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Biomedical subjects

P Sganzerla

Publications and source records attributed to P Sganzerla.

At least 37 records · Page 2Linked to original sources
PubMed1994

[Body fluid withdrawal with isolated ultrafiltration effects persistent improvement of functional capacity in patients with chronic congestive heart failure. Furosemide does not produce the same result].

In moderate congestive heart failure pulmonary overhydration may be detected at chest X-ray even if therapy is optimized to keep the urinary output normal and to prevent weight gain and dependent edema formation. Removal of overhydration of the lung may help to define its significance. This study was aimed at investigating whether a subclinical accumulation of fluid in the lung interstitium in moderate congestive heart failure interferes with the patient's functional capacity, and whether furosemide is able to promote reabsorption of the excessive fluid. Patients whose digoxin, oral furosemide and ACE-inhibitor therapeutic regimen was kept constant, were randomly allocated to ultrafiltration (8 cases) or iv bolus (mean dose = 248 mg) of supplemental furosemide (8 cases). The amount of body fluid removed with each method approximated 1.600 ml. Functional performance was assessed with cardiopulmonary exercise tests. Soon after fluid withdrawal with either procedure the filling pressures of the two ventricles and body weight were reduced and plasma renin activity, norepinephrine and aldosterone were augmented. After furosemide hormones remained elevated in the subsequent 4 days, and, during this period, patients had positive water metabolism, recovery of the elevated ventricular filling pressures, recurrence of lung congestion without any improvement in functional capacity. In ultrafiltrated patients, renin, norepinephrine and aldosterone fell below control values within the first 48 hours and water metabolism was equilibrated at a new set point (less fluid intake and diuresis without weight gain). Functional capacity in these patients was improved through favorable circulatory and ventilatory adjustments consequent on reabsorption of lung water. This may also have restored the ability of the lung to clear norepinephrine, thus restraining its facilitation of renin release. Improvement persisted at 3 months after the procedure. In congestive heart failure the set point of fluid balance is altered despite oral furosemide; supplemental iv furosemide does not shift the set point, at least in the presence of ACE-inhibition; excessive, although silent, lung water limits the functional capacity of the patient.

Aged↗
PubMed1994

[Percutaneous administration of collagen (VasoSeal): an efficacious system of hemostasis after catheterization or interventional procedures using arterial approach].

INTRODUCTION: The widespread use of PTCA and complex percutaneous interventional techniques has significantly increased peripheral vascular complications prompting the development of innovative hemostatic closure devices. METHODS: To evaluate the efficacy and safety of a bovine collagen plug (VasoSeal), we sealed 362 consecutive femoral artery puncture sites in 324 patients (240 males) (mean age 57.9 +/- 11.3 years), who underwent interventional procedures or diagnostic catheterization during acute or chronic anticoagulant treatment. RESULTS: Complete hemostasis was achieved in 2.31 +/- 1.97 minutes in 342 cases (94.4%), with a mean activated clotting time at collagen deployment of 197 +/- 56". In 20 cases, mechanical arterial compression was needed in order to obtain vascular hemostasis (mean time: 44 +/- 13 min). We observed 1 arteriovenous fistula and 1 acute arterial thrombosis (collagen related at surgical inspection) which underwent successful surgical treatment. Minor complications without clinical sequelae were: small hematomas in 13 cases (3.8%), 4 groin abscesses (1.1%) and 4 cases of lymphangitis (1.1%). CONCLUSIONS: Percutaneous collagen application at the femoral artery puncture site allows quick and effective hemostasis with low incidence of peripheral vascular complications following interventional percutaneous procedures or catheterization during anticoagulant treatment.

Administration, Cutaneous↗
PubMed1993

Control of pulmonary vasomotility in congestive heart failure.

