Apex Beat Research Articles

The use of recurrence plots and beat recordings in chronic heart failure detection

Abstract Chronic heart failure is a syndrome consisting in clinical symptoms that arise as a result of complications of many disease entities. According to the definition it is a condition in which, as a consequence of permanent heart dysfunction, cardiac output is reduced in relation to tissues’ metabolic demand. This results in subjective symptoms or proper cardiac output is sustained over higher filling pressure of the left heart ventricle. The occurrence of disease among adults in Europe and North America is 0.4-2%. Heart dysfunction detected by echocardiography appears with the frequency of 3%, and in people over 60 years of age it doubles with each decade of life, reaching 10% after 80 years of age. The aim of the study is to make an acquisition of fremitus in apex beat place and quantitative evaluation of some of their features which are correlated with the advanced syndrome. We have built the apparatus for the heart signal recording and proposed the original method of its analysis based on the theory of chaos and recurrence plots. It gave us, on the group of 85 patients, sensitivity equal to 0.896 specificity equal to 0.676 and the accuracy of diagnostics of the chronic heart failure equal up to 80%.

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.

Extended prediction rule to optimise early detection of heart failure in older persons with non-acute shortness of breath: a cross-sectional study

ObjectivesThere is a need for a practical tool to aid general practitioners in early detection of heart failure in the elderly with shortness of breath. In this study, such a...

Case 2/2016 - Scimitar Sign with Right Pulmonary Vein Drainage into the Right Atrium

Clinical data: the characteristic signs of the scimitar syndrome with right pulmonary hypoplasia were discovered in an asymptomatic patient through routine chest X-ray, in the presence of dengue. On physical examination, the patient was in good general health status, eupneic, normal skin color, with normal pulses. His weight was 54 kg, height 155 cm, blood pressure of 100/60 mmHg, heart rate of 88 bpm. The aorta was not palpable at the sternal notch. In the precordium, there were mild impulses at the left and right sternal borders and the apex beat was not palpable. Heart sounds were normal, with constant splitting of the second heart sound, with discreet and rough ejection systolic murmur in the pulmonary area. The liver was not palpable and in the lungs, breath sounds were less audible in the right lower pulmonary lobe.

Purulent pericarditis caused by Klebsiella pneumoniae in a Nigerian Child

In the Western world, cases of purulent pericarditis have become almost nonexistent with progress and advent of new immunizations against many causative organisms. We report Klebsiella pneumoniae pericarditis, a rare cause of this uncommon disease, hitherto unreported in Nigeria. K. pneumoniae, which is a rod-shaped, Gram-negative, facultative anaerobe, produces extended-spectrum beta-lactamases; hence, it is usually resistant to a lot of antibiotics and is associated with a significant case fatality rate. Our 13-year-old male patient had septic arthritis of the right hip joint came with a 3 weeks complaint of difficulty with breathing. He had respiratory distress, tachypnea, and tachycardia. Although blood pressure was normal, he had pulsus paradoxus, elevated jugular venous pressure, diffuse apex beat, and heart sounds were distant. Chest radiograph revealed an increased cardiothoracic ratio (0.86) with “water bottle” appearance. Transthoracic echocardiography confirmed pericardial effusion with cardiac tamponade. Echo-guided pericardiocentesis was done, and 340 ml of foul-smelling and creamy pus with greenish tinge was aspirated and this grew K. pneumoniae sensitive to ciprofloxacin and gentamycin but resistant to other conventional antibiotics. Recovery was complete after a week of pericardial tube drainage and 3 weeks of treatment. To the best of our knowledge, this is the first case of Klebsiella - induced pyopericardium and with successful management in a Nigerian child. Pyopericardium may follow rare causes such as K. pneumoniae infection with its unique antibiogram.

Apical Hypertrophic Cardiomyopathy.

