ABSTRACT
BACKGROUND: Acute myocardial infarction complicated by cardiogenic shock (AMI-CS) is the most common cause of mortality following AMI, and treatment algorithms vary widely. We report the results of an analysis using time-sensitive, hemodynamic goals in the treatment of AMI-CS in a single center study. METHODS: Consecutive patients with AMI-CS from November 2016 through December 2021 were included in our retrospective analysis. Clinical characteristics and outcomes were analyzed using the electronic medical records. We identified 63 total patients who were admitted to our center with AMI-CS, and we excluded patients who did not have clear timing of AMI onset or CS onset. We evaluated the rate of survival to hospital discharge based on the quantity of certain time-sensitive hemodynamic goals were met. RESULTS: We identified 63 patients who met criteria for AMI-CS, 39 (62%) of whom survived to hospital discharge. Odds of survival were closely related to the achievement of four time-dependent goals: cardiac power output (CPO) >0.6 Watts (W), pulmonary artery pulsatility index (PAPi) >1, lactate <4 mmol/L, and <2 vasopressors required. Of the 63 total patients, 36 (57%) received intra-aortic balloon pump (IABP) and 18 (29%) received an Impella CP (Abiomed) as an initial mechanical circulatory support strategy. Six patients were escalated from IABP to Impella CP for additional hemodynamic support. Nine patients were treated with vasopressors/inotropes alone. Regarding the 39 patients who survived to hospital discharge, 75% of patients met 3 or 4 goals at 24 h, whereas only 16% of deceased patients met 3 or 4 goals at 24 h. Of the 24 patients who did not survive to hospital discharge, 18 (75%) met either 0-1 goal at 24 h. There was no effect of the initial treatment strategy on achieving 3-4 goals at 24 h. CONCLUSION: Our study evaluated the association of meeting 4 time-sensitive goals (CPO >0.6 W, PAPi >1, <2 vasopressors, and lactate <4 mmol/L) at 24 h after treatment for AMI-CS with in-hospital mortality. Our data show, in line with previous data, that the higher number of goals met at 24 h was associated with improved in-hospital mortality regardless of treatment strategy.
Subject(s)
Heart-Assist Devices , Myocardial Infarction , Humans , Shock, Cardiogenic/diagnosis , Shock, Cardiogenic/etiology , Shock, Cardiogenic/therapy , Retrospective Studies , Goals , Treatment Outcome , Myocardial Infarction/complications , Myocardial Infarction/diagnosis , Myocardial Infarction/therapy , Hemodynamics , Intra-Aortic Balloon Pumping/adverse effects , Heart-Assist Devices/adverse effects , LactatesABSTRACT
MicroRNAs (miRNA) are non-coding RNAs that regulate gene expression in up to 90% of the human genome through interactions with messenger RNA (mRNA). The expression of miRNAs varies and changes in diseased and healthy states, including all stages of myocardial ischemia-reperfusion and subsequent ischemia-reperfusion injury (IRI). These changes in expression make miRNAs an attractive potential therapeutic target. Herein, we review the differences in miRNA expression prior to ischemia (including remote ischemic conditioning and ischemic pre-conditioning), the changes during ischemia-reperfusion, and the changes in miRNA expression after IRI, with an emphasis on inflammatory and fibrotic pathways. Additionally, we review the effects of manipulating the levels of certain miRNAs on changes in infarct size, inflammation, remodeling, angiogenesis, and cardiac function after either ischemia-reperfusion or permanent coronary ligation. Levels of target miRNA can be increased using molecular mimics ("agomirs"), or can be decreased by using "antagomirs" which are antisense molecules that act to bind and thus inactivate the target miRNA sequence. Other non-coding RNAs, including long non-coding RNAs and circular RNAs, also regulate gene expression and have a role in the regulation of IRI pathways. We review the mechanisms and downstream effects of the miRNAs that have been studied as therapy in both permanent coronary ligation and ischemia-reperfusion models.
Subject(s)
MicroRNAs/metabolism , Myocardial Reperfusion Injury/metabolism , Animals , Gene Expression Regulation , Humans , Ischemic Preconditioning , Myocardial Ischemia/metabolismABSTRACT
BACKGROUND: Previous studies have shown underutilization of anticoagulation therapy in patients with atrial fibrillation and a CHA2DS2-VASc score ≥2; however there exists little data regarding the inappropriate use of anticoagulation in patients with a CHA2DS2-VASc score of 0. We aimed to determine the true prevalence and predictors of inappropriate anticoagulation therapy in patients with atrial fibrillation and a CHA2DS2-VASc score of 0. METHODS: A retrospective chart review was performed on all patients with atrial fibrillation and a CHA2DS2-VASc score of 0 in our institution from January 2009 to January 2016. Demographic and clinical data were collected from the electronic medical record. We utilized multivariable logistic regression analysis to determine independent clinical predictors of inappropriate anticoagulation administration. RESULTS: 512 patients were identified with a CHA2DS2-VASc score of 0 and a diagnosis of atrial fibrillation. Of the 137 patients prescribed anticoagulation, 64 patients were identified as inappropriately treated with anticoagulation therapy after assessing for other indications of warfarin or novel anticoagulant therapy. Independent variables associated with inappropriate anticoagulation administration were age (OR 1.07; 95% CI 1.03-1.10), body mass index (OR 1.06; 95% CI 1.01-1.10), absence of current aspirin use (OR 13.50; 95% CI 6.00-30.54) and persistent atrial fibrillation (OR 2.34; 95% CI 1.11-4.94). CONCLUSIONS: Our study shows that 12% of patients with a CHA2DS2-VASc score of 0 were inappropriately prescribed anticoagulant therapy. Independent predictors of unnecessary anticoagulation were age, body mass index, absence of current aspirin use and persistent atrial fibrillation.