Patent foramen ovale in elderly: a cadaveric case report.
PFO occur during fetal development of the heart. In fetal circulation, there is normally an opening between the two atria, to allow blood to bypass the lungs. This opening usually closes around the time of birth. If PFO persist, blood continues to flow from left to right atria. This is called a shunt. If too much blood moves to the right side of the heart, pressures in the lungs build up. The shunt can be reversed so that blood flows from right to left.
Hoffman et al suggested that an atrial left-to-right shunt resulting from an incompetent foramen ovale may exist in patients without heart disease for more than a year, with eventual closure of the communication. Anatomic patency may occur for several months and 50% of all infants have probe--PFO at the end of 1st year of life. In >25 % of all persons, probably anatomic closure never occur. (6)
When the person has no other congenital defect, symptoms may be absent, particularly in children. Symptoms may begin any time after birth through childhood. If left untreated, the ASD may lead to significant morbidity and mortality. (7) A murmur heard during physical examination or imaging of the heart with Echocardiogram, Electrocardiogram, Doppler image, Cardiac catheterization, Chest x-ray and/ or MRI of the heart can indicate presence of such foramen ovale in absence of symptoms. (8)
MATERIAL AND METHODS: Specimen of normal heart were procured from dissection hall during routine teaching of MBBS 1st year students in Department of Anatomy Chhattisgarh Institute of Medical Sciences. A formalin fixed male cadaver aged 72 years was dissected. The built of the cadaver was quite normal. The exact cause of death, medical & family history of the person is not clear, since the source of cadaver is unclaimed body.
We obtained a heart after opening the thoracic cage following classical incision & dissection procedure. We were surprised to see an abnormal foramen on the superior part of fossa ovalis, when interior of right atrium was opened for study. It was a patent foramen ovale (Fig. 1) The PFO was measured by using metal scale. Other chambers were also opened and studied. The procedure of handling of cadaver for teaching & learning were in accordance with ethical standards.
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
RESULTS: On examination of right atrium, the patent foramen ovale was found at the superior part of oval fossa with easy introduction of a probe across the atrial septum. It was a slit like aperture of 1.2 cm into the atrial septal wall surrounded by a rim of tissue, the limbus of the fossa ovalis. The said foramen was 2.3 cm from tricuspid valve, 2.9 cm from superior vena caval opening and 2.3 cm from inferior vena caval opening and 1.2 cm from coronary sinus opening (Fig-2). The maximum diameter of fossa ovalis were 1.1 cm vertically and 0.9 cm horizontally. On the left atrial surface, the foramen ovale resembled flap, 1.3 cm in length and was 1.6 cm from the mitral valve. Vertically the distance between superior and inferior vena caval opening within the right atrial chamber was 7.7 cm and the internal circumference of right atrium was 7.1 cm.
Excepting the patent foramen, the heart was natural. The heart weighed 310 gm was large, soft and lacerable. The maximum circumference was 12.3 cm at the level of coronary sulcus and vertical length was 12 cm from the base to the apex. The pulmonary trunk, pulmonary arteries and aorta had normal opening. The walls of the right ventricle being thinner than usual. The condition of tricuspid and mitral orifices were normal. The patterns of right and left coronary arteries were normal. Moreover, there were no any other anomalies noticed during dissection of other regions.
DISCUSSION: The less obvious diseases occurring in the aged are often overlooked in clinical practice and have been given little mention in medical literature. Incomplete closure of foramen ovale, "probe patency," is common (>25% of adult hearts) and may be regarded as a normal variant rather than an abnormality. The patent foramen ovale is a physiological orifice, which becomes pathological if persist into adulthood. (9) Patients with a significant shunt experience symptoms over time with effort dyspnoea seen in over 75% of patients by the 5th decade. Complications may include the development of pulmonary hypertension, supraventricular arrhythmias (atrial fibrillation and atrial flutter) and right-sided heart failure from right ventricular volume overload. (10) The increase in life expectance makes the diagnosis of PFO a possible and easily manageable event in elderly patients.
