ESC/ESH 2007 Guidelines for the management of arterial hypertension   Full Text

See also: Current Guidelines for Vascular Disease

Pathogenesis of chronic Chagas heart disease

This article [1] examines the pathogenesis of chronic Chagas cardiomyopathy by performing a systematic review of the literature (MEDLINE, EMBASE, BIREME, LILACS, SCIELO) to search for relevant references on the pathogenesis and pathophysiology of Chagas disease.

From evidence gathered through studies in animal models and in anima nobile (humans), the authors note that four main pathogenetic mechanisms have been advanced to explain the development of Chagas heart disease. These include: cardiac dysautonomina, microvascular disturbances, parasite-dependent myocardial damage and immuni-mediated myocardial injury. The authors also found that “although autonomic derangements and microcirculatory disturbances constitute prominent peculiarities in Chagas cardiomyopathy, their role in the pathogenesis of chronic myocardial lesions is probably ancillary rather than fundamental in the mechanism of the disease.”

The authors conclude that “the pathogenesis of chronic Chagas heart disease is inexorably dependent on a low-grade but incessant systemic infection with documented autoimmune reaction.” Further, “parasite persistence and immunological mechanisms are inextricably related in the myocardial aggression in the chronic phase of Chagas heart disease”. They note that that most of the clinical studies have been performed in a small number of patients and suggest that “future research should appropriately focus on the exploration of the logical consequences of both underlying pathogenetic mechanisms and their clinical potential implications and therapeutic opportunities.”

[1] Marin-Neto, JA, Cunha-Neto E, Maciel BC. Pathogenesis of chronic Chagas heart disease. Circulation 2007;115:1109-1123

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See also: Development and validation of a risk score for predicting death in Chagas’ heart disease

Development and validation of a risk score for predicting death in Chagas’ heart disease

The main objective of this study [1] was to develop a risk score derived from the combination of independent predictors of death for patients with Chagas’ disease.

This retrospective study was based on clinical data of patients (n=424) who were diagnosed with Chagas’ disease and had chronic cardiac involvement, at Hospital São Salvador, a nontertiary regional referral center in central Brazil, between December 1986 and December 1991 (development cohort). At the time of enrollment, patients underwent a number of assessments to determine: electrocardiographic abnormalities (classified according to modified Minnesota code adapted for Chagas’ disease); left ventricular (LV) function; LV end-diastolic diameter; cardiomegaly; total numbers of premature ventricular complexes and episodes of nonsustained ventricular tachycardia; and heart-rate variability. These patients received treatment based on the outcome of the assessments and were followed until death or until the last ambulatory visit in 1997 or 1998. The association of potential risk factors with death was tested by Cox proportional hazards analysis. A validation cohort was established from an additional set of patients from another clinical database who were retrospectively screened according to the same inclusion and exclusion criteria as the development cohort.

During a mean follow-up of 7.9±3.2 years, 130 patients died. Of these deaths, 81 (62.3%) were sudden, 20 (15.4%) were due to progressive heart failure, 12 (9.2%) were due to other cardiovascular causes and 16 (12.3%) were due to noncardiovascular causes. Six independent prognostic factors was identified and each was assigned a number of points proportional to its regression coefficient as follows: New York Heart Association class III or IV (5 points); evidence of cardiomegaly on radiography (5 points); LV systolic dysfunction on echocardiography (3 points); nonsustained ventricular tachycardia on 24-hour Holter monitoring (3 points); low QRS voltage on electrocardiography (2 points), and male sex (2 points). Risk scores, defined as patients at low risk (0–6 points), intermediate risk (7–11 points), and high risk (12–20 points) for death were calculated for each patient. For the development cohort, the 10-year mortality rates for these groups were 10%, 44% and 84% respectively. Similarly, the validation cohort mortality rates were 9%, 37% and 85% respectively. The development cohort had a C statistic for the point system of 0.84 and the validation cohort had 0.81.

The authors conclude that their study “demonstrates that the long-term risk of death among patients with chronic Chagas’ heart disease is predicted by the presence of six clinical features.” This conclusion was validated by the independent sample of patients from a different site. While the authors note that there are some limitations to the study, e.g. selection bias might have occurred, some important prognostics were not included such as ventricular repolarization variables or inducibility of ventricular tachyarrhythmias, and assessment of the effect of therapy on survival was not controlled, “these findings may be useful to clinicians for predicting individual survival probabilities and directing therapy, to researchers for designing and interpreting clinical trials, and to policymakers for allocating limited health care resources.”

