86 hot topic(s) found with the query "Coronary artery disease"
Dose-Response Associations of Lipid Traits With Coronary Artery Disease and Mortality.
Guoyi Yang et al. JAMA Netw Open 2024 1 (1) e2352572
(Posted: Jan 20, 2024 10AM)
From the abstract: "Do apolipoprotein B (apoB), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) increase risk of coronary artery disease (CAD), all-cause mortality, or cause-specific mortality, and if so, what are the shapes of these associations? In this genetic association study using mendelian randomization including 347?797 participants of European ancestry from UK Biobank, genetically predicted apoB and LDL-C were positively associated with CAD, all-cause mortality, and cardiovascular mortality, all in a dose-dependent way. Genetically predicted TG was positively associated with CAD, although the presence of pleiotropy was suggested. "
Association Between a First-Degree Family History and Self-Reported Personal History of Obesity, Diabetes, and Heart and Blood Conditions: Results From the All of Us Research Program.
Danielle Rasooly et al. J Am Heart Assoc 2023 11 e030779
(Posted: Nov 13, 2023 8PM)
From the abstract: "We assessed the association between a self-reported family history of ODHBs and their risk in the adult population (age =20 years) of the AoU (All of Us) Research Program, a longitudinal cohort study of diverse participants across the United States. We conducted a family history-wide association study to systematically assess the association of a first-degree family history of 15 ODHBs in AoU. We use the FamWAS method to estimate 225 familial associations among 15 ODHBs. The results include overlapping associations between family history of different types of cardiometabolic conditions (such as type 2 diabetes and coronary artery disease), and their risk factors (obesity, hypertension), where adults with a family history of 1 ODHB exhibited 1.1 to 5.6 times (1.5, on average) the odds of having a different ODHB. "
Ancestry-specific polygenic risk scores are risk enhancers for clinical cardiovascular disease assessments.
George B Busby et al. Nat Commun 2023 11 (1) 7105
(Posted: Nov 06, 2023 10AM)
From the abstract: " We develop and validate ancestry-specific Polygenic Risk Scores (PRSs) for Coronary Artery Disease (CAD) using 29,389 individuals from diverse cohorts and genetic ancestry groups. The CAD PRSs outperform published scores with an average Odds Ratio per Standard Deviation of 1.57 (SD = 0.14) and identify between 12% and 24% of individuals with high genetic risk. Using this risk factor to reclassify borderline or intermediate 10 year Atherosclerotic Cardiovascular Disease (ASCVD) risk improves assessments for both CAD (Net Reclassification Improvement (NRI) = 13.14% (95% CI 9.23–17.06%)) and ASCVD (NRI = 10.70 (95% CI 7.35-14.05)) in an independent cohort of 9,691 individuals. "
Roadmap on the use of artificial intelligence for imaging of vulnerable atherosclerotic plaque in coronary arteries.
Bernhard Föllmer et al. Nat Rev Cardiol 2023 7
(Posted: Jul 27, 2023 7AM)
Artificial intelligence (AI) is likely to revolutionize the way medical images are analysed and has the potential to improve the identification and analysis of vulnerable or high-risk atherosclerotic plaques in coronary arteries, leading to advances in the treatment of coronary artery disease. In this Roadmap, we review existing evidence on the application of AI to the imaging of vulnerable plaque in coronary arteries and provide consensus recommendations developed by an interdisciplinary group of experts on AI and non-invasive and invasive coronary imaging.
Familial hypercholesterolaemia
S McErlean, BMJ, July 2023
(Posted: Jul 16, 2023 9AM)
Familial hypercholesterolemia is a common genetic condition affecting 1 in 310 people, resulting in premature coronary artery disease due to elevated cholesterol levels from birth If a parent has familial hypercholesterolemia, there is a 50% chance their child will inherit the condition. Treatment is based on lowering low density lipoprotein (LDL) cholesterol concentration, with a target of at least 50% reduction from baseline.
Improving polygenic score prediction for coronary artery disease across populations of diverse ancestry
Nature Medicine, July 10, 2023
(Posted: Jul 10, 2023 11AM)
Genome-wide polygenic scores quantify inherited risk by integrating information from many common DNA variants and hold considerable promise for enabling personalized medicine. By integrating information on coronary artery disease (CAD) and CAD-related risk traits from genetic datasets that were larger and more diverse than those used in the past, we developed an improved multi-ancestry polygenic predictor for CAD.
Contemporary Polygenic Scores of Low-Density Lipoprotein Cholesterol and Coronary Artery Disease Predict Coronary Atherosclerosis in Adolescents and Young Adults.
Rodrigo Guarischi-Sousa et al. Circ Genom Precis Med 2023 7 e004047
(Posted: Jul 10, 2023 8AM)
A multi-ancestry polygenic risk score improves risk prediction for coronary artery disease.
Aniruddh P Patel et al. Nat Med 2023 7
(Posted: Jul 07, 2023 9AM)
Identification of individuals at highest risk of coronary artery disease (CAD)—ideally before onset—remains an important public health need. Prior studies have developed genome-wide polygenic scores to enable risk stratification, reflecting the substantial inherited component to CAD risk. Here we develop a new and significantly improved polygenic score for CAD, termed GPSMult, that incorporates genome-wide association data across five ancestries for CAD (>269,000 cases and >1,178,000 controls) and ten CAD risk factors.
Clinical utility of polygenic risk scores: a critical 2023 appraisal
S Koch et al, J Comm Genetics, May 3, 2023
(Posted: May 03, 2023 7AM)
We surveyed the current state of PRSs for various diseases, including breast cancer, diabetes, prostate cancer, coronary artery disease, and Parkinson disease, with an extra focus upon the potential improvement of clinical scores by their combination with PRSs. We observed that the diagnostic and prognostic performance of PRSs alone is consistently low, as expected. Moreover, combining a PRS with a clinical score at best led to moderate improvement of the power of either risk marker. Despite the large number of PRSs reported in the scientific literature, prospective studies of their clinical utility, particularly of the PRS-associated improvement of standard screening or therapeutic procedures, are still rare.
The role of aldehyde dehydrogenase 2 in cardiovascular disease.
Jian Zhang et al. Nature reviews. Cardiology 2023 2
(Posted: Feb 26, 2023 8AM)
Aldehyde dehydrogenase 2 (ALDH2) is a mitochondrial enzyme involved in the detoxification of alcohol-derived acetaldehyde and endogenous aldehydes. The inactivating ALDH2 rs671 polymorphism, present in up to 8% of the global population and in up to 50% of the East Asian population, is associated with increased risk of cardiovascular conditions such as coronary artery disease, alcohol-induced cardiac dysfunction, pulmonary arterial hypertension, heart failure and drug-induced cardiotoxicity.
The necessity of incorporating non-genetic risk factors into polygenic risk score models
S van Dam et al, Sci Reports, February 20, 2023
(Posted: Feb 20, 2023 8AM)
The growing public interest in genetic risk scores for various health conditions can be harnessed to inspire preventive health action. However, current commercially available genetic risk scores can be deceiving as they do not consider other, easily attainable risk factors, such as sex, BMI, age, smoking habits, parental disease status and physical activity. We show improved performance at identifying the 10% most at-risk individuals for type 2 diabetes (T2D) and coronary artery disease (CAD) by including common risk factors.
