Search PubMed⌕ Search

Biomedical subjects

J Elizaga

Publications and source records attributed to J Elizaga.

17 recordsLinked to original sources
PubMed2001

Parainfluenza virus 3 infection after stem cell transplant: relevance to outcome of rapid diagnosis and ribavirin treatment.

All 456 recipients of hemopoietic stem cell transplants (SCT) at the Hammersmith Hospital, London, from January 1990 through September 1996 were reviewed for parainfluenza virus (PIV) infections. Of the 24 (5.3%) PIV type 3 (PIV3)-infected patients, 10 had upper respiratory tract infection and all survived, but 8 of 14 with pneumonia died. A same-day immunofluorescence test diagnosed PIV3 infection in 20 (83%) of the 24 cases, but virus culture diagnosed only 10 (42%) of the 24 cases after a mean delay of 12 days. Eighteen PIV3-infected patients first received ribavirin at a median of 3 days after onset of symptoms, but, nevertheless, 2 patients shed PIV3 for 4 months. Six of 10 patients with pneumonia died despite early ribavirin therapy. The cause of death was not established by autopsy; 3 patients had concurrent infections, but in 3, only PIV3 was detected. The value of immunofluorescence testing for early diagnosis and treatment of PIV3 infection after SCT is demonstrated, but the outcome was not altered.

Adolescent↗
PubMed2000

[The practical clinical guidelines of the Sociedad Española de Cardiología on interventional cardiology: coronary angioplasty and other technics].

Interventional cardiology has had an extraordinary expansion in last years. This clinical guideline is a review of the scientific evidence of the techniques in relation to clinical and anatomic findings. The review includes: 1. Coronary arteriography. 2. Coronary balloon angioplasty. 3. Coronary stents. 4. Other techniques: directional atherectomy, rotational atherectomy, transluminal extraction atherectomy, cutting balloon, laser angioplasty and transmyocardial laser and endovascular radiotherapy. 5. Platelet glycoprotein IIb/IIIa inhibitors. 6. New diagnostic techniques: intravascular ultrasound, coronary angioscopy, Doppler and pressure wire. For the recommendations we have used the classification system: class I, IIa, IIb, III like in the guidelines of the American College of Cardiology and the American Heart Association.

Angioplasty, Balloon, Coronary↗
PubMed1999

Coronary stenting during rescue angioplasty after failed thrombolysis.

Compared with primary angioplasty [percutaneous transluminal coronary angioplasty (PTCA)], rescue PTCA is associated with lower angiographic success and higher reocclusion rates, especially after thrombolysis with tissue-type plasminogen activator (tPA). Although stent placement during primary PTCA has been demonstrated to be safe and even to improve the angiographic results achieved by balloon-alone PTCA, there are few data on stent placement during rescue PTCA after failed thrombolysis. This study sought to assess the feasibility and safety of stent implantation during rescue angioplasty in myocardial infarction after failed thrombolysis. The study population consisted of 20 patients with acute myocardial infarction referred for rescue PTCA after failed thrombolysis consecutively treated with coronary stenting. The thrombolytic agent was tPA in 15 patients (75%), streptokinase in 1 (5%), and anisoylated streptokinase plasminogen activator complex (APSAC) in 1 (5%); 3 patients (15%) were included in the INTIME II study (tPA vs. lanoteplase). After stenting, aspirin 200 mg daily plus ticlopidine 250 mg b.i.d. were administered. Thirty stents (1.5+/-1.0 per patient) were implanted. Angiographic success was achieved in 19 patients (95%). Two patients (10%) died, both because of severe bleeding complications. One patient (5%) suffered a reinfarction, but no patients suffered postinfarction angina or needed new target vessel revascularization. Eighteen patients (90%) were discharged alive and free of events. All these patients remained asymptomatic and free of target vessel revascularization at 6-month follow-up. Stent placement during rescue PTCA after failed thrombolysis is feasible and safe and is associated with a good angiographic result and clinical outcome. Bleeding complications seem to be, however, the main limitation of this reperfusion strategy.

Aged↗
PubMed1998

Multi-Link Stenting in Acute Myocardial Infarction.

