Cardiovascular Biomarkers: Pathophysiology and Disease Management

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For the purposes of this review, we will confine attention to analytes measurable in blood. We can be easily reminded of the deeply embedded nature of circulating biomarkers in CVD detection and management by thinking of blood glucose, haemoglobin A1c HbA1c , low-density lipoprotein LDL , high-density lipoprotein HDL , and total cholesterol, and how these biomarkers provide diagnostic information, risk stratification and guidance to life style interventions, and pharmacotherapy in diabetes and dyslipidaemia.

Beyond these traditional markers of risk and targets of treatment, we have two cardinal evidence-based, guideline-endorsed, and widely clinically applied markers; the cardiac troponins and the cardiac natriuretic peptides. The former are now essential to the definition and diagnosis of myocardial infarction and govern immediate management strategies with respect to need for early invasive intervention in non-ST elevation coronary syndromes. What are the present and future needs? Many markers will offer some value by filling in part of the background jigsaw puzzle of pathophysiology but most will never translate to applications in routine management.

New clinical markers must provide more information, in readily available and affordable fashion, than that available in current standard practice. Marker-based information must add substantially above and beyond that from already known markers and predictors and results need to be actionable in the context of evidence-based management.

If a marker result has no possible effect on clinical care or outcomes, then it has no place in clinical practice. The assays concerned must meet high standards of precision and accuracy. Markers should have a close and specific relationship to the condition of interest. Ideally markers should be intrinsically part of the pathological process under surveillance.

Dynamic markers that faithfully reflect progression or resolution and response to treatment, of the condition of interest, are of more value than marker characteristics that endow risk but cannot be altered such as genetic variants. Alongside our increasing ability to effectively react to, and manage, acute and chronic CVD, we need to attend to the community-dwelling population and find and apply markers that enhance our ability to conduct cost-effective screening for better detection of risk and prevention of CVD than is currently achieved.

Having defined the desirable traits of future markers, we can consider needs that are unmet by our current armamentarium of markers and note the merits or deficiencies of new candidate favourites. First, in acute disease, the cardiac troponins and the cardiac natriuretic peptides have revolutionized diagnosis and management of acute coronary syndromes and heart failure. The advent of highly sensitive assays for cardiac troponins I and T are accompanied by loss of specificity for acute myocardial infarction AMI.

Elevated plasma troponin in the Emergency Department is most frequently not associated with a type 1 myocardial infarction requiring urgent admission to the coronary care unit with immediate introduction of electrocardiographic monitoring, anti-coagulation, anti-platelet therapy, beta blockade, and consideration of early transfer to the cardiac catheterization laboratory for invasive coronary angiography and possible percutaneous intervention. About two-thirds of Emergency Department attendees considered in need of rule out of AMI who have elevated plasma cardiac troponins, ostensibly crossing the threshold for consideration of acute infarction, do not have that condition and should not undergo that sequence of treatments and tests.

Careful application of clinical acumen with consideration of the electrocardiogram ECG , the complete clinical picture and the absolute degree of troponin elevation will improve diagnostic accuracy but the need for improved marker options yielding greater specificity remains obvious.

Likewise, the performance of plasma B-type natriuretic peptide BNP concentrations in the diagnosis of acute heart failure is frequently confounded or complicated by the peptide elevating effects of atrial fibrillation, renal dysfunction, and increasing age and the peptide lowering influence of preserved ejection fraction and obesity. The specific subset of HFpEF has no current proven therapy.

Markers which aid in identifying pathways and targets amenable to novel and effective treatment in HFpEF will constitute a major advance. Literally hundreds of candidates are under investigation. Complicating this picture still further is the fact that elevations of plasma concentrations of cardiac troponin and the cardiac BNPs due to non-AMI and non-acute heart failure causes still confer adverse prognosis, but the optimal investigative and therapeutic responses to such abnormal results remain to be defined. The chronic treated phases of both heart failure and coronary disease are accompanied by residual excess risk compared with the population free of these conditions.

A Look at Emerging Cardiac Biomarkers | ifdoldana.tk

Both the B-type cardiac natriuretic peptides and cardiac troponins offer prognostic information in chronic heart failure but the systematic application of those markers in the chronic setting and their role if any in guiding changes in drug doses remains unclear and unproven. In the pre-morbid stages of disease Classes A and B heart failure and there are major unmet needs for markers to improve risk stratification and guide management.

Cardiovascular risk screening has applied a coarse-grained filter for generations. At middle age, recommended CV screening includes measurement of arterial pressure, body mass index, fasting blood glucose, HbA1c, LDL, HDL and total cholesterol, and consideration of presence or absence of diabetes, smoking status, and any family history of premature coronary artery disease. The consequences of this coarse and inaccurate risk assessment, in terms of resource use, inaccurate labelling of people as sick and in need of drug therapy and unnecessary dispensing and spending on pharmacotherapy, are obvious.

