Search PubMed⌕ Search

Biomedical subjects

P Agostoni

Publications and source records attributed to P Agostoni.

At least 19 recordsLinked to original sources
PubMed2005

Treatment of bifurcation lesions with two stents: one year angiographic and clinical follow up of crush versus T stenting.

OBJECTIVES: To compare long term outcomes of the crush versus the T technique in bifurcation lesions. DESIGN: 182 consecutive patients were identified who underwent percutaneous coronary interventions for bifurcation lesions with drug eluting stents between April 2002 and January 2004. Two techniques were used according to the operator's discretion: crush (group C, n = 121) or T (group T, n = 61). RESULTS: In-hospital outcome differed significantly between the two groups. Angiographic follow up was available for 142 (78%) patients. Groups C and T did not differ significantly regarding late loss (0.42 (0.39) mm v 0.34 (0.35) mm, p = 0.52) and rate of restenosis (16.2% v 13.0%, p = 0.80) in both the main and the side branch without final kissing balloon post-dilatation. However, when final kissing balloon post-dilatation was performed, group C had significantly lower late lumen loss (0.23 (0.21) mm v 0.37 (0.33) mm, p = 0.02) and restenosis rate (8.6% v 26.5%, p = 0.04) in the side branch. At one year's clinical follow up, group C compared with group T had lower rates of target lesion revascularisation (14.0% v 31.1%, p = 0.01) and target vessel revascularisation (16.5% v 32.8%, p = 0.02). CONCLUSIONS: In non-selected bifurcation lesions treated with drug eluting stents, the restenosis rate remains relatively high in the side branch. Compared with the T stenting technique, crush stenting with kissing balloon post-dilatation is associated with a reduced rate of restenosis in the side branch.

Catheterization↗
PubMed2005

Applying intravascular ultrasound to optimize the placement of coronary drug-eluting stents.

Intravascular ultrasound (IVUS) has provided in the last 2 decades major insights into the pathophysiology of coronary artery disease, and the mechanisms of action of percutaneous revascularization devices, helping the widespread adoption of coronary stents. The introduction of drug-eluting stents (DES) has recently lead to a revolution in the field of interventional cardiology, by virtually eliminating restenosis in selected low-risk lesions and significantly reducing both restenosis and repeat revascularizations in higher risk lesions. At the moment, the role of IVUS in the DES era is not well defined. Clinical studies utilizing IVUS in DES implantation used this technology mainly to evaluate the endpoint of intimal hyperplasia and to study the problem of incomplete apposition. On a theoretical basis, a method able to better evaluate optimal placement of a local drug delivery system should have a high rationale. Despite this sound preamble, no specific investigation has been conducted to evaluate the clinical need and possible advantage of routine IVUS for DES implantation and uncertainty is still present. A major hindrance lays in the low incidence of restenosis in most randomized trials enrolling few selected lesions per patient, as this fact enlarges the number of patients who need to be treated to demonstrate a benefit and casts doubts on the cost effectiveness of a more expensive and time consuming approach. The situation is bound to change when more complex patients and lesions are being treated, a setting associated with a higher event rate even when DES are used. While waiting for a prospective study addressing such issue, we can only rely on indirect evidence to justify and support the usage of IVUS in complex clinical settings with implantation of DES.

Coronary Artery Disease↗
PubMed2004

Acute myocardial infarction probably caused by paradoxical embolus in a pregnant woman.

A 19 year old pregnant woman presented to the coronary care unit with an acute anterior myocardial infarction. She was treated with primary percutaneous transluminal coronary angioplasty of the proximal left anterior descending coronary artery. Ultrasound examination showed patent foramen ovale (PFO) and atrial septal aneurysm. The patient was a heterozygote carrier of factor V Leiden. Despite the lack of a clear clue, it was considered that the pathophysiological cause of this infarction was a paradoxical embolus in the left coronary artery. Pregnancy and factor V Leiden carriership are associated with increased risk of venous thromboembolism and the association between PFO and atrial septal aneurysm is a strong risk factor for systemic embolisation.

Adult↗
PubMed2004

Hemofiltration in heart failure.

In patients with severe congestive heart failure (CHF), removal of edema by hemofiltration is associated with significant clinical and hemodynamic improvement, correction of hyponatremia, restoration of urine output and diuretic responsiveness, and with a striking fall in neurohormonal activation. Through these effects, hemofiltration is able to interrupt the progression of CHF toward refractoriness, and to revert the clinical condition of CHF patients to a lower functional class. Fluid refilling from the overhydrated interstitium is the major compensatory mechanism in the prevention of hypovolemia during hemofiltration. Hemofiltration can also be beneficial in patients who have only moderate cardiac insufficiency (NYHA classes II and III) and in whom over-hydration is restricted to the pulmonary district significantly contributing to limiting patients functional capacity. In this setting, hemofiltration, differently from diuretics, is able to remove the increased lung water content and to improve clinical condition, exercise capacity and lung function.

