Publications

Four decades have passed since the first trial suggesting the efficacy of aspirin in the secondary prevention of myocardial infarction. Further trials, collectively summarized by the Antithrombotic Trialists' Collaboration, solidified the historical role of aspirin in secondary prevention. Although the benefit of aspirin in the immediate phase after a myocardial infarction remains incontrovertible, a number of emerging lines of evidence, discussed in this narrative review, raise some uncertainty as to the primacy of aspirin for the lifelong management of all patients with chronic coronary syndrome (CCS). For example, data challenging the previously unquestioned role of aspirin in CCS have come from recent trials where aspirin was discontinued in specific clinical scenarios, including early discontinuation of the aspirin component of dual antiplatelet therapy after percutaneous coronary intervention and the withholding of aspirin among patients with both CCS and atrial fibrillation who require anticoagulation. Recent primary prevention trials have also failed to consistently demonstrate net benefit for aspirin in patients treated to optimal contemporary cardiovascular risk factor targets, indicating that the efficacy of aspirin for secondary prevention of CCS may similarly have changed with the addition of more modern secondary prevention therapies. The totality of recent evidence supports further study of the universal need for lifelong aspirin in secondary prevention for all adults with CCS, particularly in stable older patients who are at highest risk for aspirin-induced bleeding.

No abstract is provided for this article.

No abstract is provided for this article.

Percutaneous myocardial revascularization (PMR) has emerged as a novel therapeutic strategy for patients with ischemic heart disease not amendable to traditional revascularization approaches. Despite the symptomatic improvement documented in clinical trials, underlying mechanism remains unknown.We assessed the coronary angiograms of 25 patients before and 6 months after the PMR procedures for collateral vessel formation. The Rentrop scoring system was used to score the extent of collateral vessel formation. The angiograms were analyzed by 2 independent reviewers. The change in Rentrop score and improvement in angina status was correlated.During follow-up period of 6 months, no patient died or suffered from myocardial infarction. Overall the mean Canadian Classification Society (CCS) class among the study patients was significantly improved from 3.5 to 2.4; mean difference = 1.08 (p < 0.0001). Among these, 8 (32%) had improvement of > 2 CCS classes (p = 0.003) (improvement group). The rest of the patients had either no change (n = 8; 32%) or improvement of 1 CCS class (n = 9; 36%) (no improvement group). The Rentrop score improved in 3 (12%), remained unchanged in 22 (88%) and deteriorated in 0 patient. Overall, there was no significant change in Rentrop score at 6-month follow-up; mean difference 0.13 (p = 0.08). There was also no correlation between the change in extent of collateral vessel formation and the improvement in angina status (correlation coefficient r = 0.09) at 6 months after PMR.Improvement in collateral vessel formation is unlikely to be a mechanism responsible for symptomatic improvement in patients after PMR.

Incomplete revascularisation is common after percutaneous coronary intervention (PCI). While the absolute amount of residual coronary artery disease (CAD) after PCI has been shown to be associated with worse outcomes, whether the proportion of treated CAD is prognostically important remains to be determined. We sought to quantify the proportion of CAD burden treated by PCI and to evaluate its impact on outcomes using a new prognostic instrument - the SYNTAX Revascularisation Index (SRI).The baseline SYNTAX score (bSS) and residual SYNTAX score (rSS) were determined from 2,618 angiograms of patients enrolled in the prospective ACUITY trial. The SRI was then calculated for each patient using the following formula: SRI=(1-[rSS/bSS])×100. Outcomes were examined according to three SRI groups (SRI=100% [complete revascularisation], 50-99%, and <50%). The median bSS was nine (IQR 5, 16), and after PCI the median rSS was one (IQR 0, 6). The median SRI was 85% (IQR 50, 100), and was 100% in 1,079 patients (41.2%), 50-99% in 907 patients (34.6%), and <50% in 632 patients (24.1%). One-year adverse outcomes, including death, were inversely proportional to the SRI. An SRI cut-off of <80% (present in 1,189 [45.4%] patients after PCI) had the best prognostic accuracy for prediction of death (area under the curve 0.60, 95% confidence interval [CI]: 0.53-0.67, p<0.0001). By multivariable analysis, SRI was an independent predictor of one-year mortality (hazard ratio [HR] 2.17, 95% CI: 1.05-4.35, p=0.03). However, when compared to other scores, the rSS showed superior accuracy and predictive capability for one-year mortality.The SRI is a newly described method for quantifying the proportion of CAD burden treated by PCI. Given its correlation with mortality, and pending external validation, the SRI may be useful in assessing the degree of revascularisation after PCI, with SRI ≥80% representing a reasonable goal. However, the rSS showed superior predictive capability for one-year mortality.

Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.

Abstract Inhaled corticosteroids are widely used in the treatment of bronchial asthma, but it is still uncertain whether long-term use of the inhaled corticosteroids affects bone metabolism in asthmatic patients. In this study, we examined the effect of inhaled beclomethasone dipropionate (BDP) on bone mineral density (BMD) and biochemical markers of bone metabolism in pre- and early postmenopausal asthmatic women. Thirty-six (17 premenopausal and 19 early postmenopausal) asthmatic women and 45 healthy control (24 premenopausal and 21 early postmenopausal) women were investigated. All the asthmatic patients were treated with BDP (542 ± 298 μg/day; 100–1200 μg/day) without any systemic administration of corticosteroids for at least 1 year. In premenopausal women, BMD as well as the biochemical markers of bone metabolism did not differ between control subjects and BDP-treated asthmatic patients. By contrast, in early postmenopausal women, BMD was significantly lower in BDP-treated asthmatic patients than in control subjects. In these early postmenopausal women, serum intact osteocalcin concentration was lower in the BDP-treated asthmatic patients than in the control subjects whereas urinary free pyridinoline (F-PYD) and free deoxypyridinoline (F-DPD) concentrations did not differ between the groups. Thus, early postmenopausal, but not premenopausal, asthmatic patients who were treated with inhaled BDP had reduced BMD, which was associated with a decreased level of the bone formation marker. Ovarian hormones may be protective against the adverse effect of inhaled BDP on bone metabolism in the premenopausal patients.