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Results: 1 to 10 of 240

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Autonomic Nervous System in Pulmonary Arterial Hypertension: Time to Rest and Digest.
Hemnes AR, Brittain EL
(2018) Circulation 137: 925-927
Added June 7, 2018
0 Communities
1 Members
0 Resources
0 MeSH Terms
Grounding Cardio-Oncology in Basic and Clinical Science.
Moslehi J, Amgalan D, Kitsis RN
(2017) Circulation 136: 3-5
Added December 2, 2017
0 Communities
1 Members
0 Resources
0 MeSH Terms
Loss of Cardioprotective Effects at theLocus as a Result of Gene-Smoking Interactions.
Saleheen D, Zhao W, Young R, Nelson CP, Ho W, Ferguson JF, Rasheed A, Ou K, Nurnberg ST, Bauer RC, Goel A, Do R, Stewart AFR, Hartiala J, Zhang W, Thorleifsson G, Strawbridge RJ, Sinisalo J, Kanoni S, Sedaghat S, Marouli E, Kristiansson K, Hua Zhao J, Scott R, Gauguier D, Shah SH, Smith AV, van Zuydam N, Cox AJ, Willenborg C, Kessler T, Zeng L, Province MA, Ganna A, Lind L, Pedersen NL, White CC, Joensuu A, Edi Kleber M, Hall AS, März W, Salomaa V, O'Donnell C, Ingelsson E, Feitosa MF, Erdmann J, Bowden DW, Palmer CNA, Gudnason V, Faire U, Zalloua P, Wareham N, Thompson JR, Kuulasmaa K, Dedoussis G, Perola M, Dehghan A, Chambers JC, Kooner J, Allayee H, Deloukas P, McPherson R, Stefansson K, Schunkert H, Kathiresan S, Farrall M, Marcel Frossard P, Rader DJ, Samani NJ, Reilly MP
(2017) Circulation 135: 2336-2353
MeSH Terms: ADAMTS7 Protein, Adult, Aged, Aged, 80 and over, Cells, Cultured, Coronary Disease, Coronary Vessels, Female, Gene-Environment Interaction, Genetic Loci, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Smoking
Show Abstract · Added June 6, 2017
BACKGROUND - Common diseases such as coronary heart disease (CHD) are complex in etiology. The interaction of genetic susceptibility with lifestyle factors may play a prominent role. However, gene-lifestyle interactions for CHD have been difficult to identify. Here, we investigate interaction of smoking behavior, a potent lifestyle factor, with genotypes that have been shown to associate with CHD risk.
METHODS - We analyzed data on 60 919 CHD cases and 80 243 controls from 29 studies for gene-smoking interactions for genetic variants at 45 loci previously reported to be associated with CHD risk. We also studied 5 loci associated with smoking behavior. Study-specific gene-smoking interaction effects were calculated and pooled using fixed-effects meta-analyses. Interaction analyses were declared to be significant at avalue of <1.0×10(Bonferroni correction for 50 tests).
RESULTS - We identified novel gene-smoking interaction for a variant upstream of thegene. Every T allele of rs7178051 was associated with lower CHD risk by 12% in never-smokers (=1.3×10) in comparison with 5% in ever-smokers (=2.5×10), translating to a 60% loss of CHD protection conferred by this allelic variation in people who smoked tobacco (interactionvalue=8.7×10). The protective T allele at rs7178051 was also associated with reducedexpression in human aortic endothelial cells and lymphoblastoid cell lines. Exposure of human coronary artery smooth muscle cells to cigarette smoke extract led to induction ofCONCLUSIONS: Allelic variation at rs7178051 that associates with reducedexpression confers stronger CHD protection in never-smokers than in ever-smokers. Increased vascularexpression may contribute to the loss of CHD protection in smokers.
© 2017 American Heart Association, Inc.
0 Communities
1 Members
0 Resources
16 MeSH Terms
Response by Hubers and Brown to Letter Regarding Article, "Combined Angiotensin Receptor Antagonism and Neprilysin Inhibition".
Hubers SA, Brown NJ
(2016) Circulation 134: e11-2
MeSH Terms: Aminobutyrates, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Heart Failure, Humans, Neprilysin, Receptors, Angiotensin, Tetrazoles
Added April 6, 2017
0 Communities
1 Members
0 Resources
8 MeSH Terms
Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Risk Score in Young Adults Predicts Coronary Artery and Abdominal Aorta Calcium in Middle Age: The CARDIA Study.
