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Jordi Soler-Soler

Publications and source records attributed to Jordi Soler-Soler.

At least 55 records · Page 3Linked to original sources
PubMed2003

Long-term follow-up of aortic intramural hematoma: predictors of outcome.

BACKGROUND: Aortic intramural hematoma (IMH) evolves very dynamically in the short-term to regression, dissection, or aortic rupture. The aim of the present study was to assess the long-term clinical and morphological evolution of medically treated IMH. METHODS AND RESULTS: Fifty of 68 consecutive patients with aortic IMH monitored clinically and by imaging techniques at 3, 6, and 12 months and annually thereafter were prospectively studied. Mean follow-up was 45+/-31 months. In the first 6 months, total IMH regression was observed in 14 and progression to aortic dissection in 18 patients; in 14 of these, the dissection was localized, and 12 later developed pseudoaneurysm. At the end of follow-up, the IMH had regressed completely without dilatation in 17 patients (34%), progressed to classical dissection in 6 (12%), evolved to fusiform aneurysm in 11 (22%), evolved to saccular aneurysm in 4 (8%), and evolved to pseudoaneurysm in 12 (24%). Evolution to dissection was related to echolucency (P<0.02) and to longitudinal extension of IMH (P<0.01). Multivariate analysis showed an independent association between regression and smaller maximum aortic diameter and between aneurysm formation and atherosclerotic ulcerated plaque and absence of echolucent areas in IMH. CONCLUSIONS: The most frequent long-term evolution of IMH is to aortic aneurysm or pseudoaneurysm. Complete regression without changes in aorta size is observed in one third of cases, and progression to classical dissection is less common. A normal aortic diameter in the acute phase is the best predictor of IMH regression without complications, and absence of echolucent areas and atherosclerotic ulcerated plaque are associated with evolution to aortic aneurysm.

Aortic Dissection↗
PubMed2003

Protection afforded by ischemic preconditioning is not mediated by effects on cell-to-cell electrical coupling during myocardial ischemia-reperfusion.

The end-effectors of ischemic preconditioning (IPC) are not well known. It has been recently shown that transgenic mice underexpressing the gap junction protein connexin43 (Cx43) cannot be preconditioned. Because gap junctions allow spreading of cell death during ischemia-reperfusion in different tissues, including myocardium, we hypothesized that the protection afforded by IPC is mediated by effects on gap junction-mediated intercellular communication. To test this hypothesis, we analyzed the effect of IPC (5 min ischemia-5 min reperfusion x 2) on the changes in electrical impedance (four electrode probe) and impulse propagation velocity (transmembrane action potential) induced by ischemia (60 min) and reperfusion (60 min) in isolated rat hearts. IPC (n = 8) reduced reperfusion-induced lactate dehydrogenase release by 65.8% with respect to control hearts (n = 9) (P = 0.04) but had no effect on the time of onset of rigor contracture (increase in diastolic tension), electrical uncoupling (sharp changes in tissue resistivity and phase angle in impedance recordings), or block of impulse propagation during ischemia. Normalization of electrical impedance during reperfusion was also unaffected by IPC. The lack of effect of IPC on ischemic rigor contracture and on changes in tissue impedance during ischemia-reperfusion were validated under in vivo conditions in pigs submitted to 48 min of coronary occlusion and 120 min of reperfusion. IPC (n = 12) reduced infarct size (triphenyltetrazolium) by 64.9% (P = 0.01) with respect to controls (n = 17). We conclude that the protection afforded by IPC is not mediated by effects on electrical coupling. This result is consistent with recent findings suggesting that Cx43 could have effects on cell survival independent on changes in cell-to-cell communication.

Action Potentials↗
PubMed2003

Pre-treatment with the Na+/H+ exchange inhibitor cariporide delays cell-to-cell electrical uncoupling during myocardial ischemia.