Although enhanced sympathetic tone is a well-known component of the autonomic imbalance of heart failure, its influence on pulmonary vasomotility is undefined. We investigated the pulmonary circulation in 12 patients with congestive heart failure in NYHA functional class III and in a control group of 10 normal subjects. Sympathetic influence on pulmonary vessels was studied through adrenergic activation by the arithmetic test and the cold pressor test. A rubber balloon was distended in the inferior vena cava to reduce transpulmonary flow and its influence on vascular tone. In normal individuals the arithmetic test caused pulmonary vasodilation, probably because of the mechanical effect of a largely enhanced flow: in fact, caval obstruction unmasked a neurogenic vasoconstrictor response to the arithmetic test by simply reducing the amount of cardiac output increase. In patients with heart failure, cardiac output and pulmonary arteriolar resistance remained steady during the arithmetic test, no matter what the condition of the venous return was. The cold pressor test was always a vasoconstrictor stimulus, but only in normal subjects was vasoconstriction potentiated by reducing, with caval obstruction, transpulmonary flow and its vasodilatory influence. From these data an attenuation of the sympathetic influence on pulmonary vessels in congestive heart failure seems to be likely. This might be explained as the result of modifications of pulmonary vessels rather than of reduced sympathetic excitability since circulating catecholamine levels varied to similar extents in the two groups during the tests. In congestive heart failure interstitial edema and vascular wall imbibition might increase pulmonary vessel tone and decrease vascular receptor availability. Lower reactivity to sympathetic stimuli, particularly to the vasoconstrictor ones, would ensue.

Adult↗
PubMed1993

[Intravenous ultrasonography as a method for imaging the morphoanatomical effects of coronary angioplasty].

Despite the therapeutic success of percutaneous transluminal coronary angioplasty (PTCA), the mechanisms by which PTCA increase vessel luminal size remain uncertain. To better understand the transmural morphologic changes associated with PTCA of stenosed coronary arteries, we studied with a high-frequency intravascular ultrasound catheter 18 coronary artery segments in 18 patients following balloon angioplasty. High-quality cross-sectional images were obtained from 15 coronary sites without complications in all patients. Two distinctive morphologic features following balloon angioplasty were appreciated by intravascular ultrasound imaging. The first pattern, observed in 10 cases (67%), consisted of a stretched plaque without any evidence of dissection. The second pattern, found in 5 cases (33%), demonstrated a dissection of the plaque ranging from a radial tear with separation of the 2 ends of the plaque to an extensive dissection which, in 1 case, encompassed the entire circumference of the artery. Although angiography showed a good post-angioplasty result in all cases, intravascular ultrasound evidenced a large amount of residual atheroma occupying the artery cross-sectional area. In addition, this imaging modality revealed more often than angiography the presence of calcification and dissection. These data demonstrate that PTCA creates different morphologic patterns which are related to the mechanisms of lumen enlargement and that the coronary artery anatomy after dilatation is much more complex than that observed with angiography. This study confirms that intravascular ultrasound is a feasible and safe imaging modality which provides new valuable insight into the mechanisms by which angioplasty improves vessel patency.

Aged↗
PubMed1992

[The improvement in physical exercise capacity in dilated cardiomyopathy during short-term treatment with L-thyroxine].

Reduced left ventricular function and other factors, such as vascular resistances, redistribution of cardiac output and impaired muscular metabolism, limit exercise performance in chronic heart failure. Thyroid hormones have a positive cardiac inotropic effect, stimulate protein synthesis (particularly at muscular level) and reduce peripheral vascular resistances with consequent increase of cardiac output. Therefore, it is possible that thyroid hormones can improve exercise performance in chronic heart failure. We have administered L-thyroxin (100 mcg/die) for 1 week to 9 patients affected by primary dilated cardiomyopathy. All the patients were euthyroid (T3 = 1.06 +/- 0.1 mcg/ml, T4 = 8.5 +/- 1.9 mcg/dl, TSH = 1.32 +/- 0.7 mU/ml) and in II-III NYHA functional class. Before starting the treatment and at the end of it, we performed the cardiopulmonary exercise test and the echocardiogram. We also evaluated the resting hemodynamic parameters through catheterization and the plasmatic values of thyroid hormones and noradrenaline. At the end of the treatment all patients were euthyroid, despite a significant (p less than 0.05) increase of T4 (10.5 +/- 3.2 mcg/dl) and a decrease of TSH (1.1 +/- 0.1 mU/ml). Mean values of effort parameters changed as follows: peak oxygen consumption from 19.6 +/- 1.6 to 20.6 +/- 1.3 ml/min/kg, tolerance time from 460 +/- 61 to 481 +/- 60 s. These variations were not associated with changes in resting hemodynamic parameters and noradrenaline. Left ventricular ejection fraction, calculated by echocardiography, increased from 26 +/- 6 to 28.9 +/- 8% (p less than 0.05). We conclude that in dilated cardiomyopathy short term treatment with L-thyroxin significantly improves patient's response to cardiopulmonary exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
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↗
PubMed1991

[Changes in pulmonary vascular reactivity to adrenergic stimuli in congestive heart failure].

