Circulation: Clinical Summaries
Original Research Put Into Perspective for the Practicing Clinician
- Myocardial Injury After Noncardiac Surgery and its Association With Short-Term Mortality
- Neurological Complications of Infective Endocarditis: Risk Factors, Outcome, and Impact of Cardiac Surgery: A Multicenter Observational Study
- Innate Signaling Promotes Formation of Regulatory Nitric Oxide–Producing Dendritic Cells Limiting T-Cell Expansion in Experimental Autoimmune Myocarditis
- Adoption of Radial Access and Comparison of Outcomes to Femoral Access in Percutaneous Coronary Intervention: An Updated Report from the National Cardiovascular Data Registry (2007–2012)
- Cilostazol Reduces Angiographic Restenosis After Endovascular Therapy for Femoropopliteal Lesions in the Sufficient Treatment of Peripheral Intervention by Cilostazol Study
- Predictors of Mortality and Outcomes of Therapy in Low-Flow Severe Aortic Stenosis: A Placement of Aortic Transcatheter Valves (PARTNER) Trial Analysis
- Atorvastatin, Etidronate, or Both in Patients at High Risk for Atherosclerotic Aortic Plaques: A Randomized, Controlled Trial
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Myocardial Injury After Noncardiac Surgery and its Association With Short-Term Mortality
Perioperative adverse cardiovascular events are the leading cause of morbidity and mortality after noncardiac surgery. Despite efforts to prevent the occurrence of such events, the incidence of postoperative myocardial infarction is still high. To identify patients at risk for postoperative myocardial infarction, measuring cardiac troponin routinely after noncardiac surgery has been suggested. Therefore, in our hospital we implemented routine troponin measurement monitoring on the first 3 days after surgery as part of our standard postoperative care in patients aged ≥60 years undergoing intermediate- to high-risk surgery. This observational cohort study estimated the incidence of myocardial injury after noncardiac surgery and its predictive value on the risk of death within 30 days with the use of data from routine postoperative monitoring of troponin. Postoperative myocardial injury as detected by troponin elevation was found in 19% of the patients, and overall all-cause death within 30 days occurred in 3% of the patients. Although only a minority (<10%) of the patients had typical signs of myocardial ischemia or ECG changes, we found a strong association between postoperative myocardial injury and death. We therefore conclude that patients at risk for early death after noncardiac surgery are easily identified by routine postoperative troponin measurements. Furthermore, the time interval between troponin elevation and death potentially allows physicians to modify prognosis. Implementation of postoperative monitoring of troponin as standard of care is feasible and may improve risk stratification and reclassification of patients at risk for early postoperative death. See p 2264.
Neurological Complications of Infective Endocarditis: Risk Factors, Outcome, and Impact of Cardiac Surgery: A Multicenter Observational Study
This observational study describes the incidence of neurological complications in a large, well-defined multicenter cohort of left-sided infective endocarditis. The risk factors for developing these events were analyzed carefully, and the influence of antimicrobial treatment and anticoagulant therapy in this scenario was considered. In addition, the results of early surgical intervention in this context were evaluated to assess the risk of new neurological damage that was time dependent. In the present study, vegetation size ≥3 cm, Staphylococcus aureus as the causative microorganism, and involvement of the mitral valve were risk factors related to the development of neurological complications; conversely, antimicrobial treatment reduced their incidence. Moderate to severe ischemic strokes and brain hemorrhages were associated with a significantly worse prognosis, and maintenance of anticoagulant therapy was associated with a higher incidence of hemorrhagic events. Finally, a higher mortality was observed when valvular surgery was performed within 4 weeks of a brain hemorrhage. The conclusion is that early and appropriate antimicrobial treatment is critical to avoid neurological complications in infective endocarditis and that a temporary withdrawal of anticoagulant therapy should be considered. Valvular surgery should be deferred when hemorrhage is present. See p 2272.