[1] Rassi, Jr. A, Rassi, A, Little WC et al. Development and validation of a risk score for predicting death in Chagas’ heart disease. N Engl J Med 2006;355:799-808

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Randomized trial of pulsed corticosteroid therapy for primary treatment of Kawasaki disease

This study [1] used a multicenter, randomized, double-blind, placebo-controlled trial within the Pediatric Heart Network to determine whether the addition of intravenous (IV) methylprednisolone to conventional treatment with IV immunoglobulin (IVIg; 2 g/kg/day) plus aspirin (80–100 mg/kg/day) in the treatment of acute Kawasaki disease reduces the risk of coronary artery abnormalities.

A total of 199 patients with 10 or fewer days of fever were randomly assigned to receive either 30 mg/kg of body weight of IV methyprenisolone over a 2–3 hour period (101 patients) or placebo infusion (98 patients) within strata according to age (<1 year or ≥1 year) and sex with the use of dynamic balancing at each Center. All patients received the conventional treatment until they were afebrile for 48 hours and then they received aspirin (3–5 kg) daily until the study was completed. The primary outcome variable was the larger of the z scores for the right coronary artery (RCA) and the left anterior descending coronary artery (LAD)at week 5 after randomization; coronary artery dimensions were transformed to z scores (standard-deviation units) on the basis of body surface area.

The IV methylprednisolone group and placebo group had similar mean values (1.31±1.55 and 1.39±2.0 respectively; P=0.76). The percentage of patients with coronary-artery abnormalities as defined by meeting the criteria of the Japanese Ministry of Health for aneurysms, or those associated with z scores for the proximal LAD or RCA of ≥2.5 was not significantly different between the two groups. There was similar z scores between the two groups for the proximal RCA and the LAD, similar absolute dimensions of the seven measured coronary segments, and similar changes in dimension from baseline to week 1 and 5 with the exception of the data for the posterior descending artery at week 5 and its change from baseline. Aortic-root z scores were similar in the IV methylprednisolone group and the placebo group at week 1 and week 5. The time to first hospital discharge was marginally shorter in the IV methylprednisolone group than in the placebo group, but the two groups had similar total numbers of days in the hospital and days of fever both after randomization and after the onset of illness. The groups also did not differ significantly in the percentage of patients who were retreated at least once with IVIg or in the total episodes of retreatment with IVIg. Laboratory measures were similar in the two groups at weeks 1 and 5 with the exception of lower erythrocyte sedimentation rate; lower serum IgA level at week 1 with a tendency toward a lower C-reactive protein at week 1; and a higher hemoglobin level at week 5 for the methylprednisolone group in comparison to the placebo group. The total number of adverse events did not different significantly between the two groups.

The authors concluded that “primary therapy” with pulsed IV methylprednisolone, administered as a single dose of 30 mg/kg before conventional therapy with IVIg (2 g/kg), did not improve coronary artery outcomes at week 1 or week 5 after study enrollment.” They do suggest that “children at highest risk for resistance to IVIg and for coronary abnormalities may benefit from corticosteroid therapy” and they call for prospective studies to explore the usefulness of corticosteroid or other immunomodulating therapies in this group. It should be noted, however, that the study was underpowered for subgroup analyses and for detection of between-group differences in the numbers of adverse events.

[1] Newburger JW, Sleeper LA, McCrindle BW, et al. Randomized trial of pulsed corticosteroid therapy for primary treatment of Kawasaki disease. N Engl J Med 2007;356:663-675

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The Role of PCI in Patients with Chronic Stable Angina
Dr David R. Holmes, Jr.

The role of percutaneous coronary intervention (PCI) in patients with chronic stable angina vis a vis optimal medical therapy continues to be evaluated. Most recently, this was the focus of the COURAGE trial [1,2]. In patients with chronic stable angina, particularly those with mild ischemia, multiple studies have documented that PCI is very effective in decreasing the need for subsequent revascularization procedures and also in decreasing symptoms of angina. These studies however have not shown that PCI is associated with a reduction mortality or infarction. The rates of both of these latter endpoints are very low in low risk patients with stable angina.