Association of Hypertensive Disorders of Pregnancy With Future Cardiovascular Disease.
Bilal Rayes et al. JAMA network open 2023 2 (2) e230034
(Posted: Feb 18, 2023 8AM)
Is there evidence for an association between hypertensive disorders of pregnancy (HDPs) and long-term risk of cardiovascular disease? In this large genome-wide genetic association study using mendelian randomization, HDPs were associated with higher risk of coronary artery disease and ischemic stroke but not heart failure or atrial fibrillation. Mediation analysis revealed a partial attenuation of the association between HDPs and coronary artery disease after adjustment for systolic blood pressure and type 2 diabetes. These results support the consideration of HDPs as potential risk factors for cardiovascular disease.
A machine-learning-derived, in silico marker for CAD identifies underdiagnosed patients.
Huynh Karina et al. Nature reviews. Cardiology 2023 1
(Posted: Jan 21, 2023 6AM)
Current risk prediction tools for coronary artery disease (CAD) do not measure disease on a continuous scale and use only a small number of variables for risk prediction, disregarding much of the data contained in electronic health records (EHRs). In a new study, a machine learning model trained using clinical data from EHRs generated a novel, in silico quantitative score for CAD that can quantify disease pathophysiology and clinical outcomes on a continuous spectrum.
Predictive Utility of a Coronary Artery Disease Polygenic Risk Score in Primary Prevention
NA Marston et al, JAMA Cardiology, December 28, 2022
(Posted: Dec 28, 2022 0PM)
In this cohort study of 330?201 patients, a PRS for CAD carried significantly greater predictive power in younger adults, contributing up to 30% of the myocardial infarction risk in this cohort. Younger adults with borderline and intermediate clinical risk but high polygenic risk for CAD were significantly reclassified into a risk category for which statin therapy is indicated. Although not necessary in all individuals, a targeted approach to CAD PRS testing may help guide preventive strategies such as statin initiation in younger adults with borderline to intermediate cardiovascular risk.
Finding causal genes underlying risk for coronary artery disease
PL Auer, Nature Genetics, December 6, 2022
(Posted: Dec 06, 2022 0PM)
Previous genome-wide association studies of coronary artery disease (CAD) have discovered multiple susceptibility loci but have largely failed to uncover causal genes. A new study identifies hundreds of likely causal genes underlying the genetic risk for CAD.
Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants
KG Aragam et al, Nature Genetics, December 6, 2022
(Posted: Dec 06, 2022 0PM)
The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci.
Machine Learning Algorithms for Prediction of Survival by Stress Echocardiography in Chronic Coronary Syndromes
L Cortiginai et al, J Per Med, September 16, 2022
(Posted: Sep 18, 2022 5AM)
Stress echocardiography (SE) is based on regional wall motion abnormalities and coronary flow velocity reserve (CFVR). Their independent prognostic capabilities could be better studied with a machine learning (ML) approach. The study aims to assess the SE outcome data by conducting an analysis with an ML approach. We included 6881 prospectively recruited and retrospectively analyzed patients with suspected (n = 4279) or known (n = 2602) coronary artery disease.
Personalized Medicine in Coronary Artery Disease: Where Are We in 2022?
Dmitry Shchekochikhin et al, J Per Medicine, September 1, 2022
(Posted: Sep 01, 2022 2PM)
This Special Issue of the Journal of Personalized Medicine covers several questions about personalized medicine in coronary artery disease, with a special focus on the use of non-coning RNA as biomarkers or treatment targets and novel cardiac imaging modalities that can influence daily practice.
Broad clinical manifestations of polygenic risk for coronary artery disease in the Women’s Health Initiative
SL Clarke et al, Comm Medicine, August 25, 2022
(Posted: Aug 26, 2022 8AM)
Polygenic risk for CAD is associated with a variety of biomarkers, clinical measurements, behaviors, and diagnoses related to traditional risk factors, as well as risk-enhancing factors. Analysis of adjudicated outcomes shows a graded association between atherosclerosis related outcomes, with the highest odds ratios being observed for the most severe manifestations of CAD. We find associations between increased polygenic risk for CAD and decreased risk for incident breast and lung cancer, with replication of the breast cancer finding in an external cohort.
Joint Genetic Inhibition of PCSK9 and CETP and the Association With Coronary Artery Disease: A Factorial Mendelian Randomization Study.
Cupido Arjen J et al. JAMA cardiology 2022 8
(Posted: Aug 05, 2022 8AM)
In this cohort study, a 2?×?2 factorial Mendelian randomization study including 425?354 participants from the UK Biobank, an additive association of a genetically reduced combined concentration of CETP and PCSK9 was found for lipid levels and risk of coronary artery disease, while the association of CETP with age-related macular degeneration was not mitigated. Our findings suggest that joint inhibition of CETP and PCSK9 has additive effects on lipid concentrations and clinical outcomes.
Polygenic Risk Scores for Cardiovascular Disease: A Scientific Statement From the American Heart Association
JW O'Sullivan et al, Circulation, July 18, 2022
(Posted: Jul 18, 2022 1PM)
Individuals and their physicians are increasingly presented with polygenic risk scores for cardiovascular conditions in clinical encounters. In this scientific statement, we review the contemporary science, clinical considerations, and future challenges for polygenic risk scores for cardiovascular diseases. We selected 5 cardiometabolic diseases (coronary artery disease, hypercholesterolemia, type 2 diabetes, atrial fibrillation, and venous thromboembolic disease) and response to drug therapy and offer provisional guidance to health care professionals, researchers, policymakers, and patients.
Association of the Interaction Between Familial Hypercholesterolemia Variants and Adherence to a Healthy Lifestyle With Risk of Coronary Artery Disease
AC Fahed et al, JAMA Network Open, March 16, 2022
(Posted: Mar 17, 2022 9AM)
Is adherence to a healthy lifestyle associated with lower risk of coronary artery disease in carriers and noncarriers of pathogenic DNA variants in familial hypercholesterolemia–related genes? In a case-control study of 10?175 participants and cohort study of 39?920 participants, there was a significant risk gradient of coronary artery disease according to variant carrier and lifestyle categories. Estimated risk by the age of 75 years among variant carriers ranged from 35% for those with a favorable lifestyle to 66% for those with an unfavorable lifestyle.
Impact of polygenic risk communication: an observational mobile application-based coronary artery disease study
ED Muse et al, NPJ Digital Medicine, March 11, 2022
(Posted: Mar 12, 2022 8AM)
We developed a smartphone application, MyGeneRank, to conduct a prospective observational cohort study involving the automated generation, communication, and electronic capture of response to a polygenic risk score (PRS) for coronary artery disease (CAD). We evaluated self-reported actions taken in response to personal CAD PRS information, with special interest in the initiation of lipid-lowering therapy. 19% (721/3,800) of participants provided complete responses for baseline and follow-up use of lipid-lowering therapy. 20% (n?=?19/95) of high CAD PRS vs 7.9% (n?=?8/101) of low CAD PRS participants initiated lipid-lowering therapy at follow-up (p-value?=?0.002).