Heart failure is associated with increased activity of sympathetic nervous system. As to the latter's effector organs, attention has been mainly drawn by heart and systemic circulation. In this study we investigated whether and how the neurogenic vasomotility of the lesser circulation is modified. Therefore, we compared 12 patients with heart failure in III NYHA functional class, with 10 subjects, undergoing hemodynamic study for diagnostic reasons and found to be normal. The neurogenic reactivity of pulmonary vessels was assayed by means of 2 sympathetic stimuli: arithmetic test (AT) and cold pressor test (CPT), performed both with and without obstruction to right heart venous return. This was obtained by expanding a balloon in inferior vena cava, in order to rid the neurogenic component of pulmonary vasomotility of the interference of the normally prevailing mechanical component (consisting in adaptations to flow variations). AT caused pulmonary vasodilation in normal subjects, as a passive consequence of the increase of cardiac output and, therefore, of pulmonary flow. Caval obstruction, by simply restraining this increase, induced a clearly neurogenic vasoconstrictor response. On the contrary, in failing patients, a slight vasodilation, independently from the condition of venous return, was observed. This took place in spite of the constant absence of any variations of cardiac output, which both indicates the reduction of myocardial function and helps to show the diminished nervous influence on pulmonary circulation. On the other hand, CPT had a vasoconstrictor effect in both groups, though potentiated by the reduction of transpulmonary flow in normal subjects only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Neural influences on the human pulmonary circulation as a defence reaction to volume depletion.

The role of the autonomic nervous system in the regulation of pulmonary vasomotility in man is unsettled and great emphasis is usually given to changes in flow as the main regulating mechanism. In order to simulate hypovolemia, which might reduce the mechanical influence of flow and disclose a neural mechanism, we decreased venous return through balloon distention in the inferior vena cava in 12 normal subjects, during right heart catheterization performed for diagnostic purposes. Caval obstruction was graduated to reduce cardiac output, right atrial and pulmonary arterial pressures, without altering systemic arterial pressure and heart rate. The sympathetic nervous system was activated by arithmetic and cold pressor tests. During the former, the increase in cardiac output was more than halved by venous return restraint, as compared to the unrestrained condition, and clear pulmonary vasoconstriction, instead of vasodilatation, was observed. During the cold test, cardiac output remained almost steady, in the absence as in the presence of balloon expansion. In both conditions pulmonary arteriolar resistance rose, but in the latter this increase was more than doubled. This study suggests that the autonomic nervous system is involved in the regulation of pulmonary vasomotility in man, its role being unveiled when the mechanical influence of flow is reduced by mimicking a hypovolemic state.

Adult↗
PubMed1989

Neural influences on the pulmonary vascular bed in man.

1. Impedance to venous return by distention of a balloon in the inferior vena cava (IVCB) was utilized in 10 patients, during diagnostic procedures, to reduce blood flow through the lungs at baseline and to buffer its changes during stimulation of the adrenergic system, which was obtained with mental arithmetic (AT) and cold pressor (CPT) tests. 2. When venous return was unimpeded, cardiac output rose by 2.06 1/min during the AT and remained steady during the CPT, and arteriolar resistance in the pulmonary circuit was significantly reduced and slightly raised, respectively. 3. During IVCB, baseline cardiac output decreased by 710 ml/min, it rose by 925 ml/min during the AT and again remained steady during the CPT; pulmonary arteriolar resistance was unchanged from before obstruction at baseline and was significantly augmented by both tests. In particular, AT became a clear vasoconstrictor stimulus, having originally produced vasodilatation. 4. These observations support the view that lung blood vessels in man are sensitive to adrenergic influences and that vasoconstriction can be elicited in circumstances in which the flow through the lungs is restrained. The physiological importance of the neural regulation of the pulmonary circulation in man remains undefined.

