Clinical outcomes following predilation with a novel 1.25-mm diameter angioplasty catheter.

OBJECTIVE: An unmet need is represented in angioplasty catheters that permit the predilation stage of treating complex coronary anatomy oftentimes not amenable to conventional device therapies. BACKGROUND: Lesion preparation with balloon angioplasty prior to stent placement remains the most common method of percutaneous coronary revascularization. METHODS: Clinical and angiographic outcomes were evaluated following a treatment strategy of coronary artery disease that included predilation with a low-profile, 1.25-mm angioplasty catheter prior to stent placement. The study primary end point of procedural success was defined as successful device delivery and lesion treatment, including the absence of clinically significant perforation, arrhythmia, flow-limiting dissection, or reduction in baseline Thrombolysis In Myocardial Infarction (TIMI) grade with final achievement of TIMI 3 flow. RESULTS: Among 51 patients (54 lesions), predilation using a 1.25 mm angioplasty catheter was associated with procedural and device-related success rates of 100%. In-hospital target lesion failure occurred in one patient (2.0%) related to postprocedural myocardial infarction. Patient and angiographic characteristics included diabetes, 43.1%; lesion length ≥ 20 mm, 20.4%; bifurcation lesion, 31.5%; lesion classification B2/C, 74.1%; and baseline TIMI 0/1 flow, 13.0%. No subsequent in-hospital adverse events occurred. CONCLUSIONS: Percutaneous coronary revascularization involving a predilation strategy with a low profile, 1.25-mm angioplasty catheter is associated with favorable procedural safety and efficacy and may represent an effective initial treatment for complex coronary anatomy.

Contemporary use of embolic protection devices in saphenous vein graft interventions: Insights from the stenting of saphenous vein grafts trial.

BACKGROUND: We sought to evaluate the contemporary use of embolic protection devices (EPDs) in saphenous vein graft (SVG) interventions. METHODS: We examined EPD use in the stenting of saphenous vein grafts (SOS) trial, in which 80 patients with 112 lesions in 88 SVGs were randomized to a bare metal stent (39 patients, 43 grafts, and 55 lesions) or paclitaxel-eluting stent (41 patients, 45 grafts, and 57 lesions). RESULTS: An EPD was used in 60 of 112 lesions (54%). A Filterwire (Boston Scientific) was used in 70% of EPD-treated lesions, Spider (ev3, Plymouth, Minnesota) in 12%, Proxis (St. Jude, Minneapolis, Minnesota) in 12%, and Guardwire (Medtronic, Santa Rosa, California) in 7%. Of the remaining 52 lesions, an EPD was not utilized in 13 lesions (25%) because the lesion was near the distal anastomosis, in 14 lesions (27%) because of an ostial location, in one lesion (2%) because of small SVG size, in two in-stent restenosis lesions (4%) because of low distal embolization risk, and in 22 lesions (42%) because of operator's preference even though use of an EPD was feasible. Procedural success was achieved in 77 patients (96%); in one patient a Filterwire was entrapped requiring emergency coronary bypass graft surgery and two patients had acute stent thrombosis. CONCLUSION: In spite of their proven efficacy, EPDs were utilized in approximately half of SVG interventions in the SOS trial. Availability of a proximal protection device could allow protection of approximately 25% of unprotected lesions, yet operator discretion appears to be the major determinant of EPD use.

Treatment delay in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction: a key process analysis of patient and program factors.

BACKGROUND: Most hospitals that perform primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) in the United States exceed the recommended door-to-balloon time. There is heightened interest in identifying and eliminating factors that introduce delay. METHODS: We performed a key process analysis of our primary PCI program, assessed the relative contribution of individual time intervals on total ischemic time, and identified predictors of delay. RESULTS: Median times and predictors of delay within each time interval were determined for the entire STEMI cohort ("real world") and after exclusion of patients with atypical symptoms and/or presentations of STEMI that resulted in inherent delay in diagnosis and treatment ("ideal world"). Delays in therapy were symptom onset to presentation (120 minutes [interquartile range, IQR, 60-310 minutes, ideal world] and 150 minutes [IQR 60-360 minutes, real world]; predictors of delay were peripheral vascular disease, self-transportation, daytime and weekend presentation); door-to-balloon time (118.5 minutes [IQR 96-141 minutes, ideal world] and 125 minutes [IQR 100-170 minutes, real world]; predictors of delay were female sex, previous stroke, nighttime and weekend presentation, and cardiogenic shock); and symptom onset to first balloon inflation (272 minutes [IQR 187-465 minutes, ideal world] and 297 minutes [IQR 198-560 minutes, real world]; predictors of delay were peripheral vascular disease, weekend presentation, and self-transportation). CONCLUSIONS: Key process analysis of a primary PCI program identifies treatment delays unique to the hospital and the patient population it serves.

