Cerebral Artery Occlusion
Cerebral artery occlusion refers to the blockage of an artery responsible for supplying blood to the brain. This interruption of blood flow, known as ischemia, deprives brain tissue of oxygen and nutrients, leading to brain cell damage and, if prolonged, an ischemic stroke. The severity and specific symptoms of a stroke depend on which artery is occluded and the extent of the brain region affected.
The biological basis of cerebral artery occlusion often involves atherosclerosis, a condition where fatty plaques accumulate within the arterial walls, narrowing the lumen and making the vessels stiff and prone to clot formation. These clots, or thrombi, can form directly within a cerebral artery (thrombotic stroke) or travel from another part of the body, such as the heart or carotid arteries, to the brain (embolic stroke). Genetic factors are increasingly recognized for their contribution to the risk of both atherosclerosis and ischemic stroke. For instance, research indicates a shared genetic susceptibility between ischemic stroke and coronary artery disease[1], and various genes have been identified that influence metabolic networks and the development of atherosclerosis[2].
From a clinical perspective, cerebral artery occlusion constitutes a medical emergency requiring immediate attention to restore blood flow and minimize neurological damage. Symptoms can manifest suddenly and may include weakness or numbness on one side of the body, difficulty speaking or understanding speech, vision problems, and severe headaches. Rapid diagnosis and interventions, such as thrombolytic medications or mechanical thrombectomy, are critical for improving patient outcomes. Understanding an individual’s genetic predisposition can potentially enhance risk assessment and guide personalized preventive strategies, especially given the common genetic underpinnings with other cardiovascular conditions.
The social importance of cerebral artery occlusion, primarily through its manifestation as ischemic stroke, is substantial. It is a leading cause of long-term disability and mortality globally, placing a significant burden on individuals, families, and healthcare systems due to the need for extensive rehabilitation, long-term care, and lost productivity. Public health efforts are focused on preventing occlusions by addressing modifiable risk factors such as hypertension, diabetes, high cholesterol, and smoking. Continued research into genetic factors offers the potential to identify individuals at higher risk, facilitating more targeted prevention and earlier intervention, thereby aiming to reduce the overall societal and economic impact of stroke.
Limitations
Section titled “Limitations”Understanding the genetic underpinnings of cerebral artery occlusion faces several challenges inherent to complex disease research. These limitations influence the interpretation and applicability of findings, highlighting areas for future investigation.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”Genetic association studies for cerebral artery occlusion, particularly genome-wide association studies (GWAS), require rigorous validation. Initial findings, especially those from studies with smaller sample sizes, often necessitate replication in independent cohorts to confirm their robustness and prevent the reporting of spurious associations[3]. The failure to consistently validate some reported genetic risk factors for related conditions, such as acute coronary syndrome, underscores the potential for effect-size inflation or false positives in early discoveries[4]. Such challenges highlight the critical need for large-scale replication efforts and stringent statistical thresholds to ensure the reliability of identified genetic loci.
Furthermore, the comprehensiveness of genetic data collection can impact the detection of all relevant variants. Current genotyping arrays may not fully capture the complete spectrum of common genetic variations across the genome, and are often designed with poor coverage of rare variants or structural variations [3]. This incomplete genomic coverage can lead to reduced statistical power to identify genetic factors that contribute to cerebral artery occlusion, particularly those with smaller effect sizes or lower frequencies[3]. Additionally, variations in the specific single nucleotide polymorphisms (SNPs) analyzed across different studies can complicate meta-analyses, hindering a unified and comprehensive understanding of genetic associations[5].
Generalizability Across Diverse Populations
Section titled “Generalizability Across Diverse Populations”A significant limitation in the genetic study of cerebral artery occlusion is the disproportionate representation of certain ancestral groups in research cohorts. Many large-scale genomic studies have been predominantly conducted in populations of European descent, leading to a paucity of adequately powered genomic studies in other populations, such as African Americans, despite their often higher disease rates[5]. This lack of diversity limits the generalizability of genetic findings, as associations identified in one population may not be directly transferable or hold the same predictive value in genetically distinct groups [6].