Increased family history documentation in internal medicine resident continuity clinic at a community hospital through resident-led structured genetic education program.
Chenbhanich Jirat et al. Journal of community genetics 2022
(Posted: Mar 05, 2022 7AM)
FH documentation in EMR was reviewed and compared to a 4-week baseline (Phase 0). We found that time constraint was the most reported barrier. We reviewed 1197 patient visits; FH was recorded in 34% (67/200), 52% (272/522), and 50% (239/475) during Phase 0, Phase1, and Phase 2, respectively. Genetic education significantly increased the rate of FH documentation in Phase 1 from baseline, which was maintained in Phase 2 despite removal of interventions. The mean age of patients with documented FH was younger than those without documentation (48 years vs 51 years; p?<?0.001). Documented FH of cancers and coronary artery disease lacked important details, such as age at diagnosis, in 62% (86/138) and 51% (41/81) of them, respectively. Out of 511 patients that had documented FH, we identified 66 patients (13%) where positive family history could alter medical management
Before the heart attack
EE Blaak et al, Nature Medicine, February 17, 2022
(Posted: Feb 19, 2022 7AM)
Integrated analysis of microbiome and metabolome profiles in unique cohorts reveals early and late markers of the transition towards ischemic heart disease. Ischemic heart disease (IHD), also known as coronary artery disease, can culminate in heart attack and is a major cause of morbidity and mortality worldwide. To improve clinical outcomes, more insight is required into the complex etiology of IHD. Two large-scale studies integrate extensive gut microbiome and serum metabolome profiles in the progression toward IHD, taking into account key confounders such as metabolic status and medication — and thereby providing insight into the etiology of IHD.
Clinical utility of polygenic risk scores for coronary artery disease.
Klarin Derek et al. Nature reviews. Cardiology 2021 11
(Posted: Nov 28, 2021 10AM)
In this Review, we describe technical and downstream considerations for the derivation and validation of polygenic risk scores and current evidence for their efficacy and safety. We discuss the implementation of these scores in clinical medicine for uses including risk prediction and screening algorithms for coronary artery disease, prioritization of patient subgroups that are likely to derive benefit from treatment, and efficient prospective clinical trial designs.
Mapping gene and gene pathways associated with coronary artery disease: a CARDIoGRAM exome and multi-ancestry UK biobank analysis
P Hariharan et al, Scientific Reports, August 12, 2021
(Posted: Aug 12, 2021 7AM)
We performed gene and pathway-based association (GBA) tests on publicly available Coronary ARtery DIsease Genome wide Replication and Meta-analysis consortium Exome (n?=?120,575) and multi ancestry pan UK Biobank study (n?=?442,574) summary data using versatile gene-based association study (VEGAS2) and Multi-marker analysis of genomic annotation (MAGMA) to identify novel genes and pathways associated with CAD.
Genetic testing in ambulatory cardiology clinics reveals high rate of findings with clinical management implications.
Murdock David R et al. Genetics in medicine : official journal of the American College of Medical Genetics 2021 8
(Posted: Aug 09, 2021 11AM)
We developed the "HeartCare" panel of genes associated with CVD, evaluating high-penetrance Mendelian conditions, coronary artery disease (CAD) polygenic risk, LPA gene polymorphisms, and specific pharmacogenetic (PGx) variants. We enrolled 709 individuals from cardiology clinics. Results were returned to the ordering physician and uploaded to the electronic medical record. Notably, 32% of patients had a genetic finding with clinical management implications, even after excluding PGx results, including 9% who were molecularly diagnosed with a Mendelian condition.
Expanding Discovery in Cardiovascular Genome-Wide Association Studies
P Natarajan et al, JAMA Cardiology, June 9, 2021
(Posted: Jun 10, 2021 7AM)
Genome-wide association studies of individuals of African ancestry typically living in the US are uncommon, yet they have yielded high-impact observations, including the discovery that PCSK9 loss-of-function mutations protect against coronary artery disease. Genome-wide association studies of individuals living in Africa are even rarer, representing approximately 0.4% of GWAS participants.
Response to Polygenic Risk: Results of the MyGeneRank Mobile Application-Based Coronary Artery Disease Study
ED Muse et al, MEDRXIV, April 28, 2021
(Posted: Apr 29, 2021 7AM)
We evaluated self-reported actions taken in response to personal CAD PRS information, with special interest in the initiation of lipid lowering therapy. 20% of high genetic risk (n=95) vs 7.9% of low genetic risk individuals (n=101) initiated lipid lowering therapy at follow-up (p-value = 0.002). The initiation of both statin and non-statin lipid lowering therapy was associated with degree of genetic risk.
Impact of diabetes on coronary severity and cardiovascular outcomes in patients with heterozygous familial hypercholesterolaemia.
Liu Ming-Ming et al. European journal of preventive cardiology 2021
(Posted: Apr 02, 2021 10AM)
Type 2 diabetes mellitus (T2DM) is an independent risk factor for cardiovascular disease. However, the association between T2DM and coronary artery disease (CAD) in patients with heterozygous familial hypercholesterolaemia (HeFH) has not been thoroughly evaluated. Our study aimed to assess the effect of T2DM on CAD severity and hard cardiovascular endpoints in a HeFH cohort of 432 patients.
Sexual Differences in Genetic Predisposition of Coronary Artery Disease
Y Huang et al, Circ Genetics Precision Med, December 2020
(Posted: Dec 18, 2020 8AM)
Using data from the UK Biobank, we found that the associations of genetic risk scores were stronger among men than women. Using a score of 161 loci, we observed a 2.4 times higher risk for incident CAD comparing men with high genetic risk to men with low genetic risk, but an 80 percent greater risk comparing women with high genetic risk to women with low genetic risk.
CYP2C19 Genotyping to Guide Antiplatelet Therapy After Percutaneous Coronary Interventions: One Size Rarely Fits All.
Moliterno David J et al. JAMA 2020 08 (8) 747-749
(Posted: Aug 28, 2020 8AM)
The future is pointing toward a personalized strategy for therapeutic interventions, and genotype-guided approaches should be part of this strategy—the question is how much. However, the clinical evidence at this moment does not support the routine use of personalized genotype-based selection of antiplatelet therapy for patients with coronary artery disease.
Polygenic background modifies penetrance of monogenic variants for tier 1 genomic conditions
AC Fahed et al, Nature Communications, August 20, 2020
(Posted: Aug 21, 2020 9AM)
We study 80,928 individuals to examine whether polygenic background can modify penetrance of disease in tier 1 genomic conditions — familial hypercholesterolemia, hereditary breast and ovarian cancer, and Lynch syndrome. Among carriers of a monogenic risk variant, we estimate substantial gradients in disease risk based on polygenic background — the probability of disease by age 75 years ranged from 17% to 78% for coronary artery disease, 13% to 76% for breast cancer, and 11% to 80% for colon cancer.
