Acute Coronary Syndrome Publications (24545)
Acute Coronary Syndrome Publications
The term dyspnea refers to a wide variety of subjective perceptions, some of which can be influenced by the patient's emotional state. A distinction is drawn between dyspnea of acute onset and chronic dyspnea: the latter, by definition, has been present for more than four weeks. The history, physical examination, and observation of the patient's breathing pattern often lead to the correct diagnosis, yet, in 30-50% of cases, more diagnostic studies are needed, including biomarker measurements and other ancillary tests. The diagnosis can be more difficult to establish when more than one underlying disease is present simultaneously. The causes of dyspnea include cardiac and pulmonary disease (congestive heart failure, acute coronary syndrome; pneumonia, chronic obstructive pulmonary disease) and many other conditions (anemia, mental disorders).
The many causes of dyspnea make it a diagnostic challenge. Its rapid evaluation and diagnosis are crucial for reducing mortality and the burden of disease.
The value-based price range for evolocumab was assessed using a previously published economic model. The model incorporated CPRD CV event rates and considers CV event reduction rate ratios per 1 mmol/L reduction in low-density lipoprotein-cholesterol (LDL-C) from a meta-analysis of statin trials by the Cholesterol Treatment Trialists Collaboration (CTTC), ie, CTTC relationship.
Multiple-event rates of composite CV events (ACS, IS, or coronary revascularization) per 100 patient-years were 12.3 for the high-risk ASCVD cohort, and 25.7, 13.3, and 23.3, respectively, for incident ACS, IS, and HF cohorts. Approximately one-half (42%) of the high risk ASCVD patients with a new CV event during follow-up had a subsequent CV event (ie, ≥ 2 total CV events after the index event). Combining these real-world event rates and the CTTC relationship in the economic model, the value-based price range (credible interval) under a willingness-to-pay threshold of $150,000/quality-adjusted life-year gained for evolocumab was $11,990 ($9341-$14,833) to $16,856 ($12,903-$20,678) in patients with baseline LDL-C levels ≥70 mg/dL or ≥100 mg/dL.
Real-world CVD burden is substantial. Using the observed CVD burden in CPRD and the CTTC relationship, the cost-effectiveness analysis showed that, accounting for uncertainties, the expected value-based price for evolocumab is higher than its current annual cost as long as the payer discount off list price is greater than 20%.
75 mg) adjusted for Japanese patients, evaluate the risk factors for bleeding in Japanese patients, and examine whether patients with a bleeding event are at increased risk of recurrent bleeding. This review covers published data and new analyses of the PRASFIT (PRASugrel compared with clopidogrel For Japanese patIenTs) trials of patients undergoing PCI for acute coronary syndrome or elective reasons. The bleeding risk with prasugrel was similar to that observed with the standard dose of clopidogrel (300/75 mg), including when bleeding events were re-classified using the Bleeding Academic Research Consortium criteria. The pharmacodynamics of prasugrel was not associated with the risk of bleeding events. The main risk factors for bleeding events were female sex, low body weight, advanced age, and presence of diabetes mellitus. Use of a radial puncture site was associated with a lower risk of bleeding during PCI than a femoral puncture site. Finally, the frequency and severity of recurrent bleeding events during continued treatment were similar between prasugrel and clopidogrel. In summary, this review provides important insights into the risk and types of bleeding events in prasugrel-treated patients.Trial registration numbers: JapicCTI-101339 and JapicCTI-111550.
They were randomly allocated to the control group (105 patients receiving standard education during CCR) or the study group (100 patients participating in the extended education program). The extended education program was conducted in the 2(nd) and 3(rd) week of CCR and included a package of educational materials and additional lectures.
Knowledge of basic rules for secondary cardiac prevention was better in the study group, both on admission and after CCR. Notwithstanding, a positive influence of the extended educational program was found with regard to awareness of recommended blood pressure levels and blood lipid profile (improvement of 15-20% in the study group). At baseline, the knowledge of risk factors was comparable between the groups (the percentage of correct questionnaire answers was 50 ±17% among the controls vs. 49 ±16% in the study group; p = 0.77), but improved significantly after education (52 ±17% among controls vs. 58 ±19% in the study group; p = 0.009) and remained better in the study group after a 3-month follow-up (56 ±19% among controls vs. 64 ±19% in the study group).