Different populations can possess unique genetic characteristics, meaning that susceptibility loci identified in one group might exhibit varying effect sizes or even be absent in another [6]. This population-specific genetic architecture underscores the necessity for inclusive research that encompasses diverse ancestral backgrounds. Without such broad representation, the full range of genetic risk factors contributing to cerebral artery occlusion across global populations remains incompletely characterized, potentially exacerbating health disparities if genetic insights are not equitably derived and applied.
Unaccounted Genetic and Environmental Complexity
Section titled “Unaccounted Genetic and Environmental Complexity”The genetic architecture of complex conditions like cerebral artery occlusion is intricate, with identified common variants often explaining only a portion of the estimated heritability. This phenomenon, often referred to as “missing heritability,” suggests that a substantial proportion of genetic variance remains unexplained, likely due to factors such as undetected rare variants, gene-gene interactions, or epigenetic modifications not typically captured by standard GWAS methodologies[3]. A more complete understanding requires advanced sequencing technologies and analytical approaches to explore the full spectrum of genetic variation beyond common SNPs.
Moreover, environmental factors and their complex interactions with genetic predispositions play a critical, yet frequently challenging to quantify, role in the manifestation of cerebral artery occlusion. Lifestyle choices, environmental exposures, and other non-genetic confounders can significantly modify disease risk, and their comprehensive integration into genetic models is often difficult[4]. Fully accounting for these gene-environment interactions is essential for developing a holistic understanding of disease etiology and for designing truly personalized prevention and treatment strategies that consider both an individual’s genetic makeup and their environmental context.
Variants
Section titled “Variants”Genetic variations play a crucial role in an individual’s susceptibility to various health conditions, including cerebral artery occlusion. This section explores several single nucleotide polymorphisms (SNPs) and their associated genes, detailing their potential impact on vascular health and their connection to traits like atherosclerosis and stroke.
The variant rs143594550 is located within the ADGRE3 gene, which encodes Adhesion G Protein-Coupled Receptor E3. ADGRE3 is a member of the adhesion GPCR family, typically involved in cell-cell interactions and cell adhesion, playing roles in immune responses and inflammation. A variant like rs143594550 could potentially alter the function or expression of this receptor, thereby modulating inflammatory pathways within the arterial walls. Such alterations may contribute to the development or progression of atherosclerosis, a chronic degenerative condition characterized by lipid and fibrous matrix deposition in artery walls, which is a major underlying cause of cerebral artery occlusion[3]. The influence of genes is significant in the etiology of such cardiovascular conditions[3].
Another variant, rs376477692 , is situated in a region containing OR7A8P and OR7A2P, which are olfactory receptor pseudogenes. While olfactory receptors are primarily known for their role in the sense of smell, studies increasingly show that both functional receptors and their pseudogenes can have broader roles in non-olfactory tissues, including influencing cell proliferation, migration, and inflammatory processes. Variations in these regions, even within pseudogenes, can impact gene regulation or the expression of nearby functional genes, potentially affecting cellular processes critical to vascular health. Dysregulation in these pathways could indirectly contribute to the risk of conditions like ischemic stroke, which shares genetic susceptibility with coronary artery disease[1]. Vascular mechanisms are recognized as having a key role in the pathophysiology of various related diseases [7].
The variant rs11878065 is found in proximity to the ADCYAP1 gene and LINC01904. ADCYAP1 encodes Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP), a neuropeptide with widespread functions, including potent vasodilatory, anti-inflammatory, and neuroprotective effects. LINC01904 is a long intergenic non-coding RNA (lncRNA) that regulates gene expression without coding for a protein. A variant like rs11878065 could influence the production or activity of PACAP, potentially affecting its ability to maintain vascular tone, reduce inflammation, or protect nerve cells. Similarly, it might alter the regulatory functions of LINC01904, impacting gene expression relevant to endothelial function or arterial remodeling. These genetic factors are important in the development of coronary artery stenosis, a condition linked to broader cardiovascular disease[8]. Genetic factors are known to play a role in the overall susceptibility to various forms of vascular disease[9].