Genetic Predisposition to Coronary Artery Disease in Type 2 diabetes
NR van Zuydam et al, Cir Genomics Precision Med August 2020
(Posted: Aug 14, 2020 7AM)
None of the previously characterized CAD loci was found to have specific effects on CAD in T2D individuals and a genome-wide interaction analysis found no new variants for CAD that could be considered T2D specific.
Validation of a Genome-Wide Polygenic Score for Coronary Artery Disease in South Asians
M Wang et al, JACC, August 6, 2020
(Posted: Aug 07, 2020 9AM)
Genome-wide polygenic scores (GPS) integrate information from many common DNA variants into a single number. Because rates of coronary artery disease (CAD) are substantially higher among South Asians, a GPS to identify high-risk individuals may be particularly useful in this population.
Factors Associated With Death in Critically Ill Patients With Coronavirus Disease 2019 in the US
S Gupta et al, JAMA Internal Medicine, July 15,2020
(Posted: Jul 16, 2020 6AM)
In a cohort of 2215 adults with COVID-19 who were admitted to intensive care units at 65 sites, 784 (35.4%) died within 28 days, with wide variation among hospitals. Factors associated with death included older age, male sex, obesity, coronary artery disease, cancer, acute organ dysfunction, and admission to a hospital with fewer intensive care unit beds.
Limitations of Contemporary Guidelines for Managing Patients at High Genetic Risk of Coronary Artery Disease
KG Aragam et al, JACC, June 2020
(Posted: Jun 04, 2020 1PM)
Of 47,108 study participants, 11,020 (23.4%) had CAD. The CAD PRS strongly associated with CAD (odds ratio: 1.4 per SD increase in PRS). High polygenic risk (top 20% of PRS) conferred 1.9-fold odds of developing CAD (p < 0.0001). Among primary prevention patients, high polygenic risk did not correspond with increased recommendations for statin therapy.
Polygenic Scores to Assess Atherosclerotic Cardiovascular Disease Risk: Clinical Perspectives and Basic Implications.
Aragam Krishna G et al. Circulation research 2020 Apr 126(9) 1159-1177
(Posted: Apr 29, 2020 7AM)
In this review, we describe how genomic analyses of coronary artery disease have been leveraged to create polygenic risk scores. We then discuss evaluations of the clinical utility of these scores, pertinent mechanistic insights gleaned, and practical considerations relevant to the implementation of polygenic risk scores in the health care setting.
Is family history of coronary artery disease important in the emergency department triage?
Mor Saban et al. International emergency nursing 2020 Mar 100855
(Posted: Apr 08, 2020 9AM)
Do Polygenic Risk Scores Improve Patient Selection for Prevention of Coronary Artery Disease?
SS Khan et al, JAMA Editorial, February 18, 2020
(Posted: Feb 19, 2020 0PM)
Available data do not support the clinical utility of polygenic risk scores (in their current form) in middle-aged adults of European descent. In the meanwhile, the best approach for prevention of CAD continues to be a combination of population-wide risk factor approaches and addition of drug therapies and lifestyle interventions.
Polygenic background modifies penetrance of monogenic variants conferring risk for coronary artery disease, breast cancer, or colorectal cancer
AC Fahed et al, MedRXIV, November 29, 2019
(Posted: Dec 02, 2019 8AM)
For three genomic conditions (coronary artery disease, breast cancer, and colorectal cancer) polygenic risk powerfully modifies the risk conferred by monogenic risk variants. Across the lowest to highest percentiles of polygenic risk, disease risk ranged from 17% to 78% for coronary artery disease; 13% to 76% for breast cancer; and 11% to 80% for colon cancer.
A genetic risk score predicts coronary artery disease in familial hypercholesterolaemia: enhancing the precision of risk assessment.
Ellis Katrina L et al. Clinical genetics 2019 Sep
(Posted: Oct 09, 2019 8AM)
A high GRS was associated with CAD defined clinically and angiographically in FH patients. High GRS patients may benefit from more intensive management including lifestyle modification and aggressive lipid-lowering therapy. Further assessment of the utility of the GRS requires investigation in prospective cohorts.
Association of APOL1 Risk Alleles with Cardiovascular Disease in African Americans in the Million Veteran Program.
Bick Alexander G et al. Circulation 2019 Jul
(Posted: Jul 30, 2019 8AM)
13% of African-Americans carry two copies of the APOL1 risk alleles, which are associated with increased risk of chronic kidney disease. The study We sought to test the association of APOL1 G1/G2 alleles with coronary artery disease (CAD), peripheral artery disease (PAD), and stroke among African American individuals in the Million Veteran Program (MVP).
Variability in aspirin efficacy: all in the genes?
Baigent Colin et al. European heart journal 2019 Jul
(Posted: Jul 08, 2019 3PM)
This is an editorial about the recent paper: ?Genetic variation at the coronary artery disease locus GUCY1A3 modifies cardiovascular disease prevention effects of aspirin.? Given the difficulty of selecting healthy individuals for aspirin use for primary prevention, it is of interest to consider whether subgroups defined by genetic variation might offer an alternative method of selecting people in whom the benefits of aspirin greatly exceed the bleeding risks.
High prevalence of genetic determined familial hypercholesterolemia in premature coronary artery disease.
Pirazzi Carlo et al. The application of clinical genetics 2019 1271-78
(Posted: Jun 26, 2019 9AM)
Genetic variation at the coronary artery disease risk locus GUCY1A3 modifies cardiovascular disease prevention effects of aspirin.
Hall Kathryn T et al. European heart journal 2019 Jun
(Posted: Jun 24, 2019 8AM)
In two randomized placebo-controlled trials in the setting of primary prevention, aspirin reduced the incidence of CVD events in individuals homozygous for the GUCY1A3 risk (G) allele, whereas heterozygote individuals had more events when taking aspirin.
Polygenic risk scores in coronary artery disease.
Rao Abhiram S et al. Current opinion in cardiology 2019 Apr
(Posted: Apr 24, 2019 7AM)
Application of expanded genetic analysis in the diagnosis of familial hypercholesterolemia in patients with very early-onset coronary artery disease.
Cao Ye-Xuan et al. Journal of translational medicine 2018 Dec 16(1) 345
(Posted: Dec 19, 2018 10AM)
Vascular endothelial growth factor gene transfer therapy for coronary artery disease: A systematic review and meta-analysis.
Yuan Rong et al. Cardiovascular therapeutics 2018 Oct 36(5) e12461
(Posted: Dec 19, 2018 10AM)
Genomic Risk Prediction of Coronary Artery Disease in 480,000 Adults: Implications for Primary Prevention
M Inouye et al, JACC< October 2018
(Posted: Oct 09, 2018 9AM)
Prevalence and Pharmacologic Management of Familial Hypercholesterolemia in an Unselected Contemporary Cohort of Patients With Stable Coronary Artery Disease.
De Luca Leonardo et al. Clinical cardiology 2018 Jul
(Posted: Aug 01, 2018 10AM)
Genetic stratification for primary prevention of coronary artery disease.
Roberts Robert et al. Current opinion in cardiology 2018 Jul
(Posted: Jul 19, 2018 8AM)
Genome-wide association study of coronary artery disease among individuals with diabetes: the UK Biobank.
