Myocardial Infarction Publications (218713)
Myocardial Infarction Publications
Twenty-three randomized trials were included. For agents approved prior to 2008, metformin has not been associated with measurable harm in patients with diabetes in terms of mortality and CV events (and a trend of benefit). Controversial results existed with the use of sulfonylureas, and TZDs for CV outcomes. Among agents approved after 2008, liraglutide and empagliflozin have been shown to be superior to placebo in improving CV outcomes. FDA regulatory mandate to demonstrate CV safety in order to approve new diabetes drugs led to increase number of CV outcome trials. However, these trials have placebo-controlled, non-inferiority designs aiming to show absence of CV toxicity. More studies are needed to address other questions, including comparative effectiveness, and longer term risk versus benefits.
Overall, 21,162 patients with a spontaneous MI 1 to 3 years before randomization were randomly assigned to ticagrelor 90 mg bid, ticagrelor 60 mg bid, or placebo. Compared with placebo, both doses of ticagrelor showed that they were capable of significantly reducing the primary efficacy endpoint, although with a significant increase in TIMI major bleeding. Intracranial hemorrhage or fatal bleeding did not differ across groups. These findings establish clear benefit of DAPT extension with ticagrelor beyond 1 year of treatment, which comes with a tradeoff of clinically meaningful bleeding. Altogether, current evidence suggests that the duration of DAPT remains a patient-by-patient decision based on thrombotic and bleeding risk profiles.
Although current prevalence estimates are derived from study populations with prior CIEDs, 3 trials will assess the time to a first AF diagnosis among patients receiving a CIED for purposes of AF detection. Stroke risk estimates are currently limited to patients with a prior CIED and vary widely, ranging from a hazard ratio of 0.87 (95% CI, 0.58-1.31) to 9.40 (95% CI, 1.80-47.00). Stroke risk pathogenesis may include factors that are proximately causal, upstream risk activators, and risk markers. The treatment of subclinical AF may be a useful stroke prevention strategy; however, no direct evidence of benefit from oral anticoagulation exists in this population. Two ongoing trials will assess the risk and benefit of non-vitamin K oral anticoagulants among patients at high risk for stroke with a previously placed implantable CIED, but without a prior diagnosis of clinical AF. If clinical benefit is proven, then the cost-effectiveness of screening for and the treatment of subclinical AF will require additional study.
At present, no evidence suggests that implanting a CIED to detect AF or initiating oral anticoagulation therapy among those in whom AF is detected is beneficial. Ongoing and future studies will identify people at high risk for developing subclinical AF and will evaluate the efficacy, safety, and economic value of oral anticoagulation therapy in this population.
The National Inpatient Sample database was queried to identify patients 18 years or older who were hospitalized with the principal diagnosis of STEMI. All hospitalizations for STEMI in the United States from January 1, 2003, to December 31, 2013, were included. Codes from International Classification of Diseases, Ninth Revision, Clinical Modification, were used to identify patients in the non-CKD, stage 5D CKD, or prior renal transplant groups. Data were analyzed from March to May 2016.
From 2003 to 2013, 2 319 002 patients in the non-CKD group (34.7% women; 65.3% men; mean [SD] age, 64.2 [14.4] years), 30 072 patients in the stage 5D CKD group (45.0% women; 55.0% men; mean [SD] age, 66.9 [12.5] years), and 2980 patients in the renal transplant group (27.3% women; 72.7% men; mean [SD] age, 57.5 [11.1] years) were identified who were hospitalized with STEMI. Of these, 68.9% of the patients in the non-CKD group, 39.5% in the stage 5D CKD group, and 65.2% in the renal transplant group received in-hospital reperfusion for STEMI. The renal transplant group was more likely to receive reperfusion compared with the stage 5D CKD group (adjusted odds ratio [AOR], 1.83; 95% CI, 1.67-2.01; P < .001) but less likely compared with the non-CKD group (AOR, 0.75; 95% CI, 0.68-0.83; P < .001). Risk-adjusted in-hospital mortality among the renal transplant group with STEMI was markedly lower compared with the stage 5D CKD group (AOR, 0.37; 95% CI, 0.33-0.43; P < .001) but similar compared with the non-CKD group (AOR, 1.14; 95% CI, 0.99-1.31; P = .08). Among renal transplant recipients with STEMI, the use of reperfusion increased from 53.7% in the 2003-2004 interval to 81.4% in the 2011-2013 interval (AOR, 1.33; 95% CI, 1.25-1.43; P < .001 for trend), whereas risk-adjusted in-hospital mortality remained unchanged during the study period, from 8.9% in the 2003-2004 interval to 6.1% in the 2011-2013 interval (AOR, 0.94; 95% CI, 0.85-1.05; P = .27 for trend).
In-hospital mortality rates in renal transplant recipients with STEMI are more favorable compared with those of patients with stage 5D CKD and approach those of the general population with STEMI.
