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E Roig

Publications and source records attributed to E Roig.

At least 37 records · Page 2Linked to original sources
PubMed2000

Clinical implications of increased plasma angiotensin II despite ACE inhibitor therapy in patients with congestive heart failure.

AIMS: The aim of the study was to assess the incidence and clinical implications of increased plasma angiotensin II despite chronic ACE inhibitor therapy in patients with heart failure. METHODS AND RESULTS: The studied population consisted of 70 patients (mean age 59+/-9 years). Plasma renin activity and plasma concentration of aldosterone, norepinephrine, atrial natriuretic peptide, angiotensin II, tumour necrosis factor, interleukin-6 and interleukin-1B were assessed at 6 months of ACE inhibitor therapy. Mean left ventricular ejection fraction was 24+/-5% and the end-systolic and end-diastolic diameters were 59+/-9 and 71+/-8 mm, respectively. Despite chronic enalapril or captopril therapy, 35 patients (50%) had increased plasma angiotensin II (median 33 pg. ml(-1), range 17-84), while it was in the normal range in the remaining 35 patients (median 10 pg. ml(-1), range 5-15). Plasma renin activity (P=0.005), interleukin-6 (P=0.004), New York Heart Association functional class III-IV (P=0. 006), furosemide dose (P=0.01), lack of beta-blocker therapy (P=0. 04) and norepinephrine (P=0.04) were univariately associated with increased angiotensin II. Multivariate regression analysis identified the plasma renin activity (0.0004), norepinephrine (0.02) and interleukin-6 (0.03) as independent predictors of plasma angiotensin II. During follow-up (35+/-29 months), nine (12.8%) patients died and 13 had new heart failure episodes. Increased plasma angiotensin II, despite ACE inhibitor therapy, was a significant predictor of death or heart failure according to the Kaplan-Meier survival method by log rank test (P=0.002). CONCLUSION: Fifty per cent of patients with heart failure, ha increased plasma angiotension II despite chronic ACE inhibitor therapy. These patients had higher neurohormonal activation and poor prognosis.

Angiotensin II↗
PubMed2000

A reply

Explore the source record for details and available documents.

Journal Article↗
PubMed2000

Changes in the cooling rate and medium improve the vascular function in cryopreserved porcine femoral arteries.

PURPOSE: The purpose of this study was to design an adequate technique with which to cryopreserve pig femoral arteries and to assess the influence of storage times in vascular function. METHODS: Fifty-two femoral arteries were distributed in seven groups. In group A (control), 10 arteries were studied after harvest; in groups B1 and B2, 19 arteries were suspended in RPMI 1640 plus fetal calf serum plus dimethylsulfoxide and were cryopreserved at 1 degrees C per minute or 0.3 degrees C per minute, respectively. In groups C1 to C4, 23 arteries were suspended in modified Krebs-Henseleit plus dimethylsulfoxide plus sucrose, cryopreserved at 0.7 degrees C per minute, and kept frozen for 1, 15, 60, or 180 days, respectively. After being thawed, arteries were examined for contraction and endothelial-dependent vasodilation (organ bath studies), antithrombotic properties of the endothelial layer(perfusion studies), and vessel structure (electron microscopy). RESULTS: Endothelial cells were present in both cryopreserved and control arteries. The control vessels showed a mean contraction to norepinephrine (10(-7) mol/L) of 13010 +/- 3181 mg. Arteries in groups B1 and B2 did not respond to norepinephrine. Contraction in groups C1 to C4 was as follows: C1, 5354 +/- 1222 mg; C2, 5187 +/- 2672 mg; C3, 6867 +/- 2292 mg; C4, 7000 +/- 2858 mg, which represent 50% of the control values (P <.001). Vasodilation was similar in control (99% +/- 3%) and cryopreserved arteries (C1, 90% +/- 13%; C2, 93% +/- 12%; C3, 89% +/- 15%; C4, 88% +/- 22%). Storage time did not influence vascular function. Platelet interaction was almost absent and similar in all groups. CONCLUSION: A modified cryopreservation technique preserves endothelial function independently of the storage time up to 6 months.

Acetylcholine↗
PubMed1999

Captopril administration reduces thrombus formation and surface expression of platelet glycoprotein IIb/IIa in early postmyocardial infarction stage.

