Impact of a Mobile, Cloud-Based Care-Coordination Platform on Door-to-Balloon Time in Patients With STEMI: Initial Results.

Care-coordination platforms may optimize ST-elevation myocardial infarction (STEMI) treatment delays. This study aimed to assess the impact of Stenoa use on treatment delays in STEMI patients. We conducted a retrospective cohort study on local STEMI cases for the period between September 2020 and March 2023, comparing the times from first medical contact to device, before vs after the implementation of the Stenoa platform by the catheterization laboratory (cath-lab) and emergency department.

Optimal Fluoroscopic Projections of Coronary Ostia and Bifurcations Defined by Computed Tomographic Coronary Angiography.

Objectives: The aim of this study was to define the optimal fluoroscopic viewing angles of both coronary ostia and important coronary bifurcations by using 3-dimensional multislice computed tomographic data.

Background: Optimal fluoroscopic projections are crucial for coronary imaging and interventions. Historically, coronary fluoroscopic viewing angles were derived empirically from experienced operators.

Drug-coated balloon after subintimal plaque modification in failed coronary chronic total occlusion percutaneous coronary intervention: A novel concept.

Chronic total occlusion (CTO) percutaneous coronary intervention (PCI) is a technically challenging procedure. In failed cases, plaque modification strategy (also known as "investment procedure"), defined as the intentional dilation of the subintimal space through the CTO segment, can be applied. The typical dilation device used in this strategy is a regular angioplasty balloon (either semi- or noncompliant).

Midterm Angina-Related Quality of Life Benefits After Percutaneous Coronary Intervention of Chronic Total Occlusions.

Background: Data on the impact of coronary chronic total occlusion (CTO) percutaneous coronary intervention (PCI) on quality of life (QOL) are limited. To date, studies have been limited in sample size and have focused on only a few domains of the Seattle Angina Questionnaire (SAQ). We evaluated the relationship between coronary CTO PCI and QOL in patients with symptoms of angina, incorporating all aspects of the SAQ.

CDKN2B Regulates TGFβ Signaling and Smooth Muscle Cell Investment of Hypoxic Neovessels.

Rationale: Genetic variation at the chromosome 9p21 cardiovascular risk locus has been associated with peripheral artery disease, but its mechanism remains unknown.

Objective: To determine whether this association is secondary to an increase in atherosclerosis, or it is the result of a separate angiogenesis-related mechanism.

Methods And Results: Quantitative evaluation of human vascular samples revealed that carriers of the 9p21 risk allele possess a significantly higher burden of immature intraplaque microvessels than carriers of the ancestral allele, irrespective of lesion size or patient comorbidity.

Plasma PCSK9 levels are elevated with acute myocardial infarction in two independent retrospective angiographic studies.

Objective: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a circulating protein that promotes degradation of the low density lipoprotein (LDL) receptor. Mutations that block PCSK9 secretion reduce LDL-cholesterol and the incidence of myocardial infarction (MI). However, it remains unclear whether elevated plasma PCSK9 associates with coronary atherosclerosis (CAD) or more directly with rupture of the plaque causing MI.

Cardiovascular drugs and the genetic response.

The emergence of personalized medicine mandates a complete understating of DNA sequence variation that modulates drug response. Initial forays have been made in the cardiac arena, yet much remains to be elucidated in the pharmacogenetics of cardiac drugs. Most progress has been made in describing DNA sequence variation related to the anticoagulant warfarin and the antiplatelet drug clopidogrel.

The role of genetic risk factors in coronary artery disease.

Genome-wide association studies for coronary artery disease utilizing the case control association study approach has identified 50 genetic risk variants associated with coronary artery disease or myocardial infarction. All of these genetic variants are of genome wide significance and replicated in an independent population. It is of note that 35 of these 50 genetic risk variants act through mechanisms as yet unknown.

Two chromosome 9p21 haplotype blocks distinguish between coronary artery disease and myocardial infarction risk.

Background: Variants at the 9p21 locus associate with the risk of coronary artery disease (CAD) or myocardial infarction (MI). However, atherosclerotic plaque deposition is distinct from MI (plaque rupture and thrombosis), and recent studies showed no association between these variants and MI in patients with preexisting CAD. We performed haplotype analysis at the 9p21 locus to test whether haplotypes at distinct linkage disequilibrium blocks predict these phenotypes.

Genomics in cardiovascular disease.

A paradigm shift toward biology occurred in the 1990s and was subsequently catalyzed by the sequencing of the human genome in 2000. The cost of deoxyribonucleic acid (DNA) sequencing has gone from millions to thousands of dollars with sequencing of one's entire genome costing only $1,000. Rapid DNA sequencing is being embraced for single gene disorders, particularly for sporadic cases and those from small families.

