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Biomedical subjects

Carlo Palombo

Publications and source records attributed to Carlo Palombo.

14 recordsLinked to original sources
PubMed2006

Noninvasive simultaneous assessment of wall shear rate and wall distension in carotid arteries.

A novel technique has been developed for the noninvasive real-time simultaneous assessment of both blood velocity profile and wall displacements in human arteries. The novel technique is based on the use of two ultrasound beams, one set at optimal angle for wall motion measurements and the other for blood velocity profile measurements. The technique was implemented on a linear array probe divided into two subapertures. A modified commercial ultrasound machine and a custom PC board based on a high-speed digital signal processor was used to process the quadrature demodulated echo signals and display results in realtime. Flow phantom experiments demonstrated the validity of the technique, providing wall shear rate (WSR) estimates within 10% of the theoretical values. The system was also tested in the common carotid arteries of 16 healthy volunteers (age 30 to 53 y). Results of simultaneous diameter distension and WSR measurements were in agreement with published data.

Adult↗
PubMed2005

Reduced left ventricular functional reserve in hypertensive patients with preserved function at rest.

In many hypertensive patients, left ventricular pump function is normal at rest but abnormal during exercise. Myocardial dysfunction or altered left ventricular loading may be responsible for this finding. To verify the hypothesis of impaired myocardial functional reserve in the hypertensive heart, we assessed the response of stress-adjusted midwall shortening to graded, low-dose dobutamine infusion in hypertensive subjects with normal midwall shortening at rest. Sixty-five subjects (45 never treated hypertensive subjects and 20 normotensive volunteers comparable for age) received dobutamine at 1, 2, 3, 4, and 5 microg x kg(-1) x min(-1) for 5-minute steps; within this range of infusion rates, heart rate and systemic blood pressure were stable. Two-dimensional, M-mode, and Doppler echocardiography were performed at baseline and at the end of each step. In normotensive controls, midwall shortening increased from baseline during 2 microg x kg(-1) x min(-1) dobutamine by an average of 16+/-4.5% (P<0.01); a value of 2 standard deviations below this mean response was taken as the lower limit of normal. In the hypertensive subjects, 24 had a normal midwall shortening response to dobutamine at this dose (group I) and 21 had a subnormal response (group II). Whereas blood pressure and left ventricular mass were similar in group II and group I, the former had greater relative wall thickness (P<0.01) than the latter. beta-adrenergic stimulation by very-low-dose dobutamine unmasks subtle impairment of myocardial functional reserve in hypertensive subjects with normal myocardial performance at rest. This alteration seems to be related mainly to increase in left ventricular relative wall thickness.

Adrenergic beta-Agonists↗
PubMed2005

Clinical validation of common carotid artery wall distension assessment based on multigate Doppler processing.

Mechanical properties of human large arteries result from the interaction between blood pressure, wall distensibility and shear stress. Both the arterial diameter changes through the cardiac cycle (distension) and blood flow velocities can be noninvasively investigated through Doppler ultrasound approaches. Recently, an integrated system processing in real-time all the echo signals produced along an M-line has been developed. This system has been so far demonstrated to be suitable for accurate hemodynamic studies through the detection of blood velocity profiles. This paper reports on the extension of its processing capabilities to the real-time measurement of arterial distension. Tissue motion estimation is based on a modified 2-D autocorrelation algorithm. A novel adaptive approach to track wall position over time using the sum of the high-pass filtered displacement waveform and the low-pass filtered wall position is described. By observing the blood velocity profile, a rapid and accurate positioning of the ultrasound probe and an inherent check on perpendicular observation are provided. First clinical results obtained by measuring the distension of common carotid arteries in a group of 41 volunteers are reported and measurements are validated against those provided by a dedicated wall-track reference system. Average measured distension and diameter were 499 +/- 188 microm and 6.90 +/- 0.66 mm and intraobserver intrasession reproducibility tests showed coefficients of variability of 8.5% and 5.9%, respectively. The agreement between the proposed system and the reference system, expressed as bias +/- 2 SD of the differences, was -34 +/- 141 microm for distension and 0.05 +/- 1.07 mm for diameter.

Adolescent↗
PubMed2004

The alpha1-adrenergic blocker urapidil improves contractile function in patients 3 months after coronary stenting: a randomized, double-blinded study.