Long-term administration of the angiotensin-converting enzyme inhibitor captopril in survivors of myocardial infarction (MI) reduces the risk of cardiovascular death, recurrence of MI, and unstable angina, suggesting that captopril may possess antithrombotic properties that have not been clearly elucidated. We assessed the short-term antithrombotic effects of captopril on platelet aggregation, platelet-subendothelium interaction, and the expression of major glycoproteins on platelet surface. A double-blind study was carried out in 25 patients with MI. Blood samples were taken before (baseline) and 12 days after treatment in both the control and captopril groups. Platelet aggregation was tested by conventional aggregometry using common activating agents. Platelet interaction with deeply damaged subendothelial surface was evaluated in a perfusion model, with blood maintained under flow conditions. Deposition of platelets was quantified by using computer-assisted morphometric techniques on histological sections, and it was expressed as a percentage of total vessel surface covered by platelets (CS) and as a ratio between large aggregates (T) and surface covered by platelets (100XT/CS). Glycoprotein expression was measured using flow cytometric techniques. Aggregometric responses showed no significant variations; however, in the captopril group, 100XT/CS decreased after 12 days of treatment (100XT/CS: 36+/-12.1% captopril versus 64+/-8.0% baseline; P=0.005). This parameter was also significantly decreased from that found in control group patients (100XT/CS:67=/-4.5%, P=0.008). Flow cytometry showed a 30% reduction in glycoprotein IIb/IIIa expression (P=0.02). Captopril reduced the formation of large aggregates in a perfusion system, which might be related to a down-regulation of glycoprotein IIb/IIIa complex on the platelet surface. These results suggest that captopril exerts an antiplatelet effect that may contribute to its beneficial action in MI.

Aged↗
PubMed1998

Suppression of leukotriene B4 and tumour necrosis factor alpha release in acute inflammatory responses by novel prenylated hydroquinone derivatives.

A series of prenyl hydroquinone derivatives synthesized as structural analogs of marine products were tested for their effects on inflammatory responses in vitro and in vivo. 2-Prenyl-1,4-hydroquinone (H1), 2-diprenyl-1,4-hydroquinone (H2), 2-triprenyl-1,4-hydroquinone (H3) and 2-tetraprenyl-1,4-hydroquinone (H4) scavenged reactive oxygen species and inhibited 5-lipoxygenase (5-LO) activity in human neutrophils. The inhibition of 5-LO activity was demonstrated in vivo in the mouse air pouch injected with zymosan and arachidonic acid-induced ear inflammation. The four compounds suppressed the production of tumour necrosis factor alpha (TNFalpha) in J774 cells stimulated with lipopolysaccharide (LPS) and also in vivo in the mouse air pouch injected with zymosan. In addition, all prenyl-hydroquinones inhibited the release of nitrite and PGE2 in LPS-stimulated J774 cells, without direct effects on cyclo-oxygenase-1 (COX-1), cyclo-oxygenase-2 (COX-2) or inducible nitric oxide synthase (iNOS) activities in several cell-free systems. The reduction in the length of the lateral chain in prenyl-hydroquinones (1-4 isoprene units) with respect to their marine analogs (7-8 isoprene units) has improved the anti-inflammatory activity of this class of compounds. Marine natural products may be a model to design new anti-inflammatory agents.

Animals↗
PubMed1998

Short-term effects of transdermal estrogen replacement therapy on coronary vascular reactivity in postmenopausal women with angina pectoris and normal results on coronary angiograms.

