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Biomedical subjects

A Luca

Publications and source records attributed to A Luca.

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

Physical exercise increases portal pressure in patients with cirrhosis and portal hypertension.

BACKGROUND & AIMS: In healthy subjects, exercise promotes marked hemodynamic and humoral changes characterized by an increase in cardiac output, a redistribution of blood flow to muscular territories under activity, and an increase in sympathoadrenergic activity. The aim of this study was to investigate the extent to which hemodynamic and humoral changes caused by exercise may influence portal and systemic hemodynamics in patients with cirrhosis. METHODS: In 8 patients with liver cirrhosis and portal hypertension, arterial pressure, cardiac output, portal pressure (as hepatic venous pressure gradient [HVPG]), and hepatic blood flow were measured before and at two steps of cycling exercise equivalent to 30% and 50% of their peak workload. RESULTS: Exercise (at 30% of peak work-load) significantly increased arterial pressure and cardiac output and decreased systemic vascular resistance. This was associated with a significant increase in HVPG (from 16.7 +/- 1.5 to 19.2 +/- 1.6 mm Hg; P < 0.01) and a significant reduction in hepatic blood flow (from 1291 +/- 216 to 1034 +/- 152 mL-min-1; P < 0.05). All of these changes were intensified at 50% of target workload. CONCLUSIONS: The present study shows that moderate exercise increases portal pressure and may therefore increase the risk of variceal bleeding in patients with esophageal varices. These findings suggest that cirrhotic patients with portal hypertension should be advised of potential risks during exercise.

Exercise↗
PubMed1995

Relation between portal pressure response to pharmacotherapy and risk of recurrent variceal haemorrhage in patients with cirrhosis.

In patients with variceal bleeding as a complication of hepatic cirrhosis, propranolol therapy reduces the risk of recurrent variceal haemorrhage. However, the relation between portal pressure response to pharmacological treatment and clinical events has not been well defined. This relation was prospectively investigated in 69 cirrhotic patients receiving continued propranolol therapy after an episode of variceal bleeding. Hepatic venous pressure gradient (HVPG) was measured before and at 3 months of continued drug therapy. At 3 months HVPG had fallen by 20% or more in 25 patients. During follow-up of 28 (SD 17) months rebleeding occurred in 2 of these 25 patients compared with 23 of 44 who had lesser reductions in HVPG. Cumulative probability of rebleeding at 1, 2, and 3 years was 4%, 9%, and 9% in patients with a decrease in HVPG > or = 20%, and 28%, 39%, and 66% in patients with a decrease in HVPG < 20% (p < 0.001, log-rank test). On multivariate analysis, a decrease in HVPG > or = 20% was the only independent predictor of rebleeding (relative risk 0.09, 95% CI 0.02-0.41. Of the 8 patients in whom the HVPG fell to 12 mm Hg or less, none rebled. This study suggests that measurement of the HVPG response to pharmacotherapy will provide useful prognostic information on the long-term risk of variceal rebleeding.

Administration, Oral↗
PubMed1995

[Ambulatory angiologic diagnosis using the Doppler c.w. (continuous wave) method].

A one year clinical activity of instrumental angiological diagnostics (doppler c.w. examinations) was evaluated and analysed. 970 outpatient continuous wave doppler have been performed: 37% examinations of epiaortic vessels (TSA), 31% examinations of lower limb veins, 28% examinations of lower limbs arteries. The question has been inappropriate (normal exam) in 81% of TSA, in 67% of AIA and in 52% of AIV. The authors think that the reasons for these results are a large misinformation from the physicians postulant and a consequent abuse of the instrumental method. It's therefore necessary to put a clinical filter to regulate the access to the instrumental (high technological) examinations, too often unnecessary.

Ambulatory Care↗
PubMed1995

Effects of bolus injections and continuous infusions of somatostatin and placebo in patients with cirrhosis: a double-blind hemodynamic investigation.