To more accurately identify those i destined to incur significant CVD and ii enjoy a good response to evidence-based therapy, we need vastly improved predictive tools. Can markers help? These markers measured in asymptomatic community-dwelling people were predictive of events independent of, and in addition to, consideration of conventional risk factors. Heart failure is the consequence of mechanical derangements of cardiac structure and function compounded and progressed by multi-facetted pathophysiology. The vicious cycles of pathophysiology in heart failure include contributions from at least 6 major axes: i inflammation, ii oxidative stress, iii neurohormonal activation, iv renal dysfunction, v cardiomyocyte injury, and vi matrix remodelling Figure 1.

The prototype markers of cardiac mechanical stretch and neurohormonal activation are the cardiac natriuretic peptides. The chief marker of cardiac cellular injury is cardiac troponin. These markers are in use and their established and potential applications in chronic disease and in preventive strategies ensure they will remain favourites for the foreseeable future. They are unlikely to be replaced but, as already discussed, there is ample need for supplementary markers. The natural history of many forms of evolving CVD involves persistent inflammation and oxidative stress with consequent cardiac interstitial fibrosis.

Chronic inflammation, oxidative stress, and interstitial fibrosis are key mechanisms in many forms and stages of CVD but, unlike cardiac injury or stretch, they are not yet reliably reflected by markers in routine clinical use and, at our current state of knowledge, any marker-based assessment of these pathophysiologies has no proven evidence-based therapeutic response.

After due validation it will be used to i assess severity and monitor progression of chronic disease hypertension, cardiomyopathy, cardiac valve disease, toxic cardiomyopathies, and all chronic heart failure from early to late stage, ii to monitor novel therapies and iii it is likely to become a valid surrogate endpoint for therapeutic trials of experimental therapies. New technologies enable extensive screening for markers in any given CVD. Markers can now be sought in whole blood, selected circulating cell types, plasma, serum, or in particular sub-fractions of the circulation such as populations of extracellular vesicles including exosomes.

With our new access to this expanding universe of candidates it is only a matter of time before powerful new markers, or panels of markers, are discovered and applied to improve monitoring and management of CVD. Pathophysiological pathways in heart failure and associated exemplar candidate circulating biomarkers.

Major pathways labelled in bold within blue boxes. Exemplar circulating biomarkers in standard font in black boxes. With permission, adapted from Braunwald E. Heart Failure.

Understanding Heart Disease Risk: Advanced Cardiac Biomarkers in Naturopathic Practice

Figure 7. Several are accepted as offering independent information on disease severity and prognosis, but the biomedical community considers there is still a need to further evaluate their proper role in guiding therapy. Circulating extracellular vesicles are under increasing scrutiny for possible CV biomarker applications. These bilayer membrane vesicles include and array of particles ranging from microparticles, and microvesicles, to exosomes. They may reflect disease processes in their tissues of origin. With its immediate connection to cellular events, metabolomics has considerable allure as a possible source of useful biomarkers.

A prospective study comparing and combining both troponin and metabolites in suspected AMI is needed. Product details Format Hardback pages Dimensions x x Illustrations note Illustrations, black and white; p.

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Other books in this series. Essentials of Bedside Cardiology Jules Constant. Add to basket. Cardiovascular Hemodynamics Michael D. Cardiac Drug Therapy M. Cardiovascular Genomics Mohan K. Cardiac Repolarization Ihor Gussak.

Cardiovascular Biomarkers : Pathophysiology and Disease Management

Interventional Cardiology Howard C. Valvular Heart Disease Andrew Wang. Principles of Molecular Cardiology Marschall S. Annotated Atlas of Electrocardiography Thomas M. Cardiopulmonary Resuscitation Joseph P. Platelet Function Martin Quinn. Preventive Cardiology Joanne Micale Foody. Management of Acute Pulmonary Embolism S. Back cover copy So rapidly has the number of cardiac assays available grown, and then improved, that current biomarkers not only diagnose cardiovascular disease, but also frame treatment strategies.

In Cardiovascular Biomarkers: Pathophysiology and Disease Management, a distinguished panel of internationally recognized opinion makers and experts in clinical and laboratory medicine synthesize the latest developments in the use of cardiac biomarkers by the practicing physician. The authors focus on integrating biomarkers into the contemporary clinical management of patients with cardiovascular disease, emphasizing clinical studies, evidence-based diagnostic algorithms, and critical pathways for triage and therapy, whenever available.

They also illuminate the connections between specific biomarkers and the basic pathophysiology of cardiovascular disease, explain the analytical properties of the assays relevant to clinical practice, and highlight emerging biomarkers and novel directions for biomarker development. Numerous figures, illustrations, and tables make key evidence and practical guidelines easily accessible. Authors' Disclosures or Potential Conflicts of Interest: Upon manuscript submission, all authors completed the author disclosure form. Employment or Leadership: F. Cullen, G.

Felker, G. Ginsburg, and D. Consultant or Advisory Role: F. Cullen, Abbott Diagnostics and Siemens; G. Ginsburg, Cardiodx; D. Honoraria: F.

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Apple , Louise Cullen , G. DOI: Duke University, Durham, NC;.

Utility of Biomarkers in Contemporary Management of Chronic Heart Failure

Louise Cullen. Michael Felker. Trend in the leading causes of death, by sex: US, [Heron 1 ]. CLRD, chronic lower respiratory diseases. Cardiovascular biomarker publications, — Geoffrey Ginsburg. David Morrow.