Extended education during CCR significantly improves the knowledge of cardiovascular risk factors in patients after acute coronary syndrome.
A prognostic event was defined as all-cause mortality or acute myocardial infarction(AMI).
7 trials providing data on 6935 patients fulfilled inclusion criteria. There were considerable differences between studies and this was manifest in variation in prognostic impact of elevated HFABP(Odds ratio range 1.2-15.2 for death). All studies demonstrated that HFABP provide unadjusted prognostic information and in only one study was this negated after adjusting for covariates. A combination of both negative troponin and normal HFABP conferred a very low event rate. No study evaluated the incremental value of HFABP beyond that of standard risk scores.Only one study used a high sensitive troponin assay.
There was marked heterogeneity in prognostic impact of HFABP in ACS between studies reflecting differences in sampling times and population risk. Prospective studies of suspected ACS with early sampling of HFABP in the era of high sensitivity troponin are necessary to determine the clinical value of HFABP. HFABP should not currently be used clinically as a prognostic marker in patients with suspected ACS.
Newer studies that include CKD patients have shown heterogeneity in various outcomes, making management decisions challenging. In this review, we summarize the epidemiologic significance of ACS and CAD in patients with CKD, discuss the diagnosis of ACS in this patient population, and review the therapeutic interventions in patients with CKD.
These patients were compared with age and sex matched controls with regards to the proportion of IHD in a case-control study. Chi-square and t tests were used for univariate analysis, and a logistic regression model was used for multivariate analysis. The study included 5018 patients with SLE and 25090 age and sex-frequency matched controls. The prevalence of IHD in patients with SLE was increased in comparison to controls (11.3 and 3.1%, P < 0.001). In a multivariate analysis, SLE was associated with IHD (OR 3.77, 95% confidence interval 3.34-4.26). We have confirmed that SLE patients suffer a high prevalence of IHD. Our data supports that SLE is an independent risk factor for IHD. When evaluating by gender, the risk seems even more substantial in females. No significant difference was found in the risk of IHD in SLE among the difference socioeconomic strata.
These two groups were treated with conventional antiplatelet, anticoagulation and anti-ischemic therapy, while allopurinol was added to allopurinol group based on conventional treatment. The biochemical indexes such as serum creatinine, uric acid, BNP, blood glucose and blood lipid were compared between the two groups. Indicators of oxidative stress and inflammatory response (MDA, OX-LDL, NO, hs-CRP and TNF-α) as well as cardiovascular events during 2-years follow-up were recorded.
On admission, there is no difference in serum creatinine, uric acid, BNP, blood glucose and lipid levels between the two groups (P > 0.05), and after 1 month of treatment, these levels are better in patients in the allopurinol group than the control group (P < 0.05). After treatment on day 14, 1 month, 3 months, 6 months, 1 year and 2 years follow-up, MDA, OX-LDL and hs-CRP, TNF-α in both groups have decreased, however data from the allopurinol group are significantly lower than the control group (P < 0.05). Additionally, compared with control group, allopurinol treatment significantly elevated the level of NO (P < 0.05). The total effective rates of allopurinol group are much higher than the control group both in angina pectoris (93.2% and 76% respectively) and ECG (96% and 82% respectively). Patients in allopurinol group (n=40) and control group (n=41) received stent implantation and there is no statistical difference between them. The incidence of cardiovascular events during 2-years follow-up in allopurinol group is 10% while it is 30% in the control group.
Allopurinol has remarkable effect in the treatment of ACS and can improve the Oxidative Stress and inflammatory reaction indicators of patients. The protective mechanism of allopurinol might be achieved by suppressing the secretion and release of inflammatory mediators TNF-α, hs-CRP and OX-LDL, MDA and increasing level of NO.