OBJECTIVE: Inhibition of Na(+)-H(+) exchange (NHE) delays the onset of myocardial rigor contracture during ischemia. The aim of this study was to analyse the effects of NHE inhibition on cell-to-cell electrical uncoupling during myocardial ischemia/reperfusion. METHODS: Twenty-six isolated rat hearts and 23 in situ porcine hearts were submitted to no-flow ischemia followed by reperfusion, with or without pre-treatment with cariporide (7 microM in rats and 3 mg/kg in pigs). Ischemic rigor and hypercontracture, conduction velocity and myocardial electrical impedance were monitored. RESULTS: Pre-treatment with cariporide delayed ATP depletion (luminescence assay in rat myocardium) and onset of rigor contracture (tension recordings or ultrasonic crystals) during ischemia both in rat and pig hearts (P<0.05). In addition, cariporide delayed the onset of sharp changes in tissue resistivity and phase angle in impedance recordings (four-electrode probes) from 10+/-1 to 13+/-1 min (P<0.001) in rat hearts, and from 22+/-1 to 38+/-2 min (P<0.001) in pigs. Blockade of impulse propagation (transmembrane action potentials in rat hearts) was also markedly delayed by cariporide (from 14+/-1 to 20+/-1 min, P<0.001). Reperfusion-induced LDH release in rat hearts and infarct size in pigs were markedly reduced by pre-treatment with cariporide. CONCLUSIONS: Inhibition of NHE with cariporide slows the progression of ischemic injury during myocardial ischemia, and delays the onset of cell-to-cell electrical uncoupling.

Action Potentials↗
PubMed2003

Effect of ischemia on soluble and particulate guanylyl cyclase-mediated cGMP synthesis in cardiomyocytes.

The effect of simulated ischemia [hypoxia, no glucose, extracellular pH (pH(o)) 6.4] on cGMP synthesis induced by stimulation of soluble (sGC) or particulate guanylyl cyclase (pGC) was investigated in adult rat cardiomyocytes. Intracellular cGMP content was measured after stimulation of sGC by S-nitroso-N-penicillamine (SNAP) or stimulation of pGC by natriuretic peptides [urodilatin (Uro), atrial natriuretic peptide (ANP), or C-type natriuretic peptide (CNP)] for 1 min in the presence of phosphodiesterase inhibitors. After 2 h of simulated ischemia, a decrease of >50% was observed in pGC-dependent cGMP synthesis, but no significant change was observed in sGC-dependent cGMP synthesis. The reduction in cGMP synthesis caused by simulated ischemia was mimicked by extracellular acidosis (pH(o) 6.4), which decreased pGC-mediated cGMP synthesis without altering sGC-mediated cGMP synthesis. An extreme sensitivity of pGC activity to low pH was also observed in membrane cell fractions. Hypoxia without acidosis (pH(o) 7.4) profoundly depressed cellular ATP content but did not change the response to SNAP, Uro, or ANP (selective agonists of pGC type A receptor). Only cGMP synthesis in response to CNP (a selective agonist of pGC type B receptor) was significantly reduced by ATP depletion. These data support the relevance of intracellular pH as a modulator of cGMP and suggest that, in ischemic cardiomyocytes, synthesis of cGMP would be mainly nitric oxide dependent.

Acidosis↗
PubMed2003

Migraine with aura related to the percutaneous closure of an atrial septal defect.

We report a case of a 31-year-old woman who presented migraine attacks with aura within the 48 hr after transcatheter closure of an atrial septal defect with the Amplatzer septal occluder device. The migraine attacks persisted for 3 months, and all examinations performed to rule out a thromboembolic origin of migraine were negative.

Adult↗
PubMed2003

[Evolution of systolic function and myocardial perfusion, evaluated by gated-SPECT, in the first year after acute myocardial infarction].

