susceptibility to in vitro oxidation, (2) vitamin E concentration and its efficiency in LDL, and (3) the presence of autoantibodies against oxidatively modified lipoprotein to monitor the occurrence of the oxidative processes taking place in vivo. No difference was detected between control subjects and patients concerning vitamin E concentration and the kinetics of conjugated diene formation in isolated LDL exposed to CuSO4. However, vitamin E efficiency was lower (9.6 +/- 4.2 versus 30.2 +/- 7.6 min/nmol vitamin E) and the duration of the vitamin E-independent lag phase was longer (105.5 +/- 16.5 versus 58 +/- 11.8 minutes) in the patient group. Autoantibodies against oxidatively modified lipoproteins were measured with an ELISA method using native LDL, Cu(2+)-oxidized LDL (oxLDL), or malondialdehyde-derivatized LDL (MDA-LDL) as antigens. To monitor cross-reactivity of the antibodies detected with other oxidatively modified proteins, human serum albumin (HSA) and MDA-derivatized HSA (MDA-HSA) were also employed. The antibody titer was calculated as the ratio of antibodies against modified versus native proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Cardiovascular autonomic modulation in essential hypertension. Effect of tilting.

To better understand the role played by the autonomic nervous system in essential hypertension, we used autoregressive power spectrum analysis to study the noncasual oscillations in RR interval, blood pressure, and skin blood flow in 40 subjects with mild to moderate hypertension and in 25 age-matched control subjects at low frequency (index of sympathetic activity to the heart and the peripheral circulation) and high frequency, respiratory related (index of vagal tone to the heart). RR interval, respiration, noninvasive systolic blood pressure, and skin arteriolar blood flow were simultaneously and continuously recorded with subjects in the supine position and immediately after tilting. The low-frequency component was not significantly different in the two groups either at the cardiac level (control versus hypertensive subjects: 39.1 +/- 4.3 versus 39.9 +/- 3.7 normalized units [NU]) or at the vascular level (1.52 +/- 0.17 versus 1.69 +/- 0.13 ln mm Hg2). After head-up tilting, the RR interval fluctuations were less in hypertensive subjects (low-frequency components from 39.9 +/- 3.7 to 48.4 +/- 4.1 NU, P < .05; high-frequency components from 53.9 +/- 3.7 to 44 +/- 4 NU, P < .05) than in control subjects (low-frequency components from 39.1 +/- 4.3 to 64.4 +/- 4.9 NU, P < .001; high-frequency components from 56.0 +/- 4.5 to 31.2 +/- 4.6 NU, P < .001); the low-frequency components in systolic blood pressure increased similarly in hypertensive subjects (to 2.43 +/- 0.17 ln mm Hg2, P < .0001) and in control subjects (to 2.44 +/- 0.21 ln mm Hg2, P < .01), but the low-frequency components in skin blood flow increased only in control subjects (from 5.34 +/- 0.45 to 6.55 +/- 0.53 mm Hg2, P < .01), not in hypertensive subjects (from 5.55 +/- 0.34 to 5.60 +/- 0.35 ln mm Hg2). In hypertensive subjects with left ventricular hypertrophy, the low-frequency components in systolic blood pressure did not increase after tilting (from 1.75 +/- 0.33 to 2.05 +/- 0.41 ln mm Hg2). Baroreflex sensitivity, as assessed by spectrum analysis, was significantly lower in hypertensive than in control subjects (5.17 +/- 0.49 versus 13.18 +/- 2.44 ms/mm Hg, P < .001. Power spectrum analysis did not reveal an increased sympathetic activity or reactivity either at the cardiac or at the vascular level. The decreased baroreceptor sensitivity in hypertensive subjects could explain the reduced change in sympathovagal balance in the tilt position at the cardiac level. In hypertensive subjects without left ventricular hypertrophy, cardiopulmonary reflex deactivation induced by tilting and/or amplification of sympathetic nervous tone by arteriolar structural change could have preserved the sympathetic activation at the vascular level.

Adolescent↗
PubMed1994

Metabolic risk factors in white coat hypertensives.

Metabolic disturbances such as hyperinsulinaemia, dislipoproteinaemia and glucose intolerance are often associated with essential hypertension and markedly affect cardiovascular morbidity in hypertensive patients. In order to shed some light on the prognostic significance of white coat hypertension (raised clinic and normal ambulatory blood pressure), we compared the metabolic profile in a group of white coat and sustained previously untreated hypertensives. We studied 84 newly detected hypertensive patients (49 men, 35 women, 47 +/- 8 years, range 28-59 years). Subjects with obesity (BMI > 30), NIDDM and target organ damage were excluded. Ambulatory blood pressure monitoring was performed by SpaceLabs 90207-31. Total cholesterol and triglycerides, LDL-cholesterol, HDL-cholesterol (HDL-C) and subclasses HDL2 and HDL3 cholesterol as well as apolipoprotein A1 and B were measured in fasting plasma. Glucose and insulin were determined in fasting and postload (glucose 75 g plasma. Twenty patients (24%, 8 men and 12 women) were classified as white coat hypertensives. No differences in age, BMI and waist to hip ratio were observed between white coat and sustained hypertensive patients. Plasma glucose and lipoprotein levels were similar in the two groups. Fasting and postload insulin levels were significantly lower in white coat hypertensives (fasting insulin 7.1 +/- 2.9 vs. 12 +/- 8.6 microU/ml, P < 0.02; insulin 120 minutes 48 +/- 27 vs. 65 +/- 41 microU/ml, P < 0.05); glucose/insulin rate was higher in white coat than in sustained hypertensive patients (15 +/- 7 vs. 11 +/- 7, P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[During experimental coronary occlusion dobutamine further slows down the time constant of isovolumetric relaxation].

It has been shown that the time constant (tau) of isovolumic left ventricular (LV) pressure fall is shortened by beta-adrenergic stimulation, possibly reflecting enhanced myocardial relaxation and improved uniformity within the LV wall. Conversely, acute regional ischaemia , slows tau due to mechanical nonuniformity between the nonischaemic and the ischaemic regions. In order to assess the effect of inotropic stimulation on LV pressure fall during acute regional ischaemia, 7 anaesthetized dogs (16 +/- 2 kg) were instrumented with LV and aortic micromanometers. Sonomicrometers were implanted in the areas supplied by the left circumflex and anterior descending arteries to monitor subendocardial segment length (L). After baseline recordings, acute regional ischaemia was induced by 60 s occlusion of the proximal circumflex artery. After a 30 min recovery, the same was repeated during dobutamine infusion (5 micrograms/kg/min). In order to derive tau from heart beats with comparable end-systolic pressures, a caval occlusion run was performed at each stage. The % systolic bulging of the ischaemic zone was defined as: (maximal L--end-diastolic L)/end-diastolic L x 100. The fitting of the exponential model used to derive tau was always good (r > or = 0.99). At comparable end-systolic pressures, tau was increased by acute regional ischaemia (36 +/- 2 versus 32 +/- 2 ms, p < 0.01) and reduced by dobutamine infusion (27 +/- 2 versus 32 +/- 2 ms, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