BACKGROUND: The recovery of left ventricular function (LVF) after revascularization takes time. alpha-Adrenergic blockade acutely improves coronary blood flow and LVF, whereas the effects of more prolonged alpha-adrenergic blockade on LVF recovery after stenting are unknown. METHODS: In 32 patients (age 58 +/- 12 y) with an 82% +/- 6% stenosis, ejection fraction (EF) and systolic thickening (%Th) were measured by transthoracic echocardiography before and 30 minutes to 2 hours after revascularization. In a double-blinded protocol, either 200 microg/kg urapidil or placebo was given intravenously, and LVF was measured 10 minutes later. Two hours later, oral treatment with 30 mg/d drug or placebo was started, and LVF measured again after 24 hours and 3 months. RESULTS: Before revascularization, EF was 49.4% +/- 8.5% (+/-SD) and 51.3% +/- 8.8% in the urapidil-treated and the placebo groups, respectively. Thirty minutes to 2 hours after coronary stenting, EF was unchanged. After intravenous drug administration, EF increased to 56.5% +/- 9.7%). At 24 hours and 3 months after revascularization, EF became 59.5% +/- 7.9% and 59.6% +/- 8.2% in the urapidil-treated group, respectively, whereas EF in the placebo group did not change (50.4% +/- 5.7% and 49.7% +/- 4.9%, respectively). Revascularization did not acutely improve %Th. Intravenous urapidil improved %Th from 31.4% +/- 17.6% to 44.2% +/- 11.6%, whereas there was no change in the placebo group. At 3 months, %Th was 49.5% +/- 12.9% in the urapidil-treated group and 39.7% +/- 8.9% in the placebo group. CONCLUSIONS: These data suggest that long-term alpha-adrenergic blockade might improve LVF at midterm after coronary revascularization.

Adrenergic alpha-Antagonists↗
PubMed2004

Effects of age and physical fitness on microcirculatory function.

Sedentary aging is associated with endothelial dysfunction and nitric oxide (NO) impairment. The aim of the present study was to assess the effects of regular physical exercise on nitrite/nitrate (NOx) concentrations and microcirculatory function in older men compared with young individuals. We measured NOx plasma concentrations and baseline and stimulated skin blood flow (SBF) by laser Doppler flowmetry in 39 male athletes [range, 22-72 years; maximal oxygen consumption (VO2max), 60.0 +/- 4.7 ml.min(-1).kg of body weight(-1) (mean +/- S.D.)] and 45 age- and sex-matched sedentary controls (VO2max, 38.0 +/- 7.1 ml.min(-1).kg of body weight(-1)). NOx concentrations were higher in athletes than in controls (50.4 +/- 16.3 compared with 39.0 +/- 15.4 micromol/l; P<0.005), whereas baseline SBF was comparable. Hand SBF after heating and ischaemia and foot SBF after heating were higher in athletes (P<0.0001) than in controls. By comparing the lowest and the highest tertile of age, sedentary young subjects had higher NOx concentrations than sedentary older subjects (43.3 +/- 13.4 compared with 31.8 +/- 12.2 micromol/l respectively; P<0.05). Exercise abolished this difference (49.1 +/- 9.6 micromol/l for young subjects and 52.1 +/- 11.5 micromol/l for older subjects; not significant). Resting SBF was similar in all the subgroups, but stimulated SBFs were lower in both subgroups of untrained compared with trained subjects. NOx concentrations were positively correlated with VO2max (r=0.46, P<0.001). Stimulated SBFs were correlated with NOx (r>0.30, P<0.05). These findings show that chronic exercise may improve endothelial function in older (and young) men, probably by increasing NO availability.

Adult↗
PubMed2004

Contrasting effects of acute and chronic cigarette smoking on skin microcirculation in young healthy subjects.

