冠脉评分法在急性心肌梗死应用中的相关性

目的 探讨在急性心肌梗死患者中3种冠状动脉评分方法的相关性.方法 对我院2007～2010年收治确诊为急性心肌梗死并行冠状动脉造影的301例患者的临床资料进行回顾性研究.采用相关分析,探讨3种评分方法间的相关性.结果 301例确诊为急性心肌梗死患者中,Gensini评分和Leaman评分的相关系数为0.856,ACC ...     

Depression screening in patients with coronary heart disease: a critical evaluation of the AHA guidelines

Objective

We lack evidence that routine screening for depression in patients with coronary heart disease (CHD) improves patient outcome. This lack has challenged the advisory issued by the American Heart Association (AHA) to routinely screen for depression in CHD patients. We assess the AHA advisory in the context of well-established criteria of screening for diseases.

Methods

Using principles and criteria for screening developed by the World Health Organization and the United Kingdom National Screening Committee, we generated criteria pertinent to screening for depression in CHD patients. To find publications relevant to these criteria and clinical setting, we performed a broadly based literature search on “depression and CHD,” supplemented by more focused literature searches.

Results

Evidence for an association between depression and CHD is strong. Despite this, the AHA advisory has several limitations. It did not account for the complexity of the association between depression and CHD. It acknowledged there was no evidence that screening for depression leads to improved outcomes in cardiovascular populations but still recommended routine screening without providing an alternative evidence-based explanation. It ignored the paucity of literature about the safety and cost-effectiveness of routine screening for depression in CHD and failed to define the nature and extent of resources needed to implement such a program effectively.

Conclusion

We conclude that the AHA advisory is premature. We must first demonstrate the efficacy, safety, and cost-effectiveness of screening and define the resources necessary for its implementation and monitoring. Meanwhile, organizations representing cardiologists, psychiatrists, and general practitioners must coordinate efforts to manage depression and CHD through collaborative care, and work with the policy makers to develop the necessary infrastructure and services delivery system needed to optimize the outcome of depressed and at-risk-for-depression patients suffering from CHD.     

High-sensitivity C-reactive protein and atherosclerotic disease: From improved risk prediction to risk-guided therapy

There is compelling experimental and clinical evidence suggesting a crucial role for inflammation in the initiation and also the progression of atherosclerosis. Numerous biomarkers involved at various levels of the inflammation cascade have been shown to be associated with adverse cardiovascular outcomes. Yet, to date, it is not clear whether inflammation simply accompanies the atherosclerotic process or represents a major driver. Among all blood biomarkers, C-reactive protein (CRP), the classical acute phase reactant that can be measured with high-sensitivity (hs) assays seems to be the most promising candidate. It has already found its way into the guidelines in primary prevention. Hs-CRP can also be used to identify a high-risk group for recurrent events in patients with manifest atherosclerosis. Several post hoc analyses of large-scale randomized clinical trials testing various statins have indicated that, besides low density lipoprotein (LDL) cholesterol, hs-CRP levels might also further aid in tailoring statin treatment. The large JUPITER trial has prospectively confirmed these findings in primary prevention in patients with elevated hs-CRP but normal LDL cholesterol levels. Still, statin therapy is not a specific anti-inflammatory regime acting on the inflammation cascade. Thus, to directly test the inflammation hypothesis, a novel, more proximally located cytokine-based approach is needed. Canakinumab, a fully human monoclonal antibody against interleukin-1β, might represent a promising compound in this regard and provide a proof of concept. If successful, this may become a novel strategy to treat high-risk patients with stable atherosclerotic disease to prevent recurrent events on top of standard medical care.     

Pushing harder,pushing faster,minimizing interruptions… But falling short of 2010 cardiopulmonary resuscitation targets during in-hospital pediatric and adolescent resuscitation

Aim

The objective of this study was to evaluate the effect of instituting the 2010 Basic Life Support Guidelines on in-hospital pediatric and adolescent cardiopulmonary resuscitation (CPR) quality. We hypothesized that quality would improve, but that targets for chest compression (CC) depth would be difficult to achieve.