Using a model of permanent coronary artery ligation, rupture was virtually abrogated in cd39(-/-) mice versus cd39(+/+) controls, with elevated fibrin and collagen deposition and marked neutrophil and macrophage influx. Macrophages were found to display increased surface expression of CD301 and CD206, marking a reparative phenotype, driven by increased extracellular ATP and IL-4 in the infarcted myocardium of cd39(-/-) mice. A myeloid-specific CD39-knockout mouse also demonstrated protection from rupture, with an attenuated rupture phenotype, suggesting that complete ablation of CD39 provides the greatest degree of protection in this model. Absence of CD39, either globally or in a myeloid lineage-restricted fashion, skews the phenotype toward alternatively activated (reparative) macrophage infiltration following MI. These studies reveal a previously unrecognized and unexpected role of endogenous CD39 to skew macrophage phenotype and promote a propensity to myocardial rupture after MI.
To simulate the clinical settings of acute MI followed by reperfusion therapy, we employed a rat model of left anterior descending artery occlusion for 30 min followed by reperfusion and a follow-up for 14 days. TVP1022 was initially administered postocclusion-prereperfusion, followed by chronic daily administrations. Cardiac performance and remodeling were evaluated using customary and advanced echocardiographic methods, hemodynamic measurements by Millar Mikro-Tip(®) catheter, and histopathological techniques. TVP1022 administration markedly decreased the remodeling process as illustrated by attenuation of left ventricular enlargement and cardiac hypertrophy (both at the whole heart and the cellular level). Furthermore, TVP1022 inhibited cardiac fibrosis and reduced ventricular BNP levels. Functionally, TVP1022 treatment preserved cardiac wall motion. Specifically, the echocardiographic and most of the direct hemodynamic measures were pronouncedly improved by TVP1022. Collectively, these findings indicate that TVP1022 provides prominent cardioprotection against I/R injury and post-MI remodeling in this I/R model.
An original questionnaire developed by the author was used for overall mental state assessment.
The Bender test demonstrated a significant difference in the presence and severity of visual-motor skills between the study group and the control group, while BVRT and MMSE revealed increased incidence of cognitive impairment in the study group. The Bender and BVRT (D/D)/SS (version D, method D, scaled score) scales indicated cognitive impairment in 53.3% of these patients, while the BVRT (C/A)/SS test indicated cognitive impairment in 40%. For the reference group, the values were 32.3% and 12.9%, respectively. No correlation was found between the severity of cognitive impairment and the duration of cardiac arrest.
Impairment of visual-motor skills, short-term visual memory, concentration, and visual-motor coordination occurs much more frequently and is more severe in individuals after SCA than in healthy individuals. Impairment of memory trace storage and recall after delay occurs more frequently in patients after SCA than in patients after myocardial infarction without cardiac arrest and in healthy individuals. SCA duration did not have any influence on the severity of the described disorders.
After cell death, there is very little self-regeneration of the cardiac muscle tissue, which is replaced by non-contractile connective tissue, thus weakening the ability of the heart muscle to contract fully and leading to heart failure. A number of experimental research approaches to stimulate heart muscle regeneration with the hope of regaining normal or near normal heart function in the damaged heart muscle have been attempted. Some of these very interesting studies have used a variety of stem cell types in combination with potential cardiogenic differentiation factors in an attempt to promote differentiation of new cardiac muscle for possible future use in the clinical treatment of patients who have suffered heart muscle damage from acute myocardial infarctions or related cardiovascular diseases. Although progress has been made in recent years relative to promoting the differentiation of cardiac muscle tissue from non-muscle cells, much work remains to be done for this technology to be used routinely in translational clinical medicine to treat patients with damaged heart muscle tissue and return such individuals to pre-heart-attack activity levels.
This is a prospective randomized observer-blinded study carried out in surgical Intensive Care Unit (ICU) after approval by Hospital Ethical Committee. After admission to ICU patients were randomly divided into two groups of thirty patients each-Group (C): Control group managed according to the routine protocol of sepsis and Group (E): Edaravone treated SP managed according to the routine protocol of sepsis + edaravone at dose of 30 mg/12 h intravenous infusion for 2 weeks. All patients were monitored for invasive blood pressure, central venous pressure, heart rate, temperature, urine output, total fluid balance, and routine investigation. Blood sample was taken weekly for 2 weeks to measure the following parameters: Nuclear transcription factor kappa B activity (NFKB), mitogen-activated protein kinase (MAPK), heat shock protein 72 (HSP 72) and total antioxidant capacity (TAC).
There was significant decrease (P < 0.05) in serum level of NFKB, MAPK in Group E in comparison with Group C. While serum level of HSP 72 and TAC showed significant increase (P < 0.05) in Group E compared with Group C with better outcome.
SP treatment with edaravone could significantly improve the inflammatory and oxidative states with better patient outcomes.