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs143594550 | ADGRE3 | cerebral artery occlusion |
| rs376477692 | OR7A8P - OR7A2P | cerebral artery occlusion |
| rs11878065 | ADCYAP1 - LINC01904 | cerebral artery occlusion |
Classification, Definition, and Terminology of Cerebral Artery Occlusion
Section titled “Classification, Definition, and Terminology of Cerebral Artery Occlusion”Conceptualizing Cerebral Artery Occlusion and Ischemic Stroke
Section titled “Conceptualizing Cerebral Artery Occlusion and Ischemic Stroke”Cerebral artery occlusion refers to the blockage of a blood vessel supplying the brain, which most commonly leads to an ischemic stroke .
Heterogeneity and Demographic Influences
Section titled “Heterogeneity and Demographic Influences”The genetic factors influencing cerebral artery occlusion exhibit considerable variability among individuals and diverse populations. This inter-individual variation in genetic make-up can impact the clinical manifestations of the disease and may influence responses to medical treatments, such as statin therapies[10]. Furthermore, the significance of specific genetic factors can differ across various populations, contributing to phenotypic diversity in disease presentation and progression[6]. Research on related vascular conditions, like coronary artery calcification, also points to demographic differences, such as those observed among African Americans, underscoring the ethnic heterogeneity in genetic susceptibility relevant to occlusive vascular diseases[5].
Causes of Cerebral Artery Occlusion
Section titled “Causes of Cerebral Artery Occlusion”Cerebral artery occlusion, a condition often leading to ischemic stroke, arises from a complex interplay of genetic predispositions, environmental exposures, and physiological changes. The underlying mechanism frequently involves atherosclerosis, a progressive disease characterized by the buildup of plaques within arterial walls, which can narrow the vessels or lead to the formation of blood clots that block blood flow.
Genetic Predisposition and Vascular Health
Section titled “Genetic Predisposition and Vascular Health”Genetic factors significantly influence an individual’s susceptibility to cerebral artery occlusion, often through shared biological pathways with coronary artery disease (CAD) and ischemic stroke othelial dysfunction, which collectively heighten susceptibility to plaque rupture and the formation of thrombi. While not always explicitly detailed as “age-related changes” in all studies, research on coronary artery calcification and atherosclerosis consistently highlights age as a critical determinant of vascular pathology and risk for occlusion . This pathophysiological process involves a disruption of normal homeostatic mechanisms in the vasculature, leading to the hardening and narrowing of arteries, including those supplying the brain[11]. Over time, these atherosclerotic plaques can grow, become unstable, rupture, and trigger thrombus formation, which can acutely obstruct blood flow and cause an ischemic event in the cerebral arteries. The development of subclinical atherosclerosis in major arterial territories is a significant precursor to such occlusions[11].
Cellular and Molecular Drivers of Vascular Plaque
Section titled “Cellular and Molecular Drivers of Vascular Plaque”The formation of atherosclerotic plaques is driven by intricate molecular and cellular pathways. Key biomolecules, such as modified lipids, contribute to the initiation and progression of the disease, attracting immune cells and promoting inflammation within the arterial wall[2]. Enzymes like ADAMTS7 have been identified as novel loci for coronary atherosclerosis, highlighting their role in the extracellular matrix remodeling that occurs during plaque development[12]. Furthermore, signaling pathways involving the major histocompatibility complex (MHC) suggest an immune-mediated component to coronary artery disease, indicating that inflammatory responses are critical cellular functions in vascular pathology[13].
