Page 326 - ONLINE PROCEEDING BOOK WSAVA 2017
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An Urban Experience
WSVA7-0376
CARDIOLOGY II
BIOMARKERS IN SMALL ANIMAL CARDIOVASCULAR MEDICINE
I. Ljungvall1 1Sweden
BIOMARKERS IN SMALL ANIMAL CARDIOVASCULAR MEDICINE
Ingrid Ljungvall
Associate Professor, DVM, PhD
Department of Clinical Sciences, Faculty of Veterinary Medicine and Animal Science, Swedish University of Agricultural Sciences, Uppsala, Sweden
Ingrid.ljungvall@slu.se
Introduction
Myocardial remodelling occurrs in response to primary cardiac or extra-cardiac diseases, and can stimulate release of various circulating biomarkers. The potential of using these markers for diagnosing and monitoring dogs and cats with cardiac diseases in clinical practice has over the last years gained interest. Different biomarkers can provide information about different aspects of cardiovascular diseases: Some cardiac biomarkers
will, at best, “only” have value for understanding pathophysiological aspects of heart disease, whereas others have a value in improving clinical management of patients. A combination of biomarkers (a so-called “multimarker” approach) has the potential to further improve assessment/handling of the individual cardiac patient: Each included marker can provide slightly different information from the pathologic features of the heart disease, and the combination of results can provide more information than one marker alone. The use of multimarker techniques is already widely used in veterinary medicine (such as a “hepatic panel”), and in the future we might also use such strategies for our cardiac patiens.
This presentation will focus on cardiac troponin I (cTnI) and N-terminal pro-B-type natriuretic peptide (NT- proBNP), which are the circulating cardiac biomarkers most extensively investigated, and for which evidence exists for a value in the clinical situation
Natriuretic peptides
During progression of heart disease, complex neuroendocrine activation takes place in order to maintain cardiac output and adequate tissue perfusion. Important mechanisms include up-regulation of
the sympathetic nervous system and the renin- angiotensin-aldosterone system (RAAS). Although
these compensatory mechanisms initially improve cardiovascular function, their activity leads to gradually increased peripheral vascular resistance and  uid retention with detoriation of myocardial function and promotion of adverse myocardial remodelling. Natriuretic peptides are produced and secreted into the plasma in response to volume expansion and pressure overload
in the myocardial wall, but also in response to other stimuli such as angiotension II and endothelin-1. B-type natriuretic peptide (BNP) is the natriuretic peptide that has been most intensively studied in recent years.
BNP is constitutively synthesized as high molecular weight precursors (proBNP) in atrial myocytes and
small amounts of proBNP are intracellularly stored in membrane-bound granules for later release. Increased release requires increased synthesis (in response to stretching of myocardial walls), and in patients with myocardial disease, the major site of BNP production may then switch from the atria to the ventricles. In response to stress, proBNP is cleaved into two smaller peptides, which are released into plasma: One low molecular weight, biologically active segment in the C-terminal region (C-BNP), and one biologically inactive N-terminal segment (NT-proBNP). The bioactive C-BNP of each peptide is released in equimolar quantity to
the inactive NT-proBNP. Due to the longer half-lives of inactive segments, in addition to that C-BNP is regarded as more sensitive to collection and storage methods, NT-proBNP is regarded as the more reliable analyte for diagnostic use.
The principal physiologic actions of BNP generally oppose those exerted by the RAAS and the sympathetic nervous system in order to protect the cardiovascular system from volume overload: Natriuresis and diuresis are induced by inhibited tubular sodium transport in the renal medullary-collecting ducts and suppression of renin release by the kidney and aldosterone release from the adrenal cortex. Additional action include vasorelaxation of systemic and pulmonary arterioles; leading to decreased systemic and pulmonic vascular resistance.
Plasma NT-proBNP concentrations correlate with pulmonary capillary wedge pressure, which is an indirect measurement of left atrial pressure. This is of value in
a clinical situation as the left atrial pressure increase
with increasing left sided cardiac volume overload. NT-proBNP has been established as an important biomarker in diagnosing and prognosticating congestive heart failure (CHF) in people, and NT-proBNP is also considered important in early detection of ventricular dysfunction. Results from different studies in dogs and cats indicate that increased NT-proBNP concentration can distinguish cats and dogs with CHF from those with noncardiac causes of dyspnea with a rather high degree
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42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS


































































































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