JACC - Último número
A large proportion of patients presenting with non–ST-segment elevation myocardial infarction (NSTEMI) present with multivessel disease (MVD). There is uncertainty in the role of complete coronary revascularization in this group of patients.
The aim of this study was to investigate the outcomes of complete revascularization compared with culprit vessel–only intervention in a large contemporary cohort of patients undergoing percutaneous coronary intervention (PCI) for NSTEMI.
The authors undertook an observational cohort study of 37,491 NSTEMI patients treated between 2005 and 2015 at the 8 heart attack centers in London. Clinical details were recorded at the time of the procedure into local databases using the British Cardiac Intervention Society (BCIS) PCI dataset. A total of 21,857 patients (58.3%) presented with NSTEMI and MVD. Primary outcome was all-cause mortality at a median follow-up of 4.1 years (interquartile range: 2.2 to 5.8 years).
A total of 11,737 (53.7%) patients underwent single-stage complete revascularization during PCI for NSTEMI, rates that significantly increased during the study period (p = 0.006). Those patients undergoing complete revascularization were older and more likely to be male, diabetic, have renal disease and a history of previous myocardial infarction/revascularization compared with the culprit-only revascularization group. Although crude, in-hospital major adverse cardiac event rates were similar (5.2% vs. 4.8%; p = 0.462) between the 2 groups. Kaplan-Meier analysis demonstrated significant differences in mortality rates between the 2 groups (22.5% complete revascularization vs. 25.9% culprit vessel intervention; p = 0.0005) during the follow-up period. After multivariate Cox analysis (hazard ratio: 0.90; 95% confidence interval: 0.85 to 0.97) and the use of propensity matching (hazard ratio: 0.89; 95% confidence interval: 0.76 to 0.98) complete revascularization was associated with reduced mortality.
In NSTEMI patients with MVD, despite higher initial (in-hospital) mortality rates, single-stage complete coronary revascularization appears to be superior to culprit-only vessel PCI in terms of long-term mortality rates. This supports the need for further randomized study to confirm these findings.
It has been shown that intravascular ultrasound (IVUS) and radiofrequency (RF-)IVUS can detect high-risk coronary plaque characteristics.
The authors studied the long-term prognostic value of (RF-)IVUS-derived plaque characteristics in patients with coronary artery disease (CAD) undergoing coronary angiography.
From 2008 to 2011, (RF-)IVUS was performed in 1 nonstenotic segment of a nonculprit coronary artery in 581 patients undergoing coronary angiography for acute coronary syndrome (ACS) or stable angina. The pre-defined primary endpoint was major adverse cardiovascular events (MACE), defined as the composite of all-cause death, nonfatal ACS, or unplanned revascularization. Hazard ratios (HRs) were adjusted for age, sex, and clinical risk factors.
During a median follow-up of 4.7 years, 152 patients (26.2%) had MACE. The presence of a lesion with a minimal luminal area ≤4.0 mm2 was independently associated with MACE (HR: 1.49; 95% CI: 1.07 to 2.08; p = 0.020), whereas the presence of a thin-cap fibroatheroma lesion or a lesion with a plaque burden ≥70% on its own were not. Results were comparable when the composite endpoint included cardiac death instead of all-cause death. The presence of a lesion with a plaque burden of ≥70% was independently associated with the composite endpoint of cardiac death, nonfatal ACS, or unplanned revascularization after exclusion of culprit lesion-related events (HR: 1.66; 95% CI: 1.06 to 2.58; p = 0.026). Likewise, each 10-U increase in segmental plaque burden was independently associated with a 26% increase in risk of this composite endpoint (HR: 1.26 per 10-U increase; 95% CI: 1.03 to 1.52; p = 0.022).
IVUS-derived small luminal area and large plaque burden, and not RF-IVUS–derived compositional plaque features on their own, predict adverse cardiovascular outcome during long-term follow-up in patients with CAD. (The European Collaborative Project on Inflammation and Vascular Wall Remodeling in Atherosclerosis–Intravascular Ultrasound Study [AtheroRemoIVUS]; NCT01789411)
Incremental low-density lipoprotein (LDL) cholesterol lowering with the proprotein convertase subtilisin kexin type 9 inhibitor evolocumab regresses coronary atherosclerosis in statin-treated patients.
