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Biomedical subjects

D García-Dorado

Publications and source records attributed to D García-Dorado.

At least 19 recordsLinked to original sources
PubMed2000

Randomized comparative trial of triflusal and aspirin following acute myocardial infarction.

AIMS: To compare the efficacy and tolerability of the antiplatelet agent triflusal with aspirin in the prevention of cardiovascular events following acute myocardial infarction. METHODS AND RESULTS: In this double-blind, multicentre, sequential design study, patients were randomized within 24 h of acute myocardial infarction symptom onset to receive triflusal 600 mg or aspirin 300 mg once daily for 35 days. The primary end-point was death, non-fatal myocardial reinfarction or a non-fatal cerebrovascular event. The incidences of these individual outcomes and urgent revascularization were secondary end-points. The null hypothesis of no difference between treatments in the primary combined end-point was accepted with 80% power after recruiting 2124 validated patients (odds ratio (OR) for failure [95% confidence interval (CI)]: 0.882 [0.634-1.227]). Non-fatal cerebrovascular events were significantly less frequent with triflusal (OR [95% CI]: 0.364 [0.146-0.908]; P = 0.030). There was no significant difference between treatments for death (OR [95% CI]: 0.816 [0.564-1.179]; P = 0.278), non-fatal reinfarction (OR [95% CI]: 1.577 [0.873-2.848]; P = 0.131) or revascularization (OR [95% CI]: 0.864 [0.644-1.161]; P = 0.334). Overall, both drugs were well tolerated, although there was a trend towards fewer bleeding episodes with triflusal; significantly fewer central nervous system bleeding episodes were observed in triflusal-treated patients (0.27% vs. 0.97%; P = 0.033). CONCLUSION: Triflusal and aspirin have similar efficacy in preventing further cardiovascular events after acute myocardial infarction, but triflusal showed a more favourable safety profile. Triflusal significantly reduced the incidence of non-fatal cerebrovascular events compared with aspirin.

Aged↗
PubMed1999

Attenuated severity of new acute ischemic events in patients with previous coronary heart disease receiving long-acting nitrates.

BACKGROUND: Platelet aggregation and secondary vasoconstriction are key events in the genesis of acute coronary syndromes. HYPOTHESIS: Since nitrates have vasodilatory and antiaggregant effects, treatment with long-acting nitrates at the time of onset of acute coronary syndromes could be associated with attenuation of their severity. METHODS: A consecutive series of 533 patients with acute coronary syndrome and past history of coronary artery disease admitted to the Cardiology Service of a general hospital was studied. A specific questionnaire assessed the use of nitrates and other relevant drugs, as well as other clinical variables. The diagnosis of unstable angina or acute myocardial infarction (MI) was established according to clinical, electrocardiographic, and enzymatic criteria. RESULTS: In the whole cohort, 169 patients had MI and 364 had unstable angina. Previous use of long-acting nitrates was significantly more common in patients with unstable angina (56%) than in those with MI (37%) (p < 0.0001). Multivariate analysis identified being a nonsmoker [odds ratio: 95%, confidence limits (CL) 0.37, 0.23-0.59], previous unstable angina (CL 0.62, 0.41-0.92), use of aspirin (CL 0.58, 0.41-0.92), and use of long-acting nitrates (CL 0.61, 0.40-0.93) as the independent predictors of the development of unstable angina rather than MI; of these the combination of nitrates and aspirin was the strongest predictor. CONCLUSIONS: Long-acting nitrates as well as aspirin are suggested to have a protective or modifying effect on the development of acute coronary syndromes, favoring unstable angina rather than acute MI.

Adrenergic beta-Antagonists↗
PubMed1999

Prime causes of rapid cardiomyocyte death during reperfusion.

In ischemic-reperfused myocardium, necrosis of cardiomyocytes may develop not only due to the ischemic conditions but also the specific circumstances of reperfusion. The existence of reperfusion injury becomes apparent when modifications of the conditions of reperfusion can prevent cell death otherwise occurring. Three prime causes of rapidly developing reperfusion injury are here discussed, ie, reenergization of cells at increased cytosolic Ca2+ contents, rapid normalization of tissue pH, and rapid normalization of tissue osmolality. All three causes lead to severe mechanical stress of cardiomyocytes which can cause their rapid deterioration. Propagation of cell injury among adjacent cells can cause a spreading of necrosis throughout myocardial tissue. The understanding of these initial causes of rapidly developing lethal reperfusion injury leads to new concepts for specific protection of reperfused myocardium.