OBJECTIVE: The aim of our study was to assess the effects of acute and chronic smoking on skin microvascular properties of young healthy subjects. DESIGN: An observational study, using a totally non-invasive approach, employing continuous palmar microvascular flow (laser Doppler) and arterial pressure measurements, to compute estimates of microvascular resistive (Z0) and oscillatory (impedance, i.e. ZC) properties. Measures were obtained at baseline and after iontophoretic administration of acetylcholine (ACh), an endothelium-dependent vasodilator and of sodium nitroprusside (NP), an endothelium-independent vasodilator. PARTICIPANTS: A total of 20 healthy male subjects (nine habitual smokers and 11 non-smokers; aged 27 +/- 1 and 29 +/- 2 years, respectively) in resting conditions and during administration of ACh and of NP (in two different days), before and after smoking one cigarette were evaluated. RESULTS: Smokers showed significant lower baseline Z0 and ZC than non-smokers. In non-smokers, ACh and NP iontophoresis induced a significant decrease of both Z0 and ZC, before and after smoking one cigarette (P < 0.02). Conversely, in smokers, both Z0 and ZC were not affected by ACh iontophoresis before acute smoking, while, after smoking, a significant decrease of both Z0 and ZC (P < 0.02) was detected after ACh challenge. In smokers, both Z0 and ZC were not affected by NP iontophoresis, either before or after smoking a cigarette. CONCLUSIONS: Smokers appeared characterized by a complex disruption of peripheral microcirculatory regulation, including inappropriate resting vasodilation, impaired endothelium-dependent and independent vasodilation, paradoxical recovery of endothelium-dependent vasodilation in response to acute smoking.

Acetylcholine↗
PubMed2003

Relation between left ventricular midwall function and coronary vasodilator capacity in arterial hypertension.

In systemic hypertension, depressed left ventricular midwall shortening predicts an adverse outcome and is associated with increased left ventricular relative wall thickness, which has been proposed as an independent predictor of cardiovascular risk and reduced coronary reserve. This study was designed to investigate whether depressed midwall shortening is associated with more critical impairment of coronary function and with exercise-induced myocardial ischemia. Sixty untreated hypertensive patients without coronary artery stenosis and 20 normotensive volunteers underwent exercise ECG testing, standard and transesophageal echocardiography to assess the occurrence of exercise-induced myocardial ischemia, left ventricular mass, geometry, and midwall shortening, and coronary vasodilator capacity. Compared with hypertensive patients with normal midwall shortening, those with depressed function (n=15) had higher minimum coronary resistance (1.19+/-0.27 versus 1.39+/-0.20 mm Hg/cm per second, P<0.01) and prevalence of exercise-induced myocardial ischemia (36 versus 67%, P<0.05). Within the hypertensive group, midwall shortening was inversely related to minimum coronary resistance (r=-0.42, P<0.01). Compared with patients with an exercise ECG test negative for myocardial ischemia, those with a positive test result (n=26) had higher minimum coronary resistance (1.13+/-0.21 versus 1.38+/-0.27 mm Hg/cm per second, P<0.01) and lower midwall shortening (104+/-16 versus 93+/-14%, P<0.01). We conclude that hypertensive patients with depressed midwall shortening have more severe impairment of coronary function and a higher prevalence of exercise-induced myocardial ischemia as compared with hypertensive patients with normal midwall shortening. These findings suggest that a decrease in myocardial performance may be related, at least in part, to chronic intermittent myocardial ischemia caused by a critical impairment of coronary vasodilator capacity.

Adenosine↗
PubMed2003

Ventricular repolarization is prolonged in nondipper hypertensive patients: role of left ventricular hypertrophy and autonomic dysfunction.

OBJECTIVE: The aim of this study was to investigate the influence of circadian behavior of blood pressure, left ventricular hypertrophy, and autonomic function on QTc interval duration in untreated hypertensive patients. DESIGN: Hypertensive patients underwent simultaneous blood pressure and ECG 24-h ambulatory monitoring. Patients were classified into two groups on the basis of a lack of nocturnal fall in blood pressure, as dippers and nondippers. A group of normotensive healthy subjects was studied as controls. METHODS: QT and QTc intervals were automatically computed and spectral analysis was applied to RR interval time series from the same electrocardiogram (ECG) recordings. Left ventricular mass index (LVMI) was computed by echocardiogram. RESULTS: No difference among the three groups was found concerning mean values and circadian pattern of heart rate; by contrast, QTc was significantly longer in nondippers compared to dippers or to normotensive subjects, particularly at night-time, whereas all groups exhibited similar circadian variations in heart rate. Compared to dippers, nondippers showed significantly higher LVMI, which positively correlated with QTc, and parasympathetic withdrawal, which negatively correlated with QTc. CONCLUSIONS: Nondippers show a prolonged ventricular repolarization throughout the 24-h period, absent either in dippers or normotensives. The association of left ventricular hypertrophy and vagal deactivation may lead to prolongation of QTc, potentially facilitating ventricular arrhythmias in nondipper hypertensive patients.

Adult↗
PubMed2003

Relationships between coronary flow vasodilator capacity and small artery remodelling in hypertensive patients.