INTRODUCTION AND OBJECTIVES: Systolic function and myocardial perfusion are evaluated before hospital discharge and can change during follow-up. The purpose of this study was to evaluate these parameters by gated-SPECT in the first year after acute myocardial infarction. PATIENTS AND METHOD: We studied 74 consecutive patients with a first uncomplicated acute myocardial infarction (49 infero-lateral and 25 anterior) by stress-rest 99mTc-tetrofosmin and rest-gated-SPECT before hospital discharge (6-8 days after admission) and one year after myocardial infarction. RESULTS: The ejection fraction (EF) increased > 5% in 51% of infero-lateral infarcts and 28% of non-revascularized anterior infarcts. EF increased significantly (48.4 8% to 54.6 8.7%; p < 0.0001, mean difference: 6.2; 95% IC, 2.8-9.5) and systolic volume decreased (51.3 19.2 ml to 44.3 19.4 ml; p = 0.001; mean diff.: 7.67; 95% IC, 1.5-13.8) in infero-lateral infarctions. The rest perfusion index in the necrotic region improved (2.3 0.57 to 2.17 0.58; p = 0.004; mean diff.: 0.18; 95% IC, 0.003-0.36) in infero-lateral infarcts and the ischemia index remained unchanged between the first and second studies. CONCLUSIONS: Left ventricular systolic function can change during the first year of evolution, a significant improvement being seen in infero-lateral infarctions. The ejection fraction increased > 5% in half of these patients, as opposed to only a quarter of anterior infarctions. This improvement was associated to increased myocardial perfusion at rest.

Aged↗
PubMed2003

[Post-infarction ventricular septal defect treated during the acute phase by transcatheter closure with an Amplatzer septal occluder].

A 75-year-old man had a large anterior myocardial infarction complicated by a ventricular septal defect, which was treated in the first 48 h by transcatheter closure using the Amplatzer septal occluder. Treatment was successful (with only mild residual post-procedure shunting) and coronary angioplasty with stent implantation at the point of occlusion of the middle left anterior descending artery was performed in a later intervention. However, the patient died 7 days after the procedure as a result of sepsis and ventricular failure.

Animals↗
PubMed2003

Cariporide preserves mitochondrial proton gradient and delays ATP depletion in cardiomyocytes during ischemic conditions.

The mechanism by which inhibition of Na+/H+ exchanger (NHE) reduces cell death in ischemic-reperfused myocardium remains controversial. This study investigated whether cariporide could inhibit mitochondrial NHE during ischemia, delaying H+ gradient dissipation and ATP exhaustion. Mouse cardiac myocytes (HL-1) were submitted to 1 h of simulated ischemia (SI) with NaCN/deoxyglucose (pH 6.4), with or without 7 microM cariporide, and mitochondrial concentration of Ca2+ (Rhod-2), 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) and the charge difference across the mitochondrial membrane potential (Deltapsim, JC-1) were assessed. ATP content was measured by bioluminescence and mitochondrial swelling by spectrophotometry in isolated mitochondria. Cariporide significantly attenuated the acidification of the mitochondrial matrix induced by SI without modifying Deltapsim decay, and this effect was associated to a delayed ATP exhaustion and increased mitochondrial Ca2+ load. These effects were reproduced in sarcolemma-permeabilized cells exposed to SI. In these cells, cariporide markedly attenuated the fall in mitochondrial pH induced by removal of Na+ from the medium. In isolated mitochondria, cariporide significantly reduced the rate and magnitude of passive matrix swelling induced by Na+ acetate. In isolated rat hearts submitted to 40-min ischemia at different temperatures (35.5 degrees, 37 degrees, or 38.5 degrees C) pretreatment with cariporide limited ATP depletion during the first 10 min of ischemia and cell death (lactate dehydrogenase release) during reperfusion. These effects were mimicked when a similar ATP preservation was achieved by hypothermia and were abolished when the sparing effect of cariporide on ATP was suppressed by hyperthermia. We conclude that cariporide acts at the mitochondrial level, delaying mitochondrial matrix acidification and delaying ATP exhaustion during ischemia. These effects can contribute to reduce cell death secondary to ischemia-reperfusion.

Acids↗
PubMed2002

Lack of effect of glycoprotein IIb/IIIa blockade on myocardial platelet or polymorphonuclear leukocyte accumulation and on infarct size after transient coronary occlusion in pigs.

