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Biomedical subjects

J Soler-Soler

Publications and source records attributed to J Soler-Soler.

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

Dipyridamole administration at the end of an insufficient exercise Tc-99m MIBI SPECT improves detection of multivessel coronary artery disease in patients with previous myocardial infarction.

To demonstrate that the administration of dipyridamole at the end of an insufficient maximal subjective exercise test can improve the diagnostic accuracy of single-photon emission computed tomography in patients with previous myocardial infarction, 209 consecutive patients were studied with technetium-99m methoxyisobutyl isonitrile single-photon emission computed tomography and coronary angiography. Patients were divided in 3 groups: group 1, 107 patients with sufficient exercise testing; group 2, 55 patients with insufficient exercise testing; group 3, 47 patients with insufficient exercise testing in whom intravenous dipyridamole (0.56 mg/kg over 4 minutes) was administered at the end of exercise. In groups 1 and 3 the sensitivity values for the diagnosis of multivessel disease were significantly higher (80% and 76%, respectively) than those in group 2 (59% [p = 0.009 and p = 0.02, respectively]). Specificity and predictive values were not different among the 3 groups. Thus, in patients with previous infarction in whom adequate levels of exercise could not be achieved, dipyridamole administration at the end of exercise significantly increased the sensitivity for diagnosing multivessel disease.

Cardiac Catheterization↗
PubMed2000

Urodilatin limits acute reperfusion injury in the isolated rat heart.

OBJECTIVES: Hypercontracture is an important mechanism of myocyte death during reperfusion. cGMP modulates the sensitivity of contractile myofilaments to Ca2+, and increasing cGMP concentration during the last minutes of anoxia prevents reoxygenation-induced hypercontracture in isolated cardiomyocytes. The purpose of this study was to determine whether stimulation of particulate guanylyl cyclase with the natriuretic peptide urodilatin, given at the time of reperfusion, reduces myocardial necrosis in the rat heart submitted to transient ischemia. METHODS: Isolated rat hearts (n = 38) were submitted to either 40 or 60 min of no-flow ischemia and 2 h of reperfusion, and were allocated to receive or not receive 0.05 microM urodilatin during the first 15 min of reperfusion or non-reperfusion treatment. RESULTS: A marked reduction in myocardial cGMP concentration was observed in control hearts during reperfusion after 40 or 60 min of ischemia. Urodilatin significantly attenuated cGMP depletion during initial reperfusion, markedly improved contractile recovery after 40 min of ischemia (P < 0.0309), and reduced reperfusion-induced increase in left ventricular end-diastolic pressure (P = 0.0139), LDH release (P = 0.0263), and contraction band necrosis (P = 0.0179) after 60 min of ischemia. The beneficial effect of urodilatin was reproduced by the membrane permeable cGMP analog 8-Bromo-cGMP. CONCLUSIONS: These results indicate that reduced cGMP concentration may impair myocyte survival during reperfusion. Stimulation of particulate guanylyl cyclase may appear as a new strategy to prevent immediate lethal reperfusion injury.

Analysis of Variance↗
PubMed2000

Strategy for optimal aortic regurgitation quantification by Doppler echocardiography: agreement among different methods.

BACKGROUND: Although different Doppler methods have been validated for aortic regurgitation quantification, the benefit of combining information from different methods has not been defined. METHODS: Our study included 2 phases. In the initial phase (60 patients), Doppler parameters (jet width, short-axis jet area, apical jet area, regurgitant fraction from pulmonary and mitral flow, and deceleration slope) were correlated with angiography; range values for each severity grade were defined and intraobserver and interobserver and intermachine variability were studied. In the validation phase (158 patients), defined value ranges were prospectively tested and a strategy based on considering as the definitive severity grade that in which the two best methods agreed was tested. RESULTS: Jet width had the best correlation with angiography (r = 0.91), and its ratio with the left ventricular outflow diameter did not improve the correlation (r = 0.85) and decreased reproducibility. Apical jet area and regurgitant fraction from pulmonary flow permitted acceptable quantification (r = 0.87 and 0.86, respectively) but with worse reproducibility. The other methods were not assessable in 20% to 30% of studies. Concordance with angiography decreased in jet width when the jet was eccentric (90% vs 77%, P <.01), in apical jet area when mitral valve disease was present (84% vs 65%, P <.02), and in short-axis jet area and regurgitant fraction from pulmonary flow with concomitant aortic stenosis (77% vs 44%, P <.002 and 77% vs 53%, P <.02, respectively). Agreement with angiography was very high (94 [95%] of 99) when severity grade coincided in both jet width and apical jet area. In 59 cases without concordance, regurgitant fraction from pulmonary flow was used as a third method. Overall, this strategy permitted concordance with angiography in 146 patients (92%). CONCLUSIONS: Jet width is the best predictor in aortic regurgitation quantification by Doppler echocardiography. However, better results were obtained when a strategy based on concordance between jet width and another Doppler method was established, particularly when the jet was eccentric.