OBJECTIVES: This study sought to analyze the effect of short-term transdermal estradiol treatment on in vivo coronary endothelial function in postmenopausal women with angina and normal results on coronary arteriograms. BACKGROUND: The incidence of coronary heart disease increases in women after menopause. Estrogen replacement therapy has been associated with a global reduction in cardiovascular disease incidence and mortality. In addition, coronary endothelial dysfunction has been demonstrated in a group of postmenopausal women. It has been shown that intravenous or intracoronary estrogens improve endothelial function in postmenopausal women with coronary atherosclerosis. However, the efficacy of this treatment is unknown in patients with angina and normal coronary arteries. METHODS: Endothelium-dependent coronary reactivity was analyzed in 15 postmenopausal women with angina and normal coronary arteries at baseline and after 24 h of estradiol transdermal administration (100 microg). RESULTS: Estradiol concentration increased from 22 +/- 8 pg/ml (mean +/- SEM) at baseline to 76 +/- 13 pg/ml (p < 0.01) at 24 h. At baseline, acetylcholine induced vasoconstriction, with a mean diameter reduction of -23 +/- 6% (p = 0.002). After estrogen treatment, there was no vasoconstriction with acetylcholine, with a mean diameter change of 0 +/- 4%, significantly different from the pretreatment diameter reduction observed (p = 0.003). Similarly, estimated coronary blood flow significantly increased in response to acetylcholine after estrogen treatment, with a mean change of 50 +/- 30% compared with 5 +/- 24% before estradiol administration (p = 0.04). CONCLUSIONS: Early after transdermal estrogen administration, endothelium-dependent coronary vasomotion is improved in postmenopausal women with angina and normal coronary arteries.

Aged↗
PubMed1997

Cocaine administration enhances platelet reactivity to subendothelial components: studies in a pig model.

Myocardial infarction in cocaine abusers may be related to a direct platelet-activating effect. We analysed this possibility in an experimental model. Studies were carried out in eight normal, anaesthetized pigs with a weight of 30.7 +/- 3.7 kg. Blood samples were withdrawn before and 20 min after i.v. administration of cocaine (10 mg kg-1; at 1 mg kg-1 every 2 min). Modifications in platelet responses to arachidonic acid (AA; 1.4 mmol L-1), ADP (1-4 microM), synthetic thromboxane endoperoxide analogue (U46619; 1 microM), collagen (2.5-5 micrograms mL-1), adrenaline (10 microM) and ristocetin (0.8-1 mg mL-1) were tested by conventional aggregometry. Changes in the capacity of platelets to form aggregates on damaged subendothelium were assessed by means of an ex vivo perfusion system in which blood was circulated for 10 min at 800 s-1, a shear rate similar to that found in normal coronary arteries. The interaction of platelets with perfused denuded arterial segments was morphometrically quantified and expressed as a percentage of damaged vessel surface covered by platelets (%CS). Cocaine administration did not influence platelet aggregation patterns in pigs. However, there was a significant increase in the interaction of pig platelets with subendothelial structures after cocaine infusion (%CS = 40 +/- 17% vs. 27 +/- 16% baseline; mean +/- SD; P < 0.01). Cocaine administration in this animal model increases the reactivity of platelets exposed to subendothelium. These results support the concept that the administration of cocaine to pigs has a prothrombotic effect by facilitating the interaction of platelets with damaged arteries.

Animals↗
PubMed1997

Anti-Candida albicans IgE and IgG subclasses in sera of patients with allergic bronchopulmonary aspergillosis (ABPA).

We performed immunoblotting experiments to determine specific IgE and IgG subclass responses to Candida albicans antigens in allergic bronchopulmonary aspergillosis (ABPA) patients. This is a first report describing C. albicans antigens recognized by serum IgE and IgG subclasses of ABPA patients sensitized to that yeast. Among the various antigens reacting with serum IgE, a 43-kDa component was recognized by all seven patients and can be considered a major antigen of C. albicans for this particular group of patients. By comparison, only 20% of a group of asthmatic atopics (25 patients) and 10% of a group of normal controls (10 subjects) were 43-kDa positive. Multiple banding patterns, revealing no major antigen, were observed for all four IgG subclasses except for IgG1 in one case. In particular, the 43-kDa component was not always recognized by all the patients. Furthermore, oral or inhaled steroid treatment appears to have no impact on the specific IgE immunopatterns obtained. Using immunoelectron-microscopy, we localized IgE-binding primarily in the mannoprotein-containing layers of the C. albicans cell wall. In conclusion, C. albicans-IgE and IgG subclasses may participate in the physiopathology of ABPA by exacerbating pulmonary infiltrates (IgE) and inducing eosinophil-mediated inflammatory reaction (IgG1, IgG3).

Adrenal Cortex Hormones↗
PubMed1996

Endothelial dysfunction of the non-infarct related, angiographically normal, coronary artery in patients with an acute myocardial infarction.