To understand PFO, we should have basic knowledge about developmental anatomy and physiological changes in circulation taking place after birth. Foramen ovale is a slit like opening in the atrial septum at the site of foramen secundum of the septum primum. The septum secundum surrounds the foramen secundum in a crescentic shape and leaves a slit-like opening which is covered in a valve like manner by the free edge of septum primum. In the intrauterine life, foramen ovale has the important role of transmitting highly oxygenated inferior vena caval blood to the left atrium (LA). High right atrial (RA) pressure in fetal life keeps the valve of foramen ovale open. LA pressure rises shortly after birth and the flap is lightly pushed against the septum secundum and closes the foramen ovale functionally. (11) If it does not close, it is called a patent foramen ovale (PFO).
Patent foramen ovale (PFO) is known since the time of Galen. It was first described in 1564 by Italian surgeon Leonard Botali. (12) The patent foramen ovale is the most common form of ASD usually results from abnormal resorption of septum primum during the formation of foramen secundum. (13) An atrial septal defect is an abnormal opening in the wall between the left and right atria of the heart.
If the hole is large enough, oxygen rich blood from the left atrium flows into the right atrium. This causes more work for the heart. ASDs can be located in different places on the atrial septum, and they can be different sizes. Mayo Clinic autopsy studies revealed that size of PFO increases from a mean of 3.4 mm in 1st decade to 5.8 mm in 10th decade of life, as the valve of fossa ovalis stretches with age. In addition, the prevalence decreased with age (34% in those aged 1-29 years, 25% in those 30-79 years, and 20% in those aged 80 years or more). (14) In present case report the size of PFO was 1.2 cm in a formalin fixed specimen.
Clinically four significant types of ASDs are described. The ostium secundum ASD accounts for 70% to 80% of all adult ASDs. Other less common forms of adult ASDs include ostium primum ASD (15% of ASDs), sinus venosus ASD (10% of ASDs), and the unroofed coronary sinus (<1% of ASDs). (15)
A secundum atrial septal defect is a true defect and the least severe, usually bordered by the edge of the fossa ovalis and the exposed circumference of ostium secundum. (16) The shape of the defect varies from circular to oval. Less often, strands of tissue cross the defect creating a fenestrated appearance that suggests multiple defects. Rarely, a defect can extend posteriorly and inferiorly, approaching the site of inferior vena cava entrance into the right atrium.
Our finding in this study belongs to this type of defect and was slit like. Only Patent Foramen Ovale ie; Atrioseptal defect was observed otherwise rest of the heart was found to be normal. An ostium primum atrial septal defect (ASD), is located in the most anterior and inferior aspect of the atrial septum and often associated with trisomy 21. Coronary sinus atrial septal defects (ASDs) are defects located in the portion of the atrial septum that includes the coronary sinus orifice. They are characterized by the absence of at least a portion of the common wall that separates the coronary sinus and the left atrium. Coronary sinus defects are often associated with a persistent left superior vena cava (SVC) that drains into the coronary sinus; they may also be associated with complex congenital heart lesions. (17)
Patients with small shunts may live a normal life span. Large shunts cause disability by age 40 years. Raised pulmonary vascular resistance secondary to pulmonary hypertension rarely occurs in childhood or adult life in secundum defects but is more common in primum defects. After age 40 years, pulmonary hypertension, cardiac arrhythmias (especially atrial fibrillation), and heart failure may occur in secundum defects. Paradoxic systemic arterial embolization is a concern, especially in patients with pulmonary hypertension or venous thrombosis. Paradoxical embolism is an unusual cause of cerebrovascular incidents in the elderly. (18)
There are some typical conditions when PFO can worsen hypoxemia such as valvular PS, Ebstein anomaly, RV myocardial infarction, orthodeoxia platypnoea syndrome, chronic obstructive pulmonary diseases, pulmonary hypertension (primary or secondary). (19-22) 3 factors which decide the complications arising from PFO are size of PFO, Pressure gradient between RA/LA and Direction of inferior vena cava blood flow.
In some cases of headache--migraine with aura, patient was found to have PFO also, and migraine improved on medical treatment in the form of antiplatelet and anticoagulant drugs or disappeared on the closure of PFO. (23) PFO can lead to fat embolism (Nysten, et al) and bilateral central retinal artery occlusion, thus leading to blindness. It can lead to recurrent stroke or TIA. (24) PFO is associated more with decompression sickness. PFO can worsen hypoxaemia in Scuba divers at great depths and can lead to deaths because of nitrogen gas embolism across PFO. (25)
Recently and with increasing frequency, paradoxically septic embolism through a PFO has been correlated with brain abscesses and transcatheter PFO closure has been suggested as prevention for recurrent brain abscesses. (26) In most cases ASDs are diagnosed and treated successfully with few or no complications. Early diagnosis and treatment can help to prevent complication. There are no specific ECG features of PFO. TEE (Trans-esophageal Echo) is better than transthoracic echo in diagnosing PFO. (27) Cardiac catheterization can quantitate shunt across PFO.
