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Aortic stenosis is the narrowing of the exit of the left ventricle of the heart, such that problems result. It may occur at the aortic valve as well as above and below this level. It typically gets worse over time. Symptoms often come on gradually with a decreased ability to exercise often occurring first. If heart failure, loss of consciousness, or heart related chest pain occur due to AS the outcomes are worse. Loss of consciousness typically occurs with standing or exercising. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the legs. Thickening of the valve without causing obstruction is known as aortic sclerosis.
Heart failure (HF), also known as congestive heart failure (CHF), is a syndrome, a group of signs and symptoms, caused by an impairment of the heart's blood pumping function. Symptoms typically include shortness of breath, excessive fatigue, and leg swelling. The shortness of breath may occur with exertion or while lying down, and may wake people up during the night. The severity of the heart failure is mainly decided based on ejection fraction and also measured by the severity of symptoms. Other conditions that may have symptoms similar to heart failure include obesity, kidney failure, liver disease, anemia, and thyroid disease.
Echocardiography, also known as cardiac ultrasound, is the use of ultrasound to examine the heart. It is a type of medical imaging, using standard ultrasound or Doppler ultrasound. The visual image formed using this technique is called an echocardiogram, a cardiac echo, or simply an echo.
Atrial Natriuretic Peptide (ANP) or atrial natriuretic factor (ANF) is a natriuretic peptide hormone secreted from the cardiac atria that in humans is encoded by the NPPA gene. Natriuretic peptides are a family of hormone/paracrine factors that are structurally related. The main function of ANP is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume.
Hypertrophic cardiomyopathy is a condition in which muscle tissues of the heart become thickened without an obvious cause. The parts of the heart most commonly affected are the interventricular septum and the ventricles. This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems. Specifically, within the bundle branches that conduct impulses through the interventricular septum and into the Purkinje fibers, as these are responsible for the depolarization of contractile cells of both ventricles.
Diastole is the relaxed phase of the cardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.
Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.
Bicuspid aortic valve (BAV) is a form of heart disease in which two of the leaflets of the aortic valve fuse during development in the womb resulting in a two-leaflet (bicuspid) valve instead of the normal three-leaflet (tricuspid) valve. BAV is the most common cause of heart disease present at birth and affects approximately 1.3% of adults. Normally, the mitral valve is the only bicuspid valve and this is situated between the heart's left atrium and left ventricle. Heart valves play a crucial role in ensuring the unidirectional flow of blood from the atrium to the ventricles, or from the ventricle to the aorta or pulmonary trunk. BAV is normally inherited.
Cardiac markers are biomarkers measured to evaluate heart function. They can be useful in the early prediction or diagnosis of disease. Although they are often discussed in the context of myocardial infarction, other conditions can lead to an elevation in cardiac marker level.
Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.
Valvular heart disease is any cardiovascular disease process involving one or more of the four valves of the heart. These conditions occur largely as a consequence of aging, but may also be the result of congenital (inborn) abnormalities or specific disease or physiologic processes including rheumatic heart disease and pregnancy.
Aortic valvuloplasty, also known as balloon aortic valvuloplasty (BAV), is a procedure used to improve blood flow through the aortic valve in conditions that cause aortic stenosis, or narrowing of the aortic valve. It can be performed in various patient populations including fetuses, newborns, children, adults, and pregnant women. The procedure involves using a balloon catheter to dilate the narrowed aortic valve by inflating the balloon.
Transcatheter aortic valve implantation (TAVI) is the implantation of the aortic valve of the heart through the blood vessels without actual removal of the native valve. The first TAVI was performed on 16 April 2002 by Alain Cribier, which became a new alternative in the management of high-risk patients with severe aortic stenosis. The implantated valve is delivered via one of several access methods: transfemoral, transapical, subclavian, direct aortic, and transcaval, among others.
Troponin T is a part of the troponin complex, which are proteins integral to the contraction of skeletal and heart muscles. They are expressed in skeletal and cardiac myocytes. Troponin T binds to tropomyosin and helps position it on actin, and together with the rest of the troponin complex, modulates contraction of striated muscle. The cardiac subtype of troponin T is especially useful in the laboratory diagnosis of heart attack because it is released into the blood-stream when damage to heart muscle occurs. It was discovered by the German physician Hugo A. Katus at the University of Heidelberg, who also developed the troponin T assay.