To the Editor We have read with interest the excellent review on hypertrophic cardiomyopathy (HCM)1 and wish to comment on the apical variant of the disease listed in Table 4 but not discussed in the text. This variant can be found in 15% to 25% of Chinese and Japanese cohorts with HCM but only in 3% of American cohorts.2 The typical electrocardiography (ECG) shows the loss of septal Q waves, high QRS voltage, and repolarization abnormalities with deep T-wave inversion, especially in the leads closest to the apex—V4–V6.2 Because hypertrophy is confined to the apex, dynamic left ventricular outflow tract obstruction and systolic anterior motion of the anterior mitral valve leaflet are absent. The apical pulse may be sustained on palpation, and an S4 heart sound may be heard.2 There may not be a systolic murmur. It is reasonable to expect some degree of diastolic dysfunction and the possibility of relative apical ischemia as a result of the unbalanced wall thickness-to-vascular supply ratio.3 HCM apical variant may not have a totally benign prognosis with atrial fibrillation and myocardial infarction occurring in up to one-third of patients during long-term follow-up in the Western population.3,4 In addition, in patients with atrial fibrillation, HCM (including the apical variant) may increase the risks of systemic thromboembolism and the need for long-term anticoagulation.5,6 However, there are currently no data to suggest that the perioperative risks are increased in afflicted patients without a history of syncope, chest pain, dyspnea, or heart failure. Nonetheless, in a young asymptomatic patient, the bizarre ECG pattern first seen when intraoperative ECG electrodes are placed can be alarming and may even lead to the postponement of surgery or initiation of coronary vasodilator treatment. Alternatively, a preoperative ECG may lead one to suspect HCM. However, plain echocardiography may still miss apical HCM if the apex is not adequately examined.3 A microbubble contrast-enhanced echocardiography or cardiac magnetic resonance imaging, or both, may be required to differentially diagnose apical HCM, coronary artery disease, myocardial tumor, ventricular aneurysm, ventricular noncompaction, or endomyocardial fibrosis.3 Anthony M. H. Ho, MD, FRCPC, FCCP Department of Anesthesiology and Perioperative Medicine Queen’s University and Kingston General Hospital Kingston, Ontario, Canada [email protected] Po T. Chui, MBBS, FANZCA Alex P. W. Lee, MBChB, MRCP Song Wan, PhD, MD, FRCS Departments of Anaesthesia and Intensive Care, Medicine & Therapeutics, and Surgery The Chinese University of Hong Kong and Prince of Wales Hospital Hong Kong SAR, People’s Republic of China

An infant with Cushing syndrome

Case Presentation An 8 month-old boy was referred to the endocrinology clinic for concerns of growth failure since 3 months of age. He was born full term with a birth weight of 2.67kg and a length of 45cm. His parents noticed that he was not growing well from 3 months of age. However, his weight gain remained more than satisfactory and he gained 700g in the past month. This infant was otherwise in good health, apart from atopic dermatitis, for which the parents had been applying a daily cream with good effect. He was breast fed until 2 months of age and weaned onto solids at 6 months of age. On examination, the infant had a moon face with hypertrichosis, facial telangiectasia and prominent supraclavicular fat pads. His recumbent length was 62cm (<3 percentile), his weight was 7.74 kg (25 percentile), and his head circumference was 41.0 cm (3 percentile). There was no hyperpigmentation or lentigenes, but he was hypertensive with a blood pressure of 140/90 mmHg (95 percentile for age is 99/55 mm Hg) with a heart rate of 140 beats/minute. His apex beat was not displaced and his heart sounds were normal with no murmurs. A random steroid profile demonstrated a depressed serum cortisol level of 30 nmol/L and an unmeasurably low serum ACTH level of <1.1 pmol/L. This was consistent with exogenous Cushing syndrome. An ECG showed biventricular hypertrophy and a 2-D echocardiogram confirmed severe biventricular hypertrophy with good ventricular function. On further questioning, he had been receiving twice daily applications of a topical cream for atopic dermatitis, which had been obtained over the counter, without a prescription. Subsequent analysis of the topical agent revealed the contents to be betametasone dipropionate, a high potency corticosteroid. On establishing the diagnosis of exogenous Cushing syndrome, the offending topical steroid cream was discontinued. Since he was at risk of primary adrenal failure from sudden withdrawal of steroid cream, he was started on a weaning regimen of hydrocortisone. He was also commenced on captopril which achieved good blood pressure control.

Cardiac Tamponade: A Rare Presentation of Childhood Hypothyroidism.