The COURAGE trial while it received considerable interest and was the focus of significant controversy documented similar findings to those which have been seen before. There was a striking reduction in subsequent procedures but no significant decrease in death and myocardial infarction (MI) during follow-up. There are multiple issues with the COURAGE trial. These included:

1) only a small percentage of patients screened

2) a substantial number of patients had either no angina or very mild angina

3) drug-eluting stents were used very infrequently, and

4) adherence to medical therapy was achieved in a higher percentage of patients than is usually seen or documented.

It is also important to note that patients were entered into the trial only after angiography. This has important implications for screening.

Irrespective of these issues, the results are not surprising. In patients with chronic stable angina, which is typically mild, PCI improves angina and decreases the need for subsequent revascularization procedures. This does not impact on death or MI. Optimal medical therapy is required to improve the outcome of patients irrespective of whether PCI is chosen or not.

[1] Boden WE, O’Rouke RA, Teo KK, et al. Optimal medical therapy with or without PCI for stable coronary disease. (COURAGE Trial Research Group). N Eng J Med 2007;356(15):1503-1516 (Note: You may need a subscription to access this linked reference. You are responsible for obtaining this subscription.)

[2] Optimal medical therapy with or without PCI for stable coronary disease (COURAGE Trial Research Group). http://cardiovascular-medicine.com/?p=47

See also: Increased risk in patients with high platelet aggregation receiving chronic clopidogrel therapy undergoing percutaneous coronary intervention: Is the current antiplatelet therapy adequate?

Optimal medical therapy with or without PCI for stable coronary disease (COURAGE Trial Research Group)

This study, the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial [1], examined the benefit of combining percutaneous coronary intervention (PCI) and optimal medical therapy to reduce the risks of death and nonfatal myocardial infarction (MI) in patients with stable coronary artery disease versus optimal medical therapy alone.

A total of 2,287 patients who met the eligibility criteria (objective evidence of myocardial ischemia and significant coronary artery disease) were enrolled in the study between 1999 and 2004 from 50 US and Canadian centers and randomly assigned to undergo PCI with optimal medical therapy (PCI group; n=1149) or optimal medical therapy alone (Medical-Therapy group; n=1138). These patients were followed for a period of 2.5 to 7.0 years (median 4.6 years). Baseline characteristics of the two groups were similar. The primary outcome measure was a composite of death from any cause and nonfatal MI; secondary outcome measures included a composite of death, MI, and stroke and hospitalization for unstable angina with negative biomarkers.

A total of 211 patients in the PCI group and 202 patients in the medical-therapy group experienced death or nonfatal MI. The estimate of 4.6 year cumulative primary event rates were 19% and 18.5% in the PCI group and medical therapy groups respectively (hazard ratio [HR] for the PCI group 1.05; 95% confidence interval [CI], 0.87 to 1.27; P=0.62). No significant differences were found between the PCI and medical therapy groups in the composite of death, MI or stroke (20.0% vs 19.5%; HR 1.05; 95% CI, 0.87 to 1.27; P=0.62); hospitalization for acute coronary syndrome (12.4% vs 11.8%; HR 1.07, 95% CI, 0.84 to 1.37; P=0.56); or MI (13.2% vs 12.3%; HR 1.13; 95% CI, 0.89 to 1.43; P=0.33). At the median follow-up, 21.1% of the patients in the PCI group had additional revascularization vs 32.6% of the patients in the medical therapy group (HR 0.60; 95% CI 0.51 to 0.71; P<0.001). By 5 years, no statistically significant difference was found between groups for patients that were free of angina (74% of the patients in the PCI group vs 75% of the patients in the medical-therapy group; P=0.35).

Based on these findings, the authors conclude that “as an initial management strategy, PCI added to optimal medical therapy did not reduce the primary composite end point of death and nonfatal myocardial infarction or reduce major cardiovascular events, as compared with optimal medical therapy alone, during follow-up of 2.5 to 7.0 years, despite a high baseline prevalence of clinical co-existing illnesses, objective evidence of ischemia, and extensive coronary artery disease as seen on angiography.” They also note that both groups experienced improvement in relief from angina and no significant differences were found for any secondary outcomes nor was there any significant interaction between treatment effect and prespecified subgroup variables. The authors indicate that their findings, which parallel those of other trials, reinforce existing clinical practice guidelines that “PCI can be safely deferred in patients with stable coronary artery disease, even in those with extensive, multivessel involvement and inducible ischemia, provided that intensive, multifaceted medical therapy is instituted and maintained.”