A natriuretic peptide is a hormone molecule that plays a crucial role in the regulation of the cardiovascular system. These hormones were first discovered in the 1980s and were found to have very strong diuretic, natriuretic, and vasodilatory effects. There are three main types of natriuretic peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). Two minor hormones include Urodilatin (URO) which is processed in the kidney and encoded by the same gene as ANP, and Dendroaspis NP (DNP) that was discovered through isolation of the venom from the green mamba snake. Since they are activated during heart failure, they are important for the protection of the heart and its tissues.
The ST2 cardiac biomarker is a protein biomarker of cardiac stress encoded by the IL1RL1 gene. ST2 signals the presence and severity of adverse cardiac remodeling and tissue fibrosis, which occurs in response to myocardial infarction, acute coronary syndrome, or worsening heart failure.
Cardiorenal syndrome (CRS) is an umbrella term used in the medical field that defines disorders of the heart and kidneys whereby "acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other". When one of these organs fails, the other may subsequently fail. The heart and the kidneys are involved in maintaining hemodynamic stability and organ perfusion through an intricate network. Patients who have renal failure first may be hard to determine if heart failure is concurrent. These two organs communicate with one another through a variety of pathways in an interdependent relationship. In a 2004 report from the National Heart, Lung and Blood Institute, CRS was defined as a condition where treatment of congestive heart failure is limited by decline in kidney function. This definition has since been challenged repeatedly but there still remains little consensus over a universally accepted definition for CRS. At a consensus conference of the Acute Dialysis Quality Initiative (ADQI), the CRS was classified into five subtypes primarily based upon the organ that initiated the insult as well as the acuity of disease.
Copeptin is a 39-amino acid-long peptide derived from the C-terminus of pre-pro-hormone of arginine vasopressin, neurophysin II and copeptin. Arginine vasopressin (AVP), also known as the antidiuretic hormone (ADH), is encoded by the AVP gene and is involved in multiple cardiovascular and renal pathways and abnormal level of AVP are associated with various diseases. Hence measurement of AVP would be useful, but is not commonly carried out in clinical practice because of its very short half-life making it difficult to quantify. In contrast, copeptin can be immunologically tested with ease and therefore can be used as a vasopressin surrogate marker.
Brain natriuretic peptide 32 (BNP), also known as B-type natriuretic peptide, is a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume. BNP is one of the three natriuretic peptides, in addition to ANP and CNP.
Arthur Mark Richards is a New Zealand physician, academic and medical researcher. He is a professor of cardiology and director of the Cardiovascular Research Institute at the National University of Singapore, and a professor of medicine and founder of the Christchurch Heart Institute at the University of Otago, Christchurch, New Zealand, where he holds the National Heart Foundation (NZ) Chair of Cardiovascular Studies.
References
- ↑ Bhalla V, Willis S, Maisel AS (2004). "B-type natriuretic peptide: the level and the drug--partners in the diagnosis of congestive heart failure". Congestive Heart Failure. 10 (1 Suppl 1): 3–27. doi: 10.1111/j.1527-5299.2004.03310.x . PMID 14872150.
- ↑ Atisha D, Bhalla MA, Morrison LK, Felicio L, Clopton P, Gardetto N, et al. (September 2004). "A prospective study in search of an optimal B-natriuretic peptide level to screen patients for cardiac dysfunction". American Heart Journal. 148 (3): 518–523. doi:10.1016/j.ahj.2004.03.014. PMID 15389242.
- ↑ Nakamura T, Sakamoto K, Yamano T, Kikkawa M, Zen K, Hikosaka T, et al. (May 2002). "Increased plasma brain natriuretic peptide level as a guide for silent myocardial ischemia in patients with non-obstructive hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 39 (10): 1657–1663. doi: 10.1016/s0735-1097(02)01813-2 . PMID 12020494.
- ↑ Talwar S, Squire IB, Downie PF, Davies JE, Ng LL (October 2000). "Plasma N terminal pro-brain natriuretic peptide and cardiotrophin 1 are raised in unstable angina". Heart. 84 (4): 421–424. doi:10.1136/heart.84.4.421. PMC 1729429 . PMID 10995414.
