Schemating drawing showing the location of different types of ASD, the view is into an opened right atrium. HV: right ventricle; VCS: superior caval vein; VCI: inferior caval vein; 1: upper sinus venosus defect; 2: lower sinus venosus defect; 3: secundum defect; 4: defect involving coronary sinus; 5; primum defect.Ultrasound picture of the heart, seen in a subcostal view. The apex towards the right, atria to the left. ASD secundum seen as a discuntinuation of the white band of the atrial septum. Enlarged right atrium below, enlarged pulmonary veins seen entering left atrium above. (Echocardiogram: Wikipedia editor Kjetil Lenes (Ekko) )
Find information on thousands of medical conditions and prescription drugs.

Atrial septal defect

Atrial septal defects (ASD) are a group of congenital heart diseases that involve the interatrial septum of the heart. The inter-atrial septum is the tissue that separates the right and left atria from each other. Without this septum, or if there is a defect in this septum, it is possible for blood to travel from the left side of the heart to the right side of the heart, or the other way around, resulting in mixing of arterial and venous blood. more...

Home
Diseases
A
Aagenaes syndrome
Aarskog Ose Pande syndrome
Aarskog syndrome
Aase Smith syndrome
Aase syndrome
ABCD syndrome
Abdallat Davis Farrage...
Abdominal aortic aneurysm
Abdominal cystic...
Abdominal defects
Ablutophobia
Absence of Gluteal muscle
Acalvaria
Acanthocheilonemiasis
Acanthocytosis
Acarophobia
Acatalasemia
Accessory pancreas
Achalasia
Achard syndrome
Achard-Thiers syndrome
Acheiropodia
Achondrogenesis
Achondrogenesis type 1A
Achondrogenesis type 1B
Achondroplasia
Achondroplastic dwarfism
Achromatopsia
Acid maltase deficiency
Ackerman syndrome
Acne
Acne rosacea
Acoustic neuroma
Acquired ichthyosis
Acquired syphilis
Acrofacial dysostosis,...
Acromegaly
Acrophobia
Acrospiroma
Actinomycosis
Activated protein C...
Acute febrile...
Acute intermittent porphyria
Acute lymphoblastic leukemia
Acute lymphocytic leukemia
Acute mountain sickness
Acute myelocytic leukemia
Acute myelogenous leukemia
Acute necrotizing...
Acute promyelocytic leukemia
Acute renal failure
Acute respiratory...
Acute tubular necrosis
Adams Nance syndrome
Adams-Oliver syndrome
Addison's disease
Adducted thumb syndrome...
Adenoid cystic carcinoma
Adenoma
Adenomyosis
Adenosine deaminase...
Adenosine monophosphate...
Adie syndrome
Adrenal incidentaloma
Adrenal insufficiency
Adrenocortical carcinoma
Adrenogenital syndrome
Adrenoleukodystrophy
Aerophobia
Agoraphobia
Agrizoophobia
Agyrophobia
Aicardi syndrome
Aichmophobia
AIDS
AIDS Dementia Complex
Ainhum
Albinism
Albright's hereditary...
Albuminurophobia
Alcaptonuria
Alcohol fetopathy
Alcoholic hepatitis
Alcoholic liver cirrhosis
Alektorophobia
Alexander disease
Alien hand syndrome
Alkaptonuria
Alliumphobia
Alopecia
Alopecia areata
Alopecia totalis
Alopecia universalis
Alpers disease
Alpha 1-antitrypsin...
Alpha-mannosidosis
Alport syndrome
Alternating hemiplegia
Alzheimer's disease
Amaurosis
Amblyopia
Ambras syndrome
Amelogenesis imperfecta
Amenorrhea
American trypanosomiasis
Amoebiasis
Amyloidosis
Amyotrophic lateral...
Anaphylaxis
Androgen insensitivity...
Anemia
Anemia, Diamond-Blackfan
Anemia, Pernicious
Anemia, Sideroblastic
Anemophobia
Anencephaly
Aneurysm
Aneurysm
Aneurysm of sinus of...
Angelman syndrome
Anguillulosis
Aniridia
Anisakiasis
Ankylosing spondylitis
Ankylostomiasis
Annular pancreas
Anorchidism
Anorexia nervosa
Anosmia
Anotia
Anthophobia
Anthrax disease
Antiphospholipid syndrome
Antisocial personality...
Antithrombin deficiency,...
Anton's syndrome
Aortic aneurysm
Aortic coarctation
Aortic dissection
Aortic valve stenosis
Apert syndrome
Aphthous stomatitis
Apiphobia
Aplastic anemia
Appendicitis
Apraxia
Arachnoiditis
Argininosuccinate...
Argininosuccinic aciduria
Argyria
Arnold-Chiari malformation
Arrhythmogenic right...
Arteriovenous malformation
Arteritis
Arthritis
Arthritis, Juvenile
Arthrogryposis
Arthrogryposis multiplex...
Asbestosis
Ascariasis
Aseptic meningitis
Asherman's syndrome
Aspartylglycosaminuria
Aspergillosis
Asphyxia neonatorum
Asthenia
Asthenia
Asthenophobia
Asthma
Astrocytoma
Ataxia telangiectasia
Atelectasis
Atelosteogenesis, type II
Atherosclerosis
Athetosis
Atopic Dermatitis
Atrial septal defect
Atrioventricular septal...
Atrophy
Attention Deficit...
Autoimmune hepatitis
Autoimmune...
Automysophobia
Autonomic dysfunction
Familial Alzheimer disease
Senescence
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
Medicines

