Circulation. 2008;118:1777-1778
doi: 10.1161/CIRCULATIONAHA.108.191124
doi: 10.1161/CIRCULATIONAHA.108.191124
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(Circulation. 2008;118:1777-1778.)
© 2008 American Heart Association, Inc.
Clinical Summaries
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Impact of Statin Use on Outcomes After Coronary Artery Bypass Graft Surgery |
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Impact of Statin Use...
Morphological and Physiological...Strong evidence is available to support the use of statins to reduce the risk of recurrent cardiovascular events in patients with native coronary artery disease; however, less is known about the benefits of statins after coronary artery bypass grafting (CABG). Previous randomized controlled trials investigating cholesterol reduction after CABG enrolled relatively healthy male patients <65 years of age who had undergone surgery several years earlier; however, CABG patients in the current era are older, have more coexisting conditions, and are increasingly likely to be women. We sought to clarify the role of statin therapy in this context and conducted a retrospective cohort study of 7503 CABG patients
65 years old who had and had not received statins within 1 month of hospital discharge after CABG. Our primary outcomes were all-cause mortality and freedom from major adverse cardiovascular events. Multivariable and propensity score–adjusted analysis demonstrated that statin use within 1 month of CABG discharge independently reduced the risk of all-cause mortality (adjusted hazard ratio 0.82, 95% confidence interval 0.72 to 0.94) and major adverse cardiovascular events (adjusted hazard ratio 0.89, 95% confidence interval 0.81 to 0.98) compared with nonuse. Thus, early statin therapy independently improved postoperative outcomes, and these results confirm those of earlier studies within a contemporary surgical population. Our findings endorse the view that essentially all patients should be prescribed long-term statin therapy after CABG. See p 1785. |
Morphological and Physiological Predictors of Fetal Aortic Coarctation |
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Undiagnosed coarctation can cause neonatal circulatory collapse and death, but morbidity is reduced by antenatal detection and appropriate perinatal management. Identification of isolated coarctation at obstetric screening is notoriously difficult; one 20-year regional series reported that only 6% of isolated coarctation was detected antenatally. Fetal coarctation is suspected sonographically from disproportion at 4-chamber or great arterial views. Incorporating the 3-vessel and tracheal view into obstetric screening programs enables assessment of the relative sizes of aortic and ductal arches and may reduce false-negative diagnoses, but surveillance of false-positives cases, estimated at
30%, incurs hospital costs. This article analyzes the ability of measurements and Doppler in the arches to improve diagnostic specificity. We report that the receiver-operating characteristic curves of isthmal Z scores and the isthmal-to-ductal ratio can identify cases requiring surgery at first examination and that serial measurements allow separation of normal arches from those requiring surgery or observation during infancy. Continuous isthmal Doppler flow increased the likelihood ratio of coarctation 16-fold, and visualization of a coarctation shelf was specific for those requiring surgery. Ventricular septal defect and bicuspid aortic valve were seen in 50% and 25% of true coarctation, respectively, but did not increase the specificity of diagnosis, and left superior vena cava generated false-positive cases. False-negative diagnoses of coarctation may be reduced by appreciating arch disproportion at obstetric screening using the 3-vessel and tracheal view, and false-positive diagnoses can be reduced in the tertiary center by serial measurements and detection of isthmal flow disturbance or coarctation shelf. See p. 1793. |
Real-Time Catheter Molecular Sensing of Inflammation in Proteolytically Active Atherosclerosis |
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Inflammation critically modulates atherosclerosis and is implicated in plaque rupture, a leading cause of myocardial infarction. Clinical methods to sense plaque inflammation in vivo, however, remain limited, particularly in small coronary arteries. Here, we present a new catheter-based intravascular near-infrared fluorescence (NIRF) sensing method to sense inflammation in experimental atherosclerosis in human coronary–sized vessels. In conjunction with an injectable cysteine protease–activatable NIRF agent, the fluorescence catheter sensitively and atraumatically detected NIRF signals in plaques during real-time pullback and through blood. In vivo NIRF signals were detected without the need for balloon occlusion or saline flushing and correlated well with ex vivo NIRF data. On histological analyses, microscopic NIRF signals colocalized with inflammatory plaque macrophages and plaque cathepsin B, a cysteine protease implicated in atherosclerosis. The intravascular NIRF catheter and protease-activatable agent strategy could allow detection of inflamed plaques and high-risk patients and could provide a biological readout for antiinflammatory atherosclerosis therapies. See p 1802.
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Presence of Older Thrombus Is an Independent Predictor of Long-Term Mortality in Patients With ST-Elevation Myocardial Infarction Treated With Thrombus Aspiration During Primary Percutaneous Coronary Intervention |
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Intracoronary thrombus that is 1 to several days or even weeks old is frequently aspirated in patients undergoing primary percutaneous coronary intervention for ST-elevation acute myocardial infarction within 12 hours after symptom onset. This signifies that plaque rupture and subsequent intracoronary thrombus formation on the one hand and coronary occlusion and clinical symptoms on the other hand are often segregated in time. In the present study, the long-term clinical outcome of 1315 patients with acute ST-elevation myocardial infarction after primary percutaneous coronary intervention is correlated with the histopathological findings after thrombus aspiration. The cumulative Kaplan-Meier estimate of all-cause mortality at 4 years was significantly higher in the patients with older thrombus (16.0%) compared with the patients with fresh thrombus (7.4%), with a hazard ratio of 1.82. Multivariate analysis identified the presence of older thrombus as an independent predictor (hazard ratio, 1.83) of long-term mortality, in addition to other established predictors such as patient age, diabetes mellitus, and the presence of shock. At the present time, no methods exist to establish the intracoronary presence of older thrombus noninvasively. Moreover, the pathophysiological mechanism by which older thrombus is related to mortality is unclear. Further studies may elucidate this separate pathway by which older thrombus is related to clinical outcome. See p 1810.