OBJECTIVES: We sought to assess the effect of glycoprotein (GP) IIb/IIIa blockade on myocardial platelet and polymorphonuclear leukocyte accumulation and on infarct size after coronary injury and transient coronary occlusion (CO) in pigs. BACKGROUND: It has been suggested that platelet GP IIb/IIIa blockade might reduce the severity of microvascular damage after reperfusion. METHODS: Sixteen thiopental-anesthetized, open-chest pigs, in whom platelets had been labeled with technetium-99m (99mTc) on the previous day, were submitted to catheter-induced left anterior descending coronary artery (LAD) injury followed by 55 min of CO and 5 h of reperfusion. Five minutes before reflow, the animals were blindly allocated to receive lamifiban (intravenous bolus of 250 microg/kg body weight and continuous infusion of 3 microg/kg per min) or saline. RESULTS: Lamifiban had a rapid and potent platelet anti-aggregatory effect, as demonstrated by significant prolongation of the bleeding time and profound (approximately 90%) inhibition of ex vivo platelet aggregation, and completely prevented the development of cyclic flow reductions of the LAD (0 vs. 5 +/- 1, one of them followed by re-occlusion, in control animals, p = 0.005). However, compared with animals receiving placebo, those treated with lamifiban had a similar (p = NS) content of (99m)Tc platelets in the reperfused myocardium (288 +/- 40% vs. 205 +/- 27% of the value in the control region, respectively) and similar myeloperoxidase activity (0.50 +/- 0.17 U/g vs. 0.47 +/- 0.17 U/g, respectively) and infarct size (46.8 +/- 12.0% vs. 49.8 +/- 10.5% of the area at risk, respectively). Arteriolar platelet thromboemboli were very rarely seen on histologic analysis. Lamifiban did not modify platelet P-selectin expression in additional studies. CONCLUSIONS: Platelet GP IIb/IIIa blockade has a potent antithrombotic effect at the culprit lesion, but does not significantly reduce the magnitude of microvascular platelet accumulation or myocardial damage after transient CO.

Acetates↗
PubMed2002

Ventricular fibrillation during acute coronary occlusion is related to the dilation of the ischemic region.

Myocardial stretch induces several electrophysiological changes and arrhythmias, but little is known on its possible role in triggering ventricular fibrillation (VF) during acute coronary occlusion. In thiopental-anesthetized, open-chest pigs submitted to a 40-min ligation of the left anterior descending coronary artery, the association between the early increase in end-diastolic length (measured by means of ultrasonic crystals) in the ischemic region and subsequent VF was analyzed. Animals received no treatment (n = 35) or intravenous nitroglycerin (2.5 microg/kg/min for 20 min, starting 10 min after coronary occlusion, n = 8) or Gd(3+) (80 microM/kg for 35 min, starting 5 min before occlusion, n = 15). Twenty-four animals (41 %) had VF, 16 to 39 min after coronary occlusion. The magnitude of ischemic dilation and the incidence of VF were similar among groups. End-diastolic length in the ischemic region 15 min after coronary occlusion was 115.7 +/- 1.2 % of baseline in animals with VF and 111.4 +/- 0.9 % in those without (P = 0.007), and was the strongest predictor of this arrhythmia (P = 0.003) after adjusting for treatment and other possible confounding variables. Thus, the dilation of the ischemic region is closely and independently associated with VF following coronary occlusion. Although the interventions tested in the present study failed to protect against this arrhythmia, the results strongly suggest an influence of ischemic dilation on VF.

Acute Disease↗
PubMed2002

Effect of inhibition of Na(+)/Ca(2+) exchanger at the time of myocardial reperfusion on hypercontracture and cell death.