Genetic Underpinnings of Vascular Susceptibility
Section titled “Genetic Underpinnings of Vascular Susceptibility”Genetic mechanisms play a substantial role in predisposing individuals to vascular diseases that can lead to cerebral artery occlusion. Genome-wide association studies (GWAS) have identified numerous gene functions and regulatory elements associated with an increased risk of coronary artery disease and related conditions[4], [14], [15]. For instance, novel loci associated with sudden cardiac death in the context of coronary artery disease have been discovered, pointing to specific genetic variations that influence cardiovascular stability[16]. Genes such as RTN4 and FBXL17 have been implicated in coronary heart disease, suggesting their involvement in regulatory networks affecting vascular health[6]. Additionally, the ABO blood group has been associated with myocardial infarction in the presence of coronary atherosclerosis, indicating a genetic influence on thrombotic risk[12].
Systemic Interconnections of Arterial Disease
Section titled “Systemic Interconnections of Arterial Disease”Cerebral artery occlusion is often part of a broader systemic vascular disease, with significant shared genetic susceptibility between ischemic stroke and coronary artery disease[1]. This indicates that common genetic variants and underlying pathophysiological processes can manifest in different arterial beds, affecting both the heart and the brain. The effectiveness of therapies, such as pravastatin, in reducing cardiovascular events also demonstrates the impact of systemic metabolic processes and lipid regulation on overall vascular health and the prevention of occlusive events[10]. Therefore, understanding the interconnected nature of vascular diseases and their systemic consequences is vital for addressing cerebral artery occlusion.
Pathways and Mechanisms
Section titled “Pathways and Mechanisms”Cerebral artery occlusion, often a consequence of atherosclerotic disease, involves a complex interplay of genetic predispositions and molecular pathways that govern vascular health and disease progression. Understanding these mechanisms is crucial for elucidating the underlying causes and identifying potential therapeutic targets.
Genetic Influences on Vascular Integrity and Atherogenesis
Section titled “Genetic Influences on Vascular Integrity and Atherogenesis”Cerebral artery occlusion, frequently stemming from atherosclerosis, is significantly influenced by an individual’s genetic makeup. Genome-wide association studies (GWAS) have identified numerous novel loci associated with an increased risk of coronary artery disease (CAD), a condition sharing common pathophysiological roots with cerebral artery occlusion[4]. These genetic variants likely contribute to the dysregulation of pathways critical for maintaining vascular integrity, influencing processes such as endothelial function, vascular smooth muscle cell proliferation, and extracellular matrix remodeling[11]. While specific molecular interactions are complex, these genetic predispositions can alter baseline cellular responses, potentially overwhelming compensatory mechanisms and accelerating the progression of atherosclerotic plaque formation and instability, ultimately leading to arterial occlusion [4].
Metabolic Network Dysregulation
Section titled “Metabolic Network Dysregulation”Genetic variations play a crucial role in the dysregulation of metabolic networks, which are central to the development of atherosclerosis and subsequent cerebral artery occlusion[2]. Studies have revealed novel loci associated with these metabolic networks, suggesting that inherited differences in energy metabolism, biosynthesis, and catabolism can influence disease susceptibility[2]. For instance, specific gene variants can alter lipid metabolism, affecting the synthesis, transport, and breakdown of cholesterol and other fats, which are key components of atherosclerotic plaques. The observed differential response to pravastatin therapy, a lipid-lowering drug, among individuals with distinct genetic profiles further underscores the impact of inherited metabolic regulation on disease progression and treatment efficacy[10]. These metabolic pathway alterations contribute to an environment conducive to arterial plaque accumulation and inflammation.
Inflammatory and Immune Responses in Arterial Disease
Section titled “Inflammatory and Immune Responses in Arterial Disease”Inflammation and immune responses are fundamental to the initiation and progression of arterial diseases like atherosclerosis, which can lead to cerebral artery occlusion. Genetic studies have identified a novel susceptibility locus within the Major Histocompatibility Complex (MHC) as being associated with coronary artery disease[13]. The MHC region is critical for immune system function, suggesting that variations here can influence the body’s inflammatory signaling pathways, including receptor activation and downstream intracellular cascades, in response to vascular injury or metabolic stress. Such genetic predispositions may modulate the activity of transcription factors that regulate pro-inflammatory gene expression, thereby contributing to chronic vascular inflammation and the destabilization of atherosclerotic plaques [13]. This intricate interplay between genetic factors and immune mechanisms highlights a key driver of arterial pathology.