The present double-blind study was aimed at investigating the hemodynamic and humoral effects of somatostatin or placebo in patients with cirrhosis. Patients were randomly assigned to receive either an injection of 250 micrograms of somatostatin followed by a constant infusion of somatostatin at 250 micrograms/h (n = 13), an injection of 250 micrograms of somatostatin followed by a 500 micrograms/h continuous infusion (n = 10), or an injection of placebo followed by a placebo infusion (n = 9). Placebo had no effect. Somatostatin bolus markedly decreased the hepatic venous pressure gradient: by 52% at 1 minute; P < .001; 19% at 3 minutes, P < .01; and by 13% at 5 minutes, P < .04. Azygos blood flow decreased similarly by 45% at 1 minute, P < .001; 16% at 3 minutes, P < .02; and 9.5% at 5 minutes, P = .05. Mean arterial pressure increased by 25% (P < .001). Continuous somatostatin infusions (250 or 500 micrograms/h) had no systemic effects, but significantly reduced hepatic venous pressure gradient (250 micrograms/h: -6.1%, P < .05 and 500 micrograms/h: -15%, P < .01) and hepatic blood flow (250 micrograms/h: -10%, 500 micrograms/h: -18%, P < .05). Azygos blood flow was not changed after 250 micrograms/h infusion but was reduced after 500 micrograms/h (-23%, P < .02). Somatostatin but not placebo, suppressed glucagon to normal levels. This study shows that a bolus injection of somatostatin caused an immediate and marked decrease of hepatic venous pressure gradient and azygos blood flow. Continuous infusion of somatostatin had a mild but sustained effect on splanchnic hemodynamics; this effect was more pronounced with the higher dose.

Dose-Response Relationship, Drug↗
PubMed1995

Beneficial effects of intravenous albumin infusion on the hemodynamic and humoral changes after total paracentesis.

The study investigated the hemodynamic and neurohumoral effects of albumin infusion after total paracentesis in 18 patients with cirrhosis and tense ascites. Measurements of systemic and splanchnic hemodynamics, and vasoactive neurohumoral systems were performed before and immediately after total paracentesis. The patients were then randomized to receive albumin or not, and hemodynamic and humoral measurements were repeated at 24 hours. Hemodynamic and humoral changes just after paracentesis were similar in patients later randomized to receive albumin infusion or not. Twenty-four hours after total paracentesis, patients nor receiving albumin had total significant reductions in cardiac index (-13%; P = .005), femoral blood flow (-17%; P = .004), and pulmonary capillary pressure (-16%; P = .02), which were accompanied by significant increases in plasma renin activity (PRA) and plasma aldosterone (PA) and by significant decreases in atrial natriuretic factor (ANF) and plasma sodium. By contrast, there was no significant changes in patients receiving albumin, except for an increase in ANF and a further decrease in PA. In both groups, hepatic venous pressure gradient (HVPG) and azygos blood flow decreased just after paracentesis returning to baseline at 24 hours. This study shows that albumin infusion prevents the impairment in systemic hemodynamics, vasoactive neurohumoral systems, and plasma sodium after a large-volume paracentesis, without detrimental effects on portal pressure and portocollateral blood flow.

Aged↗
PubMed1995

Noninvasive measurement of femoral blood flow and portal pressure response to propranolol in patients with cirrhosis.