ACS Multi-Linkª stent is a stainless steel balloon expandable stents composed of 12 rings connected by multiple links giving a great flexibility and radial strength. Multi-Link stenting offers good clinical and angiographic results in patients with unstable and stable angina, but there are few reports about Multi-Link stent placement in acute myocardial infarction (AMI). In this study, the experience of Multi-Link stenting during primary PTCA is described. RESULTS: 38 Multi-Link stents were placed in the culprit vessel in 34 patients with AMI. Mean age was 67 +/- 14 years, 25 (74%) were male, 12 (35%) were in Killip class III or IV and 20 (59%) had multi-vessel disease. All 38 Multi-Link stents (100%) could be successfully delivered. Angiographic success was achieved in 32 patients (94%). After stenting, stenosis decreased from 95 +/- 9% to 9 +/- 5% (p < 0.001) and minimal lumen diameter increased from 0.2 +/- 0.5 to 2.9 +/- 0.5 mm (p < 0.001). One patient (3%) suffered a subacute thrombosis requiring a new PTCA, but no patient needed surgical revascularization. Seven patients (20.6%; 95% CI: 8.7Ð37.9%) died during hospitalization, 6 of whom were in cardiogenic shock at admission. Mortality in patients with and without cardiogenic shock at admission was 85.7% (95% CI: 42.1Ð99.6%) and 3.7% (95% CI: 0.1%Ð20.0%) respectively (p < 0.001). CONCLUSION: The Multi-Link stent offers good angiographic results in patients with AMI. The in-hospital mortality in patients without cardiogenic shock at admission is low.

Journal Article↗
PubMed1997

[Registry of activities of the Hemodynamics and Interventional Cardiology Section in the year 1996].

The results of the Spanish Registry of Hemodynamic and Interventional Cardiology in 1996 are presented. The Registry collects the activity of 81 centers which constitutes all of the cardiac catheterization laboratories in Spain. The main activity was adult cardiac catheterization in 73 centers and exclusively pediatric cardiac catheterization in 8. A total of 63,961 diagnostic catheterization procedures were performed, which represents a 10.7% increase compared to 1995. This was mainly due to the increase in coronary angiographies. Coronary interventions increased by 21.4%, for a total number of 15,009 procedures. The ratio of coronary interventions per million inhabitants was 375. Success rates of coronary interventions (94%) and complications (2.9%) were similar to those registered in preceding years. In the specific field of revascularization devices, there has been a sustained and spectacular increase in the use of intracoronary stents in the last 3 years. In 1996, coronary stents were employed in 7,104 cases (47.3% of all coronary revascularization procedures) and 8,873 prosthesis were implanted, increasing two-fold the activity in that field when compared to 1995. Stent implantation was elective in 58% cases, and the complication rate was very low (1% subacute closure; 1.8% myocardial infarction and 0.9% mortality). Directional coronary atherectomy decreased by 47% in the last year whereas rotational atherectomy increased by 10% despite a reduction in the number of centers performing this technique. As in previous years, a slight decrease in adult valvuloplasties was noted. Pediatric interventional procedures (607) increased by 30% compared to the 1995 Registry.

Adult↗
PubMed1993

Q fever mimicking herpetic encephalitis.

We describe a patient with temporal lobe encephalitis associated with primary Coxiella burnetii infection who presented with CT and MRI findings suggestive of herpes simplex encephalitis and an initial improvement during treatment with acyclovir. Q fever should be considered in the differential diagnosis of patients whose manifestations suggest herpes encephalitis.

Coxiella burnetii↗
PubMed1992

Favorable effects of hyperosmotic reperfusion on myocardial edema and infarct size.