Adult↗
PubMed1989

Pulmonary vasoconstrictor overreactivity in borderline systemic hypertension.

Raised vascular pressure and resistance and vasoconstrictor overreactivity to adrenergic stimulation are hallmarks of the pulmonary circulation in sustained primary hypertension. The aim of this study was to investigate the reasons for these disorders. In 10 males with borderline systemic hypertension, pulmonary haemodynamic variables were similar to those of an age matched group of eight normotensive subjects. In normotension, arithmetic and cold pressor tests (sympathetic activators) caused slight vasodilatation and vasoconstriction, respectively. In hypertension both tests showed an obvious vasoconstrictor effect. Restriction of blood flow through the lungs by distension of a balloon in the inferior vena cava is known to increase pulmonary vasoconstrictor reactivity in normal man. As a result of this manoeuvre, pulmonary pressure fell in the normotensive controls without variation in pulmonary vascular resistance, whereas in the hypertensive group there was an increase in resistance and the pressure did not change. In normotensive subjects with caval balloon, the sympathetic activating stimuli both became constrictor and caused vascular resistance to rise to the levels attained in the hypertensive patients during adrenergic stimulation in the absence of obstruction to venous return. In the hypertensives, these stimuli were not able to enhance the pulmonary vascular resistance further. This shows that in these patients maximal vasoconstriction was already achieved through the simple restraint of blood flow with vena caval obstruction. We suggest that in the early phases of systemic hypertension lung vessels are hypercontractile so that they overreact to hypoperfusion or to sympathetic stimulation, even before there is a stable rise in pressure and resistance.

Adult↗
PubMed1989

Electrophysiologic and haemodynamic correlates in supraventricular tachycardia.

In 16 subjects with paroxysmal supraventricular tachycardia (SVT) we sought a relationship between haemodynamic changes associated with artificially induced arrhythmias and the electrophysiological properties of the related atrioventricular (AV) nodal reentry circuit. In 10 patients (group 1) induced SVT was typical (long AH) and caused a significant fall in cardiac output (-1.720 ml min-1) and arterial systolic pressure (-18 mmHg). In six subjects (group 2), induced SVT was atypical (long HA) and did not significantly alter the output of the heart and systolic pressure, despite the elicitation of similar tachycardia. The opposite AV nodal reciprocation pattern which resulted in a substantial increase in AH/HH in group 1 and in a slight rise of the same variable in group 2, may explain these haemodynamic differences. In fact, atrial and ventricular systoles occurred simultaneously and impeded the ventricular filling in the former group, while a regular subsequence of contraction was maintained in the latter group. In group 2, systolic arterial pressure and cardiac output fell to the same level as in group 1 when right atrial pacing, at a similar rate of SVT, determined an increase of AH/HH similar to that observed during typical tachycardia. Thus, the haemodynamic response to SVT differs significantly between the two types of reciprocating tachycardia, particularly as regards cardiac output and blood pressure, and is mainly influenced by the temporal relationship between atrial and ventricular systole, independent of the rate of contraction. The different conduction velocities of the reciprocating circuit limbs and their interrelation seem to be major determinants of the haemodynamic pattern of SVT.

Adult↗
PubMed1988

Pulmonary vasomotor responses to neural activation in man.

Passive adaptation to changes in flow is an established mechanism of regulation of pulmonary vasomotility. The role of the autonomic nervous system is not well defined in man. To separate the neural from the mechanical component (variation in flow) the venous return and the lung blood flow of six normal men (while undergoing haemodynamic diagnostic procedures) were impeded by a balloon tipped catheter placed in the inferior vena cava. Mental arithmetic and cold pressor tests were used as sympathetic activators. When the venous return was impeded cardiac output was reduced by a mean of 540 ml compared with baseline. During the arithmetic test the rise in cardiac output fell from 2140 ml when venous return was unimpeded to 890 ml when venous return was impeded. This stimulus changed from being a slight pulmonary vasodilator to being an unequivocal vasoconstrictor. Cold stimulation had little effect on cardiac output and caused an increase in pulmonary arteriolar resistance. This effect was more than doubled when flow through the lungs was impeded. These observations suggest that a neural regulation of the pulmonary circulation exists in man, which is disclosed (arithmetic test) or potentiated (cold pressor test) when the influence of mechanical factors is prevented or reduced.