This study investigated the correlation between changes in hepatic and systemic hemodynamics and femoral blood flow (FBF), measured by dual-beam pulsed wave Doppler, in 58 portal hypertensive patients receiving propranolol (0.15 mg/Kg intravenously; n = 44) or placebo (n = 14) under double-blind conditions. Placebo administration had no effects. Propranolol caused significant reductions (P < .0001) in hepatic venous pressure gradient (HVPG; from 19.1 +/- 4.1 to 16.2 +/- 4.2 mm Hg), azygos blood flow (from 563 +/- 204 to 387 +/- 176 mL/min), cardiac index (CI; from 4.4 +/- 1.0 to 3.3 +/- 0.8 L/m2/min), and FBF (from 237 +/- 79 to 176 +/- 58 mL/m2/min). In 17 patients HVPG decreased below 12 mm Hg and/or more than 20% of the baseline value (good response; mean change, -26 +/- 8%); in the remaining 27 patients (poor response) the mean change in HVPG was less: -9 +/- 6%. Patients with a good response had bled less often from varices, had significantly higher FBF (272 +/- 73 vs. 215 +/- 76 mL/m2/min) and lower baseline HVPG (16.8 +/- 3.9 vs. 20.6 +/- 3.6 mm Hg) than those with poor response in HVPG. The good response was also associated with greater decreases in FBF (-33 +/- 12 vs. -19 +/- 13% in poor responders), CI (-30 +/- 9 vs. -19 +/- 12%), and heart rate (-19 +/- 5 vs. -16 +/- 6%). A decrease in FBF of > 20% predicted a good response in 16 of 28 patients (positive predictive value, 57%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Circadian variations of portal pressure and variceal hemorrhage in patients with cirrhosis.

This study was aimed at investigating whether portal pressure, which is usually measured in the morning, is subject to circadian variations in patients with cirrhosis. Furthermore, a possible circadian variation for the occurrence of variceal bleeding was also investigated. Ten patients with alcoholic cirrhosis and portal hypertension had serial measurements of portal pressure, evaluated by the hepatic venous pressure gradient (the difference between wedged and free hepatic venous pressures), during a 24-hr period. In addition, a survey of the hour of occurrence of variceal hemorrhage was performed in 101 consecutive cirrhotic patients with hematemesis, in whom the precise moment of onset of bleeding could be determined, and the origin of bleeding was confirmed by emergency endoscopy. Statistical evaluation with the population-mean cosinor method allowed detection of a circadian variation in portal pressure. Portal pressure progressively declined during the afternoon and evening (from 17.9 +/- 5.3 mm Hg at 12 PM to a nadir of 16.8 +/- 4.9 mm Hg at 7 PM (p < 0.05). Thereafter, portal pressure increased during the night, returning to baseline values at 9 AM (18.1 +/- 5.1 mm Hg). The acrophase was at 8:32 AM (+/- 100 min) with an amplitude of 3.45 +/- 1.1 (% of mean +/- S.E.) (rhythm detection: p < 0.03). Similarly, the analysis of the time of occurrence of variceal hemorrhage with the use of a multiple-components rhythmometry test disclosed two peaks in the prevalence of esophageal bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of low-sodium diet and spironolactone on portal pressure in patients with compensated cirrhosis.

The aim of this study was to investigate the hemodynamic effects of spironolactone associated with a low-sodium diet (n = 14) or a low-sodium diet alone (n = 9) in patients with compensated cirrhosis and portal hypertension. Spironolactone significantly reduced the plasma volume. This effect was associated with a significant reduction in the hepatic venous pressure gradient, from 17.6 +/- 3.6 mm Hg to 15.3 +/- 3.5 mm Hg (-13% +/- 13%; p < 0.01). Azygos blood flow (-20% +/- 20%), cardiac output (-16.2% +/- 10.5%) and mean arterial pressure (-9% +/- 9%) also decreased significantly. However, there were no significant changes in hepatic blood flow. Patients receiving low-sodium diet alone experienced a mild but significant reduction in hepatic venous pressure gradient (-6.3% +/- 6%) and in mean arterial pressure (-4% +/- 5%). There were no significant changes in cardiac output and in hepatic or azygos blood flows. This study indicates that low-sodium diet plus administration of spironolactone reduces portal pressure and azygos blood flow in patients with compensated cirrhosis. Low-sodium diet alone only produces mild effects that are likely to be clinically irrelevant.

Aged↗
PubMed1994

Favorable effects of total paracentesis on splanchnic hemodynamics in cirrhotic patients with tense ascites.