Myocardial water content and infarct size were studied in 39 pigs randomly assigned to a nonintervention group, a group with an intracoronary infusion of a control solution, and a group with a hyperosmotic infusion to 450 mosM by the addition of D-mannitol. The intracoronary solutions were selectively infused into the left anterior descending coronary artery just distal to the occlusion site starting 48 min after occlusion. Reperfusion was performed 3 min later and the infusion rate progressively tapered off over the following 33 min. Multiple myocardial fragments were then obtained in nine pigs, from endocardial, mesocardial, and epicardial regions of the ischemic and control myocardium. Water content measured after 48 h of dessication was significantly greater in the reperfused [530 +/- 7 ml/100 (mean +/- SE) g dry wt] compared with control myocardium (374 +/- 3; P less than 0.0001) and similar in reperfused control and isotonic infusion groups (556 +/- 7 and 543 +/- 8 ml/100 g dry wt); it was 491 +/- 11 with intracoronary D-mannitol infusion, representing 35% less increase (P less than 0.001). In the 30 remaining pigs, area at risk and infarct size were measured 24 h later by in vivo fluorescein and in vitro triphenyltetrazolium chloride. Infarct size was similar in control and in the isotonic reperfused hearts, 6.80 +/- 1.05 and 6.22 +/- 0.76% of ventricular weight, and smaller with D-mannitol, 4.46 +/- 0.46 (P less than 0.05). The ratio of infarct size to area at risk was also smaller [0.415 +/- 0.029 vs. 0.543 +/- 0.052 and 0.547 +/- 0.045 (P less than 0.02)].(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Selective inhibition of the contractile apparatus. A new approach to modification of infarct size, infarct composition, and infarct geometry during coronary artery occlusion and reperfusion.

BACKGROUND: Myocardial reperfusion is associated with calcium overload and cell contracture, mechanisms that may precipitate cell death. In this study, we tested the hypothesis that in vivo inhibition of this contracture could lead to cell preservation in an open-chest large animal model. METHODS AND RESULTS: Regional myocardium function was measured during a selective intracoronary infusion of 2,3-butanedione monoxime (BDM), a specific inhibitor of actin-myosin coupling, in the control state (10 pigs) and in a protocol of a 51-minute coronary occlusion followed by reperfusion (40 pigs). The effects on coronary artery blood flow in the basal state were also studied (seven pigs). Intramyocardial distribution of the infusate during coronary occlusion, myocardial water content after 30 minutes of reperfusion and area at risk, infarct size, type of histological necrosis, and infarct geometry after 24 hours of reperfusion were assessed. Methods used included electromagnetic flowmeter, radiolabeled microspheres, subendocardial sonomicrometers, fluorescein, triphenyl tetrazolium chloride and Masson's trichrome staining, and computer quantification of infarct edges. In the absence of ischemia, BDM infusion inhibited regional shortening in a dose-dependent manner up to full systolic bulging while producing marked regional increase in coronary blood flow. During early reperfusion, BDM reduced end-diastolic length 76% more than the control infusion (p less than 0.05) and increased systolic bulging by 420% compared with no change in control animals. The ratio of infarct size/area at risk was reduced by 31% with BDM (p less than 0.05), with striking modifications of infarct histology and infarct geometry; specifically, the extent of contraction band necrosis was reduced by 63% from 105.5 +/- 18.2 to 39.2 +/- 13.6 mm2 (p less than 0.02), and more patches of necrosis (6.5 +/- 2.1 versus 1.6 +/- 0.4, p less than 0.05) and higher contour (7.7 +/- 1.2 versus 5.03 +/- 0.2, p less than 0.05) and fractal (12.1 +/- 1.3 versus 7.8 +/- 0.2, p less than 0.05) indexes were found. CONCLUSIONS: Selective intracoronary infusion of BDM at doses inhibiting regional wall motion decreased infarct size after reperfusion. The effects of BDM on regional function, the reduction in contraction band necrosis at histology, and the peculiar configuration of these infarcts all suggest that inhibition of contracture can interfere with cell-to-cell progression of myocardial necrosis, supporting a role for contracture in reperfusion-induced cell death.

Actins↗
PubMed1990

Determinants of hemorrhagic infarcts. Histologic observations from experiments involving coronary occlusion, coronary reperfusion, and reocclusion.

