Michael Kapeliovich

Fasting glucose is an important independent risk factor for 30-day mortality in patients with acute myocardial infarction: a prospective study.

Background—Stress hyperglycemia in patients with acute myocardial infarction has been associated with increased mortality. Most studies looked at the relationship between admission glucose (AG) and outcome; limited information is available about the clinical significance of fasting glucose (FG). Methods and Results—We prospectively studied the relationship between FG and 30-day mortality in 735 nondiabetic patients with acute myocardial infarction. FG (≥8-hour fast within 24 hours of admission) and AG were measured in each patient. At 30 days, 9 deaths (2%) occurred in patients with normal FG, and 11 (10%), 14 (13%), and 31 (29%) deaths occurred in the first, second, and third tertiles of elevated FG, respectively. Compared with normal FG (<110 mg/dL), the adjusted OR for 30-day mortality progressively increased with higher tertiles of elevated FG (first tertile, 4.6; 95% CI, 1.7 to 12.7; P=0.003; second tertile, 6.4; 95% CI, 2.5 to 16.6; P<0.0001; third tertile, 11.5; 95% CI, 4.7 to 20.0; P<0.0001). Compared with patients categorized as having normal AG (<140 mg/d), the adjusted ORs for tertiles of elevated AG were as follows: first tertile, 1.4 (95% CI, 0.5 to 3.8; P=0.54); second tertile, 3.0 (95% CI, 1.3 to 7.0; P=0.01); and third tertile, 4.4 (95% CI, 2.0 to 9.7; P<0.0001). Compared with patients with normal FG and AG, the adjusted ORs for 30-day mortality were 0.71 (95% CI, 0.15 to 3.4; P=0.67) in patients with elevated AG and normal FG, 3.4 (95% CI, 1.1 to 10.4; P=0.03) for patients with normal AG glucose and elevated FG, and 9.6 (95% CI, 3.5 to 26.0; P<0.0001) for patients with both elevated FG and AG. Comparing nested models showed that including AG failed to improve the prediction of the model based on FG (&khgr;2=5.4, 3 df, P=0.15). In contrast, the addition of FG classes to the model based on AG improved model prediction (&khgr;2=22.4, 3 df, P<0.0001). Conclusions—There is a graded relation between elevated FG and AG and 30-day mortality in patients with acute myocardial infarction. FG is superior to AG in the assessment of short-term risk. (Circulation. 2005;111:754-760.)

Impact of Red Blood Cell Transfusion on Clinical Outcomes in Patients With Acute Myocardial Infarction

Divergent views remain regarding the safety of treating anemia with red blood cell (RBC) transfusion in patients with acute coronary syndrome (ACS). We used a prospective database to study effect of RBC transfusion in patients with acute myocardial infarction (MI; n = 2,358). Cox regression models were used to determine the association between RBC transfusion and 6-month outcomes, incorporating transfusion as a time-dependent variable. The models adjusted for baseline variables, propensity for transfusion, and nadir hemoglobin previous to the transfusion. One hundred ninety-two patients (8.1%) received RBC transfusion. Six-month mortality rates were higher in patients receiving transfusion (28.1% vs 11.7%, p <0.0001). The adjusted hazard ratio (HR) for mortality was 1.9 in transfused patients (95% confidence interval [CI] 1.3 to 2.9). Interaction between RBC transfusion and nadir hemoglobin with respect to mortality (p = 0.004) was significant. Stratified analyses showed a protective effect of transfusion in patients with nadir hemoglobin < or=8 g/dL (adjusted HR 0.13, 95% CI 0.03 to 0.65, p = 0.013). By contrast, transfusion was associated with increased mortality in patients with nadir hemoglobin >8 g/dL (adjusted HR 2.2, 95% CI 1.5 to 3.3; p <0.0001). Similar results were obtained for the composite end point of death/MI/heart failure (p for interaction = 0.04). In conclusion, RBC transfusion in patients with acute MI and hemoglobin < or =8 g/dL may be appropriate. The increased mortality observed in transfused patients with nadir hemoglobin above 8 g/dL underscores the clinical difficulty of balancing risks and benefits of RBC transfusion in the setting of ACS.

Late thrombosis of sirolimus-eluting stents following noncardiac surgery

We describe two patients with in‐stent thrombosis occurring 4 and 21 months after implantation of sirolimus‐eluting stents. Both cases occurred following noncardiac surgery. In both cases, aspirin had been stopped prior to surgery. Both patient sustained a severe myocardial infarction; one died. The occurrence of late thrombosis of sirolimus‐eluting stents is of concern.

