Periprocedural Anticoagulation Management of Patients With Nonvalvular Atrial Fibrillation
WALDEMAR E. WYSOKINSKI, MD; ROBERT D. MCBANE, MD; PAUL R. DANIELS, MD; SCOTT C. LITIN, MD; DAVID O. HODGE, MS; NICOLE F. DOWLING, PHD; AND JOHN A. HEIT, MD
OBJECTIVE: To estimate the 3-month cumulative incidence of thromboembolism (TE), bleeding, and death among consecutive patients with nonvalvular atrial fibrillation (AF) who were receiving long-term anticoagulation therapy and were referred to the Thrombophilia Center at Mayo Clinic for periprocedural anticoagulation management.
PATIENTS AND METHODS: In a prospective cohort study of consecutive patients receiving long-term anticoagulation therapy who were referred to the Thrombophilia Center for periprocedural anticoagulation management over the 7-year period, January 1, 1997, to December 31, 2003, 345 patients with nonvalvular AF were eligible for inclusion. Warfarin was stopped 4 to 5 days before and was restarted after surgery as soon as hemostasis was assured. The decision to provide bridging therapy with heparin was individualized and based on the estimated risks of TE and bleeding.
RESULTS: The 345 patients with AF (mean ± SD age, 74±9 years; 33% women) underwent 386 procedures. Warfarin administration was not interrupted for 44 procedures. Periprocedural heparin was provided for 204 procedures. Patients receiving heparin were more likely to have prior TE (43% vs 24%; P<.001) and a higher CHADS2 (congestive heart failure, hypertension, age, diabetes, stroke) score (2.2 vs 1.9; P=.06). Four patients had 6 episodes of TE (3 strokes and 3 acute coronary episodes; TE rate, 1.1%; 95% confidence interval, 0.0%-2.1%). Nine patients had 10 major bleeding events (major bleeding rate, 2.7%; 95% confidence interval, 1.0%-4.4%). There were no deaths. Neither bleeding nor TE rates differed by anticoagulant management strategy. CONCLUSION: The 3-month cumulative incidence of TE and bleeding among patients with AF in whom anticoagulation was temporarily interrupted for an invasive procedure was low and was not significantly influenced by bridging therapy. Mayo Clin Proc. 2008;83(6):639-645
Comment by Joel Hernández
The idea of this study was to determine if patients anticoagulated for non-valvular AF that were going to be summited to surgical or invasive diagnostic procedures could de left without anticoagulation, or if it´s necessary to either continue oral anticoagulation or to "bridge" from oral anticoagulation to low-molecular-weight-heparin (LMWH) or non-fractioned-heparin (NFH). This was investigated because it is considered that the risk of emboly is not very high when anticoagulation is suspended for a few days, while, on the other hand, the risk of important hemorrage elevates importantly when it´s not suspended. Some patients were left anticoagulated with Warfarin (an oral anticoagulant like Sintrom) or with heparin (either LMWH or NFH), and some were left without anticoagulation. The decision of whether to anticoagulate or not was done taking into account every patient´s risk of having an emboly and the type of procedure. The conclusion was that the incidence of embolic and hemorragic events in both groups was low and there were no statistically significant differences in these two parameters between both groups. It wasn´t an experimental study, so results must be interpreted cautiously. What´s most important is that the low rates of hemorrage and emboly were probably due to an accurate determination of every patient´s risk, for which the "CHADS index" was used. C (congestive heart failure), H (hypertension), A (age; >75), D (diabetes), S (previous stroke). With 3 or more of these, a patient is considered at high risk for embolic events.
lunes, 15 de diciembre de 2008
miércoles, 12 de noviembre de 2008
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
Posted By Borja
N Engl J Med 2008;359:2195-207.
JUPITER Study Group*
Background
Increased levels of the inflammatory biomarker high-sensitivity C-reactive protein predict cardiovascular events. Since statins lower levels of high-sensitivity C-reactive protein as well as cholesterol, we hypothesized that people with elevated high-sensitivity C-reactive protein levels but without hyperlipidemia might benefit from statin treatment.
Methods
We randomly assigned 17,802 apparently healthy men and women with low-density lipoprotein (LDL) cholesterol levels of less than 130 mg per deciliter (3.4 mmol per liter) and high-sensitivity C-reactive protein levels of 2.0 mg per liter or higher to rosuvastatin, 20 mg daily, or placebo and followed them for the occurrence of the combined primary end point of myocardial infarction, stroke, arterial revascularization, hospitalization for unstable angina, or death from cardiovascular causes.
Results
The trial was stopped after a median follow-up of 1.9 years (maximum, 5.0). Rosuvastatin reduced LDL cholesterol levels by 50% and high-sensitivity C-reactive protein levels by 37%. The rates of the primary end point were 0.77 and 1.36 per 100 person- years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for rosuvastatin, 0.56; 95% confidence interval [CI], 0.46 to 0.69; P<0.00001), p =" 0.0002)," p =" 0.002)," p =" 0.02).">
Posted By Borja
N Engl J Med 2008;359:2195-207.
JUPITER Study Group*
Background
Increased levels of the inflammatory biomarker high-sensitivity C-reactive protein predict cardiovascular events. Since statins lower levels of high-sensitivity C-reactive protein as well as cholesterol, we hypothesized that people with elevated high-sensitivity C-reactive protein levels but without hyperlipidemia might benefit from statin treatment.
Methods
We randomly assigned 17,802 apparently healthy men and women with low-density lipoprotein (LDL) cholesterol levels of less than 130 mg per deciliter (3.4 mmol per liter) and high-sensitivity C-reactive protein levels of 2.0 mg per liter or higher to rosuvastatin, 20 mg daily, or placebo and followed them for the occurrence of the combined primary end point of myocardial infarction, stroke, arterial revascularization, hospitalization for unstable angina, or death from cardiovascular causes.
Results
The trial was stopped after a median follow-up of 1.9 years (maximum, 5.0). Rosuvastatin reduced LDL cholesterol levels by 50% and high-sensitivity C-reactive protein levels by 37%. The rates of the primary end point were 0.77 and 1.36 per 100 person- years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for rosuvastatin, 0.56; 95% confidence interval [CI], 0.46 to 0.69; P<0.00001), p =" 0.0002)," p =" 0.002)," p =" 0.02).">
lunes, 10 de noviembre de 2008
The Lancet 2008; 371:1587-1594
Posted by Joel Hernández
Carotid bruits as a prognostic indicator of cardiovascular death and myocardial infarction: a meta-analysis
Dr Christopher A Pickett MD a , Prof Jeffrey L Jackson MD a c, Brian A Hemann MD a b and Prof J Edwin Atwood MD a b c
Background
Although carotid bruits are deemed to be markers of generalised atherosclerosis, they are poor predictors of cerebrovascular events. We investigated whether a carotid bruit predicts myocardial infarction and cardiovascular death.