There are no risk factors for the development of PFO. It is mostly a benign condition and its incidental finding in asymptomatic patients requires no specific therapy. Moreover, in the elderly many other syndromes than paradoxical stroke mediated by PFO required full assessment. The management of PFO in aged patients should obligatory include the careful evaluation of potential co-morbidities and eventual contraindications, such as severe diastolic dysfunction due to for example to hypertensive cardiomyopathy and coronary heart disease, the main causes of diastolic dysfunction. (28)
CONCLUSION: Patients with isolated atrial septal defects (ASD) have benefited from important recent advances in the diagnosis, evaluation, & management of their conditions. The study suggests that in an elderly many co-morbidities & severe diastolic dysfunctions mediated by PFO required full assessment to evaluated as therapeutic options in presence of anatomical & functional indications. More studies should be undertaken about unresolved issues to explain the reasons for prolong survival, as PFO is present in >25 % of normal adult population.
(1.) Manuel R, Frederic D.Z and Isadore E.G: Atrial septal defect in the aged. American heart association, Circulation. 1961; 23: 665-674.
(2.) Standring S, Editor-in-Chief, Gray's Anatomy, 40th ed, Churchill Livingstone, Edinburgh, 2008, 974
(3.) Rigatelli G, Rigatelli G. Congenital heart diseases in aged patients: clinical features, diagnosis, and therapeutic indications based on the analysis of a twenty five-year Medline search. Cardiol Rev 2005; 13: 293-296.
(4.) Fisher DC, Fisher EA, Budd JH, Rosen SE, Goldman ME, The incidence of patent foramen ovale in 1000 consecutive patients: a contrast transesophageal echocardiography study, Chest 1995, 107, 1504-9.
(5.) P. T. Wilmshurst, M. J. Pearson, S Nightingale, K. P. Walsh, and W. L. Morrison, Inheritance of persistent foramen ovale and atrial septal defects and the relation to familial migraine with aura. Heart 2004; 90: 1315-1320.
(6.) W A Seldon, C Rubinstein, and A A Fraser, The incidence of atrial septal defects in adults. Br Heart J 1962; 24: 557-560.
(7.) Hoffman JI, Kaplan S. The incidence of congenital heart disease, J Am coll cardiol, 2002; 39 (12): 1890.
(8.) Moake L, Ramaciotti C, Atrial Septal Defect Treatment Options, AACN Clin Issues, 2005, 16, 2, 252-266.
(9.) Bauer, D. de F. and E.C. Astbury. (1944) Congenital variations of the heart with the maximum recorded life span based on 1000 cases in the bibliography of M.E. Abbott. Am. Heart J. 27: 688752.
(10.) Karen SL Teo*, Patrick J. Disney, Benjamin K Dundon, Matthew I Worthley, Michael A Brown, Prashanthan Sanders and Stephen G Worthley: Assessment of atrial septal defects in adults comparing cardiovascular magnetic resonance with trans esophageal echocardiography. Journal of Cardiovascular Magnetic Resonance 2010, 12: 44.
(11.) David Radzik, MD; Andre Davignon, MD, FACC; Nicolaas van Doesburg, MD; Anne Fournier, MD, FACC; Therese Marchand, RN; Gilles Ducharme, PhD, Predictive factors for spontaneous closure of atrial septal defects diagnosed in the first 3 months of life. J Am Coll Cardiol. 1993; 22 (3): 851-853.
(12.) Patten BM: The closure of the foramen ovale. Am J Anat 48: 19-44, 1931.
(13.) Moore KL, TVN Persaud, The developing human, clinically oriented embryology, 8th Ed, Elsevier Inc. India, 2009, 310-13.
(14.) Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first ten decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984; 59: 17-20.
(15.) Konstantin ides S, Geibel A, Kasper W, Just H. The natural course of atrial septal defect in adults-a still unsettled issue. Klin Wochenschr. N Engl J Med 1991 Aug 16; 69 (12): 506-10.
