Clinical Investigations: Interventional CardiologyTroponin I elevation and cardiac events after percutaneous coronary intervention
Abstract
Background Serum troponins are sensitive markers of myonecrosis and ischemia and are now widely used in clinical practice. Although percutaneous coronary intervention (PCI)-related creatine kinase-myocardial band isoenzyme (CK-MB) elevation has been associated with future cardiac events, the significance of troponin elevation in this setting is unknown. We sought to determine whether serum troponin I (Tn-I) elevation after PCI is associated with future cardiac events. Methods and Results Consecutive patients undergoing elective PCI underwent systematic postprocedure measurement of Tn-I and CK-MB levels. Serum levels were correlated with demographic, angiographic, and procedural characteristics and the development of major adverse cardiac events (MACE; defined as death, MI, or need for PCI or coronary bypass graft surgery) at 30 days, 6 months, and 1 year. In 286 consecutive procedures, postintervention myonecrosis-specific Tn-I was elevated in 13.6% of patients, and CK-MB was elevated in 12.9% of patients. Multivariable predictors of Tn-I elevation were procedural side branch occlusion and thrombus formation. Peak Tn-I and CK-MB values were well correlated (r = 0.81, P < .0001). Three-fold elevation of Tn-I after successful PCI was independently predictive of MACE (P = .01). Conclusions Tn-I elevation after elective PCI is relatively common and is associated with procedural complications such as incidental side branch occlusion and thrombus formation. In addition, this study demonstrates that a 3-fold elevation of Tn-I after successful elective PCI is predictive of future cardiac events, especially the need for early repeat revascularization. (Am Heart J 2003;145:522-8.)
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2017, JACC: Cardiovascular InterventionsCardiac Remote Ischaemic Preconditioning: Mechanistic and Clinical Considerations
2017, Heart Lung and CirculationCitation Excerpt :Administration of glibenclamide, a non-selective potassium ATP channel inhibitor, abolished the effect of RIPC, suggesting that potassium ATP channels are involved. Coronary artery stenting (PCI) can cause myocardial injury, measured as increased serum troponin [49], and this predicts future cardiovascular events and need for revascularisation [50–52]. Remote ischaemic preconditioning prior to PCI reduced post PCI troponin levels in most studies, and some studies suggested an improvement in clinical outcomes.
Brief, non-harmful ischaemic insults to an organ remote from the heart, remote ischaemic preconditioning (RIPC), has been proposed to confer protection to the heart against ischaemia-reperfusion injury. While most clinical trials of RIPC during coronary interventions (PCI) suggest benefit, recent large, multicentre trials in coronary artery bypass surgery suggest a lack of efficacy. Mechanistically, RIPC most likely promotes the release of circulating factors which modulate multiple cellular pathways in the heart, promoting cell survival. This review explores potential mechanisms underlying RIPC and includes a contemporary evaluation of clinical studies in PCI and cardiac surgery, highlighting methodological differences which may explain discrepant findings between these two clinical groups.
High-Sensitivity Troponin T and Mortality After Elective Percutaneous Coronary Intervention
2016, Journal of the American College of CardiologyThe prognostic value of high-sensitivity troponin T (hs-TnT) elevation after elective percutaneous coronary intervention (PCI) in patients with or without raised baseline hs-TnT levels is unclear.
The goal of this study was to assess whether the prognostic value of post-procedural hs-TnT level after elective PCI depends on the baseline hs-TnT level.
This study included 5,626 patients undergoing elective PCI who had baseline and peak post-procedural hs-TnT measurements available. The primary outcome was 3-year mortality (with risk estimates calculated per SD increase of the log hs-TnT scale).