The purpose of this study was to evaluate the effect of adding evolocumab to statin therapy on coronary plaque composition.
A total of 968 statin-treated coronary artery disease patients underwent serial coronary intravascular ultrasound imaging at baseline and following 76 weeks of treatment with placebo or evolocumab 420 mg monthly. Plaque composition changes were determined in 331 patients with evaluable radiofrequency analysis of the ultrasound backscatter signal.
Compared with statin monotherapy, evolocumab further reduced LDL cholesterol (33.5 mg/dl vs. 89.9 mg/dl; p < 0.0001) and induced regression of percent atheroma volume (–1.2% vs. +0.17%; p < 0.0001) and total atheroma volume (–3.6 mm3 vs. –0.8 mm3; p = 0.04). No difference was observed between the evolocumab and placebo groups in changes in calcium (1.0 ± 0.3 mm3 vs. 0.6 ± 0.3 mm3; p = 0.49), fibrous (–3.0 ± 0.6 mm3 vs. –2.4 ± 0.6 mm3; p = 0.49), fibrofatty (–5.0 ± 1.0 mm3 vs. –3.0 ± 1.0 mm3; p = 0.49), and necrotic (–0.6 ± 0.5 mm3 vs. –0.1 ± 0.5 mm3; p = 0.49) volumes. An inverse correlation was observed between changes in LDL cholesterol and plaque calcification (r = –0.15; p < 0.001).
The addition of evolocumab to a statin did not produce differential changes in plaque composition compared with statin monotherapy. This suggests that evaluation of plaque morphology using virtual histology imaging may provide no incremental information about the plaque effects of evolocumab beyond measurement of plaque burden. (GLobal Assessment of Plaque reGression With a PCSK9 antibOdy as Measured by intraVascular Ultrasound [GLAGOV]; NCT01813422)
The long-term risk of thromboembolism in patients developing new-onset post-operative atrial fibrillation (POAF) following noncardiac surgery is unknown, and data on stroke prophylaxis in this setting are lacking.
The purpose of this study was to assess the long-term risk of thromboembolism in patients developing new-onset POAF following noncardiac surgery relative to patients with nonsurgical, nonvalvular atrial fibrillation (NVAF).
Using Danish nationwide registries, the authors identified all patients who developed POAF following noncardiac surgery from 1996 to 2015. These were matched by age, sex, heart failure, hypertension, diabetes, previous thromboembolism, ischemic heart disease, and year of diagnosis to patients with nonsurgical NVAF in a 1:4 ratio. Comparative long-term risk of thromboembolism was examined by multivariable Cox regression models.
In patients undergoing noncardiac surgery, 6,048 (0.4%) developed POAF during hospitalization, with the highest incidences following thoracic/pulmonary, vascular, and abdominal surgery. A total of 3,830 patients with POAF were matched with 15,320 patients with NVAF. Oral anticoagulation therapy was initiated within 30 days post-discharge in 24.3% and 41.3% of these patients, respectively (p value <0.001). The long-term risk of thromboembolism was similar in patients with POAF and NVAF (31.7 events vs. 29.9 events per 1,000 person years; hazard ratio [HR]: 0.95; 95% confidence interval [CI]: 0.85 to 1.07). Anticoagulation therapy during follow-up was associated with a comparably lowered risk of thromboembolic events in patients with POAF (HR: 0.52; 95% CI: 0.40 to 0.67) as well as NVAF (HR: 0.56; 95% CI: 0.51 to 0.62) compared with no anticoagulation therapy.
New-onset POAF following noncardiac surgery was associated with a long-term risk of thromboembolism similar to NVAF.