Personalized cardiovascular medicine: status in 2012.

Personalized medicine is the tailoring of the diagnosis, prevention, and treatment to the characteristics of each individual patient. In this review, we provide a status report on genetic variants that influence therapy with antiplatelet agents, warfarin, and statins. Resistance to clopidogrel, an antiplatelet therapy, has been shown to be present in 25% to 30% of Caucasians and an even higher percentage in Asians.

Genomics: is it ready for primetime?

The next decade will focus on identifying the missing heritability of coronary artery disease (CAD). This process will involve a more comprehensive interrogation of common single nucleotide polymorphisms (SNPs) that impart modest biologic effect and an interrogation of rare SNPs that impart profound biologic effect. In parallel, an investigation of the underlying biology of the described association will likely yield novel pathways that provide therapeutic targets.

A genome-wide association study for coronary artery disease identifies a novel susceptibility locus in the major histocompatibility complex.

Background: Recent genome-wide association studies (GWAS) have identified several novel loci that reproducibly associate with coronary artery disease (CAD) and/or myocardial infarction risk. However, known common CAD risk variants explain only 10% of the predicted genetic heritability of the disease, suggesting that important genetic signals remain to be discovered.

Methods And Results: We performed a discovery meta-analysis of 5 GWAS involving 13 949 subjects (7123 cases, 6826 control subjects) imputed at approximately 5 million single nucleotide polymorphisms, using pilot 1000 Genomes-based haplotypes.

Insulin suppresses the expression of amyloid precursor protein, presenilins, and glycogen synthase kinase-3beta in peripheral blood mononuclear cells.

Objective: Our objective was to determine whether peripheral blood mononuclear cells express amyloid precursor protein (APP) and other mediators involved in the pathogenesis of Alzheimer's disease and whether their expression is suppressed by insulin.

Research Design And Methods: Ten obese type 2 diabetic patients were infused with insulin (2 U/h with 100 ml 5% dextrose/h) for 4 h. Patients were also infused with 5% dextrose/h or normal physiological saline for 4 h, respectively, on two other days as controls.

Improved prediction of cardiovascular disease based on a panel of single nucleotide polymorphisms identified through genome-wide association studies.

Background: Genome-wide association studies (GWAS) have identified single-nucleotide polymorphisms (SNPs) at multiple loci that are significantly associated with coronary artery disease (CAD) risk. In this study, we sought to determine and compare the predictive capabilities of 9p21.3 alone and a panel of SNPs identified and replicated through GWAS for CAD.

Gene dosage of the common variant 9p21 predicts severity of coronary artery disease.

Objectives: The purpose of this study was to test the hypothesis that 9p21 gene dosage determines the severity of coronary artery disease (CAD).

Background: The 9p21 locus is the first common genetic variant to associate with risk of CAD and/or myocardial infarction in multiple studies.

Methods: A cross-sectional study examined nondiabetic patients with CAD defined by coronary angiography to have at least 1 epicardial stenosis >50%.

The genome-wide association study--a new era for common polygenic disorders.

This review covers the advances made in the last decade utilizing the high-density single-nucleotide microarrays to screen the entire human genome for genetic risk variants and outlines future strategies to draw deeper into the human genetic front. The sequence of the human genome provides the blueprint for life, while its variation provides the spice of life. Approximately 99.

Genomics in coronary artery disease: past, present and future.

The past three years has seen the completion of a series of genome-wide association studies designed to identify genetic variants associated with risk for coronary artery disease (CAD) or its related phenotype, myocardial infarction (MI). The first and most robust genetic risk variant is located on chromosome 9p21.3.

The transcription factor GATA-2 does not associate with angiographic coronary artery disease in the Ottawa Heart Genomics and Cleveland Clinic GeneBank Studies.

The transcription factor GATA2 was reported to associate with coronary artery disease (CAD) in the family-based Genecard sample (Connelly et al. in PLoS Genet 2:e139, 2006). We asked whether GATA2 associates with sporadic cases of CAD in the Ottawa Heart Genomics Study (OHGS) and Cleveland Clinic (CC) populations.

Genomic view of factors leading to plaque instability.

The manifestations of coronary artery disease are varied. They all arise as a consequence of the deposition of atherosclerotic plaque within the vessel wall. The most feared sequela of coronary artery disease is sudden and unexpected death in the ostensibly healthy patient.

Creating a genetic risk score for coronary artery disease.

Coronary artery disease (CAD) and its sequelae represent a significant health burden. Over the past two decades, numerous studies have attempted to link DNA sequence variation with the risk of CAD and related phenotypes. There has been significant evolution in technology from the early linkage studies within kindreds, and now we are able to use high-density genotyping to facilitate large-scale genome-wide association studies.