Since the right side of the heart contains venous blood with a low oxygen content, and the left side of the heart contains arterial blood with a high oxygen content, it is beneficial to prevent any communication between the two sides of the heart and prevent the blood from the two sides of the heart from mixing with each other.

During development of the fetus, the inter-atrial septum develops to eventually separate the left and right atria. The foramen ovale remains open during fetal development to allow blood from the venous system to bypass the lungs and go to the systemic circulation. This is because prior to birth, the oxygenation of the blood is via the placenta and not the lungs. A layer of tissue begins to cover the foramen ovale during fetal development, and will close it completely soon after birth. After birth, the pressure in the pulmonary circulation drops, and the foramen ovale closes. In approximately 30% of adults the foramen ovale does not seal over. In this case, elevation of pressure in the pulmonary circulation (ie: pulmonary hypertension due to various causes, or transiently during a cough) can cause opening of the foramen ovale. This is known as a patent foramen ovale (PFO).

Pathophysiology

In normal individuals, the chambers of the left side of the heart make up a higher pressure system than the chambers of the right side of the heart. This is because the left ventricle has to produce enough pressure to eject blood to the entire body, while the right ventricle has to produce enough pressure to eject blood to only the lungs.

In the event of an atrial septal defect, blood will flow from the left atrium to the right atrium. This is called a left-to-right shunt. This extra blood will cause a volume overload of both the right atrium and the right ventricle.

Any process that increases the pressure in the left ventricle can cause worsening of the left-to-right shunt. This includes hypertension, which increases the pressure that the left ventricle has to generate in order to open the aortic valve during ventricular systole, and coronary artery disease which increases the stiffness of the left ventricle, thereby increasing the filling pressure of the left ventricle during ventricular diastole.

The right ventricle will have to push out more blood than the left ventricle due to the left-to-right shunt. This constant overload of the right side of the heart will cause an overload of the entire pulmonary vasculature. Eventually the pulmonary vasculature will develop pulmonary hypertension to try to divert the extra blood volume away from the lungs.

The pulmonary hypertension will cause the right ventricle to face increased afterload in addition to the increased preload that the shunted blood from the left atrium to the right atrium caused. The right ventricle will be forced to generate higher pressures to try to overcome the pulmonary hypertension. This may lead to right ventricular failure (dilatation and decreased systolic function of the right ventricle) or elevations of the right sided pressures to levels greater than the left sided pressures.

Read more at Wikipedia.org


[List your site here Free!]


Elevated cardiac troponin I following heavy-resistance exercise in ostium secundum type-atrial septal defect - communications to the editor - Letter to
From CHEST, 11/1/01 by Johann Auer

To the Editor:

Raised concentrations of cardiac troponin, indicating poor short-term prognosis, have been reported in patients with dilated and secondary cardiomyopathy. (1) It is assumed that these elevated levels of troponin reflect ongoing myocyte degeneration. Heavy-resistance exercise and strength training are associated with adaptive changes of cardiac structure and function. (2) Furthermore, recently published data demonstrate that more than one third of patients who received a clinical diagnosis of pulmonary embolism had presented with elevated serum troponin concentrations due to minor myocardial damage in acute right ventricular dysfunction. (3)