Fall Tove et al. Diabetologia 2018 Jul
(Posted: Jul 19, 2018 8AM)
Genetic Risk Analysis of Coronary Artery Disease in a Population-based Study in Portugal, Using a Genetic Risk Score of 31 Variants.
Pereira Andreia et al. Arquivos brasileiros de cardiologia 2018 Jul
(Posted: Jul 11, 2018 9AM)
Genetics in the prevention and management of coronary artery disease.
Roberts Robert et al. Current opinion in cardiology 2018 Jan
(Posted: Jan 21, 2018 6PM)
Genomic risk prediction of coronary artery disease in nearly 500,000 adults: implications for early screening and primary prevention
M Inouye et al, BioRXIV preprints, Jan 18, 2018
(Posted: Jan 21, 2018 9AM)
Polygenic Contribution in Individuals With Early-Onset Coronary Artery Disease
Sébastien Thériault et al, Circ Cardio Genetics, Jan 2018
(Posted: Jan 08, 2018 11AM)
The Identification of 64 Novel Genetic Loci Provides an Expanded View on the Genetic Architecture of Coronary Artery Disease
Pim van der Harst, et al, Circ Res, Dec 2017
(Posted: Dec 09, 2017 11AM)
A 45-SNP genetic risk score is increased in early-onset coronary artery disease but independent of familial disease clustering.
Christiansen Morten K et al. Atherosclerosis 2017 Feb 257172-178
(Posted: Nov 14, 2017 8AM)
Exome chip meta-analysis identifies novel loci and East Asian–specific coding variants that contribute to lipid levels and coronary artery disease
X Lu et al, Nat Genetics, Oct 30, 2017
(Posted: Oct 30, 2017 11AM)
Genetics of coronary artery disease: discovery, biology and clinical
translation
AV Khera et al, Nature Rev Genetics, 2017
(Posted: May 23, 2017 8AM)
Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms
J MM Howson et al, Nature Genetics
(Posted: May 22, 2017 2PM)
Genetics of coronary artery disease: discovery, biology and clinical translation
AV Khera et al. Nat Rev Genetics, March 2017
(Posted: Mar 13, 2017 9AM)
Association of Rare and Common Variation in the Lipoprotein Lipase Gene With Coronary Artery Disease
AV Khera et al, JAMA, March 7, 2017
(Posted: Mar 08, 2017 4PM)
Moving Beyond Clinical Risk Scores with a Mobile App for the Genomic Risk of Coronary Artery Disease
ED Muse et al, BioRXIV preprints, January 2017
(Posted: Jan 20, 2017 9AM)
Genetics and Genomics of Coronary Artery Disease.
Pjanic Milos et al. Current cardiology reports 2016 Oct (10) 102
(Posted: Oct 04, 2016 5PM)
Variant ASGR1 Associated with a Reduced Risk of Coronary Artery Disease
P. Nioi et al, NEJM, May 18, 2016
(Posted: May 19, 2016 7AM)
Inactivating Variants in ANGPTL4 and Risk of Coronary Artery Disease
FE Dewey et al, NEJM, March 2, 2016
(Posted: Mar 02, 2016 5PM)
Common genetic risk factors for coronary artery disease: new opportunities for prevention?
Hamrefors Viktor et al. Clin Physiol Funct Imaging 2015 Aug 17.
(Posted: Sep 24, 2015 10AM)
A comprehensive 1000 Genomes–based genome-wide association meta-analysis of coronary artery disease
M Nikpay et al. Nature Genetics, September 7, 2015
(Posted: Sep 07, 2015 7PM)
Prediction of Causal Candidate Genes in Coronary Artery Disease Loci.
Brænne Ingrid et al. Arterioscler. Thromb. Vasc. Biol. 2015 Aug 20.
(Posted: Sep 01, 2015 2PM)
Screening Strategies and Primary Prevention Interventions in Relatives of People With Coronary Artery Disease: A Systematic Review and Meta-analysis.
Goldfarb Michael et al. Can J Cardiol 2015 May (5) 649-57
(Posted: Jul 17, 2015 4PM)
The Genetic Basis of Coronary Artery Disease and Atrial Fibrillation: A Search for Disease Mechanisms and Therapeutic Targets.
Neelankavil Jacques et al. J. Cardiothorac. Vasc. Anesth. 2015 Jan 23.
(Posted: Jun 21, 2015 7PM)
Predicting sudden cardiac death using common genetic risk variants for coronary artery disease.
Hernesniemi Jussi A et al. Eur. Heart J. 2015 Apr 23.
(Posted: May 12, 2015 11AM)
Seven-year clinical follow-up of a Chinese homozygous familial hypercholesterolemia child with premature xanthomas and coronary artery disease--a need for early diagnosis and aggressive treatment.
Jiang Long et al. Int. J. Cardiol. 2014 Nov 15. (1) 188-91
(Posted: Feb 28, 2015 0PM)
Unraveling New Therapeutic Targets of Coronary Artery Disease by Genetic Approaches.
Lee Sang Eun et al. Circ. J. 2014 Dec 12.
(Posted: Feb 16, 2015 9AM)
Mendelian randomization studies in coronary artery disease.
Jansen Henning et al. Eur. Heart J. 2014 Aug 1. (29) 1917-24
(Posted: Feb 16, 2015 9AM)
Coronary Microvascular Disease
From NHLBI health topic site
(Posted: Jan 11, 2014 11AM)
What Is
Coronary microvascular disease (MVD) is heart disease that affects the tiny coronary (heart) arteries. In coronary MVD, the walls of the heart's tiny arteries are damaged or diseased.
Coronary MVD is different from traditional coronary heart disease (CHD), also called coronary artery disease. In CHD, a waxy substance called plaque (plak) builds up in the large coronary arteries.
Plaque narrows the heart's large arteries and reduces the flow of oxygen-rich blood to your heart muscle. The buildup of plaque also makes it more likely that blood clots will form in your arteries. Blood clots can mostly or completely block blood flow through a coronary artery.
In coronary MVD, however, the heart's tiny arteries are affected. Plaque doesn't create blockages in these vessels as it does in the heart's large arteries.
Coronary Microvascular Disease
Figure A shows the small coronary artery network (microvasculature), containing a normal artery and an artery with coronary MVD.
Figure A shows the small coronary artery network (microvasculature), containing a normal artery and an artery with coronary MVD. Figure B shows a large coronary artery with plaque buildup.
Overview
Both men and women who have coronary microvascular disease often have diabetes or high blood pressure. Some people who have coronary microvascular disease may have inherited heart muscle diseases.
Diagnosing coronary microvascular disease has been a challenge for doctors. Standard tests used to diagnose coronary heart disease aren?t designed to detect coronary microvascular disease. More research is needed to find the best diagnostic tests and treatments for the disease.
Outlook
Most of what is known about coronary MVD comes from the National Heart, Lung, and Blood Institute's Wise study (Women's Ischemia Syndrome Evaluation).
The WISE study started in 1996. The goal of the study was to learn more about how heart disease develops in women.
Currently, research is ongoing to learn more about the role of hormones in heart disease and to find better ways to diagnose coronary MVD.