Systems-Level Interactions in Cardiovascular Risk
Section titled “Systems-Level Interactions in Cardiovascular Risk”The development of cerebral artery occlusion is not typically driven by a single genetic variant or pathway, but rather by complex systems-level integration of multiple interacting factors. Extensive genome-wide association studies have revealed numerous susceptibility loci for coronary artery disease and, importantly, a shared genetic susceptibility between ischemic stroke and coronary artery disease, indicating common underlying network interactions[1]. These findings suggest significant pathway crosstalk, where dysregulation in one metabolic or inflammatory pathway can influence others, creating a hierarchical regulatory network that collectively contributes to disease risk[2]. The emergent properties of these integrated networks, such as overall vascular resilience or susceptibility to plaque rupture, are a result of these intricate genetic and environmental interactions, making the disease a multifactorial challenge.
Pathophysiological Mechanisms and Therapeutic Implications
Section titled “Pathophysiological Mechanisms and Therapeutic Implications”Understanding the specific pathways and mechanisms dysregulated in cerebral artery occlusion provides critical insights for therapeutic development. Genetic studies have identified variants that influence the pathophysiology of arterial diseases, highlighting particular molecular targets for intervention[4]. The observation that certain gene variants are associated with differential cardiovascular event reduction by pravastatin therapy, for example, demonstrates how genetic insights can personalize treatment strategies by targeting specific metabolic pathways or regulatory mechanisms[10]. Identifying these disease-relevant mechanisms, including those that influence lipid metabolism, inflammation, or vascular remodeling, allows for the development of drugs that can either correct pathway dysregulation or bolster compensatory mechanisms to prevent or mitigate arterial occlusion.
Clinical Relevance
Section titled “Clinical Relevance”Cerebral artery occlusion, a primary cause of ischemic stroke, carries significant clinical implications for patient management, risk assessment, and therapeutic strategies. Research, particularly through genome-wide association studies (GWAS), has elucidated shared genetic underpinnings with other cardiovascular conditions, offering pathways for improved patient care.
Shared Genetic Susceptibility and Comorbidity
Section titled “Shared Genetic Susceptibility and Comorbidity”Cerebral artery occlusion, often manifesting as ischemic stroke, exhibits a significant genetic overlap with coronary artery disease (CAD), including myocardial infarction (MI) and coronary artery calcification (CAC). Genome-wide association studies (GWAS) have identified common genetic variants that contribute to the susceptibility of both ischemic stroke and CAD, highlighting a shared pathological basis[1]. This shared genetic architecture underscores the importance of considering cardiovascular health comprehensively, as individuals predisposed to one condition may also be at elevated risk for the other. Understanding these overlapping phenotypes is crucial for a holistic approach to patient management and risk assessment.
Risk Stratification and Early Intervention
Section titled “Risk Stratification and Early Intervention”Identifying individuals at high risk for cerebral artery occlusion benefits significantly from genetic insights derived from large-scale association analyses. GWAS have pinpointed numerous susceptibility loci for CAD, which, given the shared genetic background, also inform risk for ischemic stroke[4]. This genetic information can be integrated into risk stratification models to identify individuals who may benefit from early and intensive preventive strategies, even before the onset of overt symptoms. For instance, genetic predispositions associated with subclinical atherosclerosis in major arterial territories can signal a higher likelihood of future occlusive events, guiding proactive monitoring and lifestyle interventions[11]. Such advanced risk stratification supports personalized medicine approaches, moving beyond traditional risk factors to incorporate an individual’s unique genetic profile. By pinpointing high-risk individuals, clinicians can tailor prevention strategies, such as aggressive management of modifiable risk factors or early initiation of pharmacological interventions, to mitigate the progression of atherosclerotic disease that can lead to cerebral artery occlusion.