[1] Boden WE, O’Rouke RA, Teo KK, et al. Optimal medical therapy with or without PCI for stable coronary disease. (COURAGE Trial Research Group). N Eng J Med 2007;356(15):1503-1516

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See also: Increased risk in patients with high platelet aggregation receiving chronic clopidogrel therapy undergoing percutaneous coronary intervention: Is the current antiplatelet therapy adequate?

Increased risk in patients with high platelet aggregation receiving chronic clopidogrel therapy undergoing percutaneous coronary intervention: Is the current antiplatelet therapy adequate?

This study [1] examines the hypothesis that “patients receiving chronic clopidogrel therapy undergoing non-emergent PCI who display high preprocedural platelet reactivity, as measured by standard light transmittance aggregometry (LTA) and thrombelastography (TEG), are at increased risk for post-PCI ischemic events.”
The study consisted of 100 consecutive patients who were >18 years of age and who received clopidogrel therapy (75 mg qd) for ≥1 month and at least 81 mg aspirin 7 days before undergoing non-emergent coronary stenting. All the study patients received clopidogrel and aspirin therapy for at least 6 months after the procedure. The primary outcome at the 1-year follow up after coronary stenting was occurrence of death, myocardial infarction, stent thrombosis, stroke, or ischemia that required a hospital stay.

At the 1-year follow up, 26 ischemic events occurred in 23 patients (23%). The patients with ischemic events had greater on-treatment present ADP-induced platelet aggregation than patients without ischemic events by LTA and TEG (P<0.001 for both measurements). In the 23 patients with ischemic events, 70% and 87% displayed high on-treatment platelet reactivity at baseline by LTA and TEG, respectively. The only variables significantly related to ischemic events were high on-treatment platelet reactivity as measured by LTA and TEG (P<0.001 for both assays). Eptifibatide administration reduced periprocedural elevation in platelet reactivity, with no significant differences in bleeding events.

The authors conclude that the “current study demonstrates that patients receiving chronic clopidogrel therapy undergoing nonemergent PCI who exhibit high on-treatment preprocedural ADP-induced platelet aggregation as measured by LTA (≥50%) ADP-induced aggregation) or TEG (≥70% ADP-induced aggregation) are at increased risk for recurrent ischemic events.” The authors note that their results are consistent with other previous studies, e.g. CREST (Clopidogrel Effect on Platelet Reactivity in Patients with Stent Thrombosis) and PREPARE POST STENTING (Platelet Reactivity in Patients with Recurrent Events Post-Stenting), that also demonstrate that there is a relationship among inadequate platelet inhibition, the occurrence of stent thrombosis and recurrent ischemic events.

This study was limited because of its small sample size, patients were not given an additional loading dose of clopidogrel, inherent differences within the study population by virtue of their need for repeat PCI could have impacted the prevalence of high platelet reactivity, flow cytometric platelet surface P-selectin and GP IIb/IIIa expression were not measured and medication was not provided and distributed by the study. The authors suggest that their “findings may have implications for the alteration in clopidogrel maintenance dose and use of glycoprotein IIb/IIIa inhibitors in selected patients” and note that addition prospective studies are needed to determine the efficacy of these regiments in patients with high on-treatment platelet reactivity.

[1] Bliden KP, DeChiara J, Tantry US, et al. Increased risk in patients with high platelet aggregation receiving chronic clopidogrel therapy undergoing percutaneous coronary intervention: Is the current antiplatelet therapy adequate? J Am Coll Cardio 2007;49:657-666

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Gender differences in hospital mortality and use of percutaneous coronary intervention in acute myocardial infarction: Microsimulation analysis of the 1999 nationwide French Hospitals Database

The goals of this study [1] were “to compare age-adjusted, gender-specific hospital mortality rates for patients hospitalized for acute myocardial infarction and to determine whether variation in mortality rates could be explained by gender differences in epidemiology, in patterns of use of percutaneous coronary intervention (PCI) or in the benefit of PCI.”