Quantification of intramyocardial hemorrhage was performed in 69 pigs submitted to various protocols of coronary artery occlusion and reperfusion. The study groups include 1) permanent occlusion; 2) reperfusion after periods of coronary occlusion of 30, 45, 60, 90, and 120 minutes; 3) reperfusion with diltiazem and with 4) methoxamine after a 60-minute occlusion period; and 5) permanent reocclusion after a 30-minute period of reperfusion. Red blood cell counts were directly assessed by visual examination of histologic slices of myocardium and in a subgroup of animals by counts of red blood cells labeled with 99m-technetium pertechnetate. Hemorrhage occurs in infarcts reperfused after a duration of 45 minutes or more of coronary occlusion and after a period of reperfusion maintained for at least 30 minutes. Red blood cell counts were maximal in the mid portions of transmural sections of the infarcts, with decreasing values toward epicardium and endocardium. Diltiazem decreased total red blood cell counts, whereas methoxamine increased it and also caused subendocardial hemorrhage. The most powerful predictors of the severity of hemorrhage after sustained reperfusion were infarct size and higher blood pressure.

Animals↗
PubMed1989

Cell-to-cell interaction: a mechanism to explain wave-front progression of myocardial necrosis.

Histological sections performed 24 h after coronary occlusion in eight pigs displayed compact infarcts extending transmurally with well-defined edges; reconstruction and inspection of the area of necrosis showed a geometric distribution of the infarcts with very irregular, interdigitating edges always in continuity with the main mass of necrosis. Reperfusion in 32 pigs after periods of coronary occlusion of 90, 60, 45, and 30 min exponentially reduced infarct size and transmural extension of the infarct but did not modify its geometry. The two-dimensional size, progression, and geometry of the infarcts could be reproduced by a computer model. In the simulated infarcts, each myocardial cell within the area at risk was represented by a pixel. The algorithm included an inner loop, which determined at random at each iteration a status of reversible or irreversible damage to all pixels. The number of iterations could reproduce infarct of various sizes. With the addition of an index of transmural sensitivity to ischemia, progression of the infarct area could also be reproduced. The only possible means of reproducing the geometry of the infarct was to enter into the program a contiguity condition requiring a direct contact between irreversibly damaged pixels. These observations suggest that the physical interaction between cells is an important determinant of progression of necrosis during coronary occlusion.

Animals↗
PubMed1988

Influence of tachycardia and arterial hypertension on infarct size in the pig.

To investigate the clinically important but controversial question of how hypertension during coronary occlusion affects infarct size 24 pigs underwent 1 h occlusion of the mid left anterior descending coronary artery and 24 h reperfusion and were randomised to one of three treatment groups. In group 1 blood pressure was increased during the occlusion period by an infusion of methoxamine; in group 2 tachycardia was induced by atrial pacing; and in group 3 no intervention was performed. The area at risk and infarct size were quantified by digital planimetry of slices of myocardium previously marked with fluorescein and with triphenyl-tetrazolium. Methoxamine maintained mean aortic blood pressure at 117 (SEM8) mmHg during occlusion, whereas the values were 80(6) mmHg in group 2 and 67(9) mmHg in group 3. Pacing increased heart rate to 146(1) beats.min-1 in group 2; it was 103(5) in group 1 and 99(8) in group 3. The pressure-rate product achieved was similar in groups 1 and 2 and significantly higher than in group 3. The pathological studies showed infarct size to be moderately but significantly larger in group 1 (14[3.5]% of the left ventricle) and similar in groups 2 (10.5[3.9]%) and 3 (10.1[2.2]%). The ratio of infarct size to area at risk was also significantly higher (0.743[0.057]) in group 1 with no differences between group 2 (0.604[0.055]) and group 3 (0.613[0.027]). At similar pressure-rate product, infarct size was thus greater with hypertension but not with pacing alone, showing a deleterious effect of increasing blood pressure in this experimental model with negligible collateral blood flow.

Animals↗
PubMed1987

Diltiazem and progression of myocardial ischemic damage during coronary artery occlusion and reperfusion in porcine hearts.