Gidding SS, Rana JS, Prendergast C, McGill H, Carr JJ, Liu K, Colangelo LA, Loria CM, Lima J, Terry JG, Reis JP, McMahan CA
(2016) Circulation 133: 139-46
MeSH Terms: Adolescent, Adult, Age of Onset, Aorta, Abdominal, Aortic Diseases, Atherosclerosis, Calcinosis, Coronary Disease, Follow-Up Studies, Humans, Middle Aged, Odds Ratio, Prognosis, Risk, Risk Assessment, Risk Factors, Severity of Illness Index, United States, Young Adult
Show Abstract · Added September 29, 2016
BACKGROUND - We explored whether, the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) coronary and abdominal risk scores measured at 18 to 30 years of age and changes in these scores would more strongly predict coronary artery calcium (CAC) and abdominal aortic calcium (AAC) assessed 25 years later, than scores measured 25 years later.
METHODS AND RESULTS - In the Coronary Artery Risk Development in Young Adults (CARDIA) study, 3008 participants had measurements of risk score components at 5-year intervals beginning at 18 to 30 years of age. CAC and AAC were assessed at 43 to 55 years of age. Odds ratios (ORs) for the presence and extent of CAC/AAC per/point higher score and c-statistics for predicting CAC/AAC were calculated. The prevalence of CAC was 28% and AAC was 53%. For each 1 point higher PDAY score, the odds of CAC were higher using baseline scores than year 25 scores (OR, 1.29; 95% confidence interval [CI], 1.25-1.33 versus OR, 1.12; 95% CI, 1.11-1.14). For AAC, ORs at years 0 and 25 were similar (OR, 1.29; 95% CI, 1.24-1.34 versus OR, 1.22; 95% CI, 1.19-1.26). C-statistic for CAC prediction was higher at year 0 than year 25 (0.731 versus 0.705) but similar at years 0 and 25 for AAC (0.665 versus 0.670). ORs for CAC were highest at baseline, and, for AAC, ORs were highest at year 10. Including change in PDAY scores with baseline scores improved prediction.
CONCLUSIONS - Atherosclerosis risk and change in risk assessed in young adulthood years before subclinical atherosclerosis imaging provide strong prediction of future subclinical atherosclerosis. CAC and AAC reflect chronic risk exposure in addition to risk measured at the time of study.
© 2015 American Heart Association, Inc.
0 Communities
2 Members
0 Resources
19 MeSH Terms
Fatty Acid Metabolic Defects and Right Ventricular Lipotoxicity in Human Pulmonary Arterial Hypertension.
Brittain EL, Talati M, Fessel JP, Zhu H, Penner N, Calcutt MW, West JD, Funke M, Lewis GD, Gerszten RE, Hamid R, Pugh ME, Austin ED, Newman JH, Hemnes AR
(2016) Circulation 133: 1936-44
MeSH Terms: Animals, Ceramides, Cohort Studies, Fatty Acids, Humans, Hypertension, Pulmonary, Mice, Mice, Transgenic, Prospective Studies, Triglycerides, Ventricular Dysfunction, Right
Show Abstract · Added April 22, 2016
BACKGROUND - The mechanisms of right ventricular (RV) failure in pulmonary arterial hypertension (PAH) are poorly understood. Abnormalities in fatty acid (FA) metabolism have been described in experimental models of PAH, but systemic and myocardial FA metabolism has not been studied in human PAH.
METHODS AND RESULTS - We used human blood, RV tissue, and noninvasive imaging to characterize multiple steps in the FA metabolic pathway in PAH subjects and controls. Circulating free FAs and long-chain acylcarnitines were elevated in PAH patients versus controls. Human RV long-chain FAs were increased and long-chain acylcarnitines were markedly reduced in PAH versus controls. With the use of proton magnetic resonance spectroscopy, in vivo myocardial triglyceride content was elevated in human PAH versus controls (1.4±1.3% triglyceride versus 0.22±0.11% triglyceride, P=0.02). Ceramide, a mediator of lipotoxicity, was increased in PAH RVs versus controls. Using an animal model of heritable PAH, we demonstrated reduced FA oxidation via failure of palmitoylcarnitine to stimulate oxygen consumption in the PAH RV.
CONCLUSIONS - Abnormalities in FA metabolism can be detected in the blood and myocardium in human PAH and are associated with in vivo cardiac steatosis and lipotoxicity. Murine data suggest that lipotoxicity may arise from reduction in FA oxidation.
© 2016 American Heart Association, Inc.
0 Communities
3 Members
0 Resources
11 MeSH Terms
Combined Angiotensin Receptor Antagonism and Neprilysin Inhibition.