Methods

Prospective in-hospital observational study comparing CPR quality 24 months before and after release of the 2010 Guidelines. CPR recording/feedback-enabled defibrillators collected CPR data (rate (CC/min), depth (mm), CC fraction (CCF, %), leaning (% > 2.5 kg)). Audiovisual feedback for depth was: 2005, ≥38 mm; 2010, ≥50 mm; for rate: 2005, ≥90 and ≤120 CC/min; 2010, ≥100 and ≤120 CC/min. The primary outcome was average event depth compared with Student's t-test.

Results

45 CPR events (25 before; 20 after) occurred, resulting in 1336 thirty-second epochs (909 before; 427 after). Compared to 2005, average event depth (50 ± 13 mm vs. 43 ± 9 mm; p = 0.047), rate (113 ± 11 CC/min vs. 104 ± 8 CC/min; p < 0.01), and CCF (0.94 [0.93, 0.96] vs. 0.9 [0.85, 0.94]; p = 0.013) increased during 2010. CPR epochs during the 2010 period more likely to meet Guidelines for CCF (OR 1.7; CI95: 1.2–2.4; p < 0.01), but less likely for rate (OR 0.23; CI95: 0.12–0.44; p < 0.01), and depth (OR 0.31; CI95: 0.12–0.86; p = 0.024).

Conclusions

Institution of the 2010 Guidelines was associated with increased CC depth, rate, and CC fraction; yet, achieving 2010 targets for rate and depth was difficult.     

Proprotein convertases in human atherosclerotic plaques: the overexpression of FURIN and its substrate cytokines BAFF and APRIL

Background

Proprotein convertase subtilisin/kexin (PCSK) enzymes cleave proproteins into mature end products. Previously, MBTPS1 and PCSK9 have been shown to regulate cholesterol metabolism and LDL receptor recycling, whereas FURIN and PCSK5 have been suggested to inactivate lipases and regulate inflammation in atherosclerosis. Here, we systematically analyzed the expression of PCSKs and their targets in advanced atherosclerotic plaques.

Methods and results

Microarray and quantitative real-time PCR experiments showed that FURIN (42.86 median fold, p = 2.1e−8), but no other PCSK, is universally overexpressed in the plaques of different vascular regions. The mRNA expression screen of PCSK target proteins in plaques identified many known factors, but it also identified the significant upregulation of the previously overlooked furin-processed B cell activating cytokines APRIL (TNFSF13, 2.52 median fold, p = 3.0e−5) and BAFF (TNFSF13B, 2.97 median fold, p = 7.6e−6). The dysregulation of FURIN did not associate with its htSNPs or the previously reported regulatory SNP (−229, rs4932178) in the promoter. Immunohistochemistry experiments showed the upregulation of FURIN in the plaque lymphocytes and macrophages where it was co-expressed with BAFF/TNFSF13B and APRIL/TNFSF13.

Conclusions

Our data unequivocally show that FURIN is the primary PCSK that is dysregulated in the immune cells of advanced human atherosclerotic plaques, which implies a role for this enzyme in plaque pathology. Therefore, drugs that inhibit FURIN in arteries may modulate the course of this disease.     

Type 2 Diabetes Mellitus and Heart Failure,A Scientific Statement From the American Heart Association and Heart Failure Society of America

Type 2 diabetes mellitus is a risk factor for incident heart failure and increases the risk of morbidity and mortality in patients with established disease. Secular trends in the prevalence of diabetes mellitus and heart failure forecast a growing burden of disease and underscore the need for effective therapeutic strategies. Recent clinical trials have demonstrated the shared pathophysiology between diabetes mellitus and heart failure, the synergistic effect of managing both conditions, and the potential for diabetes mellitus therapies to modulate the risk of heart failure outcomes. This scientific statement on diabetes mellitus and heart failure summarizes the epidemiology, pathophysiology, and impact of diabetes mellitus and its control on outcomes in heart failure; reviews the approach to pharmacological therapy and lifestyle modification in patients with diabetes mellitus and heart failure; highlights the value of multidisciplinary interventions to improve clinical outcomes in this population; and outlines priorities for future research.     