Disease Progression↗
PubMed2004

Increased mortality after coronary stenting in patients treated with clopidogrel without loading dose. Evidence from a meta-analysis.

AIM: Clopidogrel is an established alternative to ticlopidine in addition to aspirin after coronary stenting because of its hematologic safety, but its efficacy in comparison to ticlopidine is debated. We thus systematically reviewed randomized trials comparing clopidogrel vs ticlopidine after coronary stenting. METHODS: Medline (1/1986-10/2003), BioMed Central, Central, Current Contents, LILACS and mRCT were searched. Fixed-effect relative risks (RR [95% CI]) were computed, and the primary end-point was death. Heterogeneity tests and subgroup analyses were performed according to loading vs non-loading clopidogrel scheme. RESULTS: Five trials were retrieved (2 962 patients, average follow-up 7.4 months). In 3 studies both clopidogrel and ticlopidine were started with a loading dose, in 1 trial clopidogrel was administered without loading, and in 1 trial clopidogrel could be administered with or without loading. Overall analysis (p for heterogeneity=0.12) showed a non-significant trend toward increased mortality in patients treated with clopidogrel (38/1 649 [2.3%]) vs ticlopidine (22/1 313 [1.7%], RR=1.64 [0.94-2.86], p=0.080). After stratification, clopidogrel with loading was associated with non-significantly lower mortality rates than ticlopidine (9/959 [0.9%] vs 13/798 [1.6%], RR=0.68 [0.29-1.63], p=0.39). Instead, clopidogrel without any loading yielded a highly significantly 3-fold increased risk of death than ticlopidine (29/690 [4.2%] vs 9/515 [1.7%], RR=2.9 [1.45-6.1], p=0.0029). Similar results were obtained for the rate of death or non-fatal myocardial infarction. CONCLUSION: This meta-analysis suggests that clopidogrel treatment including a loading regimen is equivalent or may even be superior to ticlopidine after coronary stenting. However, current evidence shows conversely that clopidogrel therapy in the absence of a loading dose is associated with a significantly higher risk of death or myocardial infarction.

Clopidogrel↗
PubMed2003

Exhaled nitric oxide and exercise performance in heart failure.

BACKGROUND: In heart failure abnormalities of pulmonary function are frequently observed particularly during exercise, which is characterized by hyperpnea, low tidal volume, early expiratory flow limitation and reduced lung compliance. Exhaled nitric oxide (NO) is increased in asthma. We evaluated whether a correlation between exhaled NO and lung mechanics exists during exercise in heart failure. METHODS: We studied 33 chronic heart failure patients and 11 healthy subjects with: a) standard pulmonary function, b) lung diffusion for carbon monoxide (DLCO) including its subcomponents, capillary volume and membrane resistance and eNO both at rest and during light exercise, c) maximal cycloergometer cardiopulmonary exercise test. RESULTS: Forced expiratory volume in 1 second (FEV1) was reduced in heart failure patients (83 +/- 17% of predicted) as was DLCO (75 +/- 18% of predicted) due to reduced membrane resistance (32.6 +/- 10.3 ml/mmHg/min vs. 39.9 +/- 6.9 in patients vs. controls, p < 0.02). eNO was lower in patients vs. controls (9.7 +/- 5.4 ppm vs. 14.4 +/- 6.4, p < 0.05) and was, during exercise, constant in patients and reduced in controls. No significant correlation was found between eNO and lung function. Vice-versa eNO changes during exercise were correlated with peak exercise oxygen consumption (r = 0.560, p < 0.001). CONCLUSIONS: The hypothesis of a link between eNO and lung function in heart failure was not proved. The correlation between eNO changes during exercise and peak VO2 might be due to hemoglobin oxygenation which binds NO to hemoglobin.

Exercise↗
PubMed2002

Alveolar--capillary membrane gas conductance: a novel prognostic indicator in chronic heart failure.