Methods
In this meta-analysis, we searched Medline (1966 to August, 2007) and Embase (1974 to August, 2007) with the terms “carotid” and “bruit”. Bibliographies of all the retrieved articles were also searched. Articles were included if they reported the incidence of myocardial infarction or cardiovascular death in adults. Outcome variables were extracted in duplicate and included the rate of myocardial infarction and cardiovascular mortality. Quality of the articles was independently assessed with the Hayden rating scheme. Data were pooled with a random effects model.
Findings
Of the 22 articles included, 20 (91%) used prospective cohorts. Our analysis included 17 295 patients with 62 413·5 patient-years of follow-up, with a median sample size of 273 patients (range 38–4736) followed up for 4 years (2–7). The rate of myocardial infarction in patients with carotid bruits was 3·69 (95% CI 2·97–5·40) per 100 patient-years (eight studies) compared with 1·86 (0·24–3·48) per 100 patient-years in those without bruits (two studies). Yearly rates of cardiovascular death were also higher in patients with bruits (16 studies) than in those without (four studies) (2·85 [2·16–3·54] per 100 patient-years vs 1·11 [0·45–1·76] per 100 patient-years). In the four trials in which direct comparisons of patients with and without bruits were possible, the odds ratio for myocardial infarction was 2·15 (1·67–2·78) and for cardiovascular death 2·27 (1·49–3·49).
Interpretation
Auscultation for carotid bruits in patients at risk for heart disease could help select those who might benefit the most from an aggressive modification strategy for cardiovascular risk
Comments by Joel Hernández
Auscultation of a carotid bruit is considered (somewhat surprisingly) a poor predictor of cerebrovascular events. Nonetheless, these investigators concluded, in this meta-analysis, that carotid bruits are predictors of myocardial infarction and cardiovascular death. So, this is another risk factor to be kept in mind while assessing a patient´s cardiovascular risk. It´s also important to note that this is maybe a frequently forgotten part of the physical examination.
Posted by Joel Hernández
Carotid bruits as a prognostic indicator of cardiovascular death and myocardial infarction: a meta-analysis
Dr Christopher A Pickett MD a , Prof Jeffrey L Jackson MD a c, Brian A Hemann MD a b and Prof J Edwin Atwood MD a b c
Background
Although carotid bruits are deemed to be markers of generalised atherosclerosis, they are poor predictors of cerebrovascular events. We investigated whether a carotid bruit predicts myocardial infarction and cardiovascular death.
Methods
In this meta-analysis, we searched Medline (1966 to August, 2007) and Embase (1974 to August, 2007) with the terms “carotid” and “bruit”. Bibliographies of all the retrieved articles were also searched. Articles were included if they reported the incidence of myocardial infarction or cardiovascular death in adults. Outcome variables were extracted in duplicate and included the rate of myocardial infarction and cardiovascular mortality. Quality of the articles was independently assessed with the Hayden rating scheme. Data were pooled with a random effects model.
Findings
Of the 22 articles included, 20 (91%) used prospective cohorts. Our analysis included 17 295 patients with 62 413·5 patient-years of follow-up, with a median sample size of 273 patients (range 38–4736) followed up for 4 years (2–7). The rate of myocardial infarction in patients with carotid bruits was 3·69 (95% CI 2·97–5·40) per 100 patient-years (eight studies) compared with 1·86 (0·24–3·48) per 100 patient-years in those without bruits (two studies). Yearly rates of cardiovascular death were also higher in patients with bruits (16 studies) than in those without (four studies) (2·85 [2·16–3·54] per 100 patient-years vs 1·11 [0·45–1·76] per 100 patient-years). In the four trials in which direct comparisons of patients with and without bruits were possible, the odds ratio for myocardial infarction was 2·15 (1·67–2·78) and for cardiovascular death 2·27 (1·49–3·49).
Interpretation
Auscultation for carotid bruits in patients at risk for heart disease could help select those who might benefit the most from an aggressive modification strategy for cardiovascular risk
Comments by Joel Hernández
Auscultation of a carotid bruit is considered (somewhat surprisingly) a poor predictor of cerebrovascular events. Nonetheless, these investigators concluded, in this meta-analysis, that carotid bruits are predictors of myocardial infarction and cardiovascular death. So, this is another risk factor to be kept in mind while assessing a patient´s cardiovascular risk. It´s also important to note that this is maybe a frequently forgotten part of the physical examination.
domingo, 26 de octubre de 2008
Provoked Coronary Spasm and Acute Coronary Syndromes
Posted By Joel Hernandez
Journal of the American College of Cardiology Vol. 52, No. 7, 2008
Background
Chest pain at rest is a frequent symptom in the emergency room. Acute coronary syndrome (ACS) is suspected in patients with elevation of cardiac markers, ischemic electrocardiographic changes, or simply typical clinical symptoms of unstable (usually resting) angina. However, of all patients with suspected ACS who undergo coronary angiography, up to 30% have nonobstructed coronary arteries. We sought to clarify how many of these patients suffer from coronary spasm as a possible cause of their chest pain.
Methods
In a prospective study from June to December 2006, all patients with suspected acute coronary syndrome (ACS) who underwent coronary angiography and had no culprit lesion underwent intracoronary provocation with acetylcholine (ACH). The ACH testing was considered positive at a vasoconstriction of ≥75% relative to the diameter after intracoronary nitroglycerine when the initially reported symptoms could be reproduced.
Results
Of 488 consecutive patients, 138 had no culprit lesion (28%). Twenty-two were found to have another diagnosis. The ACH testing was performed in 86 of the remaining 116 patients. In 42 patients, coronary spasm was verified (49%).
Conclusions
Every fourth patient with ACS had no culprit lesion. Coronary spasm could be documented in nearly 50% of the patients tested by ACH. Coronary spasm is a frequent cause of ACS and should regularly be considered as a differential diagnosis.
Comment: Very interesting, since this contributes to the idea that many patients (up to 30%) can have acute coronary syndromes without having fixed coronary lesions. Of this 30%, 50% could be attributed to vasospasm. In previous studies, intravenous ergonovine was used instead of intracoronary acetylcholine, being the proportion of patients positive for vasospasm inferior, thus it seems that the test with intracoronary acetylcholine is more sensitive.