Studies also are under way to learn more about the causes of coronary MVD, how to treat the disease, and the expected health outcomes for people with coronary MVD.
Other Names
?Cardiac syndrome X
?Nonobstructive coronary heart disease
Heart Disease in Women
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
How Does Heart Disease Affect Women?
In the United States, 1 in 4 women dies from heart disease. In fact, coronary heart disease (CHD)?the most common type of heart disease?is the #1 killer of both men and women in the United States.
Other types of heart disease, such as coronary microvascular disease (MVD) and broken heart syndrome, also pose a risk for women. These disorders, which mainly affect women, are not as well understood as CHD. However, research is ongoing to learn more about coronary MVD and broken heart syndrome.
This article focuses on CHD and its complications. However, it also includes general information about coronary MVD and broken heart syndrome.
Coronary Heart Disease
CHD is a disease in which plaque (plak) builds up on the inner walls of your coronary arteries. These arteries carry oxygen-rich blood to your heart. When plaque builds up in the arteries, the condition is called atherosclerosis (ath-er-o-skler-O-sis).
Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque can harden or rupture (break open).
Hardened plaque narrows the coronary arteries and reduces the flow of oxygen-rich blood to the heart. This can cause chest pain or discomfort called angina (an-JI-nuh or AN-juh-nuh).
If the plaque ruptures, a blood clot can form on its surface. A large blood clot can mostly or completely block blood flow through a coronary artery. This is the most common cause of a heart attack. Over time, ruptured plaque also hardens and narrows the coronary arteries.
Heart With Muscle Damage and a Blocked Artery
Figure A is an overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. Figure B is a cross-section of the coronary artery with plaque buildup and a blood clot resulting from plaque rupture.
Figure A is an overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. Figure B is a cross-section of the coronary artery with plaque buildup and a blood clot resulting from plaque rupture.
Plaque also can develop within the walls of the coronary arteries. Tests that show the insides of the coronary arteries may look normal in people who have this pattern of plaque. Studies are under way to see whether this type of plaque buildup occurs more often in women than in men and why.
In addition to angina and heart attack, CHD can cause other serious heart problems. The disease may lead to heart failure, irregular heartbeats called arrhythmias (ah-RITH-me-ahs), and sudden cardiac arrest (SCA).
Coronary Microvascular Disease
Coronary MVD is heart disease that affects the heart's tiny arteries. This disease is also called cardiac syndrome X or nonobstructive CHD. In coronary MVD, the walls of the heart's tiny arteries are damaged or diseased.
Coronary Microvascular Disease
Figure A shows the small coronary artery network (microvasculature), containing a normal artery and an artery with coronary MVD.
Figure A shows the small coronary artery network (microvasculature), containing a normal artery and an artery with coronary MVD. Figure B shows a large coronary artery with plaque buildup.
Women are more likely than men to have coronary MVD. Many researchers think that a drop in estrogen levels during menopause combined with other heart disease risk factors causes coronary MVD.
Although death rates from heart disease have dropped in the last 30 years, they haven't dropped as much in women as in men. This may be the result of coronary MVD.
Standard tests for CHD are not designed to detect coronary MVD. Thus, test results for women who have coronary MVD may show that they are at low risk for heart disease.
Research is ongoing to learn more about coronary MVD and its causes.
Broken Heart Syndrome
Women are also more likely than men to have a condition called broken heart syndrome. In this recently recognized heart problem, extreme emotional stress can lead to severe (but often short-term) heart muscle failure.
Broken heart syndrome is also called stress-induced cardiomyopathy (KAR-de-o-mi-OP-ah-thee) or takotsubo cardiomyopathy.
Doctors may misdiagnose broken heart syndrome as a heart attack because it has similar symptoms and test results. However, there's no evidence of blocked heart arteries in broken heart syndrome, and most people have a full and quick recovery.
Researchers are just starting to explore what causes this disorder and how to diagnose and treat it. Often, patients who have broken heart syndrome have previously been healthy.
Outlook
Women tend to have CHD about 10 years later than men. However, CHD remains the #1 killer of women in the United States.
The good news is that you can control many CHD risk factors. CHD risk factors are conditions or habits that raise your risk for CHD and heart attack. These risk factors also can increase the chance that existing CHD will worsen.
Lifestyle changes, medicines, and medical or surgical procedures can help women lower their risk for CHD. Thus, early and ongoing CHD prevention is important.
Other Names
?Arrhythmia
?Broken heart syndrome, which also is called stress-induced cardiomyopathy or takotsubo cardiomyopathy
?Coronary heart disease, which also is called coronary artery disease
?Coronary microvascular disease, which also is called cardiac syndrome X or nonobstructive coronary heart disease
?Heart failure
?Sudden cardiac arrest
Heart Attack
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
Also known as Myocardial infarction
What Is
A heart attack happens when the flow of oxygen-rich blood to a section of heart muscle suddenly becomes blocked and the heart can?t get oxygen. If blood flow isn?t restored quickly, the section of heart muscle begins to die.
Heart attack treatment works best when it?s given right after symptoms occur. If you think you or someone else is having a heart attack, even if you?re not sure, call 9?1?1 right away.
Overview
Heart attacks most often occur as a result of coronary heart disease (CHD), also called coronary artery disease. CHD is a condition in which a waxy substance called plaque builds up inside the coronary arteries. These arteries supply oxygen-rich blood to your heart.
When plaque builds up in the arteries, the condition is called atherosclerosis. The buildup of plaque occurs over many years.
Eventually, an area of plaque can rupture (break open) inside of an artery. This causes a blood clot to form on the plaque's surface. If the clot becomes large enough, it can mostly or completely block blood flow through a coronary artery.
If the blockage isn't treated quickly, the portion of heart muscle fed by the artery begins to die. Healthy heart tissue is replaced with scar tissue. This heart damage may not be obvious, or it may cause severe or long-lasting problems.
Heart With Muscle Damage and a Blocked Artery
Figure A is an overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. Figure B is a cross-section of the coronary artery with plaque buildup and a blood clot.
Figure A is an overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. Figure B is a cross-section of the coronary artery with plaque buildup and a blood clot.
A less common cause of heart attack is a severe spasm (tightening) of a coronary artery. The spasm cuts off blood flow through the artery. Spasms can occur in coronary arteries that aren't affected by atherosclerosis.
Heart attacks can be associated with or lead to severe health problems, such as heart failure and life-threatening arrhythmias.
Heart failure is a condition in which the heart can't pump enough blood to meet the body's needs. Arrhythmias are irregular heartbeats. Ventricular fibrillation is a life-threatening arrhythmia that can cause death if not treated right away.
Don't Wait--Get Help Quickly
Acting fast at the first sign of heart attack symptoms can save your life and limit damage to your heart. Treatment works best when it's given right after symptoms occur.
Many people aren't sure what's wrong when they are having symptoms of a heart attack. Some of the most common warning symptoms of a heart attack for both men and women are:
?Chest pain or discomfort. Most heart attacks involve discomfort in the center or left side of the chest. The discomfort usually lasts more than a few minutes or goes away and comes back. It can feel like pressure, squeezing, fullness, or pain. It also can feel like heartburn or indigestion.