(16.) Gary Webb, Michael A, Gatzoulis. Atrial septal defects in the adult, circulation 2006, 114: 16451653.
(17.) John P. Higgins, Anvi H Thakore. Ostium secundum atrial septal defect discovered after 60 years of age, Europian Society of cardiology 16 Jul 2006.
(18.) Mark A. Vella, A. Neil Sulkel, Christopher A. Rodrigues, W. Robin McNabb and Roger R. Lewis, Patent foramina ovale in elderly stroke patients Postgrad Med J (1991) 67, 745--746.
(19.) Anderson KR, Lic JT. Pathologic anatomy of the Ebsteins anomaly of the heart revisited. Am J Cardio 1978; 41: 739.
(20.) Arnett EN, Aisner SC, Lewis KB et al. Pulmonary stenosis, atrial septal defect and left to right shunt with intact ventricular septum. Chest 1980; 78: 759.
(21.) Dick M, Fyler DC, Nadas AS. Tricuspid atresia: Clinical courses in 101 patients. Am J Cardio 1975; 36: 327.
(22.) Rudolph AM, Mayer FE, Nadas AS, Gross RE. Patent ductus arteriosus. A clinical and hemodynamic study of 23 patients in 1st year of life. Pediatrics 1958; 22: 892.
(23.) Homma S, Sacco RL, Di Tullio MR et al. Effect of medical treatment in stroke patients with PFO PFO in cryptogenic stroke study. Circulation 2002; 105: 2625-31.
(24.) Lechat P et al. Prevalence of PFO in patients with stroke. NEJM 1988; 318 (18): 1148-52.
(25.) Wilmhurst P, Byrne JC, Webb MM. Relation between interatrial shunts and decompression sickness in divers. Lancet 1989; 11: 1302-6.
(26.) Stathopoulos GT, Mandila CG, Koukoulitsios GV, Katsarelis NG, Pedonomos M, Karabinis A. Adult brain abscess associated with patent foramen ovale: a case report. J Med Case Rep 2007; 1: 68.
(27.) Fisher DC, Fisher FA, Budd JH et al. Incidence of PFO in 1000 consecutive patients. A contrast TEE study--Chest 1995; 107 (6): 1504-9.
(28.) Gianluca Rigatelli, Fabia Dell' Avvocata, Patent foramen ovale in the elderly: What to do?. Journal of Geriatric Cardiology, December 2007; 4(4):254--256.
Ranjana Singh Arya , Shiksha Jangdey , Kamal Basan , Amit Kumar , Suhasini Tayade 
[1.] Ranjana Singh Arya
[2.] Shiksha Jangdey
[3.] Kamal Basan
[4.] Amit Kumar
[5.] Suhasini Tayade
PARTICULARS OF CONTRIBUTORS:
[1.] Associate Professor, Department of Anatomy, Chhattisgarh Institute of Medical Sciences, Bilaspur, C. G.
[2.] Assistant Professor, Department of Anatomy, Chhattisgarh Institute of Medical Sciences, Bilaspur, C. G.
[3.] Demonstrator, Department of Anatomy, Chhattisgarh Institute of Medical Sciences, Bilaspur, C. G.
[4.] Assistant Professor, Department of Anatomy, Chhattisgarh Institute of Medical Sciences, Bilaspur, C. G.
[5.] Assistant Professor, Department of Anatomy, Chhattisgarh Institute of Medical Sciences, Bilaspur, C. G.
NAME ADDRESS EMAIL ID OF THE CORRESPONDING AUTHOR:
Dr. Ranjana Singh Arya, # 103, Nilgiri Appartment, Green Garden Colony, Mungeli Road, Bilaspur, C. G. Email: email@example.com
Date of Submission: 16/09/2014.
Date of Peer Review: 17/09/2014.
Date of Acceptance: 29/09/2014.
Date of Publishing: 06/10/2014.
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||CASE REPORT|
|Author:||Arya, Ranjana Singh; Jangdey, Shiksha; Basan, Kamal; Kumar, Amit; Tayade, Suhasini|
|Publication:||Journal of Evolution of Medical and Dental Sciences|
|Date:||Oct 6, 2014|
|Previous Article:||The effect of normal saline and 3.5% hypertonic saline on mucociliary clearance in sinusitis.|
|Next Article:||Indigenous tube exchanger: be safe be sure.|