Should All Atrial Fibrillation Be Considered a Life-Long Problem Requiring Prophylaxis Against Thromboembolism?15/10/2018
Patients with cardiac amyloidosis often have carpal tunnel syndrome that precedes cardiac manifestations by several years. However, the prevalence of cardiac involvement at the time of carpal tunnel surgery has not been established.
The authors sought to identify the prevalence and type of amyloid deposits in patients undergoing carpal tunnel surgery and evaluate for cardiac involvement. The authors also sought to determine if patients with soft tissue transthyretin (TTR) amyloid had abnormal TTR tetramer kinetic stability.
This was a prospective, cross-sectional, multidisciplinary study of consecutive men age ≥50 years and women ≥60 years undergoing carpal tunnel release surgery. Biopsy specimens of tenosynovial tissue were obtained and stained with Congo red; those with confirmed amyloid deposits were typed with mass spectrometry and further evaluated for cardiac involvement with biomarkers, electrocardiography, echocardiography with longitudinal strain, and technetium pyrophosphate scintigraphy. Additionally, serum TTR concentration and tetramer kinetic stability were examined.
Of 98 patients enrolled (median age 68 years, 51% male), 10 (10.2%) had a positive biopsy for amyloid (7 ATTR, 2 light chain [AL], 1 untyped). Two patients were diagnosed with hereditary ATTR (Leu58His and Ala81Thr), 2 were found to have cardiac involvement (1 AL, 1 ATTR wild-type), and 3 were initiated on therapy. In those patients who had biopsy-diagnosed ATTR, there was no difference in plasma TTR concentration or tetramer kinetic stability.
In a cohort of patients undergoing carpal tunnel release surgery, Congo red staining of tenosynovial tissue detected amyloid deposits in 10.2% of patients. Concomitant cardiac evaluation identified patients with involvement of the myocardium, allowing for implementation of disease-modifying therapy. (Carpal Tunnel Syndrome and Amyloid Cardiomyopathy; NCT02792790)
Fine particulate matter <2.5 μm (PM2.5) air pollution is the most important environmental risk factor contributing to global cardiovascular (CV) mortality and disability. Short-term elevations in PM2.5 increase the relative risk of acute CV events by 1% to 3% within a few days. Longer-term exposures over several years increase this risk by a larger magnitude (~10%), which is partially attributable to the development of cardiometabolic conditions (e.g., hypertension and diabetes mellitus). As such, ambient PM2.5 poses a major threat to global public health. In this review, the authors provide an overview of air pollution and health, including assessment of exposure, impact on CV outcomes, mechanistic underpinnings, and impact of air pollution reduction strategies to mitigate CV risk. The review concludes with future challenges, including the inextricable link between air pollution and climate change, and calls for large-scale trials to allow the promulgation of formal evidence-based recommendations to lower air pollution–induced health risks.
Observations on human and experimental atherosclerosis, biomarker studies, and now a large-scale clinical trial support the operation of immune and inflammatory pathways in this disease. The factors that incite innate and adaptive immune responses implicated in atherogenesis and in lesion complication include traditional risk factors such as protein and lipid components of native and modified low-density lipoprotein, angiotensin II, smoking, visceral adipose tissue, and dysmetabolism. Infectious processes and products of the endogenous microbiome might also modulate atherosclerosis and its complications either directly, or indirectly by eliciting local and systemic responses that potentiate disease expression. Trials with antibiotics have not reduced recurrent cardiovascular events, nor have vaccination strategies yet achieved clinical translation. However, anti-inflammatory interventions such as anticytokine therapy and colchicine have begun to show efficacy in this regard. Thus, inflammatory and immune mechanisms can link traditional and emerging risk factors to atherosclerosis, and offer novel avenues for therapeutic intervention.
Annual live meetings are a focus for many organizations and professional societies and have long been considered an essential part of lifelong learning. Live meetings offer a venue for a wide range of topics including late breaking science, traditional and novel educational formats, networking opportunities, integration of technology, engagement of the cardiovascular team, and more. Although many factors provide challenges for the future of live annual meetings, there are many opportunities as well. The unique aspects of interactions and experiences at these meetings will maintain their importance in the lifelong learning toolbox.
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