Acute Coronary Syndrome

Sirolimus-coated balloon in acute and chronic coronary syndromes: the PEACE study, a subanalysis of the EASTBOURNE registry

Background: Acute coronary syndrome (ACS) remains the primary cause of mortality worldwide. Performing complex coronary intervention in patients with ACS is considered a significant factor for worsening prognosis. This study aimed to evaluate the prognosis of patients with ACS treated with complex procedures compared to patients with chronic coronary syndrome (CCS). Methods: Among 980 patients from the Polish Complex Registry, we enrolled 829 consecutive patients who underwent complex percutaneous coronary intervention (PCI) for acute or chronic coronary syndrome with a completed one-year follow-up. The primary endpoint is defined as the major adverse cardiac event (MACE) at 12 months, a composite endpoint including all-cause death, target lesion revascularization, target vessel revascularization, and non-fatal myocardial infarction. Results: The incidence of the composite endpoint of MACE at one-year follow-up was comparable between the patients with acute and chronic coronary syndrome who underwent complex PCI (12.4% vs. 7.6%, LogRank p = 0.035). Cox multivariate analysis indicated that ACS is an independent risk factor for death at one-year follow-up. Additionally, age and comorbidities, such as heart failure and chronic kidney disease, along with procedural factors, including lesion length and pre-procedural diameter stenosis, are independent predictors of death in patients with complex lesions. Independent risk factors for MACE at one-year follow-up include age, heart failure, previous PCI, in-stent restenosis, and pre-procedural diameter stenosis. Conclusions: The prognosis of patients with acute and chronic coronary syndrome in the annual follow-up is comparable in the context of cardiovascular events. The clinical presentation of ACS is an independent risk factor for all-cause death.

Modern antithrombotic therapy for acute coronary syndromes rests on a growing body of basic and clinical evidence that rupture or erosion of the surface of a vulnerable plaque sets in motion a sequence of events culminating in thrombus formation in the culprit vessel.1 When the contents of a vulnerable plaque are exposed to the bloodstream, platelets adhere to the subendothelial matrix, release ADP and thromboxane A2, and amplify the generation of thrombin.2 As a result, a platelet aggregate begins to develop. In addition, the coagulation cascade is activated and fibrin strands are formed. Thrombin (factor IIa) plays a pivotal role in the processes described above because of its extensive procoagulant and prothrombotic actions.3 In addition to catalyzing the transformation of soluble fibrinogen into fibrin monomers and activating factor XIII to produce cross-linked fibrin, thrombin promotes clot formation by activating factors V and VIII. It is also one of the most potent agents responsible for platelet adhesion, activation, and aggregation. In vessels with a diseased endothelium, thrombin promotes the release of the vasoconstrictor endothelin 1. Importantly, thrombin also potentiates the proliferative effects of multiple growth factors and is a key mediator of early smooth muscle cell proliferation after arterial injury. There is now abundant evidence that thrombus formation can be prevented by direct or indirect inactivation of thrombin or by inhibition of thrombin production via the intrinsic or extrinsic limbs of the coagulation pathway.3 Unfractionated heparin, the standard antithrombotic agent in clinical practice, is a glycosaminoglycan, consisting of chains of alternating residues of d-glucosamine and uronic acid.4 Although familiar to the vast majority of clinicians, unfractionated heparin has several disadvantages: (1) a variable anticoagulant effect (necessitating frequent monitoring of activated partial thromboplastin time), (2) neutralization by platelet factor 4, (3) less effective inhibition …

<i>Circulation: Cardiovascular Interventions</i> Editors’ Picks

Balón liberador de sirolimus en el tratamiento del síndrome coronario agudo y crónico: el estudio PEACE, un subanálisis del registro EASTBOURNE