BACKGROUND: Arterial hypertension is frequently associated with the presence of structural alterations in small arteries. Moreover, a reduced coronary flow reserve and vasodilator capacity has been observed in essential hypertensive patients, possibly due, at least in part, to microangiopathy of small coronary vessels. The aim of the present study was to evaluate a possible relationship between subcutaneous small artery structure and coronary flow reserve or vasodilator capacity in patients with essential hypertension. METHODS AND RESULTS: A total of 20 patients with mild to moderate essential hypertension were included in the study, and underwent a biopsy of the subcutaneous fat from the gluteal region. Small arteries were dissected and mounted on a micromyograph. The media thickness, the normalized internal diameter and the media:lumen ratio (M/L) were then calculated. In addition, a transesophageal Doppler echocardiographic study, which allows the measurement of coronary flow velocity before and during maximal pharmacological vasodilatation, was performed. Coronary flow reserve (CFR) was measured as the ratio of coronary flow velocity assessed during adenosine infusion and that measured in basal conditions. From blood pressure and coronary flow velocity during adenosine infusion, minimum coronary resistance was calculated. CFR as well as minimum coronary resistance were significantly correlated to both M/L and to normalized internal diameter of subcutaneous small arteries. CONCLUSIONS: Our results are consistent with the hypothesis of a generalized remodelling of small arteries in the body, including the coronary circulation; this remodelling may play an important role in the reduction of coronary vasodilator capacity in patients with mild to moderate essential hypertension.

Adipose Tissue↗
PubMed2003

Coronary vasodilator capacity and exercise-induced myocardial ischemia are related to the pulsatile component of blood pressure in patients with essential hypertension.

OBJECTIVES: High pulsatile load is associated with structural alterations of the heart and arteries, which may cause changes in the coronary circulation and predispose to myocardial ischemia. This study was designed to investigate the relationships of coronary vasodilator capacity and exercise-induced myocardial ischemia to pulsatile and steady components of office blood pressure. METHODS: Eighty-two untreated, middle-aged hypertensive patients without coronary artery stenosis and 23 normotensive volunteers, underwent exercise electrocardiogram test and standard and transesophageal echocardiography to assess the occurrence of myocardial ischemia, left ventricular (LV) mass and geometry, total arterial compliance and coronary vasodilator capacity. RESULTS: In the hypertensive population, minimum coronary resistance (MCR) was significantly higher (P < 0.01) in the top as compared to all three lower pulse pressure (PP) quartiles (1.10 +/- 0.19, 1.21 +/- 0.23, 1.20 +/- 0.26 and 1.43 +/- 0.26 mmHg s/cm). An additional increase in MCR also occurred in the top quartile of systolic blood pressure (SBP), but not across quartiles of mean blood pressure. In regression analysis, MCR increased with PP, SBP and LV wall thickness and decreased with total arterial compliance. As compared to hypertensive patients with a negative exercise test for myocardial ischemia (n = 30), those with a positive test (n = 20) had higher MCR (1.12 +/- 0.22 versus 1.39 +/- 0.29 mmHg s/cm, P < 0.01) and lower total arterial compliance (96 +/- 22 versus 81 +/- 16%, P < 0.01). CONCLUSIONS: In untreated middle-aged hypertensive patients, coronary vasodilator capacity declines with increasing office PP and SBP. A decreased arterial compliance and increased LV wall thickness appear to be major alterations underlying this relationship. Exercise-induced myocardial ischemia is associated with higher MCR and lower arterial compliance.

Adult↗
PubMed2003

Coronary vasodilator capacity and hypertension-induced increase in left ventricular mass.

An increase in left ventricular mass represents a compensatory response of hypertensive heart to augmented loading conditions. The concept of inappropriate mass has been proposed to define an increase in left ventricular mass higher than needed to compensate for increased workload. To assess whether inappropriate left ventricular mass is associated with more severe impairment of coronary vasodilator capacity, 64 untreated middle-aged hypertensive patients without significant coronary artery stenosis and 14 normotensive volunteers comparable for age and gender were studied by transthoracic and transesophageal echocardiography to evaluate left ventricular mass, geometry, and coronary flow velocity response to adenosine. Thirty-three patients had appropriate and 31 had inappropriate increase in left ventricular mass, whereas all normotensive control subjects had appropriate left ventricular mass. Compared with control subjects, minimum coronary resistance (0.87+/-0.18 mm Hg per second/centimeter) was increased in both hypertensive subgroups, more in those with inappropriate left ventricular mass (1.34+/-0.23 versus 1.19+/-0.23 mm Hg per second/centimeter, P<0.01), who also exhibited lower afterload-corrected midwall shortening and ratio of peak early and peak late velocities of transmitral flow profile. In hypertensive patients, minimum coronary resistance was related positively to absolute and relative left ventricular wall thickness (r=+0.33 and +0.35, both P<0.01) and negatively to midwall shortening and ratio of peak early and peak late velocities of transmitral flow (r=-0.32 and -0.31, both P<0.02). Thus, in the hypertensive heart, a deviation of left ventricular mass from values compensatory for increased cardiac workload is associated with lower coronary vasodilator capacity, depressed left ventricular wall mechanics, and abnormal left ventricular diastolic filling pattern.