Hubers SA, Brown NJ
(2016) Circulation 133: 1115-24
MeSH Terms: Abnormalities, Drug-Induced, Aminobutyrates, Angioedema, Angiotensin Receptor Antagonists, Biphenyl Compounds, Bradykinin, Contraindications, Drug Combinations, Drug Costs, Drug Synergism, Enalapril, Enzyme Inhibitors, Female, Follow-Up Studies, Heart Failure, Humans, Hyperkalemia, Hypertension, Kidney, Multicenter Studies as Topic, Natriuretic Peptides, Neprilysin, Pregnancy, Prodrugs, Prospective Studies, Pyridines, Randomized Controlled Trials as Topic, Stroke Volume, Tetrazoles, Thiazepines, Valsartan
Show Abstract · Added April 6, 2017
Heart failure affects ≈5.7 million people in the United States alone. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, β-blockers, and aldosterone antagonists have improved mortality in patients with heart failure and reduced ejection fraction, but mortality remains high. In July 2015, the US Food and Drug Administration approved the first of a new class of drugs for the treatment of heart failure: Valsartan/sacubitril (formerly known as LCZ696 and currently marketed by Novartis as Entresto) combines the angiotensin receptor blocker valsartan and the neprilysin inhibitor prodrug sacubitril in a 1:1 ratio in a sodium supramolecular complex. Sacubitril is converted by esterases to LBQ657, which inhibits neprilysin, the enzyme responsible for the degradation of the natriuretic peptides and many other vasoactive peptides. Thus, this combined angiotensin receptor antagonist and neprilysin inhibitor addresses 2 of the pathophysiological mechanisms of heart failure: activation of the renin-angiotensin-aldosterone system and decreased sensitivity to natriuretic peptides. In the Prospective Comparison of ARNI With ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) trial, valsartan/sacubitril significantly reduced mortality and hospitalization for heart failure, as well as blood pressure, compared with enalapril in patients with heart failure, reduced ejection fraction, and an elevated circulating level of brain natriuretic peptide or N-terminal pro-brain natriuretic peptide. Ongoing clinical trials are evaluating the role of valsartan/sacubitril in the treatment of heart failure with preserved ejection fraction and hypertension. We review here the mechanisms of action of valsartan/sacubitril, the pharmacological properties of the drug, and its efficacy and safety in the treatment of heart failure and hypertension.
© 2016 American Heart Association, Inc.
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1 Members
0 Resources
31 MeSH Terms
Cardiovascular Complications of Novel Multiple Myeloma Treatments.
Li W, Cornell RF, Lenihan D, Slosky D, Jagasia M, Piazza G, Moslehi J
(2016) Circulation 133: 908-12
MeSH Terms: Aged, Antineoplastic Combined Chemotherapy Protocols, Cardiovascular Diseases, Female, Humans, Multiple Myeloma, Treatment Outcome
Added March 6, 2016
0 Communities
1 Members
0 Resources
7 MeSH Terms
Cardiovascular Effects of Androgen Deprivation Therapy for the Treatment of Prostate Cancer: ABCDE Steps to Reduce Cardiovascular Disease in Patients With Prostate Cancer.
Bhatia N, Santos M, Jones LW, Beckman JA, Penson DF, Morgans AK, Moslehi J
(2016) Circulation 133: 537-41
MeSH Terms: Aged, Androgen Antagonists, Aspirin, Blood Pressure, Cardiovascular Diseases, Cholesterol, Diabetes Mellitus, Exercise, Humans, Male, Prostatic Neoplasms, Treatment Outcome
Added February 4, 2016
0 Communities
2 Members
0 Resources
12 MeSH Terms
Cardio-Oncology: How New Targeted Cancer Therapies and Precision Medicine Can Inform Cardiovascular Discovery.
Bellinger AM, Arteaga CL, Force T, Humphreys BD, Demetri GD, Druker BJ, Moslehi JJ
(2015) Circulation 132: 2248-58
MeSH Terms: Animals, Antineoplastic Agents, Cardiovascular Diseases, Drug Delivery Systems, Drug Discovery, Humans, Molecular Targeted Therapy, Neoplasms, Precision Medicine, Protein Kinase Inhibitors
Show Abstract · Added March 6, 2016
Cardio-oncology (the cardiovascular care of cancer patients) has developed as a new translational and clinical field based on the expanding repertoire of mechanism-based cancer therapies. Although these therapies have changed the natural course of many cancers, several may also lead to cardiovascular complications. Many new anticancer drugs approved over the past decade are "targeted" kinase inhibitors that interfere with intracellular signaling contributing to tumor progression. Unexpected cardiovascular and cardiometabolic effects of patient treatment with these inhibitors have provided unique insights into the role of kinases in human cardiovascular biology. Today, an ever-expanding number of cancer therapies targeting novel kinases and other specific cellular and metabolic pathways are being developed and tested in oncology clinical trials. Some of these drugs may affect the cardiovascular system in detrimental ways and others perhaps in beneficial ways. We propose that the numerous ongoing oncology clinical trials are an opportunity for closer collaboration between cardiologists and oncologists to study the cardiovascular and cardiometabolic changes caused by the modulation of these pathways in patients. In this regard, cardio-oncology represents an opportunity and a novel platform for basic and translational investigation and can serve as a potential avenue for optimization of anticancer therapies and for cardiovascular research and drug discovery.
© 2015 American Heart Association, Inc.
0 Communities
1 Members
0 Resources
10 MeSH Terms