Weekly Checks Improve Real-Time Prehospital ECG Transmission in Suspected STEMI.

IntroductionField identification of ST-elevation myocardial infarction (STEMI) and advanced hospital notification decreases first-medical-contact-to-balloon (FMC2B) time. A recent study in this system found that electrocardiogram (ECG) transmission following a STEMI alert was frequently unsuccessful.HypothesisInstituting weekly test ECG transmissions from paramedic units to the hospital would increase successful transmission of ECGs and decrease FMC2B and door-to-balloon (D2B) times. METHODS: This was a natural experiment of consecutive patients with field-identified STEMI transported to a single percutaneous coronary intervention (PCI)-capable hospital in a regional STEMI system before and after implementation of scheduled test ECG transmissions. In November 2014, paramedic units began weekly test transmissions. The mobile intensive care nurse (MICN) confirmed the transmission, or if not received, contacted the paramedic unit and the department's nurse educator to identify and resolve the problem. Per system-wide protocol, paramedics transmit all ECGs with interpretation of STEMI. Receiving hospitals submit patient data to a single registry as part of ongoing system quality improvement. The frequency of successful ECG transmission and time to intervention (FMC2B and D2B times) in the 18 months following implementation was compared to the 10 months prior. Post-implementation, the time the ECG transmission was received was also collected to determine the transmission gap time (time from ECG acquisition to ECG transmission received) and the advanced notification time (time from ECG transmission received to patient arrival). RESULTS: There were 388 patients with field ECG interpretations of STEMI, 131 pre-intervention and 257 post-intervention. The frequency of successful transmission post-intervention was 73% compared to 64% prior; risk difference (RD)=9%; 95% CI, 1-18%. In the post-intervention period, the median FMC2B time was 79 minutes (inter-quartile range [IQR]=68-102) versus 86 minutes (IQR=71-108) pre-intervention (P=.3) and the median D2B time was 59 minutes (IQR=44-74) versus 60 minutes (IQR=53-88) pre-intervention (P=.2). The median transmission gap was three minutes (IQR=1-8) and median advanced notification time was 16 minutes (IQR=10-25). CONCLUSION: Implementation of weekly test ECG transmissions was associated with improvement in successful real-time transmissions from field to hospital, which provided a median advanced notification time of 16 minutes, but no decrease in FMC2B or D2B times. D'ArcyNT, BossonN, KajiAH, BuiQT, FrenchWJ, ThomasJL, ElizarrarazY, GonzalezN, GarciaJ, NiemannJT. Weekly checks improve real-time prehospital ECG transmission in suspected STEMI. Prehosp Disaster Med. 2018;33(3):245-249.

Relationship between serum low-density lipoprotein cholesterol and in-hospital mortality following acute myocardial infarction (the lipid paradox).

Lipoprotein levels are currently recognized as independent risk factors for long-term cardiovascular events after acute myocardial infarction (AMI). During the acute-phase reaction after AMI, previous studies have reported trends of decreased low-density lipoprotein cholesterol (LDL-C), increased triglycerides, and variable high-density lipoprotein cholesterol (HDL-C) levels. However, the association between LDL-C and HDL-C levels and in-hospital mortality has not been well established following AMI. The relationship between lipid levels and in-hospital all-cause mortality in 115,492 patients hospitalized for AMI (July 2002 to December 2006), registered in the National Registry of Myocardial Infarction (NRMI) 4b-5, was evaluated using multivariable-adjusted logistic regression models. Mean LDL-C was 104 ± 38, HDL-C was 41 ± 14, and triglycerides 143 ± 83 mg/dl. Compared with the lowest quartile of LDL-C (<77 mg/dl), the risk of in-hospital mortality in the second to fourth quartiles was decreased (adjusted odds ratio 0.79, 0.80, and 0.85, respectively). For HDL-C, only those in the lowest quartile (<31 mg/dl) had higher risk of in-hospital mortality (odds ratio 1.20) compared with the highest quartile (≥47 mg/dl). Results from NRMI 4b-5 suggest a lipid paradox, with lower LDL-C levels associated with increased risk of in-hospital mortality, contrary to findings outside the acute setting. Consistent with previous analyses, lowest HDL-C levels were associated with increased in-hospital mortality. In conclusion, further explorations of the relationship between very low levels of LDL-C, myocardial necrosis, and subsequent adverse cardiovascular events are warranted.

Previous myocardial infarction as a risk factor for in-hospital cardiovascular outcomes (from the National Registry of Myocardial Infarction 4 and 5).