This study was designed to investigate whether a cardioprotective intervention could delay the completion of necrosis so that subsequent reperfusion would be more useful. Thirty-six pigs were randomly allocated to treatment with diltiazem (15 micrograms/kg per min) or saline solution and to a 60 or 120 minute coronary occlusion period followed by reperfusion. The treatment was begun 15 minutes before coronary occlusion and terminated 75 minutes after reperfusion. Twenty-four hours after the procedure, the heart was sliced and incubated in triphenyltetrazolium chloride. The infarct area and the maximal transmural area of extension of the infarct were calculated by planimetry. The total number of red blood cells in a transmural section was also counted. In the pigs with a 60 minute coronary occlusion, diltiazem (compared with saline solution) significantly reduced infarct size from 9.7 +/- 1.5% of left ventricular mass to 5.9 +/- 0.6% (p less than 0.05) and the percent transmural extension from 0.72 +/- 0.05 to 0.61 +/- 0.05% (p less than 0.05). Red blood cell extravasation in the infarcted area was reduced from 161,934 +/- 59,905 to 78,525 +/- 46,484 cells/mm3 (p less than 0.05) with diltiazem and the percent transmural extension of the hemorrhagic necrosis from 70 +/- 10 to 36 +/- 15% (p less than 0.05). No such differences were observed in the 120 minute coronary occlusion groups. Mean red blood cell counts and the extent of hemorrhagic necrosis did not correlate with either infarct size or transmural extension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Myocardial reperfusion in the pig heart model: infarct size and duration of coronary occlusion.

The effect of coronary artery reperfusion on infarct size was studied in a pig heart model. Forty four open chest pigs underwent occlusion of the mid-left anterior descending artery. Fifteen minutes after occlusion the animals were randomised to one of five groups: reperfusion at 30, 45, 60, or 90 min after occlusion (groups 1-4) or permanent occlusion (group 5). Twenty four hours after coronary occlusion the pigs were killed. The heart was sectioned in slices, which were incubated in triphenyl-tetrazolium. Mean(SEM) infarct sizes calculated by planimetry were 0.46(0.42), 2.85(1.14), 9.74(1.65), 8.93(1.37), and 13.17(1.17)% of left ventricular mass in the five groups. The transmural extension of the infarct was 14.6(11.4), 42.1(12.9), 87.4(6.6), 96.2(3.2), and 100(0)% and a transmurality index used as an estimate of the mean extension of the infarct relative to wall thickness was calculated to be 0.08(0.06), 0.32(0.10), 0.72(0.06), 0.79(0.04), and 0.92(0.02) respectively. Infarct size was similar in groups 3-5, but significantly smaller in groups 1 and 2 (p less than 0.05). Infarct size and the transmurality index correlated exponentially with the duration of the occlusion (r = 0.80, p less than 0.01; and r = 0.95, p less than 0.001 respectively). These results indicate that in the pig heart model submitted to an acute coronary occlusion cell viability may be less than that suggested by previous canine studies. This observation is probably related to a less well developed collateral blood flow in the pig heart and may provide an experimental model that better resembles certain clinical conditions.

Acute Disease↗
PubMedDate not supplied

Intracoronary infusion of superoxide dismutase and reperfusion injury in the pig heart.

The effects of an intracoronary infusion of superoxide dismutase on infarct size were studied in 16 pigs submitted to a 48-min coronary occlusion of the mid left anterior descending coronary artery followed by reperfusion for 24 h. Areas at risk marked with fluorescein and infarct sizes calculated with triphenyl tetrazolium chloride staining 24 h after the occlusion were similar in the five control animals with coronary reperfusion alone, in the five animals with an intracoronary infusion of lactate Ringer initiated 3 min before reperfusion and maintained for 33 min and in the six animals with superoxide dismutase added to the solution of lactate Ringer and infused at a rate of 2500 units/min. The ratios infarct size/area at risk were respectively 0.50 +/- 0.10, 0.65 +/- 0.04 in the three study groups (NS). The extent of intramyocardial hemorrhage, evaluated by morphometric analysis was also similar 0.90 +/- 0.29 x 10(6), 0.70 +/- 0.14 and 1.62 +/- 0.42 red blood cells/mm3 of tissue (NS). The superoxide dismutase infusion, however, resulted in significantly fewer early reperfusion arrhythmias which involved 23 +/- 15 s of each minute electrocardiographic recording in the superoxide dismutase group, compared to 37 +/- 13 s in the lactate Ringer group and 45 +/- 14 s in the control group (p = 0.004). The lack of an effect of intracoronary infusion of superoxide dismutase on infarct size suggests that in this experimental model, extracellular superoxide radicals generated during early reperfusion have no major role on myocardial cell necrosis and microvascular damage. Reperfusion arrhythmias were, however, reduced.

Animals↗