Patients with diabetes mellitus (DM) are at a greater risk of mortality and cardiovascular events after percutaneous coronary intervention than those without DM. We aimed to determine whether differences exist in the long-term mortality of patients with versus without DM who present with acute myocardial infarction and receive drug-eluting stents. Data were collected on 161 patients with and 395 without DM referred for primary percutaneous coronary intervention for acute myocardial infarction and treated with drug-eluting stents. The patients with cardiac arrest or cardiogenic shock were excluded. The 1-year major cardiac event (MACE) rates, defined as death, Q-wave myocardial infarction, or target lesion revascularization, were compared between the 2 groups. The patients with DM were sicker at baseline. The MACE rates at 1 year were significantly increased in those with DM compared to those without DM. This was primarily driven by all-cause mortality. No differences in Q-wave myocardial infarction, target lesion revascularization, stent thrombosis, type of drug-eluting stents used, or procedure-related renal failure were seen. No differences were found in death or MACE rates at 1 year after adjusting for age, gender, race, systemic hypertension, peripheral artery disease, and a history of chronic renal failure between the 2 groups (weighted log-rank statistic, p = 0.37 and p = 0.37, respectively). In patients presenting with acute myocardial infarction, those with DM were sicker than those without DM. In conclusion, after correction for co-morbid conditions, no difference was seen in the 1-year MACE or death rates between those with and without DM who presented with acute myocardial infarction and were treated with drug-eluting stents.
Diabetes mellitus (DM) is a risk factor for coronary artery disease and is considered a coronary artery disease equivalent. Furthermore, in nearly every therapy trial, DM has proved to be a predictor of adverse outcomes. For example, DM appears to be an independent predictor of mortality in patients with left ventricular dysfunction after acute myocardial infarction. In the patients with DM and stable coronary artery disease, drug-eluting stent use reduces the risk of subsequent major adverse cardiac events (MACE) compared to the use of bare metal stents. In contrast, evidence of a beneficial effect of drug-eluting stents on the outcome in patients with DM with acute coronary syndrome is less clear. The results of randomized controlled trials of drug-eluting stent and bare metal stent use in acute myocardial infarction have been controversial and have not included enough patients with DM to allow subset analyses. A recent review of a large registry and a meta-analysis of available randomized trials appeared to indicate a benefit for drug-eluting stents in terms of intermediate and late outcomes. The present study was undertaken to report a large “real world” experience in patients with DM and acute myocardial infarction receiving drug-eluting stents. Their outcomes were then compared to the results of those without DM. Our aim was to evaluate whether drug-eluting stent use could reduce MACE in patients with DM compared to those without DM, as was previously reported.
Methods
A cohort of 556 consecutive patients who presented with acute myocardial infarction and received a drug-eluting stent at Washington Hospital Center from April 2003 to October 2007 were studied. After we obtained approval for a Health Insurance Portability and Accountability Act waiver from our local institutional review board, we extracted from the database the data for all patients who corresponded to the inclusion criteria and conducted a retrospective analysis of the clinical outcomes. Patients were classified into 2 groups according to the presence or absence of DM. We identified 161 patients with DM and 395 without DM.
Coronary angioplasty was performed in the conventional manner, and coronary stents or other procedures/devices were used when required. Adjunct balloon inflation was added after initial stent deployment in all cases. Optimal stent implantation was carefully monitored using an iterative technique with intravascular ultrasound monitoring in most cases. In all cases, the interventional strategy, including the use of direct stenting, before or after dilation, intravascular ultrasonography, use of ablative devices, choice of periprocedural adjunctive antiplatelet therapy, and choice of antithrombotic regimen, was at the discretion of the responsible physician. Angiographic success was defined as stenosis of ≤30% with a Thrombolysis In Myocardial Infarction flow grade 3. All patients received aspirin 325 mg/day before the intervention and continued with it indefinitely. Additional antiplatelet therapy with either clopidogrel 75 mg/day (after a loading dose of 300 to 600 mg) or ticlopidine 250 mg twice daily was instituted in all patients and was continued for ≥1 year.
The anticoagulation regimen consisted of either bivalirudin with or without low-dose heparin mixed in the contrast media or weight-adjusted unfractionated heparin. After sheath insertion, bivalirudin was administered as a bolus dose of 0.75 mg/kg and then as an intravenous infusion of 1.75 mg/kg/hour for the duration of the procedure to achieve an activated clotting time of 250 to 300 seconds for unfractionated heparin and >250 seconds for bivalirudin. The activated clotting time was routinely measured before and during percutaneous coronary intervention (Hemochron, International Technidyne, Edison, New Jersey). Aspirin was administered to all patients at the dose of 325 mg orally before percutaneous coronary intervention, with indefinite continuation encouraged. The use of glycoprotein IIb/IIIa inhibitors was at the discretion of the operator.