Journal of the American College of Cardiology Vol. 52, No. 7, 2008
Background
Chest pain at rest is a frequent symptom in the emergency room. Acute coronary syndrome (ACS) is suspected in patients with elevation of cardiac markers, ischemic electrocardiographic changes, or simply typical clinical symptoms of unstable (usually resting) angina. However, of all patients with suspected ACS who undergo coronary angiography, up to 30% have nonobstructed coronary arteries. We sought to clarify how many of these patients suffer from coronary spasm as a possible cause of their chest pain.
Methods
In a prospective study from June to December 2006, all patients with suspected acute coronary syndrome (ACS) who underwent coronary angiography and had no culprit lesion underwent intracoronary provocation with acetylcholine (ACH). The ACH testing was considered positive at a vasoconstriction of ≥75% relative to the diameter after intracoronary nitroglycerine when the initially reported symptoms could be reproduced.
Results
Of 488 consecutive patients, 138 had no culprit lesion (28%). Twenty-two were found to have another diagnosis. The ACH testing was performed in 86 of the remaining 116 patients. In 42 patients, coronary spasm was verified (49%).
Conclusions
Every fourth patient with ACS had no culprit lesion. Coronary spasm could be documented in nearly 50% of the patients tested by ACH. Coronary spasm is a frequent cause of ACS and should regularly be considered as a differential diagnosis.
Comment: Very interesting, since this contributes to the idea that many patients (up to 30%) can have acute coronary syndromes without having fixed coronary lesions. Of this 30%, 50% could be attributed to vasospasm. In previous studies, intravenous ergonovine was used instead of intracoronary acetylcholine, being the proportion of patients positive for vasospasm inferior, thus it seems that the test with intracoronary acetylcholine is more sensitive.
martes, 1 de julio de 2008
Bacteriemia following toothbrushing
posted by carlos GSG
Circulation. 2008 Jun 17;117(24):3118-25
Bacteremia Associated With Toothbrushing and Dental Extraction
Background— Antibiotic prophylaxis recommendations for the prevention of infective endocarditis are based in part on studies of bacteremia from dental procedures, but toothbrushing may pose a greater threat. The purpose of this study was to compare the incidence, duration, nature, and magnitude of endocarditis-related
bacteremia from single-tooth extraction and toothbrushing and to determine the impact of amoxicillin prophylaxis on single-tooth extraction.
Methods and Results— In this double-blind, placebo-controlled study, 290 subjects were randomized to (1) toothbrushing, (2) single-tooth extraction with amoxicillin prophylaxis, or (3) single-tooth extraction with identical placebo. Blood was drawn for bacterial culturing and identification at 6 time points before, during, and after these interventions. The focus of our analysis was on bacterial species reported to cause infective endocarditis. We identified 98 bacterial species, 32 of which are reported to cause endocarditis. Cumulative incidence of endocarditis-related bacteria from all 6 blood draws was 23%, 33%, and 60% for the toothbrushing, extraction-amoxicillin, and extraction-placebo groups, respectively (P<0.0001).>COMENTARIOS: El porcentaje de bacteriemia es 23% tras cepillado, 80% tras extracción dental sin profilaxis ATB y 33% tras extracción dental con profilaxis
- Amoxicilina reduce significativamente el riesgo de bacteriemia tras extracción dental (de 80 a 33%), ergo se confirma que debemos usarla
- No obstante, la profilaxis ATB no es completamente efectiva, incluso tras profilaxis ATB hasta un 33% de pacientes tiene bacteriemia tras extracción dental
- Aunque el cepillado no es tan agresivo como la extracción dental, hasta un 23% de pacientes tienen bacteriemias tras cepillado; además es bacteriemias sostenida en el tiempo, tienen un porcentaje mayor de bacteriemias ¡a los 60 minutos!
- Aunque el pico de bacteriemias ocurre en los primeros cinco minutos (lógico, luego actúa el sistema inmunitario del huésped), se trata de bacteriemias mantenidas, dado que hasta un 10% postcepillado tenían bacteriemia detectable ¡60 minutos tras el cepillado! (ver texto, no obstante si consideramos sólo bacterias que puedan causar EI el porcentaje a los 60 minutos es menor)
- Aunque el cepillado no supone tanto riesgo de bacteriemia como la extracción dental, dado que es mucho más frecuente (2 veces diarias vs aprox 2 veces anuales de visitas al dentista), supone un riesgo no despreciable para los pacientes con riesgo de EI, con lo cual deberán extremar su higiene bucal
- Curiosamente, hasta el 80% de la muestra del estudio es de raza negra (hombre, es un estudio hecho en el estado de Carolina, pero desde luego esa no es la proporción en la población de USA). Dado que en general suelen tener menor poder adquisitivo, ¿a lo mejor su higiene bucal es peor que la del resto de población y este estudio no se puede genralizar al resto de población?
- Y la prinicipal limitación del estudio para aplicarlo a pacientes valvulópatas con riesgo de EI: es un estudio en pacientes sanos, no en valvulópatas y estudian surrogate endopoints (bacteriemias), no si reducen hard endpoints (diagnóstico cierto de EI según criterios establecidos de Duke, necesidad de cirugía o tto ATB de EI, ICC, mortalidad, necesidad de cirugía, que implicarían una población muy amplia y un seguimiento muy largo...)
Circulation. 2008 Jun 17;117(24):3118-25
Bacteremia Associated With Toothbrushing and Dental Extraction
Background— Antibiotic prophylaxis recommendations for the prevention of infective endocarditis are based in part on studies of bacteremia from dental procedures, but toothbrushing may pose a greater threat. The purpose of this study was to compare the incidence, duration, nature, and magnitude of endocarditis-related
bacteremia from single-tooth extraction and toothbrushing and to determine the impact of amoxicillin prophylaxis on single-tooth extraction.
Methods and Results— In this double-blind, placebo-controlled study, 290 subjects were randomized to (1) toothbrushing, (2) single-tooth extraction with amoxicillin prophylaxis, or (3) single-tooth extraction with identical placebo. Blood was drawn for bacterial culturing and identification at 6 time points before, during, and after these interventions. The focus of our analysis was on bacterial species reported to cause infective endocarditis. We identified 98 bacterial species, 32 of which are reported to cause endocarditis. Cumulative incidence of endocarditis-related bacteria from all 6 blood draws was 23%, 33%, and 60% for the toothbrushing, extraction-amoxicillin, and extraction-placebo groups, respectively (P<0.0001).>COMENTARIOS: El porcentaje de bacteriemia es 23% tras cepillado, 80% tras extracción dental sin profilaxis ATB y 33% tras extracción dental con profilaxis
- Amoxicilina reduce significativamente el riesgo de bacteriemia tras extracción dental (de 80 a 33%), ergo se confirma que debemos usarla
- No obstante, la profilaxis ATB no es completamente efectiva, incluso tras profilaxis ATB hasta un 33% de pacientes tiene bacteriemia tras extracción dental
- Aunque el cepillado no es tan agresivo como la extracción dental, hasta un 23% de pacientes tienen bacteriemias tras cepillado; además es bacteriemias sostenida en el tiempo, tienen un porcentaje mayor de bacteriemias ¡a los 60 minutos!