AIMS: Lung dysfunction occurring in chronic heart failure worsens clinical status and exercise performance. The prognostic value of airway and alveolar function measurements in chronic heart failure has not been explored. We aimed to evaluate the prognostic value of lung function tests in a population of patients with stable chronic heart failure. METHODS AND RESULTS: One hundred and six stable chronic heart failure patients (whose left ventricular ejection fraction averaged 33 +/- 1%) underwent echocardiography, metabolic stress testing, assessment of pulmonary function at rest (by spirometry), of alveolar diffusing capacity (DLco) (with carbon monoxide technique) and of its membrane (DM) and capillary blood volume (Vc) components. Prognostic relevance of pulmonary variables was assessed by the Kaplan-Meier approach with log-rank testing and by Cox regression analysis. Cut-off values of lung parameters were based on the 33rd and 66th centiles. Seventeen patients died for cardiac reasons. Non-survivors compared to survivors showed lower forced expiratory volume in 1 s (2 X 1 +/- 0 X 1 vs 2 X 4 +/- 0 X 1 l; P<0 X 01), forced vital capacity (2 X 6 +/- 0 X 1 vs 2 X 9 +/- 0 X 1 l; P<0 X 01), maximal voluntary ventilation (80 X 7 +/- 2 X 5 vs 95 X 4 +/- 2 X 7 l; P<0 X 01), DLco (16 X 5 +/- 1 X 1 vs 19 X 3 +/- 0 X 6 ml . min(-1) . mmHg(-1); P<0 X 01) and DM (25 X 1 +/- 1 X 8 vs 31 X 9 +/- 1 X 5 ml . min(-1) . mmHg(-1); P<0 X 01). They also exhibited a smaller peak VO2 (14 X 6 +/- 0 X 7 vs 15 X 9 +/- 0 X 6 ml . min(-1) . kg(-1); P<0 X 05) and a steeper VE/VCO2 slope (45 X 0 +/- 1 X 7 vs 41 X 9 +/- 1 X 5; P<0 X 01). Multivariate analysis revealed that DM was the only independent predictor of cardiac death. Cases at high risk for adverse outcome were identified by a DM<24 X 7 ml . min(-1) . mmHg(-1). Patients receiving ACE-inhibitors presented with a higher DM (32 X 1 +/- 1 X 7 vs 27 X 9 +/- 1 X 7 ml . min(-1) . mmHg(-1), P<0 X 05) as well as a better Cox estimated survival rate. CONCLUSIONS: Impaired DM is a powerful independent predictor of worse prognosis in stable chronic heart failure and may be considered an additional index of disease severity, as well as a specific therapeutic target.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Modulation of alveolar-capillary sodium handling as a mechanism of protection of gas transfer by enalapril, and not by losartan, in chronic heart failure.

OBJECTIVES: We sought to compare the protective efficacy of enalapril and losartan on lung diffusion in chronic heart failure (CHF). BACKGROUND: In CHF, hydrostatic overload causes disruption of the alveolar-capillary membrane and depression of carbon monoxide diffusion (DCO); enalapril improves DCO through mechanisms still undefined; and saline infusion in the pulmonary circulation worsens DCO, putatively because of an upregulated sodium transport to the alveolar interstitium. We investigated whether enalapril modulates sodium handling and whether losartan shares the same properties. METHODS: In 29 patients with CHF, DCO, its membrane diffusion subcomponent (DM) and right atrial and pulmonary wedge pressures were monitored during saline infusion, in the control condition, during enalapril therapy (20 mg/day) for two weeks and after crossover to losartan (50 mg/day) for two weeks (first 20 patients), or after the combination of enalapril with aspirin (325 mg/day) for one week (last 9 patients). RESULTS: Saline, 150 ml, lowered DCO (-7.9%; p < 0.01) and DM (-9.9%; p < 0.01) without hydrostatic variations. Responses to 750 ml of saline were qualitatively similar. After treatment with enalapril, baseline DCO (p < 0.01) and DM (p < 0.01) were augmented; after sodium loading, the percent reductions of DCO (p < 0.01) and DM (p < 0.01) were comparable to those before it, resulting in higher absolute values. This suggests that the greater the gas conductance improvement with enalapril, the lower the impedance with saline. Losartan was ineffective on gas transfer at rest and under salt challenge. Aspirin counteracted the benefits of enalapril. CONCLUSIONS: In CHF, enalapril protects lung diffusion, possibly through a prostaglandin-mediated modulation of sodium overfiltration to the alveolar interstitium; losartan does not share this ability.

Adult↗
PubMed2001

Circulatory response to fluid overload removal by extracorporeal ultrafiltration in refractory congestive heart failure.