To investigate the role of periodontitis in the risk of acute and chronic coronary syndrome with compounding factors, including sociodemographic factors and medication use. This retrospective cohort study used nationwide, population-based data from the Korean National Health Insurance Service-Health Screening Cohort database (514,866 individuals, 40-79years). Propensity score matching was used for analysis. Information of subjects for 12years was included. Socioeconomic and clinical factors were recorded and analysed. The periodontitis group had a greater risk of overall acute coronary syndrome (hazard ratio [95% confidence interval] =1.25 [1.15, 1.35], p<.001) and non-fatal acute coronary syndrome (1.26 [1.16, 1.37], p<.001). The hazard ratio for chronic coronary syndrome was higher in patients with periodontitis (1.35 [1.25, 1.46], p<.001). The cumulative incidence of both acute and chronic coronary syndrome gradually increased, and the hazard ratios reached 1.25 and 1.35 at the 12-year follow-up, respectively. Subgroup analysis revealed that periodontitis had a significantly greater link with acute coronary syndrome incidence in males, younger adults, smokers and subjects without hypertension (p<.01) and with chronic coronary syndrome incidence in smokers, subjects without hypertension and subjects without dyslipidaemia (p<.05). Periodontitis is associated with an increased risk of acute and chronic coronary syndrome.

Background: Cognitive impairment is prevalent in survivors of acute coronary syndrome (ACS) and increases risk for poor outcomes. Lifestyle changes are recommended to patients after ACS to reduce their risk for recurrent events, but cognitively impaired patients may encounter difficulties initiating these changes. This dissertation had three aims: (1) to examine cognitive status as a predictor of lifestyle changes after ACS, (2) to examine whether caregiver support moderates the association of cognitive status and initiation of lifestyle changes, and (3) to assess the reliability of self-reported lifestyle changes in cognitively impaired patients through comparison of their reports of lifestyle change with those from their caregivers. Methods: For aims 1 and 2, Poisson regression with robust error variance was used to examine the association of cognitive status and caregiver support with patient-reported initiation of five lifestyle changes (improving diet, increasing exercise, quitting smoking, reducing stress, and attending cardiac rehabilitation) in 881 patients from TRACE-CORE, a prospective longitudinal observational study of outcomes in ACS. For aim 3, pilot data from 78 patient-caregiver dyads from TRACE-CARE, an ancillary substudy, were used to examine whether patient-caregiver congruence on reports of lifestyle changes varied according to patients’ cognitive function. Results: Patient-reported rates of lifestyle change did not vary according to cognitive status, except for participation in cardiac rehabilitation. Caregiver support improved patient-reported rates of lifestyle change among cognitively intact patients but not cognitively impaired patients. Patients’ cognitive function was positively associated with patient-caregiver congruence on reports of initiation of lifestyle changes and patients with decreased cognitive function tended to over-report initiation of lifestyle changes compared to reports by their caregivers. Conclusion: Although cognitive status was not associated with initiation of most lifestyle changes and the influence of caregiver support on initiation of lifestyle changes was only beneficial to cognitively intact patients in this cohort of ACS patients, these null findings may be explained by the questionable validity of self-report in cognitively impaired patients. This dissertation yields new knowledge about secondary prevention in ACS patients and provides insight into the challenges of conducting patient-reported outcomes research in cognitively compromised populations.

Platelet Interactions with Von Willebrand Factor: Comparing Platelet Function in Acute and Stable Coronary Syndromes

98: The Association Between Self-Reported Physical Fitness and Exercise Frequency With ACS In Emergency Department Chest Pain Patients

oronary heart disease is the leading cause of mortality and morbidity in industrialized countries, in men as well as in women.Women have their first cardiac event 6 to 10 years later than men do.Whereas the cardiovascular death rates are declining in men, they remain constant in women.In cardiovascular studies with age limits, women are naturally the minority, amounting to Ͻ40%.It is well known that distinct gender differences exist in terms of presentation of symptoms, validity of diagnostic tests, drug side effects, and complications.With respect to cardiac risk factors, women have higher rates of diabetes and hypertension but are less frequently smokers.