OBJECTIVE: There is recent evidence that Ca(2+) influx via reverse mode Na(+)/Ca(2+) exchange (NCX) at the time of reperfusion can contribute to cardiomyocyte hypercontracture. However, forward NCX is essential for normalization of [Ca(2+)](i) during reperfusion, and its inhibition may be detrimental. This study investigates the effect of NCX inhibition with KB-R7943 at the time of reperfusion on cell viability. METHODS: The effect of several concentrations of KB-R7943 added at reperfusion was studied in Fura-2 loaded quiescent cardiomyocytes submitted to 40 min of simulated ischemia (NaCN 2 mM, pH 6.4), and in rat hearts submitted to 60 min of ischemia. [Ca(2+)](i) and cell length were monitored in myocytes, and functional recovery and LDH release in isolated hearts. From these experiments an optimal concentration of KB-R7943 was identified and tested in pigs submitted to 48 min of coronary occlusion and 2 h of reperfusion. RESULTS: In myocytes, KB-R7943 at concentrations up to 15 microM reduced [Ca(2+)](i) rise and the probability of hypercontracture during re-energization (P<0.01). Nevertheless, in rat hearts, the effects of KB-R7943 applied during reperfusion after 60 min of ischemia depended on concentration and timing of administration. During the first 5 min of reperfusion, KB-R7943 (0.3-30 microM) induced a dose-dependent reduction in LDH release (half-response concentration 0.29 microM). Beyond 6 min of re-flow, KB-R7943 had no effect on LDH release, except at concentrations > or = 15 microM, which increased LDH. KB-R7943 at 5 microM given during the first 10 min of reflow reduced contractile dysfunction (P=0.011), LDH release (P=0.019) and contraction band necrosis (P=0.014) during reperfusion. Intracoronary administration of this concentration during the first 10 min of reperfusion reduced infarct size by 34% (P=0.033) in pigs submitted to 48 min of coronary occlusion. CONCLUSIONS: These results are consistent with the hypothesis that during initial reperfusion NCX activity results in net reverse mode operation contributing to Ca(2+) overload, hypercontracture and cell death, and that NCX inhibition during this phase is beneficial. Beyond this phase, NCX inhibition may impair forward mode-dependent Ca(2+) extrusion and be detrimental. These findings may help in the design of therapeutic strategies against lethal reperfusion injury, with NCX as the target.

Analysis of Variance↗
PubMed2002

A multicenter study of the tolerability of tirofiban versus placebo in patients undergoing planned intracoronary stent placement.

BACKGROUND: The use of intravenous glycoprotein IIb/IIIa-receptor antagonists has been shown to improve outcomes in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Tirofiban has shown benefit in a wide range of patients presenting with acute coronary syndromes. Although this agent has been used in patients undergoing percutaneous coronary intervention, a literature search identified no prospective data comparing tirofiban with placebo in patients undergoing planned intracoronary stent placement. OBJECTIVE: This study examined the tolerability of tirofiban in patients undergoing percutaneous intervention with planned intracoronary stent placement. METHODS: This was a multinational, multicenter, prospective, randomized, double-blind, placebo-controlled trial in patients scheduled to undergo PTCA with planned intracoronary stent placement. Patients were randomized in a 3:2 ratio to receive tirofiban as an intravenous bolus (10 microg/kg over 3 minutes) and maintenance infusion (0.10 microg/kg per minute for 36 hours) or a bolus and infusion of placebo. All patients received periprocedural aspirin and heparin and an optional postprocedural thienopyridine (ticlopidine or clopidogrel). Laboratory and safety monitoring were performed throughout the 36 hours after the procedure and at hour 40 or hospital discharge. The primary end point was the proportion of patients with bleeding, defined according to Thrombolysis in Myocardial Infarction (TIMI) trial criteria. The number of patients with cardiac events (death, myo- cardial infarction, urgent revascularization) during the first 30 days after stent placement was also assessed. RESULTS: Eight hundred ninety-four patients (536 tirofiban, 358 placebo) were enrolled, all of whom received aspirin and heparin periprocedurally and optional ticlopidine or clopidogrel after the procedure. No significant between-group differences were observed in the incidence of TIMI major bleeding (0.2% tirofiban, 0.6% placebo) or any TIMI bleeding (3.2% and 1.7%, respectively). The incidence of TIMI minor bleeding was higher with tirofiban than with placebo (2.8% vs 0.6%). The 30-day incidence of the composite end point of any cardiac event was 3.9% in both groups. CONCLUSIONS: On a background of concomitant aspirin, heparin, and a thienopyridine, tirofiban was generally well tolerated in patients undergoing PTCA with planned intracoronary stent placement. Further investigation is needed to ascertain the optimal dosing of tirofiban and heparin to achieve reductions in ischemic complications of intracoronary stenting with an acceptable incidence of bleeding complications.

Angioplasty, Balloon, Coronary↗
PubMed2002

[Baseline characteristics and determinants of outcome in a patient population admitted for heart failure to a general hospital].