Adult↗
PubMed2000

Neurally mediated depressor hemodynamic response induced by intracoronary catheter balloon inflation in pigs.

OBJECTIVES: To assess whether intracoronary catheter balloon inflation triggers a neurally mediated hemodynamic response that interacts with the ischemia-induced myocardial dysfunction. METHODS: Forty-eight chloralose anesthetized pigs underwent a 60 s intraluminal catheter balloon inflation of the proximal left anterior descending (LAD) coronary artery before and after one of these treatments: disruption of LAD pericoronary nerves with phenol (n=6), bilateral stellectomy (n=8), bilateral cervical vagotomy (n=6), atropine (n=5), and ganglionic blockade with hexamethonium (n=10). In 13 other pigs, we assessed the reproducibility of two balloon inflations spaced 15 min (n=6) or 60 min (n=7). The ECG, left ventricular (LV) pressure, and LV dP/dt were recorded during each intervention. Right ventricular (RV) pressure, RV dP/dt, and aortic blood flow were also measured in a subset of pigs. RESULTS: Balloon inflation induced an early (10 s) and reproducible (ANOVA, P<0.001) drop in systolic pressure and peak dP/dt; a decrease in aortic blood flow; a rise in end-diastolic pressure; and elevation of the ST segment. Pericoronary denervation, stellectomy and ganglionic blockade attenuated (P<0.001) the drop in LV parameters during coronary inflation, but atropine and vagotomy did not. CONCLUSIONS: A depressor hemodynamic response subserved by pericoronary nerves worsens the LV dysfunction induced by brief coronary catheter balloon inflation in anesthetized pigs. Cholinergic fibers do not appear to play a major role.

Analysis of Variance↗
PubMed2000

L-Arginine administration prevents reperfusion-induced cardiomyocyte hypercontracture and reduces infarct size in the pig.

OBJECTIVE: Stimulation of cGMP synthesis protects cardiomyocytes against reoxygenation-induced hypercontracture. The purpose of this study was to determine whether L-arginine supplementation has a protective effect against reperfusion-induced hypercontracture and necrosis in the intact animal. METHODS: Twenty-four Large-White pigs were randomized to receive either 100 mg/kg of L-arginine i.v. or vehicle 10 min before 48 min of coronary occlusion and 2 h of reperfusion. Hemodynamic variables, coronary blood flow and myocardial segment length changes (piezoelectric crystals) were monitored. Postmortem studies included quantification of myocardium at risk (in vivo fluorescein), infarct size (triphenyltetrazolium reaction), myocardial myeloperoxidase activity and histological analysis. Systemic, coronary vein, and myocardial cGMP concentration were measured in additional animals. RESULTS: Administration of L-arginine had no significant effect in hemodynamics or coronary blood flow. During reperfusion, myocardial cGMP content was reduced in the LAD as compared to control myocardium (P=0.02). L-Arginine increased myocardial cGMP content and caused a transient increase in plasma cGMP concentration during the initial minutes of reperfusion (P=0.02). The reduction in end-diastolic segment length induced by reperfusion, reflecting hypercontracture, was less pronounced in the L-arginine group (P=0.02). Infarct size was smaller in pigs receiving L-arginine (47.9+/-7.2% of the area at risk) than in controls (62.9+/-4.9%, P=0.047). There were no differences between groups in leukocyte accumulation in reperfused myocardium (P=0.80). CONCLUSION: L-Arginine supplementation reduces myocardial necrosis secondary to in situ ischemia-reperfusion by a direct protective effect against myocyte hypercontracture.

Analysis of Variance↗
PubMed2000

Dynamic intracoronary thrombosis does not cause significant downstream platelet embolization.