Prognostic Value and Therapeutic Responsiveness
Section titled “Prognostic Value and Therapeutic Responsiveness”Genetic markers hold significant prognostic value for cerebral artery occlusion, offering insights into disease progression, long-term outcomes, and individual responses to therapeutic interventions. Specific gene variants have been associated with differential cardiovascular event reduction by therapies such as pravastatin, suggesting that pharmacogenomic approaches can optimize treatment selection for preventing occlusive events[10]. This enables a more personalized approach to patient care, where treatment regimens can be tailored based on an individual’s genetic predisposition to respond to certain medications, thereby improving efficacy and reducing adverse effects. Furthermore, understanding the genetic underpinnings of conditions like coronary artery disease, which shares susceptibility with ischemic stroke, can help predict long-term implications, including severe complications such as sudden cardiac death[16]. This broader cardiovascular genetic risk profile provides a framework for predicting overall atherosclerotic burden and its potential for critical events, aiding clinicians in counseling patients and planning long-term management strategies to minimize the impact of progressive vascular disease.
Frequently Asked Questions About Cerebral Artery Occlusion
Section titled “Frequently Asked Questions About Cerebral Artery Occlusion”These questions address the most important and specific aspects of cerebral artery occlusion based on current genetic research.
1. My dad had a stroke; does that mean I’m more likely to get one?
Section titled “1. My dad had a stroke; does that mean I’m more likely to get one?”Yes, a family history of stroke, especially from a parent, can indicate a higher personal risk. Research shows a shared genetic susceptibility between ischemic stroke and other cardiovascular conditions, meaning certain genetic factors can be passed down. This doesn’t guarantee you’ll have one, but it’s an important factor to consider for prevention.
2. Can eating healthy and exercising really beat my family’s bad genes?
Section titled “2. Can eating healthy and exercising really beat my family’s bad genes?”While genetics play a significant role in stroke risk, lifestyle factors like diet and exercise are incredibly powerful. Modifiable risk factors such as hypertension, diabetes, and high cholesterol can be managed through healthy habits, even if you have a genetic predisposition. Integrating both your genetic insights and environmental choices offers the most comprehensive approach to prevention.
3. Would a DNA test tell me if I’m at risk for a stroke?
Section titled “3. Would a DNA test tell me if I’m at risk for a stroke?”A DNA test could provide insights into your genetic predisposition for conditions like atherosclerosis and ischemic stroke. Understanding these genetic factors can enhance risk assessment and help guide personalized preventive strategies. However, genetic findings are just one piece of the puzzle, and their full predictive value is still being understood.
4. I’m not European; does my background change my stroke risk?
Section titled “4. I’m not European; does my background change my stroke risk?”Yes, your ancestral background can influence your stroke risk. Many genetic studies have focused on populations of European descent, and genetic associations identified in one group may not be the same or have the same impact in others. Diverse populations can have unique genetic characteristics, so understanding your specific background is important for accurate risk assessment.
5. Why do some people get strokes even when they seem healthy?
Section titled “5. Why do some people get strokes even when they seem healthy?”Even seemingly healthy individuals can have underlying genetic predispositions that increase their risk for conditions like atherosclerosis, which can lead to a stroke. While lifestyle is crucial, genetic factors can influence metabolic networks and blood vessel health in ways that aren’t always visible externally. This highlights why a holistic view, including genetics, is important.
6. I have high cholesterol; does that mean my family history matters more?
Section titled “6. I have high cholesterol; does that mean my family history matters more?”Having high cholesterol is a significant risk factor for cerebral artery occlusion, and this risk can be compounded by a family history of stroke or heart disease. Your genetic makeup can influence how prone you are to developing high cholesterol or how your body processes fats. Therefore, managing your cholesterol becomes even more critical if you have a genetic predisposition.