Total paracentesis is widely used in the treatment of patients with cirrhosis and tense ascites. However, very little information is available regarding its consequences on splanchnic circulation, and its effects on portocollateral blood flow have not been investigated. Ten cirrhotic patients admitted because of tense ascites had measurements of hepatic and systemic hemodynamics, renal function and endogenous vasoactive neurohumoral systems at baseline, just after total paracentesis and 1 hr later. Total paracentesis caused a significant increase in cardiac output (+11%; 95% confidence interval, +4% to +19%) and a rapid fall in portal pressure, as shown by significant decreases in both the wedged hepatic venous pressure (-27% +/- 8%; p < 0.005) and the hepatic venous pressure gradient (-10%; 95% confidence interval, -3% to -18%). This was accompanied by a marked decrease in azygos blood flow (-28%; 95% confidence interval, -13% to -43%). These favorable hemodynamic effects were associated with a fall of the elevated levels of plasma renin activity (-47% +/- 9%; p < 0.05), plasma aldosterone (-31% +/- 21%; p < 0.05) and plasma norepinephrine and by a decrease in levels of serum creatinine (-24% +/- 15%; p < 0.05) and blood urea nitrogen (-4% +/- 3%; p < 0.05). These changes were maintained 1 hr later. This study indicates that in patients with cirrhosis and tense ascites total paracentesis favorably influences the systemic hemodynamics, portocollateral blood flow and portal pressure.

Aged↗
PubMed1994

Terlipressin or vasopressin plus transdermal nitroglycerin in a treatment strategy for digestive bleeding in cirrhosis. A randomized clinical trial. Liver Study Group of V. Cervello Hospital.

Between 1988 and 1990 an unblinded, randomized trial of terlipressin or vasopressin plus transdermal nitroglycerin, as part of a treatment strategy including emergency sclerotherapy for actively bleeding varices, was conducted during 165 admissions in 137 patients with cirrhosis and upper digestive bleeding. Eighty-four patient admissions were assigned to terlipressin (2 mg every 6 h) and 81 to vasopressin (0.4 to 0.8 unit per min) plus transdermal nitroglycerin (20 to 80 mg). The two groups were comparable for relevant clinical data, but there were slightly more patients with hepatocellular carcinoma or terminal conditions in the terlipressin group. After the 24-h study period, failure to control bleeding was 20/84 (25%) in the vasopressin and 14/81 (17%) in the terlipressin group (p = 0.19). Corresponding figures for patients bleeding from varices (emergency sclerotherapy in 43 and 45, respectively) were 13/55 (24%) and 5/56 (9%; p = 0.035), from other sources 5/16 (31%) and 2/15 (13%; p = 0.23), from undefined sources 2/10 (20%) and 7/13 (54%; p = 0.1). In a logistic multivariate regression model the odds ratio for terlipressin adjusted for prognostic factors was 0.45 (p = 0.07). There were seven major side effects requiring treatment discontinuation in the vasopressin and one in the terlipressin group. These results suggest that terlipressin alone is as effective as vasopressin plus transdermal nitroglycerin, with less severe side effects, in 24-h control of upper gastrointestinal bleeding in patients with cirrhosis.

Administration, Cutaneous↗
PubMed1994

Nicardipine increases hepatic blood flow and the hepatic clearance of indocyanine green in patients with cirrhosis.