This study extracted a total of 74,389 patients from the national payment database in France from all hospital admissions in 1999 with a discharge diagnosis of acute myocardial infarction (AMI). The study variables included: gender and age (demographic); heart failure, valvular disease, conduction disease, diabetes mellitus, severe hypertension, renal insufficiency, stroke and peripheral arterial disease (comorbid conditions); and cardiac catheterization, percutaneous coronary angioplasty, and stenting (procedural). In this study, PCI with stenting was considered representative of coronary intervention. Logistical regressions were performed to test for gender differences in mortality and use of coronary interventions in each age group. A series of microsimulation models were developed that estimated the PCI and mortality rates that women would experience if they were “treated like men.” Women comprised 30% of the admissions for patients diagnosed with acute myocardial infarction.

The mean age of women and men was 75 and 63 years respectively (P<0.001); women had a higher hospital mortality rate than men (14.8% vs 6.1%; P<0.001). Men received PCI more frequently than women (7.4% vs 4.8%; 24.4% vs 14.2% with stent; P<0.001). Women had a higher mortality when adjusted for age and comorbidities (P<0.001) with an excess adjusted absolute mortality of 1.95%. Of this excess, the simulation model attributed 0.46% (relative percentage, 23.6%) of the excess to the reduced use of procedures. The survival benefit related to PCI was lower among women.

The authors conclude that their “analysis confirms the higher age-adjusted mortality rate from AMI in women relative to men …” and that “the results …show that, after adjustment for age and comorbid conditions, there was a persistent mortality difference between men and women,” which strongly supports the hypothesis of gender disparity. The authors speculate, however, that even if women were treated like men, some excess mortality would remain, possibly because of smaller target-vessel size, increased vessel tortuosity and other biological differences. Nevertheless, they suggest that their results “strengthen the case for better dissemination and implementation of guidelines for AMI treatment in women.” The authors note that the strength of their findings is the size of the population and the use of microsimulation analyses. To their knowledge, the microsimulation analyses used in this study have not ever been used before in the analysis of healthcare delivery.

[1] Milcent C, Dormont B, Durand-Zaleski I, et al. Gender differences in hospital mortality and use of percutaneous coronary intervention in acute myocardial infarction: Microsimulation analysis of the 1999 nationwide French Hospitals Database. Circulation 2007;115:833-839

[2] Anderson RD, Pepine CJ, Gender differences in the treatment for acute myocardial infarction: Bias or Biology? (Editorial). Circulation 2007;115:823-826

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See also: Randomized early versus late abciximab in acute myocardial infarction treated with primary coronary intervention (RELAx-AMI Trial)

Randomized early versus late abciximab in acute myocardial infarction treated with primary coronary intervention (RELAx-AMI Trial)

This prospective randomized trial [1] on patients with acute myocardial infarction (AMI) who were treated with primary stenting compares the impact of early administration of abxicimab in the emergency room versus administration in the catheterization laboratory on angiographic outcome, microvascular reperfusion, myocardial salvage, and left ventricular (LV) function.

A total of 232 consecutive patients diagnosed with first AMI who were referred to the Misericordia e Dolce Hospital in Parto, Italy, for percutaneous coronary intervention (PCI) were enrolled in the trial between June 2003 and March 2006 and randomly assigned to the receive abxicimab either in the emergency room (early) or in the catheterization lab following coronary angiography (late) group. The primary end point was the pre-interventional angiographic finding as measured by the Thrombolysis In Myocardial Infarction (TIMI)) flow grade as well as corrected TIMI frame count (cTFC), and myocardial blush grade (MBG). The secondary end points included infarct size and LV functional recovery at 1 month.