Background/Objectives: The complement system (particularly C5b-9) is an instrumental part of the induction and progression of atherosclerosis. The fluid phase C5b-9, also known as soluble C5b-9 (sC5b-9), is a reliable indicator of terminal complement pathway activation. Response Gene to Complement (RGC)-32 is a C5b-9 effector involved in cell cycle regulation and differentiation, immunity, tumorigenesis, obesity, and vascular lesion formation. RGC-32 regulates the expression of Sirtuin1 (SIRT1), known to delay vascular aging. The aim of this study was to assess the levels of sC5b-9, RGC-32, and SIRT1 in patients with atherosclerotic chronic and acute ischemic coronary syndromes. Methods: We determined the levels of sC5b-9, serum RGC-32, and SIRT1 by enzyme-linked immunosorbent assays (ELISAs) in 41 patients with chronic atherosclerotic coronary syndromes, 36 patients with acute ischemic coronary syndromes, and 21 asymptomatic controls with no history of ischemic heart disease. Results: sC5b-9 was significantly higher in patients with acute coronary syndrome as compared to the control group (p = 0.020, AUC = 0.702). In chronic coronary ischemia patients, serum RGC-32 was correlated with the extension of coronagraphically visualized atherosclerotic lesions (r = 0.352, p = 0.035) as well as with sC5b-9 levels (r = 0.350, p = 0.025). RGC-32 concentration was significantly lower in patients with acute coronary syndrome than in the control group (p = 0.020). We also observed significantly lower serum SIRT1 concentrations in patients with chronic ischemic heart disease than in the control group (p = 0.025). Conclusions: sC5b-9 may function as a possible biomarker for myocardial tissue damage in acute coronary syndrome. In acute coronary syndrome settings, low levels of RGC-32 may indicate a protective, antifibrotic function of RGC-32 in the ischemia-damaged myocardium; however, in stable chronic disease, RGC-32 serum values appear to correlate with the extent of atherosclerotic lesions, suggesting a pro-atherogenic role for RGC-32. Chronic myocardial ischemia decreases SIRT1 protein levels in serum, which underscores the use of SIRT1-modulating drugs in these patients.

Acute coronary syndromes

Anticoagulation Use and Outcomes Among Patients with Atrial Fibrillation and Von Willebrand Disease

The PIONEER III trial demonstrated noninferiority of 12-month target lesion failure (TLF) with the Supreme DES (Sinomed), a thin-strut cobalt-chromium, biodegradable polymer, sirolimus-eluting stent, compared with a durable polymer, everolimus-eluting (XIENCE/PROMUS) stent (DP-EES). The relative safety and effectiveness of the Supreme DES in patients with acute coronary syndromes (ACS) and those with chronic coronary syndromes (CCS) is not known. PIONEER III was a prospective, multicenter, international, 2:1 randomized trial stratified by clinical presentation. The primary end point was TLF at 12 months (a composite of cardiac death, target vessel myocardial infarction, or ischemia-driven target lesion revascularization). A total of 1628 patients were enrolled, including 41% of patients with ACS (unstable angina and non-ST-elevation myocardial infarction) randomized to Supreme DES (n = 441) versus DP-EES (n = 232) and 59% of patients with CCS randomized to Supreme DES (n = 645) versus DP-EES (n = 310). Patients with ACS were younger, fewer presented with less diabetes, hypertension, and previous revascularization, but more were current smokers. The primary end point of TLF (6.4% vs 4.4%; P = .1), major adverse cardiac events (8.5% vs 6.5%; P = .16), and stent thrombosis (0.4% vs 0.9%; P = .25) at 12 months were similar in the ACS and CCS groups. There was no difference in TLF at 12 months between Supreme DES and DP-EES among patients with ACS (6.6% vs 6.0%; P = .89) and those with CCS (4.5% vs 4.3%; P = .83); interaction P = .51 for TLF by clinical presentation. Compared with the DP-EES, the Supreme DES seemed safe and effective with a similar TLF at 12 months in both patients with ACS and those with CCS.