The present study investigated the hemodynamic effects of nicardipine, a new calcium channel blocker, and placebo in 14 patients with cirrhosis. Sixty minutes after nicardipine administration (20 mg orally; n = 8), there was a significant increase in hepatic blood flow (25 +/- 21%; p < 0.05) and azygos blood flow (33 +/- 40%; p < 0.05) but no significant change in the hepatic venous pressure gradient. As a result of the increase in hepatic blood flow and the lack of change in the hepatic venous pressure gradient, nicardipine significantly reduced hepatic sinusoidal resistance (-14 +/- 15%; p < 0.05). Enhanced liver perfusion was associated with a significant increase in the hepatic clearance of indocyanine green (from 241 +/- 81 to 265 +/- 92 ml/min, p < 0.05). A mild, well-tolerated decrease in mean arterial pressure (-10 +/- 6%, p < 0.05), without significant changes in cardiac output, systemic vascular resistance and heart rate, was also observed. Placebo administration (n = 6) did not cause significant changes in systemic or hepatic hemodynamics. The results of the present study show that nicardipine, unlike other calcium channel blockers, effectively increases hepatic blood flow and the hepatic clearance of indocyanine green in patients with cirrhosis. The acute beneficial effects of nicardipine should be confirmed in chronic studies.

Aged↗
PubMed1993

Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis.

BACKGROUND: Changes in intra-abdominal pressure (IAP) have significant circulatory effects. However, whether this may influence the gastroesophageal collateral blood flow in patients with cirrhosis has not been studied. METHODS: In 14 portal hypertensive cirrhotics, serial hemodynamic measurements were obtained in baseline conditions 30 minutes after the mechanical increase of IAP by 10 mm Hg and 30 minutes after returning IAP to baseline levels. RESULTS: Increasing IAP caused similar increases in free and wedged hepatic venous pressures (+10.3 mm Hg and +11.0 mm Hg, respectively; P < 0.005), without changing the hepatic venous pressure gradient (HVPG). However, there were significant decreases in cardiac output (-18%; P < 0.005) and hepatic blood flow (-20%; P < 0.05), whereas azygos blood flow, an index of gastroesophageal collateral blood flow, increased markedly (+23%; P < 0.005). The opposite occurred after releasing the high IAP. CONCLUSION: In portal hypertensive cirrhotics, acute changes in IAP did not change HVPG but markedly modified splanchnic and systemic hemodynamics. Brief elevations of IAP may have deletereous effects, as shown by the increase in azygos blood flow and the decrease in cardiac output and hepatic blood flow, whereas reduction of a high IAP causes the opposite changes and may be beneficial.

Abdomen↗
PubMed1993

New approaches in the pharmacologic treatment of portal hypertension.

To alleviate the risk of variceal bleeding, the portal pressure gradient--usually evaluated as the hepatic venous pressure gradient (HVPG)--must be reduced to < or = 12 mmHg. Although beta-blocking agents are accepted therapy for preventing first or subsequent bleeding episodes, propranolol therapy decreases final HVPG to < or = 12 mmHg in only 12% of patients, while only 24% of patients have a > or = 20% reduction in HVPG and nearly 40% show no reduction in HVPG. This has stimulated research on alternative or additional treatments. Nitrates such as isosorbide dinitrate reduce portal pressure by decreasing resistance to portal and collateral blood flow and by promoting reflex splanchnic vasoconstriction. However, while nitrates are effective in the acute situation, tolerance leading to refractoriness develops over the long term unless they are combined with diuretics or other agents in the treatment of portal hypertension. Propranolol and isosorbide-5-mononitrate combined cause a substantially greater reduction in HVPG than monotherapy with either drug in both acute and long-term use. Presumably concomitant isosorbide-5-mononitrate administration opposes the increase in portal resistance induced by propranolol. Spironolactone, which has been shown to lower HVPG in patients with cirrhosis, produces a reduction in plasma volume that attenuates the increased cardiac output associated with cirrhosis and triggers vasoactive mechanisms that decrease splanchnic blood flow. Potentially, spironolactone may maintain and enhance the decrease in portal pressure achieved by nitrates or propranolol. Triple therapy with a beta-blocker, a nitrate and spironolactone may be feasible.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1993

Reduction of variceal pressure by propranolol: comparison of the effects on portal pressure and azygos blood flow in patients with cirrhosis.