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Long-Term Clinical Outcomes After Drug-Eluting and Bare-Metal Stenting in Massachusetts |
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The late safety of drug-eluting stents (DES) has been a matter of recent controversy. Randomized trials have not been powered to detect differences in mortality compared with bare-metal stents (BMS) and have been limited to lower-risk patients. This population-based study collected prospective clinical and procedural data on all patients who underwent percutaneous coronary intervention with stents from April 1, 2003, through September 30, 2004, at nongovernment hospitals in Massachusetts. Rates of mortality, myocardial infarction, and repeat revascularization procedures on the treated vessel were ascertained over the 2 years after stent placement. The goal of the study was to determine long-term patient outcomes by stent type in a population representative of current US medical practice. Because the choice of stent was not assigned randomly, a propensity score–matched analysis was performed to compare DES- and BMS-treated patients with similar characteristics. One-to-one matching was performed with a logistic regression model created from 63 variables to identify unique pairs of DES and BMS patients with similar baseline characteristics. A total of 17 793 patients who underwent placement of DES or BMS were identified; patients who received both stent types were excluded. Sixty-five percent of patients (11 556) received DES compared with 35% (6237) who received BMS. A total of 5549 DES patients matched to 5549 BMS patients were analyzed for each of the 2-year outcomes. The 2-year risk-adjusted mortality, myocardial infarction, and target-vessel revascularization rates each were lower for patients treated with DES than for those treated with BMS. See p 1817.
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Impact of Pretreatment With Clopidogrel on Initial Patency and Outcome in Patients Treated With Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction: A Systematic Review |
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Although randomized data are lacking, patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction are often pretreated with a loading dose of clopidogrel. In this systematic review, we compared the incidence of initial coronary artery patency and short-term outcome in treatment groups of studies in which patients received pretreatment with clopidogrel with those in which patients did not receive clopidogrel before initial coronary angiography. A total of 38 treatment groups comprising 8429 patients were included. We found that initial patency and clinical outcome were improved in treatment groups that received pretreatment with clopidogrel. This is in line with the experience of pretreatment with clopidogrel in elective patients, non–ST-elevation coronary syndromes, and thrombolytic studies. The results of this systematic review strongly suggest that it is appropriate to give a loading dose of clopidogrel in patients as early as possible after ECG confirmation of ST-elevation myocardial infarction. The safety and efficacy of a higher loading dose of 600 mg clopidogrel before primary percutaneous coronary intervention and the relative merits of prasugrel versus clopidogrel are currently being investigated in randomized trials. See p 1828.
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Increased Inflammatory Gene Expression in ABC Transporter–Deficient Macrophages: Free Cholesterol Accumulation, Increased Signaling via Toll-Like Receptors, and Neutrophil Infiltration of Atherosclerotic Lesions |
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Plasma high-density lipoprotein (HDL) levels have a strong inverse relationship to the incidence of heart attack and stroke, but the underlying mechanisms are poorly understood. Results from our previous reports suggest that 2 ATP-binding cassette transporters, ABCA1 and ABCG1, are central to the antiatherogenic effects of HDL, at least in part by mediating macrophage cholesterol efflux and protecting macrophage foam cell formation. However, the past decade has witnessed a dramatic increase in our understanding of the importance of inflammation in all stages of atherosclerotic heart disease, and HDL has been reported to have antiinflammatory properties. In the present study, we demonstrated that cholesterol accumulation in the plasma membrane of Abcg1–/– and Abca1–/–Abcg1–/– macrophages leads to increased levels and signaling of Toll-like receptor 4 and an increased inflammatory response after exposure to lipopolysaccharide. Significantly, neutrophils became prominent in lesions of Abcg1–/– bone marrow–transplanted mice after a peripheral inflammatory stimulus, most likely reflecting the underlying neutrophilia in these mice as well as the secretion of potent neutrophil chemokines, macrophage inflammatory protein-1
and macrophage inflammatory protein-2, by Abcg1–/– macrophages. These data suggest that similar changes in human atherosclerotic plaques could be involved in plaque destabilization in subjects with low HDL levels after a peripheral inflammatory stimulus and suggest that treatments that raise HDL levels, such as niacin and cholesteryl ester transfer protein inhibitors, have the potential to decrease atherosclerosis not only by promoting cholesterol efflux via ABCA1 and ABCG1 but also by suppressing inflammatory and chemokine gene responses in macrophage foam cells. See p 1837. |
Cardiovascular Stress Hyperreactivity in Babies of Smokers and in Babies Born Preterm |
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Large-scale epidemiological studies convincingly indicate that the seeds of cardiovascular and other diseases may be planted very early in life, before or around the time of birth. Events or insults that occur during this formative developmental period are thought to alter ("program") the body’s structure and physiology, which in turn increases vulnerability to stress and accelerates disease onset. The developmental programming concept has broad public health implications because it raises the prospect of improving the early diagnosis, treatment, and perhaps prevention of disease. This article provides some of the first direct evidence of perinatal programming of human cardiovascular physiology by revealing distinct vascular reactivity patterns in infants born preterm, small for dates, and to mothers who smoked during pregnancy. These are the 3 most common complications of pregnancy and causes of poor infant outcome in the world today. Signs of subtle cardiovascular dysfunction can be spotted surprisingly early in these groups of infants, within days or weeks (rather than months or years) of birth. The long-term significance of this dysfunction is uncertain at present, but it could plausibly be an early marker of later susceptibility to complications such as raised blood pressure. See p 1848.
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