Adenosine↗
PubMed2003

Myocardial ultrasonic backscatter in hypertension: relation to aldosterone and endothelin.

A disproportionate accumulation of fibrillar collagen is a characteristic feature of hypertensive heart disease, but the extent of myocardial fibrosis may differ in different models of hypertension. In experimental studies, aldosterone and endothelins emerge as important determinants of myocardial fibrosis. Changes in myocardial extracellular matrix and collagen deposition can be estimated noninvasively by analysis of the ultrasonic backscatter signal, which arises from tissue heterogeneity within the myocardium and describes myocardial texture. This study was designed to investigate the relations between myocardial integrated backscatter and circulating aldosterone and immunoreactive endothelin in human hypertension. The study population consisted of 56 subjects: 14 healthy normotensive volunteers and 42 hypertensive patients (14 with primary aldosteronism, 7 with renovascular hypertension, and 21 with essential hypertension). The patients with essential and secondary hypertension were matched for age, gender, body mass index, and blood pressure. Myocardial integrated backscatter at diastole was 19.8+/-2.0 and 20.8+/-2.9 decibels in normotensive control subjects and patients with essential hypertension and significantly higher in patients with primary aldosteronism (27.4+/-3.8 decibels, P<0.01) and renovascular hypertension (26.8+/-4.8 decibels, P<0.01). In the population as a whole, as well as in the hypertensive subpopulation, myocardial integrated backscatter was directly related to plasma aldosterone (r=0.73 and 0.71, P<0.01 for both) and immunoreactive endothelin (r=0.60 and 0.56, P<0.01 for both). The data of this study suggest that in human hypertension, circulating aldosterone and immunoreactive endothelin may induce alterations in left ventricular myocardial texture, possibly related to increased myocardial collagen content.

Adult↗
PubMed2002

Effects of selective alpha1- and alpha2-adrenergic blockade on coronary flow reserve after coronary stenting.

BACKGROUND: Coronary flow reserve (CFR) is not normalized shortly after coronary stenting. We hypothesized that alpha-adrenergic coronary vasoconstriction acts to limit CFR. METHODS AND RESULTS: We assessed flow velocity by Doppler wires and cross-sectional area by angiography in 46 patients undergoing coronary culprit lesion stenting (81+/-4% stenosis). Hyperemia was induced by adenosine (24 micro g IC or 140 micro g/kg per minute IV) before and after stenting. Finally, either the alpha(1)-antagonist urapidil (10 mg IC) or the alpha(2)-antagonist yohimbine (3 mg IC) was randomly combined with adenosine. In 8 subjects with angiographically normal coronary arteries, CFR was increased from 3.21+/-0.30 to 3.74+/-0.43 by yohimbine and to 4.58+/-0.65 by urapidil, respectively (P=0.0001). Patients were divided according to the cutoff of CFR > or =3.0 (n=18) or <2.5 (n=28). Revascularization per se did not change CFR. However, 15 minutes after stenting, CFR decreased to 2.05+/-0.55 from CFR 3.64+/-0.58, whereas in patients with CFR 2.39+/-0.51, it remained unchanged. Yohimbine improved CFR to 3.26+/-0.42 and to 3.41+/-0.58 in patients with >3.0 and <2.05+/-0.55 baseline CFR, respectively. Urapidil improved CFR to 3.52+/-0.30 and 3.98+/-1.07, respectively. CONCLUSIONS: Urapidil and yohimbine attenuated the CFR impairment occurring after revascularization by increasing both the epicardial vasodilator effect of adenosine and the blood flow velocity, thus suggesting that the adrenergic system plays an important role in limiting the capacity of the coronary circulation to dilate.

Adenosine↗