Prior to PCI, angiographic analysis showed a significantly better initial TIMI flow grade 3 (early group 24% vs late group 10%; P=0.01), cTFC (early group 78±30 frames vs late group 92±21 frames; P=0.001) and MBG 2 or 3 (early group 15% vs late group 6%; P=0.02), which favored the early group. Multivariate analysis identified only early abciximab administration as an independent predictor of initial TIMI flow grade 3 (odds ratio 2.90; 95% CI 1.3-6.6; P=0.001). Post-PCI, however, tissue perfusion parameters were significantly improved in the early group on a consistent basis, as evaluated by 60-minute ST-segment reduction ≤70% (early group 50% vs late group 35%; P=0.03) and MBG 2 or 3 (early group 79% vs late group 58%; P=0.001). At 1 month, LV function recovery was significantly greater in the early group (mean gain ejection fraction early group 8±7% vs late group 6±7%, P=0.02; mean gain wall motion score index early group 0.4±0.03 vs late group 0.3±0.3, P=0.03). No statistically significant differences were found for cumulative major adverse cardiac events (death, recurrent myocardial infarction, repeat PCI, coronary artery bypass surgery and stroke) or for bleeding complications.

The authors concluded that the findings of this study suggest that “in patients with first AMI treated with PCI, early abxicimab administration in the emergency room compared with late in the catheterization laboratory significantly improves preprocedural angiographic epicardial flow … and tissue perfusion …” and improves post-interventional parameters of myocardial reperfusion. They note that their findings are similar to those found in other large randomized trials that demonstrate the benefit of abciximab in AMI. The authors acknowledge that the study was limited by the sample size that was not powered to detect differences in mortality or hard clinical end points; operator physicians who were not blinded to the treatment assignment, which may have introduced investigator bias; event reporting was by the investigators without involvement of any independent adjudication committee; and the study was designed before the use of a clopidogrel loading dose as standard therapy for patients undergoing PCI. The authors concluded, however, that “in patients with AMI treated with primary PCI, early abciximab administration improves pre-PCI angiographic findings and 1-month LV function, possibly by starting early recanalization of the IRA [infarct-related artery].”

[1] Maioli M, Bellandi F, Leoncini M, et al. Randomized early versus late abciximab in acute myocardial infarction treated with primary coronary intervention (RELAx-AMI Trial). J Am Coll Cardiol 2007;49(14):1517-1524

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Drug-Eluting Coronary Stents: Update
Dr. David Holmes, Jr.

There has been intense controversy about drug-eluting stents (DES) and the issue of stent thrombosis (ST). This began to surface in 2006 and then culminated in a Food & Drug Administration panel meeting [1] and then multiple publications (see recent entries). The issues around ST have been complicated by several factors:

1. The specific patient group in which the questions are asked; e.g. large multicenter registries versus carefully selected randomized clinical trials and patients in whom the indication for DES is “off label” versus “on label”. The data on ST varies depending on these considerations.

2. The length of follow-up. The timing of events varies – with bare metal stents (BMS) there are more adverse early events – with DES, the timing may be shifted later.

3. The definition of stent thrombosis and the completeness of ascertainment of specific cases.

4. The specific drug-eluting stent device evaluated.

5. Specific adjunctive therapy, particularly dual anti-platelet drugs, including dose and duration.

This controversy has had an actual measurable impact on the frequency of the use of DES. This has actually decreased slightly while the use of BMS has increased commensurately.
The following observations, however, can be made:

1. ST occurs with both BMS and DES. In patients receiving DES, the incidence may be shifted somewhat later.

2. In careful selected patient populations, the frequency of death and myocardial infarction during follow-up between those patients treated with DES and BMS is very similar.

3. In unselected patient population registries, the frequency of adverse events tends to be higher for both BMS and DES than seen in carefully selected randomized trials.

4. Dual antiplatelet therapy for an extended period of time appears to be a cornerstone treatment for patients with DES.

The issue of ST is an incredibly important one because of the often very severe adverse consequences of it. At the present time, new approaches are being tested including changes in polymer, changes in drug, and changes in metal backbone. Subsequent studies will evaluate the role of these changes in technology for prevention of this significant, albeit, very infrequent problem.

[1] FDA Statement on Coronary Drug-Eluting Stents (September 14, 2006)

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See also: Safety and efficacy of Sirolimus- and Paclitaxel-eluting coronary stents

A pooled analysis of data comparing Sirolimus-eluting stents with bare-metal stents

Are drug-eluting stents associated with a higher rate of late thrombosis than bare metal stents

Long-term outcomes with drug-eluting stents versus bare-metal stents in Sweden

Stent thrombosis in randomized clinical trials of drug-eluting stents

Analysis of 14 trials comparing sirolimus-eluting stents with bare-metal stents