?Upper body discomfort. You may feel pain or discomfort in one or both arms, the back, shoulders, neck, jaw, or upper part of the stomach (above the belly button).
?Shortness of breath. This may be your only symptom, or it may occur before or along with chest pain or discomfort. It can occur when you are resting or doing a little bit of physical activity.
Other possible symptoms of a heart attack include:
?Breaking out in a cold sweat
?Feeling unusually tired for no reason, sometimes for days (especially if you are a woman)
?Nausea (feeling sick to the stomach) and vomiting
?Light-headedness or sudden dizziness
?Any sudden, new symptom or a change in the pattern of symptoms you already have (for example, if your symptoms become stronger or last longer than usual)
Not all heart attacks begin with the sudden, crushing chest pain that often is shown on TV or in the movies, or other common symptoms such as chest discomfort. The symptoms of a heart attack can vary from person to person. Some people can have few symptoms and are surprised to learn they've had a heart attack. If you've already had a heart attack, your symptoms may not be the same for another one.
Quick Action Can Save Your Life: Call 9?1?1
If you think you or someone else may be having heart attack symptoms or a heart attack, don't ignore it or feel embarrassed to call for help. Call 9?1?1 for emergency medical care. Acting fast can save your life.
Do not drive to the hospital or let someone else drive you. Call an ambulance so that medical personnel can begin life-saving treatment on the way to the emergency room. Take a nitroglycerin pill if your doctor has prescribed this type of treatment.
Other Names
?Myocardial infarction (MI)
?Acute myocardial infarction (AMI)
?Acute coronary syndrome
?Coronary thrombosis
?Coronary occlusion
Atherosclerosis
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
Also known as Arteriosclerosis, Hardening of arteries
What Is
Atherosclerosis is a disease in which plaque builds up inside your arteries. Arteries are blood vessels that carry oxygen-rich blood to your heart and other parts of your body.
Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrows your arteries. This limits the flow of oxygen-rich blood to your organs and other parts of your body.
Atherosclerosis can lead to serious problems, including heart attack, stroke, or even death.
Atherosclerosis
Atherosclerosis diagram.Figure A shows a normal artery with normal blood flow. The inset image shows a cross-section of a normal artery. Figure B shows an artery with plaque buildup. The inset image shows a cross-section of an artery with plaque buildup.
Atherosclerosis-Related Diseases
Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms, legs, pelvis, and kidneys. As a result, different diseases may develop based on which arteries are affected.
Coronary Heart Disease
Coronary heart disease (CHD), also called coronary artery disease, occurs when plaque builds up in the coronary arteries. These arteries supply oxygen-rich blood to your heart.
Plaque narrows the coronary arteries and reduces blood flow to your heart muscle. Plaque buildup also makes it more likely that blood clots will form in your arteries. Blood clots can partially or completely block blood flow.
If blood flow to your heart muscle is reduced or blocked, you may have angina (chest pain or discomfort) or a heart attack.
Plaque also can form in the heart's smallest arteries. This disease is called coronary microvascular disease (MVD). In coronary MVD, plaque doesn't cause blockages in the arteries as it does in CHD.
Carotid Artery Disease
Carotid (ka-ROT-id) artery disease occurs if plaque builds up in the arteries on each side of your neck (the carotid arteries). These arteries supply oxygen-rich blood to your brain. If blood flow to your brain is reduced or blocked, you may have a stroke.
Peripheral Artery Disease
Peripheral artery disease (P.A.D.) occurs if plaque builds up in the major arteries that supply oxygen-rich blood to your legs, arms, and pelvis.
If blood flow to these parts of your body is reduced or blocked, you may have numbness, pain, and, sometimes, dangerous infections.
Chronic Kidney Disease
Chronic kidney disease can occur if plaque builds up in the renal arteries. These arteries supply oxygen-rich blood to your kidneys.
Over time, chronic kidney disease causes a slow loss of kidney function. The main function of the kidneys is to remove waste and extra water from the body.
Overview
The cause of atherosclerosis isn't known. However, certain traits, conditions, or habits may raise your risk for the disease. These conditions are known as risk factors.
You can control some risk factors, such as lack of physical activity, smoking, and an unhealthy diet. Others you can't control, such as age and a family history of heart disease.
Some people who have atherosclerosis have no signs or symptoms. They may not be diagnosed until after a heart attack or stroke.
The main treatment for atherosclerosis is lifestyle changes. You also may need medicines and medical procedures. These treatments, along with ongoing medical care, can help you live a healthier life.
Outlook
Improved treatments have reduced the number of deaths from atherosclerosis-related diseases. These treatments also have improved the quality of life for people who have these diseases. However, atherosclerosis remains a common health problem.
You may be able to prevent or delay atherosclerosis and the diseases it can cause. Making lifestyle changes and getting ongoing care can help you avoid the problems of atherosclerosis and live a long, healthy life.
Other Names
?Arteriosclerosis
?Hardening of the arteries
Cardiac Catheterization
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
Also known as Cardiac Cath
What Is Cardiac Catheterization?
Cardiac catheterization (KATH-eh-ter-ih-ZA-shun) is a medical procedure used to diagnose and treat some heart conditions.
A long, thin, flexible tube called a catheter is put into a blood vessel in your arm, groin (upper thigh), or neck and threaded to your heart. Through the catheter, your doctor can do diagnostic tests and treatments on your heart.
For example, your doctor may put a special type of dye in the catheter. The dye will flow through your bloodstream to your heart. Then, your doctor will take x-ray pictures of your heart. The dye will make your coronary (heart) arteries visible on the pictures. This test is called coronary angiography (an-jee-OG-rah-fee).
The dye can show whether a waxy substance called plaque (plak) has built up inside your coronary arteries. Plaque can narrow or block the arteries and restrict blood flow to your heart.
The buildup of plaque in the coronary arteries is called coronary heart disease (CHD) or coronary artery disease.
Doctors also can use ultrasound during cardiac catheterization to see blockages in the coronary arteries. Ultrasound uses sound waves to create detailed pictures of the heart's blood vessels.
Doctors may take samples of blood and heart muscle during cardiac catheterization or do minor heart surgery.
Cardiologists (heart specialists) usually do cardiac catheterization in a hospital. You're awake during the procedure, and it causes little or no pain. However, you may feel some soreness in the blood vessel where the catheter was inserted.
Cardiac catheterization rarely causes serious complications.
Cardiomyopathy
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
What Is
Cardiomyopathy refers to diseases of the heart muscle. These diseases have many causes, signs and symptoms, and treatments.
In cardiomyopathy, the heart muscle becomes enlarged, thick, or rigid. In rare cases, the muscle tissue in the heart is replaced with scar tissue.
As cardiomyopathy worsens, the heart becomes weaker. It's less able to pump blood through the body and maintain a normal electrical rhythm. This can lead to heart failure or irregular heartbeats called arrhythmias. In turn, heart failure can cause fluid to build up in the lungs, ankles, feet, legs, or abdomen.
The weakening of the heart also can cause other complications, such as heart valve problems.