- Aunque el pico de bacteriemias ocurre en los primeros cinco minutos (lógico, luego actúa el sistema inmunitario del huésped), se trata de bacteriemias mantenidas, dado que hasta un 10% postcepillado tenían bacteriemia detectable ¡60 minutos tras el cepillado! (ver texto, no obstante si consideramos sólo bacterias que puedan causar EI el porcentaje a los 60 minutos es menor)
- Aunque el cepillado no supone tanto riesgo de bacteriemia como la extracción dental, dado que es mucho más frecuente (2 veces diarias vs aprox 2 veces anuales de visitas al dentista), supone un riesgo no despreciable para los pacientes con riesgo de EI, con lo cual deberán extremar su higiene bucal
- Curiosamente, hasta el 80% de la muestra del estudio es de raza negra (hombre, es un estudio hecho en el estado de Carolina, pero desde luego esa no es la proporción en la población de USA). Dado que en general suelen tener menor poder adquisitivo, ¿a lo mejor su higiene bucal es peor que la del resto de población y este estudio no se puede genralizar al resto de población?
- Y la prinicipal limitación del estudio para aplicarlo a pacientes valvulópatas con riesgo de EI: es un estudio en pacientes sanos, no en valvulópatas y estudian surrogate endopoints (bacteriemias), no si reducen hard endpoints (diagnóstico cierto de EI según criterios establecidos de Duke, necesidad de cirugía o tto ATB de EI, ICC, mortalidad, necesidad de cirugía, que implicarían una población muy amplia y un seguimiento muy largo...)
viernes, 27 de junio de 2008
intracoronary reopro bolus in STEMI
posted by Pepa
Circulation. 2008Published online before print June 16, 2008, doi: 10.1161/CIRCULATIONAHA.107.747642
Intracoronary Compared With Intravenous Bolus Abciximab Application in Patients With ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. The Randomized Leipzig Immediate Percutaneous Coronary Intervention Abciximab IV Versus IC in ST-Elevation Myocardial Infarction Trial
Background—Abciximab reduces major adverse cardiac events in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention (PCI). Intracoronary abciximab bolus application results in high local drug concentrations and may be more effective than a standard intravenous bolus.
Methods and Results—Patients undergoing primary PCI were randomized to either intracoronary (n=77) or intravenous (n=77) bolus abciximab administration with subsequent 12-hour intravenous infusion. The primary end point was infarct size and extent of microvascular obstruction as assessed by delayed enhancement magnetic resonance. Secondary end points were ST-segment resolution at 90 minutes, Thrombolysis in Myocardial Infarction flow and perfusion grades after PCI, and the occurrence of major adverse cardiac events within 30 days. The median infarct size was 15.1% (interquartile range, 6.1% to 25.2%) in the intracoronary versus 23.4% (interquartile range, 13.6% to 33.2%) in the intravenous group (P=0.01). Similarly, the extent of microvascular obstruction was significantly smaller in intracoronary compared with intravenous abciximab patients (P=0.01). Myocardial perfusion measured as early ST-segment resolution was significantly improved in intracoronary patients with an absolute ST-segment resolution of 77.8% (interquartile range, 66.7% to 100.0%) versus 70.0% (interquartile range, 45.2% to 83.5%; P=0.006). The Thrombolysis in Myocardial Infarction flow after PCI was not different between treatment groups (P=0.51), but there was a trend toward an improved perfusion grade (P=0.09). There also was a trend toward a lower major adverse cardiac event rate after intracoronary versus intravenous abciximab application (5.2% versus 15.6%; P=0.06; relative risk, 0.33; 95% CI, 0.09 to 1.05).
Conclusions—Intracoronary bolus administration of abciximab in primary PCI is superior to standard intravenous treatment with respect to infarct size, extent of microvascular obstruction, and perfusion.
COMMENTS: Despite a small sample size, there is a strongo trend towards a reduction in clinical endpoints in patients receiving IC reopro as compared with those receiving classical IV bolus.
Another important point is that MRI was used as the technique for evaulating infarct size.
Circulation. 2008Published online before print June 16, 2008, doi: 10.1161/CIRCULATIONAHA.107.747642
Intracoronary Compared With Intravenous Bolus Abciximab Application in Patients With ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. The Randomized Leipzig Immediate Percutaneous Coronary Intervention Abciximab IV Versus IC in ST-Elevation Myocardial Infarction Trial
Background—Abciximab reduces major adverse cardiac events in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention (PCI). Intracoronary abciximab bolus application results in high local drug concentrations and may be more effective than a standard intravenous bolus.
Methods and Results—Patients undergoing primary PCI were randomized to either intracoronary (n=77) or intravenous (n=77) bolus abciximab administration with subsequent 12-hour intravenous infusion. The primary end point was infarct size and extent of microvascular obstruction as assessed by delayed enhancement magnetic resonance. Secondary end points were ST-segment resolution at 90 minutes, Thrombolysis in Myocardial Infarction flow and perfusion grades after PCI, and the occurrence of major adverse cardiac events within 30 days. The median infarct size was 15.1% (interquartile range, 6.1% to 25.2%) in the intracoronary versus 23.4% (interquartile range, 13.6% to 33.2%) in the intravenous group (P=0.01). Similarly, the extent of microvascular obstruction was significantly smaller in intracoronary compared with intravenous abciximab patients (P=0.01). Myocardial perfusion measured as early ST-segment resolution was significantly improved in intracoronary patients with an absolute ST-segment resolution of 77.8% (interquartile range, 66.7% to 100.0%) versus 70.0% (interquartile range, 45.2% to 83.5%; P=0.006). The Thrombolysis in Myocardial Infarction flow after PCI was not different between treatment groups (P=0.51), but there was a trend toward an improved perfusion grade (P=0.09). There also was a trend toward a lower major adverse cardiac event rate after intracoronary versus intravenous abciximab application (5.2% versus 15.6%; P=0.06; relative risk, 0.33; 95% CI, 0.09 to 1.05).
Conclusions—Intracoronary bolus administration of abciximab in primary PCI is superior to standard intravenous treatment with respect to infarct size, extent of microvascular obstruction, and perfusion.
COMMENTS: Despite a small sample size, there is a strongo trend towards a reduction in clinical endpoints in patients receiving IC reopro as compared with those receiving classical IV bolus.