- ↑ Kim H, Yang DH, Park Y, Han J, Lee H, Kang H, et al. (November 2006). "Incremental prognostic value of C-reactive protein and N-terminal proB-type natriuretic peptide in acute coronary syndrome". Circulation Journal. 70 (11): 1379–1384. doi: 10.1253/circj.70.1379 . PMID 17062957.
- ↑ Ruwald MH, Goetze JP, Bech J, Nielsen OW, Madsen BK, Nielsen LB, et al. (January 2014). "NT-ProBNP independently predicts long-term mortality in patients admitted for coronary angiography". Angiology. 65 (1): 31–36. doi:10.1177/0003319712462758. PMID 23070682. S2CID 33475819.
- 1 2 Hadziselimovic E, Greve AM, Sajadieh A, Olsen MH, Kesäniemi YA, Nienaber CA, et al. (April 2022). "Association of Annual N-Terminal Pro-Brain Natriuretic Peptide Measurements With Clinical Events in Patients With Asymptomatic Nonsevere Aortic Stenosis: A Post Hoc Substudy of the SEAS Trial". JAMA Cardiology. 7 (4): 435–444. doi:10.1001/jamacardio.2021.5916. PMC 8851368 . PMID 35171199.
- ↑ "N-terminal-pro-BNP". LABORATORY SERVICES HANDBOOK. The University of Iowa (UIHC), Department of Pathology. 28 May 2020. Archived from the original on 2008-10-11. Showing 95th percentiles. Epic Lab Code: LAB649.
- 1 2 Lee MA (2009). Basic Skills in Interpreting Laboratory Data. Amer Soc of Health System. p. 220. ISBN 978-1-58528-180-0.
- ↑ Maisel AS, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, Duc P, et al. (July 2002). "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure". The New England Journal of Medicine. 347 (3): 161–167. doi: 10.1056/NEJMoa020233 . PMID 12124404.
- 1 2 3 Moses EJ, Mokhtar SA, Hamzah A, Abdullah BS, Yusoff NM (2011). "Usefulness of N-Terminal-Pro-B-Type Natriuretic Peptide as a Screening Tool for Identifying Pediatric Patients With Congenital Heart Disease". Laboratory Medicine. 42 (2): 75–80. doi: 10.1309/LMW0U87COTHXGELF .
- ↑ Hadziselimovic E, Greve AM, Sajadieh A, Olsen MH, Kesäniemi YA, Nienaber CA, et al. (April 2022). "Association of Annual N-Terminal Pro-Brain Natriuretic Peptide Measurements With Clinical Events in Patients With Asymptomatic Nonsevere Aortic Stenosis: A Post Hoc Substudy of the SEAS Trial". JAMA Cardiology. 7 (4): 435–444. doi:10.1001/jamacardio.2021.5916. PMC 8851368 . PMID 35171199.
- ↑ Bergler-Klein J, Klaar U, Heger M, Rosenhek R, Mundigler G, Gabriel H, Binder T, Pacher R, Maurer G, Baumgartner H (2004-05-18). "Natriuretic Peptides Predict Symptom-Free Survival and Postoperative Outcome in Severe Aortic Stenosis". Circulation. 109 (19): 2302–2308. doi:10.1161/01.CIR.0000126825.50903.18. ISSN 0009-7322. PMID 15117847.
- ↑ Murray H, Cload B, Collier CP, Sivilotti ML (July 2006). "Potential impact of N-terminal pro-BNP testing on the emergency department evaluation of acute dyspnea". CJEM. 8 (4): 251–258. doi: 10.1017/s1481803500013798 . PMID 17324304.
- ↑ "B-type Natriuretic Peptide (BNP) & NT-proBNP Test Implementation". Alberta Health Services. Archived from the original on 22 April 2015. Retrieved 3 January 2013.
- ↑ George H (2010). "NT-proBNP The Finest Cardiovascular Screening and Reflexive Test In the History of Life Underwriting" (PDF). Insureintell. Retrieved 11 July 2016.
- ↑ Clark M, Kaufman V, Fulks M, Dolan VF, Stout RL (2014). "NT-proBNP as a predictor of all-cause mortality in a population of insurance applicants". Journal of Insurance Medicine. 44 (1): 7–16. PMID 25004594.