Acid-Base Equilibrium↗
PubMed1999

L-arginine limits myocardial cell death secondary to hypoxia-reoxygenation by a cGMP-dependent mechanism.

The objective of this study was to investigate the effect of L-arginine supplementation on myocardial cell death secondary to hypoxia-reoxygenation. Isolated rat hearts (n = 51) subjected to 40 min of hypoxia and 90 min of reoxygenation received 3 mM L-arginine and/or 1 microM 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; a selective inhibitor of soluble guanylyl cyclase) throughout the experiment or during the equilibration, hypoxia, or reoxygenation periods. The incorporation of L-[3H]arginine into myocytes during energy deprivation was investigated in isolated adult rat myocytes. The addition of L-arginine to the perfusate throughout the experiment resulted in higher cGMP release (P < 0.05), reduced lactate dehydrogenase release (P < 0.05), and increased pressure-rate product (P < 0.05) during reoxygenation. These effects were reproduced when L-arginine was added only during equilibration, but addition of L-arginine during hypoxia or reoxygenation had no effect. Addition of ODQ either throughout the experiment or only during reoxygenation reversed the beneficial effects of L-arginine. L-[3H]arginine was not significantly incorporated into isolated myocytes subjected to energy deprivation. We conclude that L-arginine supplementation protects the myocardium against reoxygenation injury by cGMP-mediated actions. To be effective during reoxygenation, L-arginine must be added before anoxia.

Animals↗
PubMed1997

[Role of noninvasive examinations in the management of ischemic heart disease. III. Assessment of myocardial viability].

Assessment of myocardial viability is a field of growing interest. This article summarizes the pathophysiology of myocardial stunning and hibernation; both phenomena are associated with the presence of dysfunctional, viable myocardium. The techniques that are currently available for the assessment of viability, and the clinical situations in which these assessments may be more useful are discussed.

Animals↗
PubMed1996

Intravenous amiodarone in treatment of recent-onset atrial fibrillation: results of a randomized, controlled study.

OBJECTIVES: This study was designed to determine the efficacy of intravenous amiodarone in the management of recent-onset atrial fibrillation. BACKGROUND: The optimal approach for acute atrial fibrillation has not been established. Amiodarone is a unique antiarrhythmic agent with activity in both supraventricular and ventricular tachyarrhythmias, but its value for the restoration of sinus rhythm in patients with recent-onset atrial fibrillation has not been demonstrated. METHODS: Sample size was calculated to detect a 25% increase in reversion rate with amiodarone with a statistical power of 80%. One hundred consecutive patients with recent-onset (<1 week) atrial fibrillation and not taking antiarrhythmic agents were randomized to receive either intravenous amiodarone, 5 mg/kg body weight in 30 min followed by 1,200 mg over 24 h, or an identical amount of saline. Both groups received intravenous digoxin, 0.5 mg initially, followed by 0.25 mg at 2 h and 0.25 mg every 6 h thereafter, to complete 24 h while the ventricular rate was >100 beats/min. Amiodarone and digoxin blood levels were determined. Both groups were homogeneous regarding underlying heart disease, time from onset to treatment, initial ventricular rate and left atrial size. RESULTS: By the end of the 24-h treatment period, 34 patients (68%, 95% confidence interval [CI] 53% to 80%) in the amiodarone group and 30 (60%, 95% CI 45% to 74%) in the control group had returned to sinus rhythm (p = 0.532). Mean times (+/-SD) of conversion were 328 +/- 335 and 332 +/- 359 min, respectively (p =0.957). Among patients who did not convert to sinus rhythm, treatment with amiodarone was associated with a slower ventricular rate (82 +/- 15 beats/min in the amiodarone group vs. 91 +/- 23 beats/min in the control group, p = 0.022). After restoration of sinus rhythm, atrial fibrillation recurred during a 15-day follow-up period in 4 (12%) of 34 patients (95% CI 3% to 27%) in the amiodarone group and in 3 (10%) of 30 (95% CI 2% to 26%) in the control group (p = 0.861). CONCLUSIONS: Intravenous amiodarone, at the doses used in this study, produces a modest but not significant benefit in converting acute atrial fibrillation to sinus rhythm.