OBJECTIVE: A mural intracoronary thrombus is a potential source of platelet emboli that may obstruct downstream microvessels, but this phenomenon has not been characterized. The present study aimed to assess the magnitude of myocardial platelet accumulation downstream of a mural intracoronary thrombus and its modification by a concomitant transient coronary occlusion (OC) or by treatment with aspirin. METHODS: The myocardial content of 99mTc-labelled platelets was analyzed in 26 pigs submitted to intimal injury of the left anterior descending coronary artery (LAD) followed by no intervention (n=6), 25-min OC (n=6), or 48-min OC preceded (n=8) or not (n=6) by intravenous administration of 250 mg aspirin. RESULTS: After 2 h, 24 animals had had 12+/-1 cyclic flow reductions (CFRs) reflecting dynamic LAD thrombosis. Myocardial platelet content in the inferior region was similar among groups. Platelet content in the LAD region was not significantly different to that in the inferior region (129+/-19%, P=NS) in the no intervention group, but was increased following OC (172+/-20 and 312+/-71% after 25- and 48-min OC, respectively, P<0.05). Pre-treatment with aspirin lessened the number of CFRs but did not reduce platelet accumulation in LAD myocardium (483+/-148%). Myocardial platelet accumulation was not associated with the magnitude of platelet deposition in the LAD nor with the number of CFRs, but was correlated with myeloperoxidase activity (r=0.91, P<0.001) and with infarct size (r=0.52, P=0.05). Histological analysis frequently showed sparse platelets or small platelet or leukoplatelet aggregates in small vessels, but arteriolar emboli were rare. In none of seven additional experiments coronary angiography showed obstructions of arterial branches during CFRs. CONCLUSION: The magnitude of platelet embolization from a mural intracoronary thrombus into downstream myocardium is small despite the presence of repetitive CFRs.

Analysis of Variance↗
PubMed2000

[Morphologic classification of hypertrophic cardiomyopathy with myocardial single photon emission tomography. Comparison with echocardiographic classification].

INTRODUCTION AND OBJECTIVES: The aim of this study was to compare different morphologic types of hypertrophic cardiomyopathy obtained by single photon emission tomography to those obtained by echocardiogram. MATERIALS AND METHODS: In 76 (64%) out of 119 patients with hypertrophic cardiomyopathy the echocardiogram permitted an optimal visualization of all left ventricular segments in the short axis view and consequent classification to one of the six morphological types: type I (septal anterior hypertrophy), type II (septal anterior and septal posterior hypertrophy), type III (septal and antero-lateral hypertrophy), type IV (antero-lateral and/or septal posterior hypertrophy), type V (concentric hypertrophy) and type VI (apical hypertrophy). Without knowledge of echo data, two experienced observers included the short axis of single photon emission tomography images at rest (99mTc-tetrofosmin) to one of those types. RESULTS: Global concordance between echocardiogram and single photon emission tomography was 75%. Type III was the most frequent both in echo (76%) and in single photon emission tomography (74%) and type III produced the majority of discrepancies. SPET identified 4 patients with a predominant septal and inferior hypertrophy, that did not correspond to any of the 6 types of echocardiographic classification and had been previously classified as type III by echo in 3 cases and as type V in 1 case. CONCLUSIONS: There was agreement between echo and single photon emission tomography in the morphological classification of most of the patients (75%) with hypertrophic cardiomyopathy. Nevertheless, some discrepancies were observed for the type III echocardiogram.

Cardiomyopathy, Hypertrophic↗
PubMed2000

[Myocardial SPET in hypertrophic cardiomyopathy].

INTRODUCTION AND OBJECTIVES: The aim of this study was to evaluate the diagnostic accuracy of myocardial SPET in patients with hypertrophic cardiomyopathy (HC). PATIENTS AND METHODS: One hundred and six consecutive patients (aged 53 +/- 12 years, 50 women, 66 with dynamic obstruction) with an echocardiographic diagnosis of HC were studied with exercise-rest myocardial SPET with 99mTc-tetrofosmin. Forty-six (43%) of these patients had chest pain and in 31 (29%) a coronary angiography was performed. Fifty-six per cent of the patients were treated with beta-blockers and 23% with verapamil. RESULTS: Angina during the exercise test was observed in only 8% of the patients. Perfusion defects were observed in 35% of the patients. Only 8 (26%) out of the 31 patients with angiography had coronary artery disease (stenosis > 50%). When fixed and reversible defects were considered as positive, the sensitivity was 50%, the specificity was 65%, the positive predictive value was 33% and the negative predictive value was 79%. CONCLUSIONS: Myocardial perfusion defects can be observed in more than one third of medically treated patients with HC. Only a quarter of catheterized patients, even with chest pain, have associated coronary artery disease. The accuracy of SPET for the diagnosis of coronary artery disease in hypertrophic cardiomyopathy is low. Thus, the value of this technique is limited in these patients.