Patients were divided into 4 groups: nonelevated baseline and post-procedural hs-TnT levels (hs-TnT ≤0.014 μg/l; n = 742); nonelevated baseline but elevated post-procedural hs-TnT levels (peak post-procedural hs-TnT >0.014 μg/l; n = 2,721); elevated baseline hs-TnT levels (hs-TnT >0.014 μg/l) with no further rise post-procedure (n = 516); and elevated baseline hs-TnT levels with a further rise post-procedure (n = 1,647). A total of 265 deaths occurred: 6 (1.6%) in patients with nonelevated baseline and post-procedural hs-TnT levels; 54 (3.8%) in patients with nonelevated baseline but elevated post-procedural hs-TnT levels; 50 (16.0%) in patients with elevated baseline hs-TnT levels with no further rise post-procedure; and 155 (18.2%) in patients with elevated baseline hs-TnT levels with a further rise post-procedure (p < 0.001). After adjustment, baseline hs-TnT levels (hazard ratio [HR]: 1.22; 95% confidence interval [CI]: 1.09 to 1.38; p < 0.001) but not peak post-procedural hs-TnT levels (HR: 1.04; 95% CI: 0.85 to 1.28; p = 0.679) were associated with an increased risk of mortality. Peak post-procedural hs-TnT findings were not associated with mortality in patients with nonelevated (HR: 0.93; 95% CI: 0.69 to 1.25; p = 0.653) or elevated (HR: 1.24; 95% CI: 0.91 to 1.69; p = 0.165) baseline hs-TnT levels.
In patients with coronary artery disease undergoing elective PCI, an increase in post-procedural hs-TnT level did not offer prognostic information beyond that provided by the baseline level of the biomarker.
Prognostic Value of High-sensitivity Troponin T After Percutaneous Coronary Intervention in Patients With Stable Coronary Artery Disease
2016, Revista Espanola de CardiologiaEstá por clarificar el valor pronóstico de la troponina T de alta sensibilidad tras una intervención coronaria percutánea en pacientes con enfermedad coronaria estable. Esta cuestión clínicamente relevante se ha investigado en 3.463 pacientes consecutivos a los que se practicó una intervención coronaria percutánea.
En este estudio se incluyó a pacientes con enfermedad coronaria estable y un valor basal de troponina T de alta sensibilidad menor que el límite superior de referencia del percentil 99 (0,014 μg/l). Se determinó la troponina T de alta sensibilidad antes de la intervención y luego al cabo de 6, 12 y 24 h. El objetivo principal fue la mortalidad por cualquier causa.
Se clasificó a los pacientes en un grupo con un valor máximo de troponina T tras la intervención ≤ percentil 99 (n = 742), un grupo con un valor máximo de troponina T tras la intervención entre > percentil 99 y 5 veces el percentil 99 (n = 1.928) y un grupo con un valor máximo de troponina T tras la intervención > 5 veces el percentil 99 (n = 793). La edad avanzada, el índice de masa corporal más bajo, el valor de troponina basal, las lesiones complejas, las lesiones en bifurcación y la longitud del stent se asociaron de manera independiente a concentraciones de troponina T aumentadas después de la intervención. La mediana de seguimiento fue de 15,5 meses. Hubo 56 muertes: 5 pacientes (1,7%) con valor máximo de troponina T tras la intervención ≤ percentil 99, 35 (4,5%) con valor máximo de troponina T tras la intervención entre > percentil 99 y 5 veces el percentil 99, y 16 (4,3%) del grupo con valor máximo de troponina T tras la intervención > 5 veces el percentil 99 (hazard ratio = 1,50; intervalo de confianza del 95%, 1,01-2,25; p = 0,047). Tras el ajuste, el valor máximo de troponina T tras el procedimiento no mostró asociación independiente con la mortalidad tras la intervención coronaria percutánea (p = 0,094).
En los pacientes con enfermedad coronaria estable y sin elevación basal de la troponina T de alta sensibilidad, la elevación de esta después de una intervención coronaria percutánea no se asoció a mayor mortalidad tras el procedimiento.
The prognostic value of high-sensitivity troponin T after percutaneous coronary intervention in patients with stable coronary artery disease is unclear. We investigated this clinically relevant question in 3463 consecutive patients undergoing percutaneous coronary intervention.
This study included patients with stable coronary artery disease and baseline high-sensitivity troponin T below the 99th percentile upper reference limit (0.014 μg/L). High-sensitivity troponin T was measured before and at 6, 12 and 24 hours after the procedure. The primary outcome was all-cause mortality.