Another important point is that MRI was used as the technique for evaulating infarct size.
Clopidogrel Vs. Ticlopidine
posted by Borja
Journal of the American College of CardiologyVolume 41, Issue 6, 19 March 2003, Pages 969-973
A randomized comparison of clopidogrel and aspirin versus ticlopidine and aspirin after the placement of coronary artery stents
Abstract
Objectives
The aim of the present study was to compare clopidogrel and ticlopidine after coronary stenting with regard to cardiovascular death during long-term follow-up.
Background
Randomized trials comparing clopidogrel and ticlopidine with a restricted use of intravenous glycoprotein IIb/IIIa inhibition have reported a trend toward a higher incidence of thrombotic stent occlusion with clopidogrel at 30 days.
Methods
After successful coronary stent implantation, 700 patients with 899 lesions were randomly assigned to receive a four-week course of either 500 mg ticlopidine (n = 345) or 75 mg clopidogrel (n = 355) in addition to 100 mg aspirin. Cardiovascular death was the primary end point and was recorded during a median follow-up period of 28 months.
Results
Cardiovascular death occurred in eight patients with ticlopidine versus 26 patients with clopidogrel (hazard ratio with ticlopidine compared with clopidogrel, 0.30; 95% confidence interval [CI], 0.14 to 0.66; P = 0.003). After adjustment for co-variables, ticlopidine reduced the risk of cardiovascular death by 63% compared with clopidogrel. The combined end point of cardiovascular death or nonfatal myocardial infarction was present in 19 patients assigned ticlopidine, compared with 40 patients assigned clopidogrel (hazard ratio, 0.45; P = 0.005). The hazard ratio for all-cause mortality with ticlopidine as compared with clopidogrel was 0.30 (95% CI, 0.14 to 0.64; P = 0.002).
Conclusions
After the placement of coronary artery stents in unselected patients, ticlopidine was associated with a significantly lower mortality than clopidogrel. This raises concern about the current practice of substituting clopidogrel for ticlopidine after stenting and highlights the need for further long-term studies.
COMMENT: This paper received almost no attention in the literature. Important to note that clopidogrel was administered with no loading dose, while ticlopidine treatment was started by a 500 mg alodaing dose. However, in a table enclosed in the paper, it is clear that the events curve start to diverge quite late (more than 2 months after stent implantation). In this scenario, it seems highly unlikely that the absence of loading dose of clopidogrel has something to do.
Journal of the American College of CardiologyVolume 41, Issue 6, 19 March 2003, Pages 969-973
A randomized comparison of clopidogrel and aspirin versus ticlopidine and aspirin after the placement of coronary artery stents
Abstract
Objectives
The aim of the present study was to compare clopidogrel and ticlopidine after coronary stenting with regard to cardiovascular death during long-term follow-up.
Background
Randomized trials comparing clopidogrel and ticlopidine with a restricted use of intravenous glycoprotein IIb/IIIa inhibition have reported a trend toward a higher incidence of thrombotic stent occlusion with clopidogrel at 30 days.
Methods
After successful coronary stent implantation, 700 patients with 899 lesions were randomly assigned to receive a four-week course of either 500 mg ticlopidine (n = 345) or 75 mg clopidogrel (n = 355) in addition to 100 mg aspirin. Cardiovascular death was the primary end point and was recorded during a median follow-up period of 28 months.
Results
Cardiovascular death occurred in eight patients with ticlopidine versus 26 patients with clopidogrel (hazard ratio with ticlopidine compared with clopidogrel, 0.30; 95% confidence interval [CI], 0.14 to 0.66; P = 0.003). After adjustment for co-variables, ticlopidine reduced the risk of cardiovascular death by 63% compared with clopidogrel. The combined end point of cardiovascular death or nonfatal myocardial infarction was present in 19 patients assigned ticlopidine, compared with 40 patients assigned clopidogrel (hazard ratio, 0.45; P = 0.005). The hazard ratio for all-cause mortality with ticlopidine as compared with clopidogrel was 0.30 (95% CI, 0.14 to 0.64; P = 0.002).
Conclusions
After the placement of coronary artery stents in unselected patients, ticlopidine was associated with a significantly lower mortality than clopidogrel. This raises concern about the current practice of substituting clopidogrel for ticlopidine after stenting and highlights the need for further long-term studies.
COMMENT: This paper received almost no attention in the literature. Important to note that clopidogrel was administered with no loading dose, while ticlopidine treatment was started by a 500 mg alodaing dose. However, in a table enclosed in the paper, it is clear that the events curve start to diverge quite late (more than 2 months after stent implantation). In this scenario, it seems highly unlikely that the absence of loading dose of clopidogrel has something to do.
martes, 17 de junio de 2008
CIRC RES: Role of mast cells in abd aortic aneurysms
Posted by Borja.
(Circulation Research. 2008;102:1368.)
Adventitial Mast Cells Contribute to Pathogenesis in the Progression of Abdominal Aortic Aneurysm
Abdominal aortic aneurysm (AAA) is histologically characterized by medial degeneration and various degrees of chronic adventitial inflammation, although the mechanisms for progression of aneurysm are poorly understood. In the present study, we carried out histological study of AAA tissues of patients, and interventional animal and cell culture experiments to investigate a role of mast cells in the pathogenesis of AAA. The number of mast cells was found to increase in the outer media or adventitia of human AAA, showing a positive correlation between the cell number and the AAA diameter. Aneurysmal dilatation of the aorta was seen in the control (+/+) rats following periaortic application of calcium chloride (CaCl2) treatment but not in the mast cell–deficient mutant Ws/Ws rats. The AAA formation was accompanied by accumulation of mast cells, T lymphocytes and by activated matrix metalloproteinase 9, reduced elastin levels and augmented angiogenesis in the aortic tissue, but these changes were much less in the Ws/Ws rats than in the controls. Similarly, mast cells were accumulated and activated at the adventitia of aneurysmal aorta in the apolipoprotein E–deficient mice. The pharmacological intervention with the tranilast, an inhibitor of mast cell degranulation, attenuated AAA development in these rodent models. In the cell culture experiment, a mast cell directly augmented matrix metalloproteinase 9 activity produced by the monocyte/macrophage. Collectively, these data suggest that adventitial mast cells play a critical role in the progression of AAA.
COMMENT:
In this paper, the authors prove, in a mouse model of AAA (abdominal aorta aneurysm), that mast cells are required for the development of AAA. Mast cells have been implicated in various pathjological proccessess, mainly in those in which inflammation is exacerbated.
It would be really interesting to know whether mast cells are also involved in the development of LV aneurysms (i.e. post-MI). Maybe, those patients showing aneurismatic remodelling of the LV post-MI have a increase in the degranulation of mast cells (potentially treatable condition).