Effect of glucose-insulin-potassium (GIK) infusion on biomarkers of cardiovascular risk in ST elevation myocardial infarction (STEMI): insight into the failure of GIK.

Glucose-insulin-potassium (GIK) infusion favourably affects several biomarkers associated with risk in the setting of myocardial infarction (MI). In the context of a recent trial demonstrating no benefit of GIK, we assessed the impact of GIK on inflammation, neurohormonal activation and myonecrosis in ST elevation myocardial infarction (STEMI). In a local substudy of an international randomised trial, 25 patients with STEMI were randomised to receive a 24-hour infusion of GIK vs. no GIK. C-reactive protein (hs-CRP), N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin T (TnT) were assayed at baseline and at 24 hours. The two groups were well matched for baseline characteristics and infarct location. There were no statistically significant differences at baseline or at 24 hours in levels of hs-CRP, NT-proBNP or cTnT, with similar and significant increases in all three biomarkers by 24 hours in both groups. In conclusion, GIK had no discernible effect on biomarkers associated with inflammation, neurohormonal activation or myonecrosis, three pathways associated with adverse outcomes in STEMI.

Effect of glucose-insulin-potassium infusion on plasma free fatty acid concentrations in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction.

To determine the effect of glucose-insulin-potassium infusion on circulating levels of free fatty acids in the setting of contemporary management of ST-elevation myocardial infarction, we randomly assigned 20 patients who were undergoing primary angioplasty to glucose-insulin-potassium infusion or to standard care. Treatment with glucose-insulin-potassium was associated with significantly lower levels of free fatty acid after 24 hours compared with standard care.

Increases in myocardial workload induced by rapid atrial pacing trigger alterations in global metabolism.

OBJECTIVE: To determine whether increases in cardiac work lead to alterations in the plasma metabolome and whether such changes arise from the heart or peripheral organs. BACKGROUND: There is growing evidence that the heart influences systemic metabolism through endocrine effects and affecting pathways involved in energy homeostasis. METHODS: Nineteen patients referred for cardiac catheterization were enrolled. Peripheral and selective coronary sinus (CS) blood sampling was performed at serial timepoints following the initiation of pacing, and metabolite profiling was performed by liquid chromatography-mass spectrometry (LC-MS). RESULTS: Pacing-stress resulted in a 225% increase in the median rate·pressure product from baseline. Increased myocardial work induced significant changes in the peripheral concentration of 43 of 125 metabolites assayed, including large changes in purine [adenosine (+99%, p = 0.006), ADP (+42%, p = 0.01), AMP (+79%, p = 0.004), GDP (+69%, p = 0.003), GMP (+58%, p = 0.01), IMP (+50%, p = 0.03), xanthine (+61%, p = 0.0006)], and several bile acid metabolites. The CS changes in metabolites qualitatively mirrored those in the peripheral blood in both timing and magnitude, suggesting the heart was not the major source of the metabolite release. CONCLUSIONS: Isolated increases in myocardial work can induce changes in the plasma metabolome, but these changes do not appear to be directly cardiac in origin. A number of these dynamic metabolites have known signaling functions. Our study provides additional evidence to a growing body of literature on metabolic 'cross-talk' between the heart and other organs.

Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: insights from a coronary sinus sampling study.

OBJECTIVES: The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release. BACKGROUND: A new hs-cTnT assay offers greater sensitivity than current assays. METHODS: Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing. RESULTS: cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups. CONCLUSIONS: Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.