Dear Editor, Myxedema heart disease is a well-known entity. Pericardial effusions have been reported in 50-73% of pediatric patients with hypothyroidism in various series (1, 2), but none of these describes the symptomatic pericardial effusions or cardiac tamponade. A 5- year-old female child presented with complaints of periorbital puffiness and mild abdominal distension intermittently for last 6 months. She was symptomatically treated with diuretics off and on without much benefit. This time she reported to pediatric emergency with progressively increasing respiratory distress for last 5 days. There was no history of any fever, decreased urine output, orthopnea, or Koch’s contact. She was third live issue of non-consanguineous marriage born by normal vaginal delivery following uncomplicated pregnancy. She was immunized for age with no significant family history. She had history of global development delay; development age corresponded to 3 years. On examination she was afebrile with HR of 70/min, RR of 44/min and BP of 80/60 mmHg with pulsus paradoxus. She had coarse facies with dilated neck veins. Her skin was dry and coarse. She had short stature with height less than 3rd centile and normal weight. Her cardiovascular examination revealed silent precordium. Her cardiac border was extending 1.5 cm beyond right sternal margin and 2 cm beyond apex beat on left side on percussion. Her heart sounds were muffled with no murmur. Her abdominal examination revealed free fluid in abdomen. Rest of systemic examination was normal. Chest X ray revealed massive cardiomegaly with CT ratio of 678%. Immediate ECHO done on urgent basis, revealed large pericardial effusion with collapse of right atrium during diastole with ejection fraction of 65% and intrinsically normal heart. ECHO guided pericardiocentesis drained 150 ml of fluid. The fluid was clear with 3.3 mg/dl of proteins, 110 mg/dl cholesterol, 20 RBC/µL, 14 lymphocytes/µL, 7 neutrophils/µL and rest of pericardial examination were normal. Rest of hematological and urinary examination was normal. Searching for tuberculosis was also negative. In view of features suggested of hypothyroidism on clinical examination and non infectious nature of pericardial fluid, her thyroid profile was done which was suggested of hypothyroidism with T3 = 0.92 nmol/L (1.39-3.7nmol/L), T4 = 3.2 µg/dl (5.5-12.8µg/dl), TSH= 40 mIU/L(0.7-6.4 mIU/L). Her anti TPO antibodies were negative and USG neck revealed mild enlargement of thyroid gland. She was started on L-thyroxine with dosage of 4 µg/kg/d. She responded to treatment with thyroid replacement and her pericardial effusion disappeared after 2 months on repeat ECHO. She is on regular follow up and showing improvement in each regards. Although mild to moderate pericardial effusions of no clinical significance are frequently reported in pediatric myxedema heart disease, but cardiac tamponade is rare. Literature reports only 2 adolescent girls with cardiac tamponade in association with hypothyroidism, but none has been reported in young children. Author reports a rare case of cardiac tamponade in a young child with previously unrecognized hypothyroidism. Besides bradycardia, minimal pericardial effusions are most common cardiac manifestations of clinical hypothyroidism in adults. Most of pediatric age group patients presenting with this belonged to neonatal period or to Down’s syndrome (1, 2). Myxedema heart disease was first described by Zondek in 1918 and was completely defined by Fahr in 1925 (3). The pathophysiological derangements responsible for pericardial effusions are increased egress of proteins from blood, decreased lymphatic clearance of proteins and abnormal electrolyte metabolism (4). At molecular level, commonly observed signs or symptoms in hypothyroidism are attributed to changes in expression of various gene products, which includes alpha myosin heavy chain, beta-1 adrenergic receptors, voltage gated potassium channels and sarcoplasmic reticulum calcium ATPase (5). The rarity of cardiac tamponade in hypothyroidism is attributed to slow accumulation of fluid and marked distensibility of pericardium (6). Alexander first described ‘Gold paint effusion’ to describe the golden brown appearance of pericardial fluid due shimmering satin cholesterol crystals (7). High cholesterol content of pericardial fluid have been attributed to disturbance of lipid metabolism; probably churning action of heart causing precipitation of cholesterol from pericardial fluid. Treatment of cardiac tamponade due to hypothyroidism involves urgent pericardiocentesis followed by thyroxine replacement. Treatment of pericardial effusion with thyroxine replacement leads to resolution of effusion in 2-12 months (5). In conclusion myxedema heart disease should be suspected in any child with symptoms suggestive of hypothyroidism, presenting with even hemodynamic-ally significant pericardial effusion or cardiac tamponade. Patients with hypothyroidism-associated pericardial effusion should be monitored for development of cardiac tamponade.