If this is interesting for the gang, we could discuss a pilot study in the pig model of MI (Hans can take the "alternativa" in the tuesdays 7am meetings)........
(Circulation Research. 2008;102:1368.)
Adventitial Mast Cells Contribute to Pathogenesis in the Progression of Abdominal Aortic Aneurysm
Abdominal aortic aneurysm (AAA) is histologically characterized by medial degeneration and various degrees of chronic adventitial inflammation, although the mechanisms for progression of aneurysm are poorly understood. In the present study, we carried out histological study of AAA tissues of patients, and interventional animal and cell culture experiments to investigate a role of mast cells in the pathogenesis of AAA. The number of mast cells was found to increase in the outer media or adventitia of human AAA, showing a positive correlation between the cell number and the AAA diameter. Aneurysmal dilatation of the aorta was seen in the control (+/+) rats following periaortic application of calcium chloride (CaCl2) treatment but not in the mast cell–deficient mutant Ws/Ws rats. The AAA formation was accompanied by accumulation of mast cells, T lymphocytes and by activated matrix metalloproteinase 9, reduced elastin levels and augmented angiogenesis in the aortic tissue, but these changes were much less in the Ws/Ws rats than in the controls. Similarly, mast cells were accumulated and activated at the adventitia of aneurysmal aorta in the apolipoprotein E–deficient mice. The pharmacological intervention with the tranilast, an inhibitor of mast cell degranulation, attenuated AAA development in these rodent models. In the cell culture experiment, a mast cell directly augmented matrix metalloproteinase 9 activity produced by the monocyte/macrophage. Collectively, these data suggest that adventitial mast cells play a critical role in the progression of AAA.
COMMENT:
In this paper, the authors prove, in a mouse model of AAA (abdominal aorta aneurysm), that mast cells are required for the development of AAA. Mast cells have been implicated in various pathjological proccessess, mainly in those in which inflammation is exacerbated.
It would be really interesting to know whether mast cells are also involved in the development of LV aneurysms (i.e. post-MI). Maybe, those patients showing aneurismatic remodelling of the LV post-MI have a increase in the degranulation of mast cells (potentially treatable condition).
If this is interesting for the gang, we could discuss a pilot study in the pig model of MI (Hans can take the "alternativa" in the tuesdays 7am meetings)........
CIRC RES PAPER: Tbx family in conduction system development
Posted by Hans.
(Circulation Research. 2008;102:1340.)
Transcription Factor Tbx3 Is Required for the Specification of the Atrioventricular Conduction System.
The cardiac conduction system consists of distinctive heart muscle cells that initiate and propagate the electric impulse required for coordinated contraction. The conduction system expresses the transcriptional repressor Tbx3, which is required for vertebrate development and controls the formation of the sinus node. In humans, mutations in Tbx3 cause ulnar–mammary syndrome. Here, we investigated the role of Tbx3 in the molecular specification of the atrioventricular conduction system. Expression analysis revealed early delineation of the atrioventricular bundle and proximal bundle branches by Tbx3 expression in human, mouse, and chicken. Tbx3-deficient mice, which die between embryonic day 12.5 and 15.5, ectopically expressed genes for connexin (Cx)43, atrial natriuretic factor (Nppa), Tbx18, and Tbx20 in the atrioventricular bundle and proximal bundle branches. Cx40 was precociously upregulated in the atrioventricular bundle of Tbx3 mutants. Moreover, the atrioventricular bundle and branches failed to exit the cell cycle in Tbx3 mutant embryos. Finally, Tbx3-deficient embryos developed outflow tract malformations and ventricular septal defects. These data reveal that Tbx3 is required for the molecular specification of the atrioventricular bundle and bundle branches and for the development of the ventricular septum and outflow tract. Our data suggest a mechanism in which Tbx3 represses differentiation into ventricular working myocardium, thereby imposing the conduction system phenotype on cells within its expression domain.
COMMENTS:
Tbx is a family of development represors. Their role in heart development is to block the differentiation of conduction cells into working myocardium. Hence, when Tbx (3 in this case) is absent, the cells continue their lineage becoming working myocardium, with the subsequent absence of sinus or AV node cells.
Tbx has been also implicated in the development of interventricular septum and RV outflow tract.
(Circulation Research. 2008;102:1340.)
Transcription Factor Tbx3 Is Required for the Specification of the Atrioventricular Conduction System.
The cardiac conduction system consists of distinctive heart muscle cells that initiate and propagate the electric impulse required for coordinated contraction. The conduction system expresses the transcriptional repressor Tbx3, which is required for vertebrate development and controls the formation of the sinus node. In humans, mutations in Tbx3 cause ulnar–mammary syndrome. Here, we investigated the role of Tbx3 in the molecular specification of the atrioventricular conduction system. Expression analysis revealed early delineation of the atrioventricular bundle and proximal bundle branches by Tbx3 expression in human, mouse, and chicken. Tbx3-deficient mice, which die between embryonic day 12.5 and 15.5, ectopically expressed genes for connexin (Cx)43, atrial natriuretic factor (Nppa), Tbx18, and Tbx20 in the atrioventricular bundle and proximal bundle branches. Cx40 was precociously upregulated in the atrioventricular bundle of Tbx3 mutants. Moreover, the atrioventricular bundle and branches failed to exit the cell cycle in Tbx3 mutant embryos. Finally, Tbx3-deficient embryos developed outflow tract malformations and ventricular septal defects. These data reveal that Tbx3 is required for the molecular specification of the atrioventricular bundle and bundle branches and for the development of the ventricular septum and outflow tract. Our data suggest a mechanism in which Tbx3 represses differentiation into ventricular working myocardium, thereby imposing the conduction system phenotype on cells within its expression domain.
COMMENTS:
Tbx is a family of development represors. Their role in heart development is to block the differentiation of conduction cells into working myocardium. Hence, when Tbx (3 in this case) is absent, the cells continue their lineage becoming working myocardium, with the subsequent absence of sinus or AV node cells.