Patients were divided into a group with peak postprocedural troponin T ≤ 99th percentile (n = 742), a group with peak postprocedural troponin T > 99th to 5 × 99th percentile (n = 1928), and a group with peak postprocedural troponin T > 5 × 99th percentile upper reference limit (n = 793). Advanced age, smaller body mass index, baseline troponin level, complex lesions, bifurcation lesions and stented length were independently associated with elevated troponin T levels after the procedure. The median follow-up was 15.5 months. There were 56 deaths: 5 deaths (1.7%) among patients with peak postprocedural troponin T ≤ 99th percentile, 35 deaths (4.5%) among patients with peak postprocedural troponin T > 99th to 5 × 99th percentile and 16 deaths (4.3%) among patients with peak postprocedural troponin T > 5 × 99th percentile upper reference limit (hazard ratio = 1.50; 95% confidence interval, 1.01-2.25; P = .047). After adjustment, peak postprocedural troponin T level was not independently associated with mortality after percutaneous coronary intervention (P = .094).
In patients with stable coronary artery disease and without elevated baseline high-sensitivity troponin T, elevated high-sensitivity troponin T level after percutaneous coronary intervention was not associated with postprocedural mortality.
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The effect on periprocedural myocardial infarction of intra-coronary nicorandil prior to percutaneous coronary intervention in stable and unstable angina
2013, Journal of CardiologyIntravenous nicorandil infusion dilates the coronary artery and reduces inflammation, coronary spasm, and arrhythmia. Periprocedural myocardial infarction (PMI) is a frequent and prognostically important complication of percutaneous coronary intervention (PCI). This prospective randomized study was designed to evaluate the efficacy of intracoronary nicorandil on PMI after elective PCI.
Eighty-one patients with stable or unstable angina undergoing PCIs of the left anterior descending artery were randomly assigned to the nicorandil group (n = 41) or the control group (n = 40). In the nicorandil group, 4 mg of intracoronary nicorandil was infused prior to PCI. Post-PCI, peak levels of creatine kinase (CK)-MB and troponin I were measured and angiographic findings were analyzed. Side branch status was also assessed. All PCIs were successful. One cerebrovascular infarction and one acute ST segment elevation myocardial infarction with acute stent thrombosis occurred in the nicorandil group. No deaths occurred, and no other major cardiac adverse events were observed in either group over 6 months follow-up. The post-PCI peak CK-MB and troponin I levels were not significantly different between the two groups. There were no significant differences between the nicorandil and control subjects in side branch occlusion or flow reduction, or in the jail index.
Intra-coronary nicorandil infusion had no significant effect on PMI and cardiac enzymes after PCI in patients with stable or unstable angina.
P2X<inf>7</inf> inhibition in stellate ganglia prevents the increased sympathoexcitatory reflex via sensory-sympathetic coupling induced by myocardial ischemic injury
2013, Brain Research BulletinPurinergic signaling has been found to participate in the regulation of cardiovascular function. In this study, using a rat myocardial ischemic injury model, the sympathoexcitatory reflex mediated by P2X7 receptor via sensory-sympathetic coupling between cervical dorsal root ganglia (DRG) nerves and stellate ganglia (SG) nerves was explored. Our results showed that the systolic blood pressure, heart rate, serum cardiac enzymes concentrations, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) concentrations were increased, and the expression levels of P2X7 mRNA and protein in DRG and SG were up-regulated after myocardial ischemic injury. Administration of brilliant blue G (BBG), a selective P2X7 antagonist, decreased the elevation of systolic blood pressure, heart rate, serum cardiac enzyme, IL-6 and TNF-α, and inhibited the up-regulated expression of P2X7 mRNA and protein in DRG and SG after myocardial ischemic injury. Retrograde tracing test showed that there were calcitonin gene-related peptide sensory nerves and substance P sensory nerves sprouting from DRG to SG, which played an important role in the development of myocardial ischemic injury. The up-regulated P2X7 receptor expression levels on the surface membrane of satellite glial cells contributed to the activation of sensory-sympathetic coupling, which in turn facilitated the sympathoexcitatory reflex. BBG can inhibit the activation of satellite glial cells and interrupt the generation of sensory-sympathetic coupling in the cervical sympathetic ganglia after the myocardial ischemic injury. Taken together, these findings may provide a new therapeutic approach for treating coronary heart disease, hypertension and other cardiovascular diseases.