Survival of patients undergoing rescue percutaneous coronary intervention: development and validation of a predictive tool.

OBJECTIVES: This study sought to develop a tool for predicting an individual's risk of mortality following rescue percutaneous coronary intervention (PCI). BACKGROUND: Although fibrinolytic therapy is appropriate and improves survival for certain ST-segment elevation myocardial infarction patients, a substantial proportion suffer ongoing myocardial ischemia, a class I indication for emergent percutaneous coronary intervention (rescue PCI). METHODS: Using the National Cardiovascular Data Registry (NCDR), rescue PCI was defined as nonelective PCI following failed fibrinolysis in patients with continuing or recurrent myocardial ischemia. Multivariable logistic regression was used to determine mortality predictors and the C-statistic for model discrimination. The NCDR-RESCUE (Real-World Estimator of Survival in Catheterized STEMI Patients Following Unsuccessful Earlier Fibrinolysis) score was developed using a shortened list of 6 pre-angiographic variables and 70% of the cohort; performance was subsequently validated against the remaining 30%. RESULTS: Among 166,516 PCI procedures on patients with an admission diagnosis of ST-segment elevation myocardial infarction, 8,007 (4.8%) represented rescue PCI. In-hospital mortality occurred in 464 (5.8%). Factors in the final model were age, glomerular filtration rate, history of congestive heart failure, insulin-treated diabetes, cardiogenic shock, and salvage status. The NCDR-RESCUE score effectively segregated individuals into 6 clinically meaningful risk categories, with 0.4% (0.0% to 1.3%), 1.6% (0.9% to 2.4%), 7.6% (5.3% to10.4%), 27.5% (20.7% to 35.1%), 64.2% (49.8% to 76.9%), or 100% (59.0% to 100.0%) risk, respectively, of in-hospital mortality (mean ± 95% confidence interval, C-index = 0.88, Hosmer-Lemeshow p = 0.898). CONCLUSIONS: In-hospital mortality risk among individuals undergoing rescue PCI varies from minimal to extreme and can be easily calculated using the NCDR-RESCUE score. This information can be of value in counseling patients, families, and referring caregivers.

Prolonged therapy with erythropoietin is safe and prevents deterioration of left ventricular systolic function in a porcine model of myocardial infarction.

BACKGROUND: Erythropoietin (EPO) has generated interest as a novel therapy after myocardial infarction (MI), but the safety and efficacy of prolonged therapy have not been studied in a large animal model of reperfused MI. METHODS AND RESULTS: MI was induced in pigs by a 90-minute balloon occlusion of the left anterior descending coronary artery. Sixteen animals were randomized to either EPO or saline (control group). Inflammatory markers, bone marrow cell mobilization, and left ventricular function (by both echocardiography and pressure-volume measurements) were assessed at baseline, 1 and 6 weeks post-MI. EPO therapy was associated with a significant increase in hemoglobin and mononuclear counts. D-dimer and C-reactive protein levels did not differ between groups. At week 6, EPO therapy prevented further deterioration of left ventricular ejection fraction (39 +/- 2% vs. 33 +/- 1%, P < .01) and improved wall motion score index (P < .02). Histopathology revealed increased areas of viable myocardium, vascular density, and capillary-to-myocyte ratio in the EPO therapy compared with the control (all P < .05). CONCLUSION: Prolonged EPO therapy after MI in a large animal model is safe and leads to an increase in viable myocardium, increased vascular density, and prevents further deterioration of left ventricular function. These results support future clinical studies in post-MI patients.

Cancer patients with markedly elevated B-type natriuretic peptide may not have volume overload.

OBJECTIVES: Elevated B-type natriuretic peptide (BNP) levels are established as a marker for volume overload and left ventricular (LV) dysfunction in patients with predominately cardiac diseases. Little is known about markedly elevated BNP values in patients with multiple comorbidities. METHODS: A total of 99 patients, admitted to M. D. Anderson Cancer Center, were identified as having a BNP value >1000 pg/mL during the year 2003. Clinical characteristics, including the presence of volume overload and sepsis, as well as echocardiographic parameters were measured. Principal outcome was defined as 30-day mortality. RESULTS: The median BNP (pg/mL) of the group was 2270 (range, 1010-5000), and there was no association between elevation of the BNP level and the presence of volume overload or LV dysfunction (P = not significant). The large majority of patients (n = 71, 72%) had no volume overload and normal or nearly normal LV function (n = 60, 61%). A majority were also identified as having sepsis (n = 52, 53%). There was no echocardiographic parameter that consistently correlated with BNP levels or volume overload. There was a highly significant association with sepsis and mortality in patients with markedly elevated BNP values, and this conferred a 2.71-fold increased risk of mortality. CONCLUSIONS: In patients admitted with multiple comorbidities and markedly elevated BNP values, there is no significant association with clinical evidence of volume overload or LV dysfunction. An elevated BNP level in patients with sepsis was significantly associated with mortality.

Risk of bleeding complications is not increased in patients undergoing rescue versus primary percutaneous coronary intervention for acute myocardial infarction.

BACKGROUND: Concern for major bleeding complications (MBC) may lead to withholding of anticoagulation and fibrinolytic therapy in preparation for primary percutaneous coronary intervention (PCI), potentially resulting in unacceptable delays in achieving reperfusion. OBJECTIVES: The primary objective of this study was to evaluate MBC associated with primary and rescue PCI and how timing to revascularization affects this variable. METHODS: We evaluated 659 consecutive patients presenting within 24 hours of an acute ST elevation myocardial infarctions (MI). One hundred and eighty-three patients presented for rescue PCI and 476 for primary PCI. Eighty-seven rescue PCI patients were treated within 6 hours of their first dose of fibrinolytic. Demographics, procedural variables, outcomes, and major adverse cardiovascular events (MACE) were compared between the primary and rescue PCI groups and between early and late presenters in the rescue PCI group. RESULTS: We observed that the incidence of MBC was 8% in patients undergoing rescue PCI and 6% in primary PCI (P=0.35). There were no significant differences in bleeding associated with GP IIb/IIIa receptor antagonist use, procedural success, or MACE. Similarly, in patients presenting for early or late rescue PCI there was no significant difference in MBC, procedural success, or MACE. CONCLUSIONS: We concluded that early or late rescue PCI and primary PCI have similar rates of MBC and overall in-hospital outcomes for patients presenting within 24 hours of acute MI. Delaying the timing of a rapid reperfusion strategy in an effort to decrease the incidence of MBC complications is generally not justified.

The use of brachytherapy to treat renal artery in-stent restenosis.

The percutaneous treatment of renal artery stenosis has become the accepted revascularization strategy by most physicians treating this disorder. Unfortunately, as renal artery angioplasty and stent implantation become increasingly prevalent the Achilles heel of angioplasty, in-stent restenosis, also rises. There are currently no data suggestive of the optimal treatment strategy for renal artery in-stent restenosis. However, given the similarities in the pathophysiology between renal artery and coronary artery in-stent restenosis, brachytherapy is considered a reasonable option. This is the strategy that has been suggested and used by a number of operators. This case report describes two examples of renal artery in-stent restenosis treated with angioplasty and brachytherapy.