Adult↗
PubMed1988

[Neural influences on pulmonary vasomotility in man].

In man, the extent, the physiological role and even the existence of neural influences on the pulmonary vasomotility are not defined. A major obstacle to these evaluations is passive adaptation of the lung vessels to changes in flow, making it hard to separate the active from the passive component of vasomotion during adrenergic activation. In this study, which was carried out in 8 patients during diagnostic procedures, the inflation of a balloon in the inferior vena cava was utilized to reduce blood flows through the lungs and to buffer its changes consequent to stimulation of the adrenergic system. Neural activation was obtained with the mental arithmetic and the cold pressor tests. When venous return was unimpeded, cardiac output rose by 2,060 ml during the former and remained stable during the latter test, and arteriolar resistance in the pulmonary circuit was significantly reduced and slightly increased, respectively. Under vena cava obstruction, cardiac output decreased in the baseline by 600 ml; it rose by 925 ml during the arithmetic test and again remained stable during the cold test; pulmonary arteriolar resistance was unchanged since before obstruction in the baseline and was significantly augmented by both test. These observations support the view that lung blood vessels in man are sensitive to adrenergic influences and the vasoconstrictor component of these becomes effective in circumstances in which the flow through the lungs reduced. The physiological importance of these influences remains unclear.

Adolescent↗
PubMed1987

Increased cardiac electrical instability concomitant with pacing induced repolarisation abnormalities.

The relation between the occurrence of repolarisation abnormalities after right ventricular pacing and spontaneous arrhythmias was investigated in 16 patients in whom the sick sinus syndrome was suspected. All patients had normal QRS complexes and T waves in the electrocardiogram before pacing and required atrial stimulation and His bundle recording for diagnostic purposes. Patients were randomised into a study group or a control group. In the eight patients in the study group right ventricular pacing was performed for 12 hours, and was followed by inversion of the T wave in surface leads II, III, aVF, and V2-V5 and lengthening of the QTc interval. The frequency and complexity of ventricular arrhythmias increased after pacing in six patients who had ventricular extrasystoles in the baseline Holter recording. As the configuration of the T wave became normal the frequency of ventricular extrasystoles returned to baseline values. In the control group of eight patients ventricular pacing was not performed after the electrophysiological study and no changes were seen in T wave configuration and in the frequency of spontaneous arrhythmias. These results suggest that the post-pacing repolarisation abnormalities reflect abnormal electrical properties of the ventricle and that in some cases they lead to increased electrical instability.

Adult↗
PubMed1987

Analgesic and hemodynamic effects of buprenorphine in acute infarction of the heart.

The analgesic, hemodynamic and respiratory effects of buprenorphine (0.3 mg i.v.) were monitored in 15 coronary care unit-admitted patients presenting with myocardial infarction who were in functional class I according to the Killip classification. At the time of the study, 8 of them had unequivocal precordial pain (group 1); the remaining 7 were painfree (group 2). The agent showed a prompt and potent analgesic action. It also induced a slight decrease in mean aortic pressure associated with a reduction in systemic vascular resistance and an increase in cardiac index, a rise in the pulmonary arterial pressure and arteriolar resistance and right atrial pressure, a reduction in arterial pO2 and pH and an increase in pCO2. Tension-time-indices of the left and right ventricles varied in parallel with variations in aortic and pulmonary artery pressure, respectively. These responses were probably unrelated to analgesia since they were similar in groups 1 and 2. Changes in systemic circulation were such as to possibly decrease the contractile effort and the oxygen need of the left ventricle and the size of infarction. On the contrary, the rise in pulmonary arterial pressure imposes a hemodynamic burden on the right ventricle that, depending on the patient's condition, may assume clinical importance. It is felt that the use of buprenorphine in myocardial infarction should be restricted to uncomplicated and selected cases.

Buprenorphine↗