We report on a 71-year-old man with a 9-year history of ostium secundum type-atrial septal defect and increased right ventricular size. The patient was admitted to our hospital because of dyspnea and chest discomfort after heavy-resistance exercise, moving furniture. The patient's BP was 120/80 mm Hg, his pulse rate was 82 beats/min, and his breathing rate was 18 breaths/min. The first heart sound was loud, the second heart sound was widely split without widening during inspiration, and a pulmonary systolic ejection murmur was present. ECG revealed complete right bundle-branch block and signs of right ventricular hypertrophy. No changes in the repolarization pattern could be documented compared with ECGs recorded previously. Echocardiography showed increased right ventricular size, moderate right ventricular dysfunction, and tricuspid regurgitation, indicative of increased right ventricular stroke volume. A pulmonary-to-systemic flow ratio of 2:1, due to an ostium secundum type-atrial septal defect, could be accurately diagnosed by Doppler echocardiography. Symptoms disappeared spontanously within a few minutes after hospital admission without therapy.

Laboratory examination revealed elevated serum concentrations of cardiac troponin I (2.2 ng/mL; normal < 1.6 ng mL) and myocardial band (MB) isoenzyme of creatine kinase (13 U/L; normal < 5 U/L). MB isoenzyme of creatine kinase peaked (17 U/L) 4 h after hospital admission, and the level of troponin I raised to a peak concentration of 6.4 ng/mL. Other laboratory findings, including inflammatory markers and coagulation tests, were within normal ranges. Coronary angiography showed normal epicardial coronary vessels with no signs of atherosclerotic lesions, and a cineangiogram revealed no wall motion abnormalities.

For several reasons, we do not believe that ischemia caused the elevation of cardiac enzymes. First, a normal coronary angiogram finding does not definitely rule out previous coronary artery occlusion, but it makes myocardial ischemia or myocardial infarction unlikely, particularly in the absence of known risk factors for atherosclerosis. (4,5) Second, neither echocardiography nor cineangiography revealed any wall-motion abnormalities indicative of segmental myocardial damage, Third, elevated concentrations of cardiac troponin have been reported in patients with dilated cardiomyopathy, secondary cardiomyopathies, and acute right ventricular dysfunction. (1,3)

To our knowledge, this is the first report in which heavy-resistance exercise induced a raise of levels of serum cardiac troponin and MB isoenzyme of creatine kinase in a patient with preexisting dilatation and dysfunction of the right ventricle due to a ostium secundum type-atrial septal defect with left-to-right shunt.

The management of atrial septal defects in older patients is debated persistently, and clinical trials (6,7) have demonstrated conflicting data. We do not have absolute proof to guide our decisions; therefore, we must rely on our experience as well as on the available evidence in deciding how to treat these patients. (8) Further studies are needed to determine whether the management of these patients should be guided by clinical signs or by biochemical markers, like troponins.

Correspondence to: Johann Auer, MD, Second Medical Department, Division of Cardiology and Intensive Care; General Hospital Wels, Grieskirchnerstra[beta]e 42, A-4600 Wels, Austria; e-mail: johann.auer@khwels.at

REFERENCES

(1) Sato Y, Yamada T, Taniguchi R, et al. Serum concentration of cardiac troponin T inpatients with cardiomypoathy: a possible mechanism of acute heart failure. Heart 1998; 80:209-210

(2) Pluim BM, Zwinderman AH, van der Laarse A, et al. The athlete's heart: a meta-analysis of cardiac structure and function. Circulation 1999; 100:336-344

(3) Meyer T, Binder L, Hruska N, et al. Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction. J Am Coll Cardiol 2000; 36:1632-1636

(4) Cheitlin MD, Sokolow M, McIlroy MB. Coronary heart disease. In: Cheitlin MD, Sokolow M, McIlroy MB, eds. Clinical cardiology, 6th ed. Norwalk, CT: Appleton and Lange, 1993; 181

(5) Michaelson SP, Karsh DL, Wolfson S, et al. Recurrent myocardial infarction with normal coronary arteriography. N Engl J Med 1977; 297:916-917

(6) Shah D, Azhar M, Oakley CM, et al. Natural history of secundum atrial septal defect in adults after medical or surgical treatment: a historical prospective study. Br Heart J 1994; 71:224-227

(7) Jemielity M, Dyszkiewicz L, Perek B, et al. Do patients over 40 years of age benefit from surgical closure of atrial septal defects? Heart 2001; 85:300-303

(8) Webb G. Do atients over 40 ears of a e benefit from closure of an atrial septal defect. Heart 2001; 85:249-250

COPYRIGHT 2001 American College of Chest Physicians
COPYRIGHT 2001 Gale Group

Return to Atrial septal defect
Home Contact Resources Exchange Links ebay