Tbx has been also implicated in the development of interventricular septum and RV outflow tract.
miércoles, 11 de junio de 2008
Estratificacion MADIT II
Como es un articulo muy interesante, mando el pdf del JACC sobre la estratificacion de pacientes del MADIT II, con las caracteristicas de pacientes en quienes es mas beneficioso el implante de CDI dentro del perfil MADIT II.
http://jmrubioc.googlepages.com/MADITII_EStratificacionclinica_JACC0.pdf
http://jmrubioc.googlepages.com/MADITII_EStratificacionclinica_JACC0.pdf
Articulo Revision Coronary CT
La Dra Sanchez-Borque nos manda este articulo de revision del Heart de este mes sobre TAC coronario, con informacion sobre historia, tecnologia básica, aplicaciones...
http://heart.bmj.com/cgi/content/full/94/6/781
http://heart.bmj.com/cgi/content/full/94/6/781
martes, 10 de junio de 2008
Aliskiren y valsartan
Aliskiren Combined with Losartan in Type 2 Diabetes and Nephropathy
Hans-Henrik Parving, M.D., D.M.Sc., Frederik Persson, M.D., Julia B. Lewis, M.D., Edmund J. Lewis, M.D., and Norman K. Hollenberg, M.D., Ph.D., for the AVOID Study Investigators*
Background Diabetic nephropathy is the leading cause of end-stage renal disease in developed countries. We evaluated the renoprotective effects of dual blockade of the renin−angiotensin−aldosterone system by adding treatment with aliskiren, an oral direct renin inhibitor, to treatment with the maximal recommended dose of losartan (100 mg daily) and optimal antihypertensive therapy in patients who had hypertension
and type 2 diabetes with nephropathy.
Methods We enrolled 599 patients in this multinational, randomized, double-blind study. After a 3-month, open-label, run-in period during which patients received 100 mg of losartan daily, patients were randomly assigned to receive 6 months of treatment with aliskiren (150 mg daily for 3 months, followed by an increase in dosage to 300 mg daily for another 3 months) or placebo, in addition to losartan. The primary outcome was a reduction in the ratio of albumin to creatinine, as measured in an earlymorning urine sample, at 6 months.
Results The baseline characteristics of the two groups were similar. Treatment with 300 mg of aliskiren daily, as compared with placebo, reduced the mean urinary albumin-tocreatinine ratio by 20% (95% confidence interval, 9 to 30; P<0.001), with a reduction of 50% or more in 24.7% of the patients who received aliskiren as compared with 12.5% of those who received placebo (P<0.001). A small difference in blood pressure was seen between the treatment groups by the end of the study period (systolic, 2 mm Hg lower [P = 0.07] and diastolic, 1 mm Hg lower [P = 0.08] in the aliskiren group). The total numbers of adverse and serious adverse events were similar in the groups.
Conclusions Aliskiren may have renoprotective effects that are independent of its bloodpressure−lowering effect in patients with hypertension, type 2 diabetes, and nephropathywho are receiving the recommended renoprotective treatment.
Comentario Dra Ana Pastor
COMENTARIOS:
-La proteinuria persistente es el final de la nefropatía diabética, un estado que se caracteriza por el aumento progresivo de la TA, una disminución del filtrado glomerular, y un riesgo elevado de acontecimientos adversos cardiovasculares.
- Este estudio a doble ciego muestra una reducción de albuminuria en grupo control vs placebo, que sigue siendo significativa tras ajustarse a TAS en cada grupo. Es decir, que la reducción de la proteinuria es independiente al efecto antihipertensivo del fármaco y del losartán.
-En este estudio no se incluyeron pacientes con K mayor de 5.1 ni pacientes con filtardo glomerular <30ml/min. Por lo que el efecto sobre el potasio sérico y en pacientes con función renal deprimida no ha sido estudiado.
Hans-Henrik Parving, M.D., D.M.Sc., Frederik Persson, M.D., Julia B. Lewis, M.D., Edmund J. Lewis, M.D., and Norman K. Hollenberg, M.D., Ph.D., for the AVOID Study Investigators*
Background Diabetic nephropathy is the leading cause of end-stage renal disease in developed countries. We evaluated the renoprotective effects of dual blockade of the renin−angiotensin−aldosterone system by adding treatment with aliskiren, an oral direct renin inhibitor, to treatment with the maximal recommended dose of losartan (100 mg daily) and optimal antihypertensive therapy in patients who had hypertension
and type 2 diabetes with nephropathy.
Methods We enrolled 599 patients in this multinational, randomized, double-blind study. After a 3-month, open-label, run-in period during which patients received 100 mg of losartan daily, patients were randomly assigned to receive 6 months of treatment with aliskiren (150 mg daily for 3 months, followed by an increase in dosage to 300 mg daily for another 3 months) or placebo, in addition to losartan. The primary outcome was a reduction in the ratio of albumin to creatinine, as measured in an earlymorning urine sample, at 6 months.
Results The baseline characteristics of the two groups were similar. Treatment with 300 mg of aliskiren daily, as compared with placebo, reduced the mean urinary albumin-tocreatinine ratio by 20% (95% confidence interval, 9 to 30; P<0.001), with a reduction of 50% or more in 24.7% of the patients who received aliskiren as compared with 12.5% of those who received placebo (P<0.001). A small difference in blood pressure was seen between the treatment groups by the end of the study period (systolic, 2 mm Hg lower [P = 0.07] and diastolic, 1 mm Hg lower [P = 0.08] in the aliskiren group). The total numbers of adverse and serious adverse events were similar in the groups.
Conclusions Aliskiren may have renoprotective effects that are independent of its bloodpressure−lowering effect in patients with hypertension, type 2 diabetes, and nephropathywho are receiving the recommended renoprotective treatment.
Comentario Dra Ana Pastor
COMENTARIOS:
-La proteinuria persistente es el final de la nefropatía diabética, un estado que se caracteriza por el aumento progresivo de la TA, una disminución del filtrado glomerular, y un riesgo elevado de acontecimientos adversos cardiovasculares.
- Este estudio a doble ciego muestra una reducción de albuminuria en grupo control vs placebo, que sigue siendo significativa tras ajustarse a TAS en cada grupo. Es decir, que la reducción de la proteinuria es independiente al efecto antihipertensivo del fármaco y del losartán.
-En este estudio no se incluyeron pacientes con K mayor de 5.1 ni pacientes con filtardo glomerular <30ml/min. Por lo que el efecto sobre el potasio sérico y en pacientes con función renal deprimida no ha sido estudiado.
Articulo Clopidogrel JACC Junio 08
Volume 51, Issue 23, June 10, 2008
CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY
Long-Term Outcomes by Clopidogrel Duration and Stent Type in a Diabetic Population With De Novo Coronary Artery Lesions
Somjot S. Brar, MD*,*, John Kim, MD, Simerjeet K. Brar, BS, Ray Zadegan, MD, Michael Ree, BS, In-Lu A. Liu, MS, Prakash Mansukhani, MD, Vicken Aharonian, MD, Ric Hyett, BS and Albert Yuh-Jer Shen, MDObjectives: The purpose of this study was to determine whether long-term clinical outcomes differed between bare-metal stents (BMS) and drug-eluting stents (DES) by duration of clopidogrel use among diabetic patients.