This study investigated the correlation between changes in hepatic hemodynamics and esophageal variceal pressure--measured with a noninvasive, pressure-sensitive endoscopic gauge--in 37 portal-hypertensive cirrhotic patients receiving propranolol (0.15 mg/kg, intravenously; n = 21) or placebo (n = 16) under strict double-blind conditions. Placebo administration had no effect on hepatic venous pressure gradient, azygos blood flow or variceal pressure. Propranolol caused a significant reduction in hepatic venous pressure gradient (from 19.6 +/- 1 to 17.3 +/- 1 mm Hg, p < 0.001), azygos blood flow (from 0.61 +/- 0.06 to 0.39 +/- 0.03 L/min, p < 0.001) and variceal pressure (from 13.1 +/- 0.9 to 10.2 +/- 0.9 mm Hg, p < 0.001). In eight patients (propranolol nonresponders) hepatic venous pressure gradient was not modified or decreased by less than 10% after propranolol (mean change, -4.1 +/- 1.6%). However, we found no significant differences between propranolol responders and nonresponders with regard to the decrease in variceal pressure (3.3 +/- 0.7 vs. 2.3 +/- 1.4 mm Hg) and azygos blood flow (0.23 +/- 0.07 vs. 0.21 +/- 0.07 L/min). As expected, in most propranolol responders (11 of 13), reduction in hepatic venous pressure gradient was accompanied by a similar response in variceal pressure (> 10% decrease). However, among propranolol nonresponders, in terms of reduction in hepatic venous pressure gradient, four out of eight patients had decreases greater than 10% in variceal pressure. The results of this study confirm that reduction in hepatic venous pressure gradient by propranolol is associated with a significant decrease in variceal pressure and azygos blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Hepatic, splanchnic and systemic haemodynamic abnormalities in portal hypertension.

Portal hypertension is characterized by a pathological increase in portal venous pressure that leads to the formation of portosystemic collaterals that divert portal blood to the systemic circulation, bypassing the liver. Increased vascular resistance to portal blood flow is the initiating factor in portal hypertension. Increased resistance along the hepatic and portocollateral circulation is in part modifiable by pharmacological agents. An additional factor is splanchnic vasodilatation with increased portal blood inflow, which contributes to the maintenance and aggravation of the portal hypertension. Endogenous vasodilators are thought to be responsible for the splanchnic hyperaemia of portal hypertension. Vasodilatation is also prominent in the stomach and lungs, and plays an important role in the pathophysiology of portal hypertensive gastropathy and of the hepatopulmonary syndrome. The systemic circulation is markedly hyperkinetic, with reduced arterial pressure and peripheral resistance and increased cardiac output. The plasma volume is expanded due to renal sodium retention. The expanded plasma volume enables the increase in cardiac output, and represents another mechanism contributing to the increase in portal pressure.

Blood Flow Velocity↗
PubMed1992

[Cardiovascular adjustments in hypertensive patients. An echocardiographic study].

Echocardiography was used to asses parameters of cardiovascular function in order to identify the main cardiac adjustment mechanisms to arterial hypertension. In addition to morphological parameters of septal and parietal thickness and diameter, telesystolic (Ses) and telediastolic (Spk) stress, EF, Vcfm, the index of left ventricular mass (ILVM), hypertrophy ratio (h/r), contractility index (Do), peripheral resistances (RPT) and Tarazi's index (SAC) were evaluated. In comparison to control subjects, higher levels of PwTs, h/r, SAC, RPT and ILVM (at the limit of significance) were found in hypertensive patients, which were reflected by higher Spk and Do values. From the further analysis of data to identify patients with signs of left ventricular hypertrophy (h/r greater than 0.40 and/or ILVM greater than 140) it was concluded that the hypertrophy ratio (h/r) is the functional parameter which most closely reveals the type of myocardial adjustment. Irrespective of absolute values of ILVM, the adequacy of myocardial hypertrophy to the dimensions of the cavity is accompanied by the normalisation of stress and the return of Do values close to normal levels. Hearts with low h/r those with the highest stress levels, as well as preesting the lowest EF and the highest Do values.

Adult↗