Adult↗
PubMed1996

[Normal values of valvular flow velocities determined by Doppler echocardiography: relations with heart rate and age].

INTRODUCTION AND OBJECTIVES: The velocity-time integral (VTI) and the mean velocity of valvular flow are widely-used variables in Doppler-echocardiography. The aim of the present work was to determine normal VTI and mean velocity values of valvular flow and their relation to age, sex, heart rate and body surface area. METHODS: One hundred and fifty-six patients (84 men, 72 women; age range: 6-86 y; mean: 37 +/- 20) without cardiovascular disease were studied by Doppler echocardiography. VTI and the mean velocity of left and right ventricular outflow tract, and mitral and tricuspid valvular flow were determined by pulsed-wave Doppler. Aortic and pulmonary valvular flow were assessed by continuous wave Doppler. RESULTS: Mean value of aortic valvular flow VTI (22 +/- 4 cm) was slightly higher than that of pulmonary valvular flow (20 +/- 4 cm). Mean VTI values of left and right ventricular outflow tract and mitral valvular flow were similar (16 +/- 3, 15 +/- 3 and 15 +/- 3 cm, respectively) with an acceptable correlation (r = 0.76-0.83). VTI of tricuspid valvular flow was clearly lower than the rest (10 +/- 3 cm; p < 0.001). Linear regression analysis showed the VTI to be inversely related to heart rate and age, and mean velocity positively related to heart rate and inversely to age. While VTI remained relatively stable up to the age of 60 and decreased sharply thereafter, mean velocity decreased progressively with age. VTI values were identical for both sexes; however, mean velocity was higher in women up to the age of 60. CONCLUSIONS: VTI is a Doppler parameter independent of body surface area, inversely related to heart rate, not sex-related and remains stable up to the age of 60. Normal mean velocity values should be defined in relation to heart rate and age. Normal values of these Doppler parameters should be borne in mind for non-invasive assessment of cardiovascular function.

Adolescent↗
PubMed1996

[Normal values of valvular annular areas. Comparison of the results of a necropsy and an echocardiographic series].

INTRODUCTION AND OBJECTIVES: Measurement of valvular annular area is necessary for valvular flow volumen quantification by Doppler echocardiography. The aim of this work was to compare normal valvular annular area values obtained in a necropsic and an echocardiographic series and to ascertain whether a relationship exists between these areas and several anthropometric variables. METHODS: Necropsic series: valvular annular area was measured in 20 hearts from deceased patients (age range: 9-79 years; mean 52 +/- 18) without cardiovascular disease. Echocardiographic series: Valvular annular area was determined in 156 patients (age range: 6-86 years; mean 37 +/- 20) without cardiovascular disease. RESULTS: Necropsic series: multiple regression analysis showed valvular annular area values to be related mainly to height (p < 0.001) but also to weight (p < 0.01). Correlations between valvular annular area and body surface were low (r = 0.64-0.75). Aortic annular area index was slightly lower than the pulmonary annular area index and half that of the mitral annular area index (2.2 +/- 0.4, 2.5 +/- 0.5 and 4.4 +/- 0.8 cm2/m2, respectively). Tricuspid annular area index was the largest (6.7 +/- 1.0 cm2/m2). ECHOCARDIOGRAPHIC SERIES: Multiple regression analysis also showed a relationship between valvular annular area and height (p < 0.00001) and weight (p < 0.004). Correlations between valvular annular real values and body surface were poor (r = 0.45-0.71). Mean values of aortic, pulmonary and mitral valvular annular area indices were similar to those obtained in the necropsic series (2.1 +/- 0.2, 2.1 +/- 0.3, 4.1 +/- 0.6 cm2/m2, respectively). However, the tricuspid annular area index was clearly lower (4.5 +/- 0.6 cm2/m2, p < 0.001). CONCLUSIONS: Valvular annular area is influenced mainly by height, but also by weight. The correlation between these values and body surface is poor. Aortic annular area is similar to the pulmonary annular area and half that of the mitral annulus. Normal values determined by echocardiography and necropsy are similar, although tricuspid annular area by apical view is smaller than that obtained in the necropsic series.