Background: There is concern that DES are associated with late adverse events such as death and myocardial infarction (MI) secondary to stent thrombosis. However, data on outcomes in diabetic patients remain limited.
Methods: We identified 749 patients with diabetes mellitus who underwent stent implantation with either BMS (n = 251) or DES (n = 498) from October 2002 to December 2004. We performed survival analysis on the full cohort and on those event-free from death, MI, or repeat revascularization at 6 months (n = 671).
Results: By clopidogrel duration, the event rate for death or MI was 3.2% in the >9-month group, 9.4% in the 6- to 9-month group, and 16.5% in the <6-month>9-month group, 4.3% in the 6- to 9-month group, and 10.0% in the <6-month group, p < 0.001. When taking BMS clopidogrel non-users as a referent in the multivariate analysis, the hazard ratio (95% confidence interval [CI]) for death and nonfatal MI for DES clopidogrel users, DES clopidogrel nonusers, and BMS clopidogrel users were: HR 0.22 (95% CI 0.08 to 0.62, p = 0.005), HR 0.39 (95% CI 0.13 to 1.13, p = 0.08), and HR 0.25 (95% CI 0.08 to 0.81, p = 0.02), respectively.
Conclusions: Longer duration of clopidogrel use was associated with a lower incidence of death or MI in both the BMS and DES groups. Among clopidogrel nonusers, the incidence of death/MI or death did not differ by stent type.
COMENTARIOS de Dr Piñero:
- Estamos hablando de pacientes diabéticos, en donde más indicados están los DES (por la alta tasa de reestenosis que presentan estos pacientes)
- Cuánto mayor tiempo se use Clopidogrel parece que menor es la tasa de IAM/muerte TANTO para DES como BMS. PERO ¿por qué recomendaban tanto tiempo el clopidogrel a los paciente con BMS? (¿por ser SCA?, si es así habría que dar de todas todas 1 año de clopidogrel independeientemente del tipo del Stent, si no me equivoco)
- Aunque no se encuentran diferencias estadísticamente significativas de IAM/Mortalidad entre los pacientes que no toman clopidogrel, independientemente del tipo de Stent, sí que parece que existe un efecto favorable de los DES (a pesar de no tomar Clopidogrel; HR 0.39 (95% CI 0.13 to 1.13, p = 0.08)).
Esto podría ser importante y a discutir, porque en principio en todos los pacientes que no van a poder tomar clopidogrel ni se plantea el poner un DES- Se trata de un estudio observacional, no es un ensayo clínico, por lo que hay que tener cuidado con la interpretación de los resultados.
CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY
Long-Term Outcomes by Clopidogrel Duration and Stent Type in a Diabetic Population With De Novo Coronary Artery Lesions
Somjot S. Brar, MD*,*, John Kim, MD, Simerjeet K. Brar, BS, Ray Zadegan, MD, Michael Ree, BS, In-Lu A. Liu, MS, Prakash Mansukhani, MD, Vicken Aharonian, MD, Ric Hyett, BS and Albert Yuh-Jer Shen, MDObjectives: The purpose of this study was to determine whether long-term clinical outcomes differed between bare-metal stents (BMS) and drug-eluting stents (DES) by duration of clopidogrel use among diabetic patients.
Background: There is concern that DES are associated with late adverse events such as death and myocardial infarction (MI) secondary to stent thrombosis. However, data on outcomes in diabetic patients remain limited.
Methods: We identified 749 patients with diabetes mellitus who underwent stent implantation with either BMS (n = 251) or DES (n = 498) from October 2002 to December 2004. We performed survival analysis on the full cohort and on those event-free from death, MI, or repeat revascularization at 6 months (n = 671).
Results: By clopidogrel duration, the event rate for death or MI was 3.2% in the >9-month group, 9.4% in the 6- to 9-month group, and 16.5% in the <6-month>9-month group, 4.3% in the 6- to 9-month group, and 10.0% in the <6-month group, p < 0.001. When taking BMS clopidogrel non-users as a referent in the multivariate analysis, the hazard ratio (95% confidence interval [CI]) for death and nonfatal MI for DES clopidogrel users, DES clopidogrel nonusers, and BMS clopidogrel users were: HR 0.22 (95% CI 0.08 to 0.62, p = 0.005), HR 0.39 (95% CI 0.13 to 1.13, p = 0.08), and HR 0.25 (95% CI 0.08 to 0.81, p = 0.02), respectively.
Conclusions: Longer duration of clopidogrel use was associated with a lower incidence of death or MI in both the BMS and DES groups. Among clopidogrel nonusers, the incidence of death/MI or death did not differ by stent type.
COMENTARIOS de Dr Piñero:
- Estamos hablando de pacientes diabéticos, en donde más indicados están los DES (por la alta tasa de reestenosis que presentan estos pacientes)
- Cuánto mayor tiempo se use Clopidogrel parece que menor es la tasa de IAM/muerte TANTO para DES como BMS. PERO ¿por qué recomendaban tanto tiempo el clopidogrel a los paciente con BMS? (¿por ser SCA?, si es así habría que dar de todas todas 1 año de clopidogrel independeientemente del tipo del Stent, si no me equivoco)
- Aunque no se encuentran diferencias estadísticamente significativas de IAM/Mortalidad entre los pacientes que no toman clopidogrel, independientemente del tipo de Stent, sí que parece que existe un efecto favorable de los DES (a pesar de no tomar Clopidogrel; HR 0.39 (95% CI 0.13 to 1.13, p = 0.08)).
Esto podría ser importante y a discutir, porque en principio en todos los pacientes que no van a poder tomar clopidogrel ni se plantea el poner un DES- Se trata de un estudio observacional, no es un ensayo clínico, por lo que hay que tener cuidado con la interpretación de los resultados.
sábado, 7 de junio de 2008
Presentacion
Hola a todos:
Bienvenidos al Blog del Servicio de Cardiología de la Fundación Jiménez Díaz - CAPIO, dedicado a aportar comentarios, discusiones ... sobre artículos y temas de actualidad en Cardiología. Creemos que tenemos que adentrarnos en el futuro y poder disponer de todas las herramientas actuales que permitan la mayor transmisión y difusión de conocimientos y que además permita poder discutir sobre los mismos para asi enriquecerlos entre todos. El trabajo debe ser diario pero debe y puede ser compartido y hecho por todos aquellos que quieran participar en el mismo. Esto tan sólo es el comienzo y poco a poco conseguiremos si nos lo proponemos hacer algo mas que una página web, y es un auténtico "foro" de discusión donde nos sintamos parte de un todo dedicado a la ampliación de conocimientos.
Suscribirse a:
Entradas (Atom)