Incidence of early left ventricular thrombus after acute anterior wall myocardial infarction in the primary coronary intervention era

BACKGROUND Rapid reperfusion has been shown to decrease mortality and improve left ventricular (LV) function. Previous studies have reported that LV thrombus (LVT) is a major complication of ST-segment elevation acute anterior wall myocardial infarction (AMI). There are little data on LVT in the current primary percutaneous coronary intervention (PPCI) era. We sought to demonstrate the incidence of LVT after AMI in patients treated with PPCI compared with those treated with thrombolysis or with conservative management. METHODS In a 6-year period, 642 patients with anterior wall AMI and echocardiography were treated with PPCI (n = 297), thrombolysis (n = 128), or conservative treatment (n = 217). Left ventricular thrombus was defined as an echodense mass adjacent to an abnormally contracting myocardial segment. RESULTS The rate of LVT among anterior wall AMI was 6.2%. Predictors for LVT were reduced ejection fraction (adjusted relative risk 0.71, 95% CI 0.52-0.96) and severe mitral regurgitation (adjusted relative risk 2.48, 95% CI 1.0-6.44). There was no statistical difference in LVT rate according to treatment: 21 (7.1%) of 297 patients in the PPCI group, 10 (7.8%) of 128 patients in the thrombolytic group, and 9 (4.1%) of 217 patients in the conservative group (P = .28). Those in the thrombolytic group were characterized by shorter duration from symptom onset and were generally also treated with heparin/low-molecular weight heparin. CONCLUSIONS This is the largest report to evaluate the incidence of LVT formation after AMI. In the current era of rapid reperfusion by PPCI, the rate of thrombus formation is similar to that reported in the past and not different than for patients currently treated conservatively or with thrombolysis.

Late stent thrombosis after implantation of a sirolimus-eluting stent

Late stent thrombosis in the era of routine high‐pressure stent deployment and combined antiplatelet therapy with thienopyridines and aspirin has become a rare but feared complication. We describe a patient with acute myocardial infarction due to late stent thrombosis 6 weeks after deployment of a sirolimus‐eluting stent and 2 weeks after the discontinuation of clopidogrel. This is the first report of late thrombosis of a sirolimus‐eluting stent. Catheter Cardiovasc Interv 2003;60:505–508.

Fasting Glucose in Acute Myocardial Infarction: Incremental value for long-term mortality and relationship with left ventricular systolic function

OBJECTIVE—Elevation of blood glucose is a common metabolic disorder among patients with acute myocardial infarction (AMI) and is associated with adverse prognosis. However, few data are available concerning the long-term prognostic value of elevated fasting glucose during the acute phase of infarction. RESEARCH DESIGN AND METHODS—We prospectively studied the relationship between fasting glucose and long-term mortality in patients with AMI. Fasting glucose was determined after an ≥8 h fast within 24 h of admission. The median duration of follow-up was 24 months (range 6–48). All multivariable Cox models were adjusted for the Global Registry of Acute Coronary Events (GRACE) risk score. RESULTS—In nondiabetic patients (n = 1,101), compared with patients with normal fasting glucose (<100 mg/dl), the adjusted hazard ratio for mortality progressively increased with higher tertiles of elevated fasting glucose (first tertile 1.5 [95% CI 0.8–2.9], P = 0.19; second tertile 3.2 [1.9–5.5], P < 0.0001; third tertile 5.7 [3.5–9.3], P < 0.0001). The c statistic of the model containing the GRACE risk score increased when fasting glucose data were added (0.8 ± 0.02–0.85 ± 0.02, P = 0.004). Fasting glucose remained an independent predictor of mortality after further adjustment for ejection fraction. Elevated fasting glucose did not predict mortality in patients with diabetes (n = 462). CONCLUSIONS—Fasting glucose is a simple robust tool for predicting long-term mortality in nondiabetic patients with AMI. Fasting glucose provides incremental prognostic information when added to the GRACE risk score and left ventricular ejection fraction. Fasting glucose is not a useful prognostic marker in patients with diabetes.

Stent deployment failure: reasons, implications, and short- and long-term outcomes.

Stents have revolutionized percutaneous coronary interventions (PCI), impacting on both acute and long‐term results. However, despite improvements in stent design, stent deployment failure is not an unusual event. The aim of the present study was to assess the frequency and causes of stent deployment failure, as well as the outcome of these patients. Between 1997 and 2001, a total of 3,537 patients underwent stent‐assisted PCI and delivery of 5,275 stents was attempted. In the majority of patients (118; 78.1%), stenting was performed as provisional; in the remaining 33 (21.8%) as a bailout procedure. A total of 175 (3.3%) stents in 151 (4.3%) patients failed. Failure to deliver the stent to the lesion site was the main cause in 139 patients (92%) and failure either to expand adequately the stent or premature disengagement of the stent from the balloon in only 12 patients (8%). Peripheral stent embolization occurred in 10 (0.3%) patients. Deployment of a different stent in place of the failed one was attempted in 122 patients and was successful in the majority (108; 88.5%). In‐hospital major adverse cardiac events were observed in six patients (4%): three patients required emergency coronary artery bypass surgery, two had a myocardial infarction (MI), and one patient underwent urgent repeat coronary intervention. At a mean follow‐up of 32.2 ± 17.7 months, 22 major adverse cardiac event occurred in 17 patients (11.2%): 1 cardiac death, 3 patients had an MI, and 18 patients required target vessel revascularization. One‐year event‐free survival for the whole group was 91.2%. Patients with stent embolization did not have any major adverse cardiac or vascular events. Thus, the rate of stent deployment failure in our series was 3.3%, mainly due to failure to deliver the stent to the site. Another stent was successfully deployed in the majority of cases and these patients had favorable short‐ and long‐term outcomes. Cathet Cardiovasc Intervent 2003;59:324–328.