INTRODUCTION AND OBJECTIVES: To assess baseline characteristics, management patterns, and clinical outcomes after 18 months in patients diagnosed as heart failure in a tertiary hospital in Catalonia, Spain. METHODS: The records of all 265 patients admitted to the Hospital General Vall d'Hebron from July through December 1998 with a diagnosis of heart failure who met study criteria were identified and analyzed. Patients were interviewed by telephone 18 months later. RESULTS: The mean age of the study population was 75 12 years, 42% were male, 19% were admitted for causes other than heart failure, and 62% had significant comorbidity. Ventricular function was assessed in 68% (preferentially patients with a better prognosis), and was considered normal in 41%. Angiotensin-converting enzyme inhibitors or angiotensin II antagonists were used in 54%, and beta-blockers in 4%. The 18-month mortality was 46% (77% cardiac mortality). Multivariate predictors of death were older age, severe or previous heart failure, and serious comorbidity. At 18 months, 69% of survivors were in functional classes I or II. CONCLUSIONS: 1) As in other geographic areas, patients in this study were an older population with poor survival; 2) local patterns of care definitely need improvement; 3) comorbidity is important for prognosis, and 4) a significant proportion of survivors enjoy an acceptable quality of life long after discharge.

Aged↗
PubMed2002

[Methods of reporting research-results and their influence on decision-making by cardiologists prescribing drugs for primary and secondary prevention].

OBJECTIVES: To assess the influence of the form of presentation of the results of clinical trials on the quantitative perceptions of cardiologists regarding the efficacy of drugs for the primary and secondary prevention of coronary heart disease and their likelihood of prescribing them. METHOD: We conducted a survey of 1,408 cardiologists in Spain who were randomly allocated of three questionnaires that used different measurements to evaluate the impact of published clinical trials. RESULTS: Five-hundred and fifty-nine questionnaires (40%) were suitable for analysis. On a scale of 0 to 10, the following mean efficacy estimates were obtained from questionnaire items that focused, respectively, on the results of clinical trials in terms of relative risk reduction, absolute risk reduction, and number needed to treat: primary prevention with statins: 6.79, 6.38 and 5.43; primary prevention with aspirin: 6.84, 5.06 and 4.25; secondary prevention with statins: 8.16, 7.76 and 7.54; secondary prevention with ACE inhibitors: 7.11, 7.81 and 7.19, and secondary prevention with beta-blockers: 7.22, 7.43 and 6.98. The likelihood that a drug treatment would be prescribed was not influenced very much by the form of presentation of the trial results. CONCLUSIONS: Presenting the results of clinical trials in the form of relative risk reduction, as compared with presenting results in terms of absolute risk reduction or number needed to treat, led to overestimation of the efficacy of interventions without influencing the likelihood of prescribing a given drug therapy.

Adrenergic beta-Antagonists↗
PubMed2002

Platelets activated by transient coronary occlusion exacerbate ischemia-reperfusion injury in rat hearts.

Platelets (Plt) accumulate in reperfused myocardium but their effect on myocardial necrosis has not been established. We tested the hypothesis that the effect of Plt depends on their activation status. Pig Plt were obtained before 48 min of coronary occlusion (pre-CO-Plt), 10 min after reperfusion (R-Plt), or after a 60-min sham operation (sham-Plt). Plt were infused into isolated rat hearts (n = 124) and subsequently submitted to 60 min of ischemia and 60 min of reperfusion. P-selectin expression was higher (P = 0.02) in R-Plt than in pre-CO-Plt or sham-Plt. Lactate dehydrogenase (LDH) release during reperfusion was similar in hearts receiving pre-CO-Plt, sham-Plt, or no Plt, but R-Plt increased LDH release by 60% (P = 0.004). Activation of pre-CO-Plt with thrombin increased P-selectin expression and LDH release (P < 0.001), and these results were unaffected by tirofiban. There was a close correlation between P-selectin expression and LDH release (r = 0.84; P < 0.001), and myocardial Plt accumulation (r = 0.85; P < 0.001). We conclude that the deleterious effect of Plt on reperfused myocardium depends on their activation status as represented by P-selectin expression, which is enhanced by ischemia-reperfusion.

Animals↗