Systematic Review for the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines

BackgroundThe 2013 American College of Cardiology/American Heart Association guidelines for the treatment of blood cholesterol found little evidence to support the use of nonstatin lipid-modifying medications to reduce atherosclerotic cardiovascular disease (ASCVD) events. Since publication of these guidelines, multiple randomized controlled trials evaluating nonstatin lipid-modifying medications have been published.MethodsWe performed a systematic review to assess the magnitude of benefit and/or harm from additional lipid-modifying therapies compared with statins alone in individuals with known ASCVD or at high risk of ASCVD. We included data from randomized controlled trials with a sample size of >1,000 patients and designed for follow-up >1 year. We performed a comprehensive literature search and identified 10 randomized controlled trials for intensive review, including trials evaluating ezetimibe, niacin, cholesterol-ester transfer protein inhibitors, and PCSK9 inhibitors. The prespecified primary outcome for this review was a composite of fatal cardiovascular events, nonfatal myocardial infarction, and nonfatal stroke.ResultsThe cardiovascular benefit of nonstatin lipid-modifying therapies varied significantly according to the class of medication. There was evidence for reduced ASCVD morbidity with ezetimibe and 2 PSCK9 inhibitors. Reduced ASCVD mortality rate was reported for 1 PCSK9 inhibitor. The use of ezetimibe/simvastatin versus simvastatin in IMPROVE-IT (Improved Reduction of Outcomes: Vytorin Efficacy International Trial) reduced the primary outcome by 1.8% over 7 years (hazard ratio: 0.90; 95% CI: 0.84–0.96], 7-year number needed to treat: 56). The PSCK9 inhibitor evolocumab in the FOURIER study (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk) decreased the primary outcome by 1.5% over 2.2 years (hazard ratio: 0.80; 95% CI: 0.73–0.88; 2.2=year number needed to treat: 67). In ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab), alirocumab reduced the primary outcome by 1.6% over 2.8 years (hazard ratio: 0.86; 95% CI: 0.79–0.93; 2.8-year number needed to treat: 63). For ezetimibe and the PSCK9 inhibitors, rates of musculoskeletal, neurocognitive, gastrointestinal, or other adverse event risks did not differ between the treatment and control groups. For patients at high risk of ASCVD already on background statin therapy, there was minimal evidence for improved ASCVD risk or adverse events with cholesterol-ester transfer protein inhibitors. There was no evidence of benefit for the addition of niacin to statin therapy. Direct comparisons of the results of the 10 randomized controlled trials were limited by significant differences in sample size, duration of follow-up, and reported primary outcomes.ConclusionsIn a systematic review of the evidence for adding nonstatin lipid-modifying therapies to statins to reduce ASCVD risk, we found evidence of benefit for ezetimibe and PCSK9 inhibitors but not for niacin or cholesterol-ester transfer protein inhibitors.     

Contemporary Management of Ischemic Mitral Regurgitation at Coronary Artery Bypass Grafting

BackgroundRecent guidelines for the treatment of moderate or severe ischemic mitral regurgitation (IMR) in patients undergoing coronary artery bypass grafting (CABG) have changed. This study assessed the real-world impact of changing guidelines on the management of IMR during CABG over time. We hypothesized that the utilization of mitral valve repair for IMR would decrease over time, whereas mitral valve replacement for severe IMR would increase.MethodsPatients undergoing CABG in a statewide collaborative database (2011-2020) were stratified by severity of IMR. Trends in mitral valve repair or replacement were evaluated. To account for differences of the patients, propensity score–matched analyses were used to compare patients with and without mitral intervention.ResultsA total of 11,676 patients met inclusion criteria, including 1355 (11.6%) with moderate IMR and 390 (3.3%) with severe IMR. The proportion of patients undergoing mitral intervention for moderate IMR decreased over time (2011, 17.7%; 2020, 7.5%; P_trend = .001), whereas mitral replacement for severe IMR remained stable (2011, 11.1%; 2020, 13.3%; P_trend = .14). Major morbidity was higher for patients with moderate IMR who underwent mitral intervention (29.1% vs 19.9%; P = .005). In a propensity analysis of 249 well-matched pairs, there was no difference in major morbidity (29.3% with mitral intervention vs 23.7% without; P = .16) or operative mortality (1.2% vs 2.4%; P = .5).ConclusionsConsistent with recent guideline updates, patients with moderate IMR were less likely to undergo mitral repair. However, the rate of replacement for severe IMR did not change. Mitral intervention during CABG did not increase operative mortality or morbidity.