Aged↗
PubMed2000

Prognostic significance of ST segment depression in lateral leads I, aVL, V5 and V6 on the admission electrocardiogram in patients with a first acute myocardial infarction without ST segment elevation.

OBJECTIVES: We sought to investigate the short-term prognostic value of the admission electrocardiogram (ECG) in patients with a first acute myocardial infarction (MI) without ST segment elevation. BACKGROUND: ST segment depression on hospital admission predicts a worse outcome in patients with a first acute MI, but the prognostic information provided by the location of ST segment depression remains unclear. METHODS: In 432 patients with a first acute MI without Q waves or > or = 0.1 mV of ST segment elevation, we evaluated the ability of the initial ECG to predict in-hospital death. RESULTS: The presence, magnitude and extent of ST segment depression were associated with an increased mortality, but the only electrocardiographic variable that was significant in predicting death after adjusting for baseline predictors was ST segment depression in two or more lateral (I, aVL, V5, or V6) leads (odds ratio 3.5, 95% confidence interval 1.2 to 10.6). Patients with lateral ST segment depression (n = 91, 21%) had higher rates of death (14.3% vs. 2.6%, p < 0.001), severe heart failure (14.3% vs. 4.1%, p < 0.001) and angina with electrocardiographic changes (20.0% vs. 11.6%, p = 0.04) than did the remaining patients, even though they had similar peak creatine kinase, MB fraction levels (129 +/- 96 vs. 122 +/- 92 IU/liter, p = NS). In contrast, ST segment depression not involving the lateral leads did not predict a poor outcome. Among patients who were catheterized, those with lateral ST segment depression had a lower left ventricular ejection fraction (57 +/- 12% vs. 66 +/- 13%, p = 0.001) and more frequent left main coronary artery or three-vessel disease than did the remaining patients (60% vs. 22%, p < 0.001). CONCLUSIONS: In patients with a first non-ST segment elevation acute MI, ST segment depression in the lateral leads on hospital admission predicts a poor in-hospital outcome.

Aged↗
PubMed2000

Thrombin formation and fibrinolytic activity in patients with acute myocardial infarction or unstable angina: in-hospital course and relationship with recurrent angina at rest.

OBJECTIVES: The goal of this study was to investigate possible differences in thrombin generation or fibrinolytic capacity in patients with unstable angina (UA) or acute myocardial infarction (AMI) with or without recurrent angina at rest. BACKGROUND: Angina at rest in patients with AMI or UA is generally produced by a reduction in coronary flow, but it is unclear whether patients with or without this event differ in their thrombin generation or in their fibrinolytic capacities, which might influence the course of the culprit lesion. METHODS: Thrombin-antithrombin complex (TAT), D-dimer, fibrinogen and plasminogen activator inhibitor (PAI-1) antigen plasma levels were determined in 40 patients with AMI and in 23 with UA on admission, at 10 days and at three months. RESULTS: First day values for TAT, fibrinogen and D-dimer were comparable in patients with AMI and in those with UA. At 10 days they increased significantly in each group, and at 3 months they decreased to a similar extent. First day PAI-1 levels, however, were highest in both groups and declined in AMI patients at 10 days and at three months, whereas they also decreased at 10 days in UA patients but not any further at three months. Ten patients with AMI (25%) and 12 with UA (52%) developed in-hospital angina at rest. First day values for TAT, fibrinogen and D-dimer were similar in patients with or without angina, but PAI-1 levels were higher in the former subset (p < 0.008). At 10 days, however, TAT (p < 0.013) and D-dimer (p < 0.013) were higher in patients who developed angina than in those who did not. CONCLUSIONS: The higher inhibition of fibrinolytic activity in the first day in patients with AMI or UA who will develop recurrent angina suggests that maintenance of a prothrombotic status may contribute to its mechanisms, perhaps by preventing passivation of the culprit thrombus/plaque. This is consistent with greater thrombin generation and greater levels of fibrynolitic products at 10 days observed in these patients compared with those who attain early stability.

Aged↗
PubMed2000

Protective effect of HOE642, a selective blocker of Na+-H+ exchange, against the development of rigor contracture in rat ventricular myocytes.