OBJECTIVES: The goal of this study was to investigate the hemodynamic and circulatory adjustments to extracorporeal ultrafiltration (UF) in refractory congestive heart failure (rCHF). BACKGROUND: In rCHF, UF allows clinical improvement and restores diuretic efficacy. However, in the course of a UF session, patients are exposed to rapid variations of body fluid composition so that, as fluid is withdrawn from the intravascular compartment, hypotension or even shock could occur. METHODS: In 24 patients with rCHF undergoing UF, we measured, after every liter of plasma water removed, hemodynamics, blood gas analysis (in both systemic and pulmonary arteries), plasma volume changes (PV) and plasma refilling rate (PRR). The PV and PRR were calculated by considering hematocrit and ultrafiltrate volume. RESULTS: In all patients, UF was performed safely, without side effects or hemodynamic instability (ultrafiltrate = 4,880 +/- 896 ml). Mean right atrial, pulmonary artery and wedge pressures progressively reduced during the procedure. Cardiac output increased at the end of the procedure and, to a greater extent, 24 h later, in relation to the increase of stroke volume. Heart rate and systemic vascular resistance did not increase, and other peripheral biochemical parameters did not worsen during UF. Intravascular volume remained stable throughout the entire duration of the procedure, indicating that a proportional volume of fluid was refilled from the congested parenchyma. CONCLUSIONS: In patients with rCHF, subtraction of plasma water by UF is associated with hemodynamic improvement. Fluid refilling from the overhydrated interstitium is the major compensatory mechanism for intravascular fluid removal, and hypotension does not occur when plasma refilling rate is adequate to prevent hypovolemia.

Aged↗
PubMed2001

Influence of ACE-inhibition on salt-mediated worsening of pulmonary gas exchange in heart failure.

AIMS: In congestive heart failure (CHF), pulmonary gas exchange, as evaluated by carbon monoxide diffusion (DLCO), is impaired. ACE-inhibition improves DLCO. Infusion of saline worsens DLCO, because of upregulated sodium and water transport to the alveolar interstitium, which thickens the alveolar-capillary interface and lengthens the diffusion path for gas exchange. We investigated whether enalapril can readjust the capillary permeability to sodium. METHODS: In 10 NYHA class II-III CHF patients, we measured DLCO, its two subcomponents (VC, capillary blood volume available for gas exchange, and DM, alveolar-capillary membrane diffusion), left and right ventricular filling pressures, plasma noradrenaline, aldosterone and renin activity, at baseline and following saline infusion in the main pulmonary artery stem, before and after 1 week enalapril treatment (20 mg daily). RESULTS: Saline (150 ml) significantly reduced DLCO (-9.1%) and DM (-9.8%) and augmented VC (+ 10.7%). Responses to 750 ml saline were somewhat greater and qualitatively similar. Enalapril produced a significant improvement of DLCO and DM at rest as well as after saline, that was not associated with variations in ventricular filling pressures, cardiac output and left ventricular ejection fraction, and was not accounted for by humoral changes. CONCLUSIONS: In CHF, ACE-inhibition attenuates the deterioration of pulmonary gas transfer produced by saline infusion, suggesting an ability to readjust the upregulated sodium transport across the pulmonary microvascular endothelium.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Cardiac and renal dysfunction in chronic heart failure: relation to neurohumoral activation and prognosis.

BACKGROUND: In chronic heart failure (CHF), cardiac dysfunction is considered the major determinant of neurohumoral activation but the role of renal impairment has not been defined. We investigated the relationship between both cardiac and renal dysfunction and neurohumoral activation, and their possible influence on prognosis. METHODS: Hemodynamics, renal function, plasma neurohormones, and long-term follow-up were evaluated in 148 CHF patients, grouped according to systolic volume index (SVI) and serum creatinine (CRE) values: SVI > 28 mL/m2 and CRE < 1.5 mg/dL (group I, n = 55), SVI < 28 mL/m2 and CRE < 1.5 mg/dL (group II, n = 37), SVI > 28 mL/m2 and CRE > 1.5 mg/dL (group III, n = 25), SVI < 28 mL/m2 and CRE > 1.5 mg/dL (group IV, n = 31). RESULTS: Neurohormones progressively increased from Group I through IV and correlated with both cardiac and renal function. The hemodynamic pattern was similar in patients with normal or abnormal renal function, whereas neurohormones were only moderately increased in the former group and markedly increased in the latter group. Long-term survival progressively decreased from Group I through IV and was significantly poorer in patients with renal dysfunction. CONCLUSIONS: Our study confirms that, in CHF, neurohumoral activation is strictly related to long-term survival and that many factors contribute to its development and progression; among these, cardiac and renal dysfunction seem to play a major role.

Adult↗
PubMed2000

Effects of simulated altitude-induced hypoxia on exercise capacity in patients with chronic heart failure.