BACKGROUND: Patients with acute myocardial infarction and single-vessel disease may have early atherosclerosis in other angiographically normal coronary arteries. METHODS: Coronary endothelial responses were analysed in 20 non-diabetic patients with an acute myocardial infarction and one-vessel disease. In an angiographically normal, non-infarct related, coronary artery serial acetylcholine doses of 10(-7) M, 10(-6) M, 10(-5) M and 10(-4) M and nitroglycerin 40 micrograms were infused over 3 min. The responses of the coronary vessel were measured with quantitative angiography. Coronary blood flow was also measured with a Doppler catheter in 11 of the 20 patients. RESULTS: Four patients showed a trend towards vasodilation during acetylcholine infusion in the proximal and distal segments: from 2.49 +/- 0.23 mm to 2.95 +/- 0.42 mm and 2.43 +/- 0.56 mm to 2.81 +/- 0.66 mm, respectively. Coronary vascular resistance decreased to 57 +/- 4% (P = 0.03). The other 16 patients presented vasoconstriction in the proximal and distal segments: 2.61 +/- 0.75 mm to 2.03 +/- 0.65 mm (P = 0.0001), and 2.40 +/- 0.58 to 1.81 +/- 0.56 mm (P = 0.0036), respectively. Nitroglycerin caused vasodilation in the proximal (2.69 +/- 0.61 mm, P = 0.017, ANOVA) and distal segments (2.48 +/- 0.45 mm, P = 0.009, ANOVA). Coronary vascular resistance increased to 141 +/- 43% (P = 0.03) over the basal value in this group of patients. CONCLUSION: Endothelial dysfunction of the epicardial and resistance vessels was found in angiographically normal coronary arteries of patients with one-vessel disease in 75% of this population.

Adult↗
PubMed1996

The role of endogenous nitric oxide in the response of coronary blood flow to tachycardia.

BACKGROUND: The role of endogenous nitric oxide as mediator of flow-dependent dilation is well established. However, its role in the adaptation of coronary blood flow to tachycardia is less well defined. This study was designed to determine whether nitric oxide is a mediator in pacing-induced hyperaemia. METHODS: Twenty pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing measurements. Their heart rate was increased by 20 beats every 5 min. Coronary blood flow was measured basally and at each pacing interval before and after each of the following interventions: intracoronary saline infusion (n = 6), N omega-nitro-L-arginine methyl ester infusion (L-NAME, 20 micrograms/kg per min intracoronarily, n = 9) and infusion of L-NAME plus L-arginine (0.3 mg/kg per min intracoronarily, n = 5). RESULTS: The coronary peak flow increased with atrial pacing. The maximum increase in coronary blood flow with pacing was significantly reduced after infusion of L-NAME (159 +/- 33 versus 143 +/- 30%), whereas no change was observed in the saline group (163 +/- 28 versus 172 +/- 29%). However, it increased significantly in the group receiving L-NAME plus L-arginine (147 +/- 29 versus 182 +/- 40%). CONCLUSIONS: In the pig, the increase in coronary blood flow and therefore the vasodilation of the microvasculature that accompanies tachycardia depend, partly, on the release of endogenous nitric oxide.

Animals↗
PubMed1996

Improvement of exercise-induced ischaemia and myocardial perfusion after aminophylline.

BACKGROUND: Previous studies have suggested that aminophylline improves exercise-induced ischaemia by preventing the redistribution of the coronary flow from ischaemic to non-ischaemic myocardium. The purpose of the study was to assess whether aminophylline improves myocardial perfusion in zones supplied by collateral circulation. METHODS: Twenty-three patients with an occluded coronary artery and collateral circulation from a non-diseased vessel underwent two symptom-limited exercise 99mTc-MIBI, single-photon emission computed tomography (SPECT) myocardial scintigraphy experiments, which were preceded by an intravenous infusion of either aminophylline (5 mg/kg over 20 min) or saline solution in a randomized double-blind control procedure. The MIBI SPECT images were analysed by two experienced observers who were blinded to each other's data. RESULTS: All patients underwent cardiac catheterization. For 16 patients this was because of stable angina and the remaining eight were post-myocardial infarction patients with a positive exercise test. Aminophylline significantly increased the time to the onset of ischaemia in the 15 patients with a positive exercise test (mean +/- SD, 6.5 +/- 1.9 compared with 5.3 +/- 1.8 min, P < 0.005); and ischaemia occurred at higher rate-pressure product (230 +/- 68 compared with 195 +/- 68 HB x mmHg, P < 0.03). After aminophylline, exercise ST-segment depression was 1.1 +/- 0.5 mV, compared with 1.5 +/- 0.8 mV after placebo (P < 0.01). All patients had perfusion defects that resolved partially or completely in the rest images. The imaging score was significantly lower after aminophylline infusion than after placebo (9.7 +/- 9 compared with 12.1 +/- 10, P < 0.01). CONCLUSIONS: Aminophylline significantly delayed the time to onset of exercise-induced ischaemia and improved perfusion in zones supplied by collateral circulation. Aminophylline-like drugs may be useful in the treatment of selected patients with ischaemic heart disease.