The objective of this study was to investigate the effect of Na+-H+ exchange (NHE) and HCO3--Na+ symport inhibition on the development of rigor contracture. Freshly isolated adult rat cardiomyocytes were subjected to 60 min metabolic inhibition (MI) and 5 min re-energization (Rx). The effects of perfusion of HCO3- or HCO3--free buffer with or without the NHE inhibitor HOE642 (7 microM) were investigated during MI and Rx. In HCO3--free conditions, HOE642 reduced the percentage of cells developing rigor during MI from 79 +/- 1% to 40 +/- 4% (P < 0.001) without modifying the time at which rigor appeared. This resulted in a 30% reduction of hypercontracture during Rx (P < 0.01). The presence of HCO3- abolished the protective effect of HOE642 against rigor. Cells that had developed rigor underwent hypercontracture during Rx independently of treatment allocation. Ratiofluorescence measurement demonstrated that the rise in cytosolic Ca2+ (fura-2) occurred only after the onset of rigor, and was not influenced by HOE642. NHE inhibition did not modify Na+ rise (SBFI) during MI, but exaggerated the initial fall of intracellular pH (BCEFC). In conclusion, HOE642 has a protective effect against rigor during energy deprivation, but only when HCO3--dependent transporters are inhibited. This effect is independent of changes in cytosolic Na+ or Ca2+ concentrations.

Animals↗
PubMed1999

Long-term follow-up of idiopathic chronic pericardial effusion.

BACKGROUND: A large idiopathic chronic pericardial effusion can be defined as a collection of pericardial fluid that persists for more than three months and has no apparent cause. We conducted a prospective study of the natural history and treatment of this disorder. METHODS: Between 1977 and 1992, we prospectively evaluated and enrolled patients with large idiopathic chronic pericardial effusion. We performed pericardiocentesis in most of the patients. We performed pericardiectomy when large pericardial effusion reappeared after pericardiocentesis. Follow-up ranged from 18 months to 20 years (median, 7 years). RESULTS: During the study period, we evaluated a total of 1108 patients with pericarditis, 461 of whom had large pericardial effusion. Twenty-eight of these patients (age range, 7 to 85 years; median, 61) had large idiopathic chronic effusion and were included in the study. The duration of effusion ranged from 6 months to 15 years (median, 3 years). At the initial evaluation, 13 patients were asymptomatic. Overt tamponade was found in eight patients (29 percent). Therapeutic pericardiocentesis, performed in 24 patients, was followed by the disappearance of or marked reduction in the effusion in 8. Five of the 24 patients underwent early pericardiectomy, and in 11 large pericardial effusion reappeared. Cardiac catheterization, performed in 16 patients, showed elevated intrapericardial pressure (4.75+/-3.79 mm Hg) and reduced transmural pressure (1.0+/-2.50 mm Hg) before pericardiocentesis. Both of these abnormalities in pressure improved significantly after pericardiocentesis. Pericardiectomy, performed in 20 patients, yielded excellent long-term results. At the end of the follow-up period, 10 patients had died, but none had died from pericardial disease. CONCLUSIONS: Large idiopathic chronic pericardial effusion is well tolerated for long periods in most patients, but severe tamponade can develop unexpectedly at any time. Pericardiocentesis alone frequently results in the resolution of large effusions, but recurrence is common and pericardiectomy should be considered whenever a large effusion recurs after pericardiocentesis.

Adolescent↗
PubMed1999

Propagation of cardiomyocyte hypercontracture by passage of Na(+) through gap junctions.