Adolescent↗
PubMed1996

[Should individuals without evidence of coronary disease and with risk factors receive continuous treatment with aspirin? Arguments in favor].

There is general agreement on the efficacy of aspirin treatment in patients with coronary heart disease, but the indications of aspirin in individuals without coronary heart disease are debated. This paper analyses data from the main studies which investigated the usefulness of aspirin in the primary prevention of coronary heart disease. Particular attention is paid to the risks and benefits of aspirin treatment in different clinically relevant subgroups of patients. It is concluded that, according to available information, the use of aspirin must be integrated in a global strategy for the primary prevention of coronary heart disease and should be probable recommended in males older than 50 years old presenting a higher risk of coronary heart disease (due to the number and intensity of risk factors) and low risk of adverse effects.

Age Factors↗
PubMed1995

Effect of osmotic stress on sarcolemmal integrity of isolated cardiomyocytes following transient metabolic inhibition.

OBJECTIVE: Exposure to hypotonic medium induces sarcolemmal rupture in metabolically inhibited cardiomyocytes. This study investigated the effect of osmotic stress applied during reoxygenation and the possible cooperation between cell swelling and hypercontracture to produce sarcolemmal disruption. METHODS: Freshly isolated adult rat myocytes were submitted to 60 min of metabolic inhibition (NaCN 2 mM). Reoxygenation was simulated by changing to one of 3 inhibitor free buffers: (1) normo-osmotic (312 mOsm); (2) hypo-osmotic (80 mOsm); (3) low Na+ normo-osmotic (312 mOsm). The contribution of hypercontracture-induced reoxygenation on sarcolemmal rupture was investigated in myocytes submitted to hypo-osmotic reoxygenation in presence of 2,3-butanedione monoxime 30 mM, a blocker of contractility. Recovery from mechanical fragility was studied by exposing cells to hypotonic buffer 20 or 40 min after restoration of metabolic activity, in either presence or absence of 2,3-butanedione monoxime. Two control groups without metabolic inhibition were used. One was exposed to osmotic stress after 60 min incubation in control conditions, the other was induced to hypercontract by exposure to hypo-osmotic, high-calcium buffer. Cell viability was assessed by the Trypan blue test. RESULTS: Before any intervention 81.9(1.2)% of cells were rod-shaped. After 60 min of metabolic inhibition most cells developed rigor contracture and only 16.4(1.8)% remained rod-shaped. Restoration of metabolic activity induced hypercontracture of most cells with rigor independently of buffer osmolality. Cell viability, however, significantly differed among groups: only 25.9(4.4)% of cells reoxygenated with hypo-osmotic buffer were viable vs. 74.1(7.6)% in the normo-osmotic reoxygenation group, and 82.9(2.9)% in the control group. Addition of 2,3-butanedione monoxime 30 mM during hypo-osmotic reoxygenation prevented hypercontracture and preserved cell viability. Delaying osmotic stress 20 or 40 min after the onset of reoxygenation did not improve viability [19.3(3.9) and 34.9(1.3)%, respectively]. Contractile blockade with 2,3-butanedione monoxime during the first 20 or 40 min of reoxygenation was associated with a reduction in the number of hypercontracted cells after the removal of the inhibitor but did not increase the proportion of hypercontracted viable cells (25% and 27%, respectively). CONCLUSIONS: (1) Osmotic stress following transient metabolic inhibition produces sarcolemmal disruption, and this effect is not related to the low Na+ concentration present in the hypo-osmotic buffer; (2) reoxygenation-induced hypercontracture cooperates with cell swelling to produce sarcolemmal disruption; and (3) osmotic fragility persists for at least 40 min after restoration of metabolic activity.

Animals↗
PubMed1995

[Effects of reoxygenation-induced osmotic edema on cell viability. Study using isolated myocytes].