The impact of body mass index on clinical outcomes after acute myocardial infarction.

BACKGROUND Several studies indicated that an elevated body mass index (BMI) is associated with a lower rate of mortality in patients with acute myocardial infarction (AMI). However, the existence of the obesity paradox in AMI patients remains controversial. METHODS We examined the association of BMI and clinical outcomes in 2157 patient with AMI (mean follow-up of 26 months). BMI was categorized into 9 groups (<18.5, 18.5 to 20.9, 21.0 to 23.4, 23.5 to 24.9, 25.0 to 26.4, 26.5 to 27.9, 28.0 to 29.9, 30.0 to 34.9, and ≥35.0 kg/m2). Cox regression was used to calculate hazard ratios (HR) for the various BMI categories, adjusting for the clinical variables, left ventricular ejection fraction, and hemoglobin level. RESULTS BMI had a U-shaped association with mortality. Relative to the lowest mortality group (BMI of 26.5 to 27.9 kg/m2), the adjusted HRs for mortality were increased only in the lower (HR 2.3; 95% CI 1.3-4.2) and upper (HR 1.8; 95% 1.2-2.9) BMI categories. There was a significant interaction between BMI and anemia (P=0.0003) such that the U-shaped relationship between BMI and mortality was present mainly in patients with anemia. Patients in the lower and upper BMI categories and concomitant anemia had a striking increase in mortality (adjusted HR 5.1, 95% CI 1.9-11.7 and 3.2, 95% CI 1.5-7.0, respectively). CONCLUSION Both obesity and underweight are associated with increased mortality in patients with AMI. The risk of mortality is particularly high among underweight and obese patients with anemia.

The Relation between Serum Phosphorus Levels and Clinical Outcomes after Acute Myocardial Infarction

Background Elevated serum phosphorus levels have been linked with cardiovascular disease and mortality with conflicting results, especially in the presence of normal renal function. Methods We studied the association between serum phosphorus levels and clinical outcomes in 1663 patients with acute myocardial infarction (AMI). Patients were categorized into 4 groups based on serum phosphorus levels (<2.50, 2.51–3.5, 3.51–4.50 and >4.50 mg/dL). Cox proportional-hazards models were used to examine the association between serum phosphorus and clinical outcomes after adjustment for potential confounders. Results The mean follow up was 45 months. The lowest mortality occurred in patients with serum phosphorus between 2.5–3.5 mg/dL, with a multivariable-adjusted hazard ratio of 1.24 (95% CI 0.85–1.80), 1.35 (95% CI 1.05–1.74), and 1.75 (95% CI 1.27–2.40) in patients with serum phosphorus of <2.50, 3.51–4.50 and >4.50 mg/dL, respectively. Higher phosphorus levels were also associated with increased risk of heart failure, but not the risk of myocardial infarction or stroke. The effect of elevated phosphorus was more pronounced in patients with chronic kidney disease (CKD). The hazard ratio for mortality in patients with serum phosphorus >4.5 mg/dL compared to patients with serum phosphorus 2.50–3.50 mg/dL was 2.34 (95% CI 1.55–3.54) with CKD and 1.53 (95% CI 0.87–2.69) without CKD. Conclusion We found a graded, independent association between serum phosphorus and all-cause mortality and heart failure in patients after AMI. The risk for mortality appears to increase with serum phosphorus levels within the normal range and is more prominent in the presence of CKD.

Relation of Statin Therapy to Risk of Heart Failure After Acute Myocardial Infarction

Recent studies suggest that statin therapy reduces hospitalizations for heart failure (HF). However, few data exist regarding the role of statins in preventing HF after acute myocardial infarction (AMI). In addition, the potential impact of left ventricular (LV) ejection fraction (EF) and coexisting functional mitral regurgitation (MR) on the efficacy of statin therapy was not considered. We prospectively studied 1,563 patients with AMI. The primary endpoint was readmission for the treatment of HF. The effect of statin therapy initiated before hospital discharge was evaluated using a Cox model, adjusting for clinical variables, a propensity score for statin therapy, LVEF, and MR grade. Patients with recurrent infarctions were censored. Statins were prescribed in 1,048 patients (67.1%) before hospital discharge. During a median follow-up of 17 months, admissions for HF were lower in patients receiving statins (6.5% vs 14.8%; unadjusted hazard ratio 0.45, 95% confidence interval 0.32 to 0.63, p <0.0001). In a multivariable Cox model, statin therapy was associated with a significant reduction of hospitalization for HF (HR 0.62, 95% confidence interval 0.43 to 0.89, p = 0.009). There was a significant interaction between MR and statin therapy (p = 0.039), such that the beneficial effect of statins on HF hospitalizations was most pronounced in patients without concomitant MR and absent in patients with hemodynamically significant MR. In conclusion, in patients with AMI statin therapy initiated before hospital discharge significantly reduces subsequent hospitalizations for HF. The effect of statins is driven largely by the reduction in events in patients without concomitant hemodynamically significant MR.