Prolonged ischemia increases cytosolic Ca(2+) concentration in cardiomyocytes. Cells with severely elevated cytosolic Ca(2+) may respond to reperfusion, developing hypercontracture, sarcolemmal disruption, and death. Cardiomyocytes are efficiently connected through gap junctions (GJs) to form a functional syncytium, and it has been shown that hypercontracture can be propagated to adjacent myocytes through a GJ-mediated mechanism. This study investigated the mechanism of propagation of cell injury associated with sarcolemmal rupture in end-to-end connected pairs of isolated rat cardiomyocytes. Microinjection of extracellular medium into one of the cells to simulate sarcolemmal disruption induced a marked increase in cytosolic Ca(2+) (fura-2) and Na(+) (SBFI) in the adjacent cell and its hypercontracture in <30 seconds (22 of 22 cell pairs). This process was not modified when Ca(2+) release from the sarcoplasmic reticulum was blocked with 10 micromol/L ryanodine (5 of 5 cell pairs), but it was fully dependent on the presence of Ca(2+) in the extracellular buffer. Blockade of L-type Ca(2+) channels with 10 micromol/L nifedipine did not alter propagation of hypercontracture. However, the presence of 15 to 20 micromol/L KB-R7943, a highly selective blocker of reverse Na(+)/Ca(2+) exchange, prevented propagation of hypercontracture in 16 of 20 cell pairs (P<0.01) without interfering with GJ permeability, as assessed by the Lucifer Yellow transfer method. Addition of the Ca(2+) chelator EGTA (2 mmol/L) to the injection solution prevented hypercontracture in the injected cell but not in the adjacent one (n=5). These results indicate that passage of Na(+) through GJ from hypercontracting myocytes with ruptured sarcolemma to adjacent cells, and secondary entry of [Ca(2+)](o) via reverse Na(+)/Ca(2+) exchange, can contribute to cell-to-cell propagation of hypercontracture. This previously unrecognized mechanism could increase myocardial necrosis during ischemia-reperfusion in vivo and be the target of new treatments aimed to limit it.

Animals↗
PubMed1999

Gender differences in survival in advanced heart failure. Insights from the FIRST study.

BACKGROUND: Previous natural history studies in broad populations of heart failure patients have associated female gender with improved survival, particularly in patients with a nonischemic etiology of ventricular dysfunction. This study investigates whether a similar survival advantage for women would be evident among patients with advanced heart failure. METHODS AND RESULTS: The study analysis is based on the Flolan International Randomized Survival Trial (FIRST) study which enrolled 471 patients (359 men and 112 women) who had evidence of end-stage heart failure with marked symptoms (60% NYHA class IV) and severe left ventricular dysfunction (left ventricular ejection fraction 18+/-4.9%). A Cox proportional-hazards model, adjusted for age, gender, 6-minute walk, dobutamine use at randomization, mean pulmonary artery blood pressure, and treatment assignment, showed a significant association between female gender and better survival (relative risk of death for men versus women was 2.18, 95% CI 1.39 to 3.41; P<0.001). Although formal interaction testing was negative (P=0.275), among patients with a nonischemic etiology of heart failure, the relative risk of death for men versus women was 3.08 (95% CI 1.56 to 6.09, P=0.001), whereas among those with ischemic heart disease, the relative risk of death for men versus women was 1.64 (95% CI 0.87 to 3.09, P=0.127). CONCLUSIONS: Women with advanced heart failure appear to have better survival than men. Subgroup analysis suggests this finding is strongest among patients with a nonischemic etiology of heart failure.

Aged↗
PubMed1999

Infective endocarditis due to Staphylococcus aureus: deleterious effect of anticoagulant therapy.

BACKGROUND: The use of anticoagulant therapy in patients with infective endocarditis (IE) is a controversial issue. OBJECTIVE: To study the impact of anticoagulant therapy on the clinical outcome, mortality, and cause of death in a series of patients with native and prosthetic left-sided Staphylococcus aureus IE. METHODS: This report is based on all consecutive cases of IE diagnosed at our hospital between 1975 to 1997. Clinical data, including the use of anticoagulant therapy at the time of diagnosis, were prospectively obtained, and antibiotic treatment and surgical indications were uniform throughout the study period. Computed tomographic scans of all clinical records were reviewed. RESULTS: Of 637 consecutive patients with IE, 56 had left-sided S aureus IE affecting native valves in 35 patients and prosthetic valves in 21 patients. Of the patients with prosthetic valve IE, 19 (90%) were taking oral anticoagulant therapy at the time of diagnosis while no patient with native valve IE was receiving such treatment. There were no differences between native valve IE and prosthetic valve IE in age, sex, embolic episodes, and number of central nervous system complications. Mortality was higher in prosthetic valve IE than in native valve IE (71% vs 37%; P=.02). No patient with native valve IE died due to central nervous system complications, while 73% (11 of 15 patients) with prosthetic valve IE died due to central nervous system complications. The difference in the distribution of the type of death (stroke vs other) was significant (P<.007). CONCLUSIONS: Our results suggest that in left-sided S aureus IE anticoagulant therapy is closely associated with death due to neurologic damage. According to our data, as soon as the clinical diagnosis of S aureus IE is indicated the use of anticoagulant therapy should be immediately stopped until the septic phase of the disease is overcome.

Acute Disease↗