Patients with acute coronary syndromes have a substantial disease burden and are at continued risk of future cardiovascular events. In this setting, the relation between previous myocardial infarction (MI) and the risk of subsequent in-hospital adverse cardiovascular outcomes has not been definitively established. The data were analyzed from 427,778 hospitalized patients presenting with acute MI from July 2002 to December 2006, who were enrolled in the National Registry of Myocardial Infarction 4-5 study. Multivariate logistic regression models were developed to examine the association between a history of MI and in-hospital all-cause mortality, recurrent MI, and congestive heart failure/pulmonary edema. Covariate adjustments were made for demographic characteristics, co-morbidities, prearrival medications, and health status at presentation. Similarly, multivariate linear regression models were used to evaluate the length of stay. Of the 232,927 patients with acute MI included in the present study after exclusions, 24.7% reported a history of MI. In-hospital mortality was not significantly different between the patients with and without a history of MI (adjusted odds ratio 0.99, 95% confidence interval 0.95 to 1.04, p = 0.75). However, patients with a previous MI had a small increased risk of in-hospital recurrent MI (adjusted odds ratio 1.18, 95% confidence interval 1.08 to 1.29, p <0.001) and congestive heart failure/pulmonary edema (adjusted odds ratio 1.23, 95% confidence interval1.19 to 1.28, p <0.001) compared with patients with no history of MI. In conclusion, a history of MI did not significantly affect in-hospital mortality after admission for an acute MI.

Intracoronary delivery of bone-marrow-derived stem cells.

Ischemic heart disease is the single greatest killer of Americans and its complications are a major cause of congestive heart failure and ventricular arrhythmias while signifiicantly contributing to increased health care costs and reduced patient quality of life. Advances in medical therapy, although signifiicant over the past decade, are still inadequate in regards to targeting the prime underlying pathology, the irreversible loss of damaged or dead cardiomyocytes. Research into the use of cell transplantation therapy to treat cardiac diseases, with the goal of improving cardiac function, shows promise. The aim of this review will be to discuss the potential therapeutic effects of myocardial stem cell and progenitor cell therapy delivered by an intracoronary route with special reference to treatment of infarcted myocardium.

"Double wire" angio-seal closure technique after balloon aortic valvuloplasty.

OBJECTIVES: To report the feasibility of a collagen-mediated closure device using a modified Angio-Seal closure technique for access site management following percutaneous balloon aortic valvuloplasty (BAV). BACKGROUND: With the advent of percutaneous aortic valve replacement therapies, there has been a resurgence of interest in BAV procedures. Vascular complications, including bleeding, are a common source of morbidity post procedure as a result of the requirement for large bore femoral artery access. The use of vascular closure devices may reduce bleeding complications. METHODS: We describe a new technique for vascular closure in this setting. At the conclusion of the valvuloplasty procedure, two 0.035'' wires are inserted through the femoral artery sheath. A conventional collagen-mediated closure device (8F Angio-Seal) is deployed over the first wire and along side the second wire. If immediate hemostasis is not achieved, a second device is loaded onto the second wire and deployed to achieve hemostasis. RESULTS: Percutaneous BAV was performed in 21 patients. Hemostasis was successfully achieved in all patients with either a single 8F Angio-Seal closure device (18 patients) or after placement of a second device (three patients). CONCLUSIONS: The modified "Double Wire" Angio-Seal technique is a feasible method for hemostasis following percutaneous BAV.

Darapladib.

IMPORTANCE OF THE FIELD: Atherosclerosis is an inflammatory-immune mediated disease process. Plaque rupture is responsible for the clinical events of ischemic death, myocardial infarction, acute coronary syndromes and ischemic strokes. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) seems to play a major role in the development of such high-risk lesions, in both the coronary and carotid arteries. Darapladib is a selective inhibitor of Lp-PLA(2). AREAS COVERED IN THIS REVIEW: An overview of darapladib by reviewing the studies (1990 - 2009) that have provided the rationale for the development of darapladib; and a discussion of its potential merit as a new therapeutic drug to target high-risk atherosclerosis. WHAT THE READER WILL GAIN: The reader should gain an understanding of the importance of inflammation during atherogenesis as well as of the biology of Lp-PLA(2) and its proatherogenic role. Additional insights will be gained into the role of selective inhibitors of Lp-PLA(2) as new therapeutic agents. TAKE HOME MESSAGE: Darapladib is a selective inhibitor of Lp-PLA(2) and represents a new class of therapeutic agents that target inflammation to treat high-risk atherosclerosis.

Atherosclerotic plaque development.

Atherosclerosis is now recognized as an inflammatory/immunomodulatory reaction to the presence of oxidized low-density lipoproteins within the arterial wall, often times in the setting of such risk factors as family history, hypercholesterolemia, high blood pressure, diabetes mellitus and smoking. The progression to high-risk lesions such as thin-fibrous cap atheromas results in an increased risk of sudden death, acute myocardial infarction and ischemic stroke. The interplay of macrophages, T lymphocytes and mast cells play a central role in both the development but more importantly in the progression of coronary and carotid artery disease to high-risk phenotypes.