Case 5/2015 Late Outcome of Corrected Aortopulmonary Window in A 23-Year-Old Female Patient Who Underwent Surgery in Childhood

Clinical data: At 10 months of age, the patient underwent correction of a large aortopulmonary window and mitral valve regurgitation secondary to volume overload, which caused severe heart failure. The post-operative clinical outcome was favorable. Prior to operation, her clinical picture was of concern because of severe malnutrition (weight of 5,500 g), congestive heart failure (tachypnea of 60 bpm), hepatomegaly (liver palpable at 4 cm of the right costal margin), severe cardiomegaly, and increased pulmonary vasculature. Cardiovascular examination showed left ventricular (LV) enlargement; thrill and systolic murmur in the mitral area; accentuated S2; marked LV overload on electrocardiogram (ECG); mitral regurgitation due to incomplete leaflet coaptation; and pulmonary systolic pressure of 60 mmHg. At surgery, the 2-cm-diameter window between the pulmonary trunk and ascending aorta (Ao) was closed, and plication of the posterior ring of the mitral valve was performed. There was an immediate clinical response with hemodynamic stabilization, resolution of the heart murmur and heart failure, and subsequent normal weight gain. Medication for congestive heart failure was discontinued at 4 years of age, when the cardiac silhouette had returned to normal. To date, the patient tolerates routine exercises well and does not report any symptoms. Physical examination: good general state of health, normal breathing, acyanotic, normal pulses. Weight: 53 kg; height: 165 cm; blood pressure on right arm (BPRA): 105/75 mmHg; heart rate (HR): 76 bpm. Aorta not palpable on the suprasternal notch. The apical impulse was not palpable in the precordium, and there were no systolic impulses. Normal heart sounds, no heart murmurs. Liver not palpable.

Primigravida with 40 Weeks of Gestation with SeverePreeclampsia with Dextro Cardia and SitusInversus: An Unusual Case Report

We present a 19yr old Primi Gravida with 40 weeks of gestation was referred to labour room Women & Children Hospital, affiliated to J.J.M.M.C, Davangere in view of high blood pressure for further management. She had ANC's in a nearby PHC. Her past medical history was not significant and general physical examination revealed severe PE, an apex beat located on 5th right intercostals space, suspected dextrocardia. Caesarean section was done in view of severe PE with Unfavourable cervix. During post-partum period, chest radiograph confirmed dextrocardia and also revealed the gastric air bubble on right side which suggestive of situs inversus totalis. Abdominal ultrasonography revealed a left sided liver, gall bladder with a right side location of spleen, aorta, and inferior venecava relationship altered.

Unusual cause of chest pain mimicking acute myocardial infarction: congenital left ventricular aneurysm.

A 36-year-old man without any cardiac history presented to the emergency room with ongoing chest pain. The Electrocardiography (ECG) showed diffuse ST segment elevations on the anterior leads compatible with acute anterolateral wall myocardial infarction [Table/Fig-1]. The patient was a current smoker with a family history of coronary artery disease (CAD). He had a stable hemodynamic status with normal blood pressure and pulse rate. Initial examination revealed mild systolic murmur along the left sternal border as well as lateral displacement of the apical pulse. Lung auscultation was completely normal and all peripheral pulses were palpable. He was evaluated with transthoracic echocardiography that showed reduced ejection fraction of 38% with hypokinesis of the anterior wall along with a diffuse aneurysmal apical segment [Table/Fig-2]. Depending on the high clinical suspicion of acute myocardial infarction, the patient underwent emergency coronary angiography that revealed normal coronary arteries. In order to further define the anatomy, cardiac magnetic resonance imaging (MRI) was performed [Table/Fig-3][Video-1 and 2]. Left ventricular cavity was seen to expand at the apical level associated with thinning of the myocardium concordant with a true aneurysm. The aneurysmal pouch had a size of 4x5 cm without any thrombus inside. The myocardium did not display contrast enhancement excluding evidence for fibrosis or scar tissue. The wall thickness at the apex was measured as 2 mm showing a risk for ventricular rupture. Since there was no history of trauma or recent infarction, the patient was estimated as having a congenital aneurysm. As the aneurysmal sac was a substrate for arrhythmia and thrombus formation, it was decided to be surgically repaired. The patient underwent a Dor procedure represented by reconstruction of the ventricular cavity with endoventricular patch-plasty [1]. Perioperative course was free of complications. The patient was discharged uneventfully provided that the left ventricular volumes were reduced along with improvement in systolic function. [Table/Fig-1]: 12-lead ECG of the patient on presentation showing marked ST elevations on the D1-aVL and V4-6 derivations [Table/Fig-2]: Transthoracic echocardiographic image of the apical aneurysm shown by asterisk in the apical four-chamber view [Table/Fig-3]: Cardiac magnetic resonance image showing thinning of the myocardium at the apex (arrows) along with an aneurysmal pouch (asterisk) This case appears to call attention to a rare cardiac malformation that can present to the emergency room with typical signs and symptoms of acute myocardial infarction. In the literature, congenital left ventricular aneurysms have a wide-spectrum of presentations [2,3]. Although mostly asymptomatic [4], life-threatening ventricular arrhythmias [5], embolic events due to thrombus formation [6] and sudden cardiac death due to rupture [7] have been reported so far. In our case, CAD risk factors of the patient as well as the ECG findings led to an initial misdiagnosis of acute myocardial infarction.The precise diagnosis of a congenital left ventricular aneurysm in such a case necessitates demonstration of the true aneurysm by cardiac MRI and exclusion of CAD by angiography.