Aminophylline↗
PubMed1995

[Do patients with duodenal ulcer transmit Helicobacter pylori to their relatives?].

The prevalence of IgG antibodies to Helicobacter pylori was determined with an enzyme-linked immunosorbent assay in 80 families who lived together with 40 duodenal ulcer patients in whom Helicobacter pylori had been cultured from a gastric biopsy (34 spouses, 31 children, 10 parents, 4 sisters and 1 brother) and in 112 controls from the same habitat and with similar age. The antibodies were positive in 38.4% of the relatives and in 36.6% of the controls, the difference was not significant. Among spouses of patients, 38.4% of those aged 25-39 years and 66.6% of those aged 40-67 years were positive, whereas controls showed a 29.2% and a 58.3% of positives respectively. The differences between both groups were not significant. Among children, 17.2% were positive and in parents 50%, whereas among controls with a similar age 26.3% and 62.5% respectively were positive. The differences between relatives and controls were not significant. We conclude that in our environment among consanguineous families living together and between spouses, person-to-person spread of Helicobacter pylori does not usually occur or it happens uncommonly.

Adolescent↗
PubMed1993

Feasibility of early discharge after acute Q wave myocardial infarction in patients not receiving thrombolytic treatment.

OBJECTIVES: The purpose of this study was to analyze the feasibility of early discharge (4 days) after acute myocardial infarction in patients not receiving thrombolytic therapy by first identifying predictors of short-term prognosis and then testing the derived risk profile in an independent cohort of patients. BACKGROUND: Previous studies have shown that early discharge after acute myocardial infarction is possible. However, physicians are reluctant to shorten the standard 7- to 10-day hospital stay, presumably because of difficulty in selecting low risk patients. METHODS: From January 1985 to November 1986, 358 patients with acute myocardial infarction who did not receive thrombolytic therapy were screened. Those with a Q-wave infarction showing no complications on day 4 were considered candidates for early discharge and were transferred to the ward for a mean of 12 days. During this period, we looked for any event (cardiac or noncardiac) that would have prompted readmission if the patient had been previously discharged. Univariate and multiple regression analysis were performed to identify predictors of these events among 25 baseline variables. The derived risk profile was tested in an independent validation cohort. RESULTS: One hundred five (29.3%) of the 358 patients were free of symptoms on day 4, and 29 (27.6%) had at least one cardiac event, including four deaths and one reinfarction. Multivariate analysis selected diabetes, ejection fraction < 40% and age as independent predictors of events. Using the risk profile, 18 (13.2%) of the 136 validation cohort patients were categorized as low risk, and only 1 of them had a major event (progressive angina). Sensitivity for the risk profile was high (91%), but specificity was low (34%). CONCLUSIONS: The use of simple clinical variables may allow the safe reduction of hospital stay after infarction in selected patients. However because the proportion of candidates for early discharge is small (12.6%), it seems unlikely that the current policies on length of hospital stay will change in the near future.

Cohort Studies↗
PubMed1993

Prognostic value of exercise radionuclide angiography in low risk acute myocardial infarction survivors.