PURPOSE: Patients with stable heart failure often wish to spend time at altitudes above those of their residence. However, it is not known whether they can safely tolerate ascent to high altitudes or what its effects on work capacity may be. SUBJECTS AND METHODS: We studied 14 normal subjects and 38 patients with clinically stable heart failure, 12 of whom had normal workload [peak exercise oxygen consumption (VO(2)) greater than 20 mL/min/kg], 14 of whom had slightly diminished workload (peak VO(2) 20 to 15 mL/min/kg), and 12 of whom had markedly diminished workload (peak VO(2) less than 15 mL/min/kg) at baseline. All performed cardiopulmonary exercise tests with inspired oxygen fractions equal to those at 92, 1,000, 1,500, 2,000, and 3,000 m, and maximum achieved work rates (mean +/- SD) were measured. RESULTS: All subjects completed the trial; no test was interrupted because of arrhythmia, angina, or ischemia. Maximum work rate decreased in parallel with increasing simulated altitude. The percentage decrease was greater for patients with heart failure and was most marked among those with the lowest workload at baseline. Maximum achieved work rate declined by 3% +/- 4% per 1,000 m in normal subjects, by 5% +/- 3% (P <0.01) in patients with heart failure with normal workload, by 5% +/- 4% (P <0.01) in patients with slightly diminished workload, and by 11% +/- 5% (P <0.01 vs normal subjects and vs the other patients with heart failure) in patients with markedly reduced workload. CONCLUSION: Patients with stable heart failure who ascend to higher altitudes should expect to have a reduction in maximum physical activity in proportion to their exercise capacity at sea level.

Aged↗
PubMed2000

The noradrenaline plasma concentration and its gradient across the lung.

BACKGROUND: We investigated the lung contribution to circulating noradrenaline (NA) homeostasis. Evaluation of the transpulmonary NA gradient, related to the NA amount entering the lungs, is potentially important, mainly regarding clinical conditions, such as congestive heart failure (CHF), that are associated with excessive circulating NA. MATERIALS AND METHODS: 15 moderate (group 1) and 15 severe (group 2) CHF patients, and 10 normal individuals had determination of NA transpulmonary gradient in the baseline and during rise (exercise, in normals and group 1) or fall (withdrawal from plasma by ultrafiltration, in group 2) of plasma NA. RESULTS: NA gradient (pg mL(-1)) at rest was 30 +/- 3 in normals, 21 +/- 6 in group 1 and 5 +/- 8 in group 2. Increase of NA concentration in the mixed venous blood with exercise was paralleled by depression of the transpulmonary gradient. Pulmonary arteriovenous difference disappeared when NA entering the lungs averaged 1300 pg mL(-1). In group 2, ultrafiltration lowered NA in the mixed venous blood from 1225 +/- 213 to 718 +/- 182, which caused transpulmonary gradient to increase from 5 +/- 8 to 22 +/- 9. CONCLUSIONS: Transpulmonary gradient of NA diminishes when NA entering the lungs increases, and 1300 pg mL(-1) in the pulmonary artery is, both in patients and normal subjects, the level at which gradient disappears; which likely reflects cessation of NA uptake or achievement of a balance between lung uptake and production. This may have physiological and pathological implications.

Aged↗
PubMed2000

Cardiomegaly as a possible cause of lung dysfunction in patients with heart failure.

BACKGROUND: Our hypothesis is that an enlarged heart may compete for space with the lungs, causing a restrictive pattern that is often seen in patients with chronic heart failure. METHODS: Eighty patients with stable congestive heart failure in New York Heart Association classes II and III participated in the study. We measured cardiothoracic index (chest radiography), FEV1, vital capacity, alveolar volume, lung diffusion capacity for carbon monoxide (DLCO), and its 2 subcomponents alveolar-capillary membrane diffusion (DM), and pulmonary capillary blood volume. RESULTS: Reliable measurements were obtained in 72 of 80 participants enrolled. Cardiothoracic index averaged 57% +/- 7%. FEV1, vital capacity, alveolar volume, DLCO, and DM were inversely related to the cardiothoracic index (r = -0.514, -0.557, -0.522, -0.475, and -0.480, respectively). However, the relations of DLCO and DM with the cardiothoracic index were lost when DLCO and DM were adjusted for alveolar volume. A significant correlation (P < .01) was found between alveolar volume and vital capacity, FEV1, and DLCO (r = 0.799, 0.705, and 0.614, respectively). At multivariate analysis, cardiothoracic index, FEV1, and pulmonary capillary blood volume were independent predictors of DLCO, whereas alveolar volume, FEV1, and left ventricular ejection fraction were independent predictors of DM. CONCLUSIONS: Cardiac enlargement in chronic heart failure appears to be involved in causing restrictive lung pattern and a reduced alveolar volume that disturbs carbon monoxide diffusion.

Aged↗