Examination of the heart.

Examination of the heart.

Abstract 17289: A Baffling Heart: a 30 Year-old Man with Biventricular Heart Failure and Severe Pulmonary Hypertension

A thirty year-old man with an unknown surgery for congenital heart disease presented with intermittent chest pain and progressive decline in his exercise tolerance. Cardiovascular examination revealed a soft S1, loud S2 without splitting, right ventricular heave, a sustained and laterally displaced apical impulse and clubbing of his fingers. An echocardiogram showed d-transposition of the great arteries (d-TGA), a dilated, sub-pulmonic left ventricle (LV) with reduced function, smaller than expected sub-aortic right ventricle with reduced function, and elevated sub-pulmonic left ventricular systolic pressure without LV outflow tract obstruction. Cardiac MRI revealed d-TGA status post Senning repair, biventricular dysfunction without baffle obstruction, no evidence of repaired atrial or ventricular septal defect or delayed gadolinium enhancement. Cardiac catheterization showed a suprasystemic pulmonary artery pressure, a pulmonary vascular resistance of 18.4 Wood units and a small right to left shunt due to a baffle leak. No coronary disease was found on angiography. The patient was diagnosed with severe pulmonary arterial hypertension and biventricular dysfunction. This pattern of heart failure was discordant from the expected sequelae of palliated congenital heart defects as pulmonary arterial hypertension and LV dysfunction are both uncommon long-term complications after atrial switch. Systematic evaluation for a unifying cause of the patient’s pattern of heart failure was unrevealing until the patient presented with decompensated heart failure and evidence of stimulant withdrawal. Urine toxicology was positive for methamphetamine and the patient was diagnosed with methamphetamine induced pulmonary arterial hypertension and subpulmonic LV dysfunction. This case demonstrates the importance of understanding the common, long-term patterns of heart failure in repaired congenital heart disease and the need to search for alternative etiologies when the pattern is inconsistent. This case further shows the toxic effects of methamphetamine on the pulmonary vasculature and myocardium, which in our patient resulted in a highly unique pattern of sub-pulmonic LV dysfunction and pulmonary arterial hypertension.

86-Year-Old Man With Atrial Fibrillation and Dyspnea on Exertion

dicine, te ester, o t in ne, , MN A n 86-year-old man with a history of atrial fibrillation (AF) and lower extremity venous stasis ulcers presented to our primary care clinic to establish care. He had dyspnea on exertion that had worsened from baseline limiting his capacity to perform basic activities of daily living including getting dressed. He also had progressive lower extremity swelling for several years and had received ongoing treatment of his venous stasis ulcers from a local vascular surgeon. The patient was taking metoprolol tartrate, 25 mg twice a day, for symptomatic AF diagnosed at an outside institution. His other medications included fish oil and aspirin, 325 mg daily. He reported no nonsteroidal antiinflammatory drug use or excessive salt intake. He had not experienced any cough, sputumproduction, angina, syncope, presyncope, paroxysmal nocturnal dyspnea, orthopnea, or sleep apnea and did not use tobacco or alcohol. On examination, thepatientwas able to speak in full sentences but with difficulty. His blood pressure was 135/89 mm Hg, pulse rate was 93 beats/min, respiratory rate was 18 breaths/min, and oxygen saturation was 97% while breathing room air. His body mass index was 26 kg/m. Cardiovascular examination revealed an irregularly irregular rhythm, normal S1 and S2, and no murmurs, rubs, gallops, or heaves. The point of maximal impulse was enlarged and laterally displaced. There was mild jugular venous distention with a jugular venous pressure of 9 cm and normal waveforms. On pulmonary examination, bibasilar crackles without wheeze were noted. Abdominal examination findings were normal. Examination of the lower extremities revealed 3þ pitting edema involving both knees and healing venous stasis ulcers.