OBJECTIVE: To investigate the hypothesis that reperfusion edema may kill myocytes. METHODS: Adult Sprague-Dawley rat hearts were perfused with a calcium free dissociation buffer containing collagenase 0.03% in a Langedorff system. Intact cells were selected and myocytes were cultured in adherent pretreated dishes. After 3 hours, 80% of cells were rod-shaped. Anoxia was simulated by means of metabolic inhibition by adding NaCN 2 mM to the control media, and reoxygenation by substituting this media with one of the following media non containing NaCN: 1) normo-osmotic (312 mOsm); 2) hypoosmotic (80 mOsm); 3) normo-osmotic with low Na+ (312 mOsm). A group of cells was kept with control media without metabolic inhibition and then submitted to simulated reoxygenation with hypoosmotic media (control group). The number of rod, square and round-shaped cells was monitored, and cell viability was assessed after 5 min of reoxygenation by the Trypan blue test. RESULTS: After 60 min of metabolic inhibition there were no differences in the % of cells without hypercontracture among groups reoxygenated with normo-osmotic, hypoosmotic, low Na+ normo-osmotic and control media (84 +/- 16, 74 +/- 10, 76 +/- 14 and 90 +/- 6% respectively (p = NS). After 5 min of reoxygenation, these values decreased (p < 0.001) to 19 +/- 6, 11 +/- 9 and 13 +/- 3% (p = NS), respectively, in groups with normo-osmotic, hypoosmotic, and low Na+ normo-osmotic reoxygenation, but were not modified in the control group (78 +/- 4). The % of viable cells (Trypan negative) preserved after 5 min of reoxygenation was 67 +/- 29% in the group with normo-osmotic reoxygenation, 31 +/- 23% in the group with hypoosmotic reoxygenation, and 85 +/- 12% in the group with low Na+ normo-osmotic reoxygenation (p < 0.001). Exposing cells without metabolic inhibition to hypoosmotic media resulted in no significative reduction of cell viability. CONCLUSION: Hypoosmotic reoxygenation following prolonged metabolic inhibition may kill viable myocytes. This effect is not due to the low Na+ concentration in the hypoosmotic medium.

Animals↗
PubMed1993

Analysis of myocardial oedema by magnetic resonance imaging early after coronary artery occlusion with or without reperfusion.

OBJECTIVE: The aim was to analyse the relationship between magnetic resonance (MR) imaging parameters and myocardial water content early after coronary occlusion with or without reperfusion. METHODS: 21 pigs were used. After 78 min of coronary occlusion (n = 7) or 48 min of coronary occlusion and 30 min of reperfusion (n = 14) the heart was excised. In seven animals in the reperfusion protocol the area at risk was perfused for 5 min with an anoxic buffer, starting 5 min after coronary occlusion. Serial T2 weighted and density weighted images of the heart were obtained from apex to base, by using a 1.5 tesla magnetic resonance imager. Water content was measured in samples from control and at-risk myocardium and relaxation parameters were measured in corresponding areas of the magnetic resonance images. RESULTS: Water content was 399(SEM 2) ml x 100 g-1 dry tissue in control myocardium, 427(8) in ischaemic myocardium, and 511(8) in reperfused myocardium (p < 0.001). Reperfused myocardium that had received intracoronary infusion contained less water than myocardium that did not: 498(9) v 534(4) ml x 100 g-1 (p = 0.003). T2 relaxation time and T2 weighted signal intensity in the different sampling sites of magnetic resonance images correlated well with water content in the corresponding myocardial samples (r = 0.76 and r = 0.83) and with the relative volume of extracellular space, as calculated by quantitative histology (r = 0.58 and r = 0.59, p < 0.001). The increase in T2 weighted signal intensity in the area at risk with respect to control myocardium allowed differentiation between ischaemic and reperfused myocardium [9(8)% v 63(3)% respectively]. The area at risk measured by MR imaging correlated very well with that determined at pathology by the fluorescein method (r = 0.92). CONCLUSIONS: Magnetic resonance imaging allows evaluation of myocardial oedema associated with acute coronary occlusion and reperfusion, and analysis of its spatial distribution. Changes in myocardial water content occurring early during acute myocardial infarction allow quantification of the area at risk and detection of reperfusion by magnetic resonance imaging.

Animals↗