Patients with an uneventful course during hospital stay, which represent from 30 to 50% of all myocardial infarction survivors, still have an incidence of new coronary events up to 7% during the first year of follow-up. To assess the value of radionuclide angiography in predicting new coronary events in this low risk population, 93 patients without evidence of left ventricular failure or recurrent postinfarction angina underwent rest and exercise radionuclide angiography and treadmill exercise testing before hospital discharge. During follow-up (16 +/- 5 months, range 12 to 32) 14 patients developed new coronary events: two patients died, four had a new myocardial infarction and the remaining eight had unstable angina. There were no differences regarding clinical variables, the results of the exercise test and the resting ejection fraction, between patients with or without new coronary events; however, patients without events during follow-up exercised longer during both exercise treadmill test and exercise radionuclide angiography. Resting end-diastolic and end-systolic volume indexes were higher in patients presenting coronary events (122 +/- 50 vs 92 +/- 32 ml.m-2, P < 0.05, 69 +/- 47 vs 47 +/- 26 ml.m-2, P < 0.05). These patients also had a higher incidence of wall motion abnormalities in more than one area (64 vs 28%, P < 0.02). During exercise, ejection fraction increased significantly in patients with an uneventful outcome (49 +/- 13 to 56 +/- 14%, P < 0.01), while it did not change in their counterparts (46 +/- 14 to 45 +/- 14%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Diagnostic value of technetium-99m-MIBI as a myocardial perfusion imaging agent: comparison of long and short intervals between rest and stress injections.

To assess the diagnostic value of technetium-99m-MIBI (99mTc-MIBI) as a myocardial perfusion imaging agent, and if rest and exercise scans could be performed on the same day, 21 patients with coronary artery disease were studied. Qualitative planar 201-thallium (201Tl) scans, coronary angiography, or both were also performed (median between studies 11 days). In 10 patients an injection of 740 mBq of 99mTc-MIBI at stress was followed by a second injection of 740 mBq at rest 24 h later (long interal) (LI). In 11 patients injection of 370 mBq at rest was followed 3 h later by an injection of 740 mBq at stress (short interval) (SI). Exercise scans were performed to similar maximal work load (LI = 6.6 +/- 1.8 METs; SI = 6.3 +/- 1.7 METs; 201Tl = 6.8 +/- 1.2 METs; p = NS) and double product (LI = 19551 +/- 7370; SI = 19900 +/- 6797; 201Tl = 19965 +/- 5282; p = NS). Overall, 99mTc-MIBI and 201Tl agreed in 92% of the patients tested and in 165 of 180 (92%) left ventricular segments in both 99mTc-MIBI protocols using short and long intervals between injections. In 15 patients with significant stenosis, 99mTc-MIBI correctly identified 13 patients (sensitivity of 87%). Thus, 99mTc-MIBI is a useful imaging agent with similar diagnostic value as 201Tl. In spite of its lack of myocardial redistribution, 99mTc-MIBI rest and exercise scans performed on the same day seem to have a similar concordance rate with 201Tl as when performed on separate days.

Adult↗
PubMed1992

[The predictive value of ventricular function during exercise after a myocardial infarct].

To assess the prognostic value of exercise left ventricular function, and if this test improves the prognostic value of clinical data and exercise test, 146 patients (mean age 56 +/- 9 years) underwent rest and exercise radionuclide angiography, 10 days after myocardial infarction. During follow-up (mean 16 +/- 5 months), 32 patients had new coronary events: 5 died, 9 had a new myocardial infarction and the remaining 18 developed unstable angina (Class III-IV of the CCS classification). Patients with new coronary events had more frequently severe left ventricular failure (Killip III-IV) (15% vs 3%; p less than 0.05) and postinfarction angina (32% vs 9%; p less than 0.01) than their counterparts. There were no differences regarding rest ejection fraction between both groups of patients. Exercise ejection fraction increased significantly (50 +/- 14% to 56 +/- 16%, p less than 0.001), while there was no change in patients with new coronary events (46 +/- 16% to 43 +/- 15%, NS). Logistic regression analysis including only clinical data identified postinfarction angina (p less than 0.01) and left ventricular failure (Killip III-IV) (p less than 0.01) as independent predictors of new coronary events. The sensitivity and specificity of the regression equation obtained with clinical data were 43% and 90%, respectively. Analyzing data from clinical variables, as well as exercise test and both, rest and exercise radionuclide angiography, logistic regression analysis identified, exercise ejection fraction (p less than 0.001), postinfarction angina (p less than 0.01) and rest ejection fraction (p less than 0.05) as independent predictors of new coronary events.(ABSTRACT TRUNCATED AT 250 WORDS)

Chi-Square Distribution↗