An analysis of additional risk factors for the development of ischemic heart disease (IHD) is needed in connection with unfavorable dynamics in the prevalence of this disease. Objective. To study the features of IHD clinical course in patients with chronic coronary syndrome and acute coronary syndrome without ST-segment elevation depending on the quantitative profile of vitamin D in the blood serum. Material and methods. A number of men equal 192 (mean age 55.1±3.4 years), who were divided into 3 groups, were examined: 1st group — with acute coronary syndrome without ST-segment elevation (n=93; mean age 55.37±3.14 years); 2nd group — with chronic coronary syndrome (n=63; mean age 55.12±3.50 years) and 3rd group — control group which consisted of conditionally healthy individuals without cardiac pathology (n=36; mean age 52.8±4.2 years). Vitamin D (25(OH)D) blood serum concentration as well as proinflammatory cytokine levels (interleukin-8, tumour necrosis factor-aloha), anti-inflammatory cytokine (interleukin-4), homocysteine, vascular endothelial growth factor (VEGF) and endothelin were determined in all study participants. Instrumental examination of patients with IHD included electrocardiography, echocardiography and selective coronary angiography. Results. Vitamin D deficiency has been more commonly found in patients with acute coronary syndrome without ST-segment elevation than in patients with chronic coronary syndrome and control group (80.6% and 27.3%; χ2=56.46; p&lt;0.001). Insufficiency of vitamin D has been more often noted in patients with chronic coronary syndrome than in patients with acute coronary syndrome without ST-segment elevation and in individuals of control group (54.5 and 12.9%; χ2=37.736; p&lt;0.001). The lowest 25(OH)D level has been determined in patients with acute coronary syndrome without ST-segment elevation compared to patients with chronic coronary syndrome and control group (18.62±9.70; 21.59±6.02; 64.39±18.03 ng/ml; F=75.64; p&lt;0.001). Correlations between 25(OH)D and the number of coronary arteries with stenosis up to 69% (R=–0.26; p&lt;0.05), the number of coronary arteries with stenosis up to 90—99% (R=–0.29; p&lt;0.05), the number of hemodynamically significant stenoses (R=–0.25; p&lt;0.05), degree of stenosing of the left main coronary artery (R=–0.23; p&lt;0.05), degree of stenosing of the proximal segment of left anterior descending artery in % (R=–0.23; p&lt;0.05), degree of stenosing of the diagonal artery (R=–0.27; p&lt;0.05), degree of stenosing of the obtuse marginal artery (R=–0.26; p&lt;0.05), degree of stenosing of the distal segment of right coronary artery (R=–0.29; p&lt;0.05), degree of stenosing of the middle segment of right coronary artery (R=–0.24; p&lt;0.05), restenosis (R=–0.26; p&lt;0.05) have been established. Patients with vitamin D deficiency had more severe coronary bed lesion compared to patients with vitamin D insufficiency or its adequate level, which was manifested in an increase in the number of coronary arteries with stenosing up to 69% (0.76 95% CI 0.58—0.94; 0.36 95% CI 0.22—0.50; 0.58 95% CI 0.34—0.83; p&lt;0.01), the number of coronary arteries with stenosing degree in the range of 70—79% (0.56; 95% CI 0.43—0.69; 0.41; 95% CI 0.28—0.52; 0.33; 95% CI 0.22—0.44; p&lt;0.05), the number of coronary arteries with stenosing degree in the range of 90—99% (0.42 95% CI 0.34—0.49; 0.27 95% CI 0.19—0.35; 0.25 95% CI 0.15—0.35; p&lt;0.01), the number of hemodynamically significant stenoses (1.51 95% CI 1.36—1.66; 1.27 95% CI 1.15—1.38; 1.17 95% CI 1.08—1.25; p&lt;0.01). Conclusion. Vitamin D deficiency is associated with the increased level of proinflammatory and anti-inflammatory cytokines, increase of adverse vascular factors blood level, which causes progression of coronary atherosclerosis in patients with ischemic heart disease. Men with ischemic heart disease are more likely to develop acute coronary syndrome without ST-segment elevation at 25(OH)D level of 20.49 ng/ml.