Innate Signaling Promotes Formation of Regulatory Nitric Oxide–Producing Dendritic Cells Limiting T-Cell Expansion in Experimental Autoimmune Myocarditis
A growing body of evidence suggests that heart-specific T-cell–mediated autoimmunity promotes progression of myocarditis after infection with cardiotropic viruses. Using the mouse model of experimental autoimmune myocarditis, we describe a novel mechanism of autoreactive T-cell regulation that depends on nitric oxide released from a specific inflammatory dendritic cell subset and stromal cells. In the experimental autoimmune myocarditis model, both the Th1 cytokine interferon-γ and Mycobacterium tuberculosis antigens controlled nitric oxide production. Mechanistically, M. tuberculosis antigens exerted their specific effects through Toll-like receptor 2 (TLR2) signaling. In humans, acute and fulminant myocarditis most commonly present with a lymphocytic pattern that includes T cells. In most cases, fulminant and acute myocarditis is associated with viral infections caused by enteroviruses, parvoviruses, HHV-6, HHV-7, H1N1 influenza, and others. Recognition of viruses by immune cells, however, is usually TLR2 independent. In contrast to viruses, bacterial infections seldom trigger acute or fulminant myocarditis. Myocardial tuberculosis, in particular, represents a rare and primarily systemic disease entity with a usually slowly progressive course. On the basis of our model, we might explain this clinical observation with possible TLR2-mediated attenuation of autoreactive T cells through bacterial antigens in myocarditis. Nevertheless, and despite its protective early role in myocarditis, innate, ie, TLR–mediated signaling can promote pathological remodeling and aggravate development of the typical end-stage heart failure phenotype in inflammatory dilated cardiomyopathy. Taken together, insights from the experimental autoimmune myocarditis model might explain why viral but not bacterial infections usually trigger fulminant and acute myocarditis. See p 2285.
Adoption of Radial Access and Comparison of Outcomes to Femoral Access in Percutaneous Coronary Intervention: An Updated Report from the National Cardiovascular Data Registry (2007–2012)
Radial access for percutaneous coronary intervention is associated with reduced vascular complications; however, previous reports have shown that <2% of percutaneous coronary intervention (PCI) procedures in the United States are performed via the radial approach. Our aims were to evaluate temporal trends in the radial approach to PCI (r-PCI) and compare procedural outcomes between r-PCI and transfemoral PCI. We conducted a retrospective cohort study from the CathPCI registry (n=2 820 874 procedures from 1381 sites) between January 2007 and September 2012. After multivariable adjustment, r-PCI use in the studied cohort of patients was associated with a lower risk of bleeding (adjusted odds ratio, 0.51; 95% confidence interval, 0.49–0.54) and lower risk of vascular complications (adjusted odds ratio, 0.39; 95% confidence interval, 0.31–0.50) in comparison with transfemoral PCI. There are several important findings in this large, contemporary observational study of a national multicenter PCI registry. First, since early reports, there has been a 13-fold increase over a period of 6 years in the use of r-PCI. Second, there is substantial interhospital and geographic variation in the use of r-PCI. Third, r-PCI is associated with consistently lower rates of bleeding and vascular complications in comparison with transfemoral PCI, without compromising procedural success rates. Finally, the greatest benefit of r-PCI in terms of absolute reduction of bleeding and vascular complications is seen in high-risk groups of patients ≥75 years of age, women, and patients with acute coronary syndrome, in whom paradoxically the use and growth of r-PCI are the lowest. These findings indicate that wider adoption of r-PCI in interventional practice presents an opportunity to potentially improve overall PCI safety. See p 2295.