The study end point for analysis was MACE, defined as a composite of death, Q-wave myocardial infarction, and target lesion revascularization. A dedicated data-coordinating center (Data Center, MedStar Research Institute, Washington, DC) performed all data management and analyses. The prespecified clinical and laboratory data during hospitalization were obtained from hospital charts reviewed by independent research personnel who were unaware of the study objectives. DM was defined as either a previous diagnosis of DM treated with diet, oral agents, or insulin or a new diagnosis of DM if the fasting glucose level was >140 mg/dl on 2 different occasions during hospitalization. Death was defined as all causes of mortality. Acute myocardial infarction was defined as chest pain with ≥1 mm of ST-segment elevation on ≥2 contiguous electrocardiographic leads, chest pain refractory to medical therapy with associated ST-segment depression in leads V 2 to V 5 (consistent with posterior injury), or new left bundle branch block. Patients presenting with cardiogenic shock or cardiac arrest requiring cardiopulmonary resuscitation were excluded. Patients for whom primary angioplasty was not the first-line therapy were also excluded. Target lesion revascularization and target vessel revascularization were characterized by repeat percutaneous or surgical intervention of the treated lesion or vessel, respectively, and were clinically driven. All clinical events were adjudicated by source documentation by independent physicians who were not involved in the procedures.
Statistical analysis was performed using Statistical Analysis Systems, version 9.1 (SAS Institute, Cary, North Carolina). Data are expressed as the mean ± SD for continuous variables and as percentages for categorical variables. Student’s t test was used to compare continuous variables, and the chi-square test or Fischer’s exact test was used to compare categorical variables. p Values <0.05 were considered to indicate statistical significance. Cox proportional hazard analysis was used to identify predictors of MACE. Cox proportional regression models were used to control for differences between the 2 groups. Event-free survival curves were constructed using Kaplan-Meier curves.
Results
The baseline clinical characteristics were comparable, although the patients with DM were more likely to be older, obese, women, and African American, were more likely to have greater rates of systemic hypertension, hyperlipidemia, peripheral artery disease, heart failure, and chronic renal insufficiency, and were less likely to be current smokers ( Table 1 ). The patients with DM were also more likely to be taking a calcium channel blocker. In addition, the baseline hemoglobin A1c was 9.09 ± 8.65% in those with DM and 5.92 ± 1.50% in those without DM. Approximately 1/3 of the patients with DM were identified as insulin dependent (n = 51 of 161). The patients with DM were more likely to have a greater number of diseased vessels and vein graft intervention. The use of paclitaxel- or sirolimus-eluting stents was similar between the 2 groups. Intravascular ultrasonography and postdilation were performed more frequently in the DM group ( Table 2 ).
| Variable | DM (n = 161) | No DM (n = 395) | p Value |
|---|---|---|---|
| Age (years) | 63.58 ± 12.65 | 61.00 ± 14.21 | 0.046 ⁎ |
| Men | 92/161 (57.1%) | 280/395 (70.9%) | 0.002 ⁎ |
| Body mass index (kg/m 2 ) | 30.99 ± 7.01 | 28.34 ± 5.54 | <0.001 ⁎ |
| Current smoker | 39/161 (24.2%) | 153/395 (38.7%) | 0.001 ⁎ |
| African American | 68/161 (42.2%) | 76/395 (19.2%) | <0.001 ⁎ |
| Systemic hypertension † | 148/160 (92.5%) | 301/395 (76.2%) | <0.001 ⁎ |
| Hyperlipidemia | 142/158 (89.9%) | 310/392 (79.1%) | 0.003 ⁎ |
| Previous congestive heart failure | 17/154 (11.0%) | 24/372 (6.5%) | 0.074 |
| Previous myocardial infarction | 118/152 (77.6%) | 289/377 (76.7%) | 0.810 |
| Previous coronary artery bypass | 32/161 (19.9%) | 37/395 (9.4%) | <0.001 ⁎ |
| Previous percutaneous coronary intervention | 38/150 (25.3%) | 57/378 (15.1%) | 0.006 ⁎ |
| Family history of coronary artery disease | 73/149 (49.0%) | 173/373 (46.4%) | 0.589 |
| Peripheral vascular disease | 33/159 (20.8%) | 31/391 (7.9%) | <0.001 ⁎ |
| History of chronic renal insufficiency | 38/159 (23.9%) | 33/393 (8.4%) | <0.001 ⁎ |
| Ejection fraction | 0.43 ± 0.13 | 0.45 ± 0.11 | 0.278 |
| Angiotensin-converting enzyme inhibitors | 107/154 (69.5%) | 267/388 (68.8%) | 0.880 |
| Angiotensin-receptor blockers | 16/135 (11.9%) | 27/343 (7.9%) | 0.171 |
| β Blockers | 134/154 (87.0%) | 338/388 (87.1%) | 0.975 |
| Calcium channel blocker | 19/137 (13.9%) | 24/345 (7.0%) | 0.016 ⁎ |
| Statins | 151/152 (99.3%) | 370/372 (99.5%) | 1.000 |
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