7. Could I know my risk before any symptoms show up?
Section titled “7. Could I know my risk before any symptoms show up?”Yes, understanding your genetic predisposition could potentially help identify your risk before any symptoms appear. This knowledge, combined with assessing other risk factors like blood pressure and cholesterol, allows for more targeted prevention strategies. Early identification can lead to interventions that minimize future neurological damage.
8. Are there hidden reasons why some families get strokes more often?
Section titled “8. Are there hidden reasons why some families get strokes more often?”Yes, beyond common genetic variants, there can be “hidden” genetic factors contributing to stroke risk in families. These might include rare genetic variants, complex interactions between multiple genes, or epigenetic modifications that aren’t easily captured by standard genetic tests. Researchers are continually exploring these intricate genetic architectures to fully understand family patterns.
9. Does my stressful job increase my risk for a stroke?
Section titled “9. Does my stressful job increase my risk for a stroke?”While the direct genetic link between stress and stroke risk is complex, environmental factors like chronic stress can interact with your genetic predispositions. Stress can contribute to high blood pressure and unhealthy lifestyle choices, which are known risk factors for cerebral artery occlusion. Fully accounting for these gene-environment interactions is crucial for a holistic understanding of your risk.
10. My doctor says my blood pressure is high; am I more prone to stroke because of my genes?
Section titled “10. My doctor says my blood pressure is high; am I more prone to stroke because of my genes?”High blood pressure is a major modifiable risk factor for stroke, and your genetic makeup can influence your susceptibility to developing it. Some individuals are genetically predisposed to higher blood pressure, making them more vulnerable to its effects. Understanding this genetic link can help you and your doctor tailor more effective management and prevention strategies.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Dichgans M, et al. “Shared genetic susceptibility to ischemic stroke and coronary artery disease: a genome-wide analysis of common variants.”Stroke, 2013.
[2] Inouye M, et al. “Novel Loci for metabolic networks and multi-tissue expression studies reveal genes for atherosclerosis.”PLoS Genet, 2012.
[3] Wellcome Trust Case Control Consortium. “Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls.” Nature, 2007.
[4] Samani NJ, et al. “Genomewide association analysis of coronary artery disease.”N Engl J Med, 2007.
[5] Wojczynski, M. K., et al. “Genetics of coronary artery calcification among African Americans, a meta-analysis.”BMC Med Genet, vol. 14, 2013.
[6] Domarkiene I, et al. “RTN4 and FBXL17 Genes are Associated with Coronary Heart Disease in Genome-Wide Association Analysis of Lithuanian Families.”Balkan J Med Genet, 2014.
[7] Debette, S. et al. “Common variation in PHACTR1 is associated with susceptibility to cervical artery dissection.” Nat Genet, 2014.
[8] Hager J, et al. “Genome-wide association study in a Lebanese cohort confirms PHACTR1 as a major determinant of coronary artery stenosis.” PLoS One, 2012.
[9] Erdmann J, et al. “New susceptibility locus for coronary artery disease on chromosome 3q22.3.”Nat Genet, 2009.
[10] Shiffman D, et al. “Genome-wide study of gene variants associated with differential cardiovascular event reduction by pravastatin therapy.”PLoS One, 2012.
[11] O’Donnell CJ, et al. “Genome-wide association study for coronary artery calcification with follow-up in myocardial infarction.”Circulation, 2011.
[12] Reilly MP, et al. “Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies.”Lancet, 2011.
[13] Davies RW, et al. “A genome-wide association study for coronary artery disease identifies a novel susceptibility locus in the major histocompatibility complex.”Circ Cardiovasc Genet, 2012.
[14] Schunkert H, et al. “Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease.”Nat Genet, 2011.
[15] Lu X, et al. “Genome-wide association study in Han Chinese identifies four new susceptibility loci for coronary artery disease.”Nat Genet, 2012.
[16] Huertas-Vazquez, A., et al. “Novel loci associated with increased risk of sudden cardiac death in the context of coronary artery disease.”PLoS One, 2013.