Cilostazol Reduces Angiographic Restenosis After Endovascular Therapy for Femoropopliteal Lesions in the Sufficient Treatment of Peripheral Intervention by Cilostazol Study
Femoropopliteal (FP) lesions are found in 60% to 70% of patients with symptomatic peripheral artery disease. Although implantation of nitinol stents has improved the long-term outcome of endovascular therapy for FP lesions, there remains a 20% to 50% incidence of restenosis at 1 year as an important challenge for endovascular intervention. Current guidelines do not recommend any specific medical intervention to reduce the incidence of restenosis after endovascular therapy for FP disease. The Sufficient Treatment of Peripheral Intervention by Cilostazol (STOP-IC) study investigated whether cilostazol reduces the 12-month angiographic restenosis rate after percutaneous transluminal angioplasty with provisional nitinol stenting for FP lesions. The angiographic patency rate at 1 year after endovascular therapy was 80% in patients receiving cilostazol treatment in comparison with 51% in patients not receiving it, and cilostazol significantly reduced angiographic restenosis after endovascular therapy for FP disease. The cilostazol group also had a significantly higher event-free survival rate at 12 months, although the rate of cardiovascular events was similar in the 2 groups (83% versus 71%; P=0.02). Cilostazol reduced angiographic restenosis after percutaneous transluminal angioplasty with provisional nitinol stenting for FP lesions. See p 2307.
Predictors of Mortality and Outcomes of Therapy in Low-Flow Severe Aortic Stenosis: A Placement of Aortic Transcatheter Valves (PARTNER) Trial Analysis
Patients with symptomatic and severe aortic stenosis may have low mean transvalvular gradients and reduced stroke volume (low flow) resulting from left ventricular systolic dysfunction, high afterload, and pronounced left ventricular concentric remodeling or measurement errors. Little is known about the prognostic value of low flow independently of gradient and ejection fraction or the response of these patients to surgical or transcatheter aortic valve replacement. In this analysis of the Placement of Aortic Transcatheter Valves (PARTNER) trial, we found that low flow (defined by a stroke volume index ≤35 mL/m2) is independently associated with a 50% increase in 2-year all-cause mortality. In inoperable patients, transcatheter aortic valve replacement improved survival relative to medical management. In high-risk patients, transcatheter aortic valve replacement and surgical aortic valve replacement had similar outcomes. Finally, similar results were observed in patients with paradoxical low-flow (normal ejection fraction) severe aortic stenosis. These findings suggest that an assessment of flow based on stroke volume index may be useful in the evaluation of patients with severe aortic stenosis. In addition, surgery and transcatheter aortic valve replacement should be considered in patients with low flow despite their increased mortality compared with patients with normal flow. See p 2316.
Atorvastatin, Etidronate, or Both in Patients at High Risk for Atherosclerotic Aortic Plaques: A Randomized, Controlled Trial
In the present randomized, clinical trial, treatment with atorvastatin plus etidronate, compared with atorvastatin and etidronate monotherapies, showed that atorvastatin could reduce thoracic aortic plaques in which fatty constituents were common and etidronate bisphosphonate could reduce abdominal aortic plaques in which calcified plaques were frequently observed. Treatment with statins reduces serum low-density lipoprotein cholesterol levels and atherosclerotic plaques in the carotid artery, coronary artery, and thoracic aorta. However, it has not been shown to reduce atherosclerotic plaques in the abdominal aorta. To the best of our knowledge, this is the first randomized, clinical trial to demonstrate that the combination therapy of atorvastatin plus etidronate induced the regression of not only thoracic but also abdominal aortic plaques. Bisphosphonates are currently considered the drug of choice for the prevention and treatment of osteoporosis and related fractures. However, accumulating evidence shows that bisphosphonates have the potential to reduce atherosclerotic plaques and vascular calcification. In addition, only first-generation bisphosphonates (etidronate and clodronate) seem to have this ability. It was reported that calcified atherosclerotic plaques in the abdominal aorta were associated with the incidence of cardiovascular events and the independent predictor of coronary heart disease. Therefore, the reduction of calcified atherosclerotic plaques in the abdominal aorta might be beneficial in reducing mortality caused by cardiovascular events. See p 2327.
- © 2013 American Heart Association, Inc.
- Myocardial Injury After Noncardiac Surgery and its Association With Short-Term Mortality
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