Overview
The types of cardiomyopathy are:
?Hypertrophic cardiomyopathy
?Dilated cardiomyopathy
?Restrictive cardiomyopathy
?Arrhythmogenic right ventricular dysplasia
?Unclassified cardiomyopathy
Cardiomyopathy can be acquired or inherited. "Acquired" means you aren't born with the disease, but you develop it due to another disease, condition, or factor. "Inherited" means your parents passed the gene for the disease on to you. Many times, the cause of cardiomyopathy isn't known.
Cardiomyopathy can affect people of all ages. However, people in certain age groups are more likely to have certain types of cardiomyopathy. This article focuses on cardiomyopathy in adults.
Outlook
Some people who have cardiomyopathy have no signs or symptoms and need no treatment. For other people, the disease develops quickly, symptoms are severe, and serious complications occur.
Treatments for cardiomyopathy include lifestyle changes, medicines, surgery, implanted devices to correct arrhythmias, and a nonsurgical procedure. These treatments can control symptoms, reduce complications, and stop the disease from getting worse.
Other Names
Other Names for Dilated Cardiomyopathy
?Alcoholic cardiomyopathy. This term is used when overuse of alcohol causes the disease.
?Congestive cardiomyopathy.
?Diabetic cardiomyopathy.
?Familial dilated cardiomyopathy.
?Idiopathic cardiomyopathy.
?Ischemic cardiomyopathy. This term is used when coronary heart disease (also called coronary artery disease) or heart attack causes the disease.
?Peripartum cardiomyopathy. This term is used when the disease develops in a woman shortly before or after she gives birth.
?Primary cardiomyopathy.
Other Names for Hypertrophic Cardiomyopathy
?Asymmetric septal hypertrophy
?Familial hypertrophic cardiomyopathy
?Hypertrophic nonobstructive cardiomyopathy
?Hypertrophic obstructive cardiomyopathy
?Idiopathic hypertrophic subaortic stenosis
Other Names for Restrictive Cardiomyopathy
?Idiopathic restrictive cardiomyopathy
?Infiltrative cardiomyopathy
Other Names for Arrhythmogenic Right Ventricular Dysplasia
?Arrhythmogenic right ventricular cardiomyopathy
?Right ventricular cardiomyopathy
?Right ventricular dysplasia
Coronary Heart Disease
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
Also known as Coronary Artery Disease
What Is
Coronary heart disease (CHD) is a disease in which a waxy substance called plaque builds up inside the coronary arteries. These arteries supply oxygen-rich blood to your heart muscle.
When plaque builds up in the arteries, the condition is called atherosclerosis. The buildup of plaque occurs over many years.
Atherosclerosis
Figure A shows the location of the heart in the body. Figure B shows a normal coronary artery with normal blood flow. The inset image shows a cross-section of a normal coronary artery. Figure C shows a coronary artery narrowed by plaque. The buildup of plaque limits the flow of oxygen-rich blood through the artery. The inset image shows a cross-section of the plaque-narrowed artery.
Figure A shows the location of the heart in the body. Figure B shows a normal coronary artery with normal blood flow. The inset image shows a cross-section of a normal coronary artery. Figure C shows a coronary artery narrowed by plaque. The buildup of plaque limits the flow of oxygen-rich blood through the artery. The inset image shows a cross-section of the plaque-narrowed artery.
Over time, plaque can harden or rupture (break open). Hardened plaque narrows the coronary arteries and reduces the flow of oxygen-rich blood to the heart.
If the plaque ruptures, a blood clot can form on its surface. A large blood clot can mostly or completely block blood flow through a coronary artery. Over time, ruptured plaque also hardens and narrows the coronary arteries.
Overview
If the flow of oxygen-rich blood to your heart muscle is reduced or blocked, angina or a heart attack can occur.
Angina is chest pain or discomfort. It may feel like pressure or squeezing in your chest. The pain also can occur in your shoulders, arms, neck, jaw, or back. Angina pain may even feel like indigestion.
A heart attack occurs if the flow of oxygen-rich blood to a section of heart muscle is cut off. If blood flow isn?t restored quickly, the section of heart muscle begins to die. Without quick treatment, a heart attack can lead to serious health problems or death.
Over time, CHD can weaken the heart muscle and lead to heart failure and arrhythmias. Heart failure is a condition in which your heart can't pump enough blood to meet your body?s needs. Arrhythmias are problems with the rate or rhythm of the heartbeat.
Outlook
Lifestyle changes, medicines, and medical procedures can help prevent or treat coronary heart disease. These treatments may reduce the risk of related health problems.
Other Names
?Atherosclerosis
?Coronary artery disease
?Hardening of the arteries
?Heart disease
?Ischemic (is-KE-mik) heart disease
?Narrowing of the arteries
Coronary Heart Disease Risk Factors
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
What Are Coronary Heart Disease Risk Factors?
Coronary heart disease risk factors are conditions or habits that raise your risk of coronary heart disease (CHD) and heart attack. These risk factors also increase the chance that existing CHD will worsen.
CHD, also called coronary artery disease, is a condition in which a waxy substance called plaque (plak) builds up on the inner walls of the coronary arteries. These arteries supply oxygen-rich blood to your heart muscle.
Plaque narrows the arteries and reduces blood flow to your heart muscle. Reduced blood flow can cause chest pain, especially when you're active. Eventually, an area of plaque can rupture (break open). This causes a blood clot to form on the surface of the plaque.
If the clot becomes large enough, it can block the flow of oxygen-rich blood to the portion of heart muscle fed by the artery. Blocked blood flow to the heart muscle causes a heart attack.
Overview
There are many known CHD risk factors. You can control some risk factors, but not others. Risk factors you can control include:
?High blood cholesterol and triglyceride levels (a type of fat found in the blood)
?High blood pressure
?Diabetes and prediabetes
?Overweight and obesity
?Smoking
?Lack of physical activity
?Unhealthy diet
?Stress
The risk factors you can't control are age, gender, and family history of CHD.
Many people have at least one CHD risk factor. Your risk of CHD and heart attack increases with the number of risk factors you have and their severity. Also, some risk factors put you at greater risk of CHD and heart attack than others. Examples of these risk factors include smoking and diabetes.
Many risk factors for coronary heart disease start during childhood. This is even more common now because many children are overweight and don?t get enough physical activity.
Researchers continue to study and learn more about CHD risk factors.
Outlook
Following a healthy lifestyle can help you and your children prevent or control many CHD risk factors.
Because many lifestyle habits begin during childhood, parents and families should encourage their children to make heart healthy choices. For example, you and your children can lower your risk of CHD if you maintain a healthy weight, follow a healthy diet, do physical activity regularly, and don't smoke.
If you already have CHD, lifestyle changes can help you control your risk factors. This may prevent CHD from worsening. Even if you're in your seventies or eighties, a healthy lifestyle can lower your risk of dying from CHD.
If lifestyle changes aren't enough, your doctor may recommend other treatments to help control your risk factors.
Your doctor can help you find out whether you have CHD risk factors. He or she also can help you create a plan for lowering your risk of CHD, heart attack, and other heart problems.
If you have children, talk with their doctors about their heart health and whether they have CHD risk factors. If they do, ask your doctor to help create a treatment plan to reduce or control these risk factors.