A rare case of Kartagener′s syndrome

A young boy presented with cough and intermittent breathlessness for 3 months. He used to suffer from frequent cough and cold since childhood. Clinical examination revealed bilateral coarse basal crepitations and rhonchi. His apex beat was on right 5th intercostal space in mid-clavicular line. Investigation revealed situs inversus, bi-lateral bronchiectasis, and chronic sinusitis. His semen analysis revealed the complete absence of sperm. The Saccharin test revealed impaired nasal ciliary movement. Considering all the finding, he was diagnosed as a case of Kartagener's syndrome. We are reporting this case because of its rarity and rare presence of aspermia in Kartagener's syndrome.

Case 2/2014 - 20-year-old Woman with Corrected Transposition, Pulmonary Atresia and Aortopulmonary Collateral Arteries

Clinical data: In the course of life, the patient developed three types of clinical manifestations. The first one was characterized by dyspnea and tachypnea, from birth to five months of age, increased pulmonary flow and heart failure, with cardiomegaly and hepatomegaly. The second phase was characterized by stability without significant symptoms, which lasted until the age of three, presumptive of balanced aortopulmonary flow. The third phase, with decreased pulmonary flow, had mild cyanosis that worsened two years ago. Exertion fatigue was noted for four years ago. The patient maintained saturation above 85% and up to 75% two years ago, hemoglobin = 17 g/dL and hematocrit = 62%. Physical examination: Eupneic, cyanotic +++, normal pulses, no jugular venous distention. Weight: 54 kg; height: 160 cm; BP: 115/60 mmHg; HR: 78 bpm; oxygen saturation = 78%. Aorta was palpated ++ in the suprasternal notch. In precordium, apical impulse in the 4th right intercostal space and discrete systolic impulses at the right sternal edge. Second hyperphonetic heart sound, +++, at pulmonary area, increases toward the lower left sternal edge. Discrete and mild continuous murmur, +/++, at pulmonary area, irradiating to the back. Liver was not palpated.

Case 3/2015 A 32-year-old Female Patient with Coarctation of the Aorta, Bicuspid Aortic Valve and Dilatation of the Ascending Aorta

Clinical data: The patient reports that a heart murmur had been heard at childhood; however, the diagnosis of coarctation of the aorta was made 1 month ago by echocardiogram and CT scan, performed due to recent complaints of tired legs. She performed physical activities on a regular basis and did not report headache. She was not receiving any specific medication. Physical examination: Normal breathing; acyanotic; brisk pulses in upper limbs, absent in lower limbs. Weight: 58 kg; height: 166 cm; blood pressure (BP) in right arm equal to that in left arm = 140/80 mmHg, BP in legs: 80 mmHg; heart rate (HR): 78 bpm; oxygen saturation: 96%. Aorta clearly palpable on the suprasternal notch. Thrill and grade 1/4 mild systolic murmur on the suprasternal notch. The apical impulse was not palpable in the precordium, and there were no systolic impulses on the left sternal border. Normal heart sounds; grade 1/4 systolic murmur in the aortic area and back, both on the right and left sides. Liver not palpable.

Case 3/2014 - 26-year-old man with pulmonary atresia and ventricular septal defect in late postoperative evolution.

Clinical data: Surgical correction of pulmonary atresia with ventricular septal defect and aortopulmonary collateral arteries was performed in three steps. The first one, with 19 months, with the unification of major collateral artery in the right upper lobe (8 mm) to the right pulmonary artery (RPA), which nurtured the right lower lobe, and Blalock-Taussig anastomosis from the right subclavian artery with its own collateral artery. The second one, with 27 months, with unification of the collateral artery to the left lower lobe with the left pulmonary artery (LPA) of 4 mm and Blalock-Taussig to the left with 6 mm tube in the pulmonary hilum. The third one, with nine years, with no. 18 valved corrugated pericardium tube placement and expansion of LPA and RPA anastomosis with right upper lobe artery. Immediate evolution was considered good, with pulmonary systolic pressure of 22 mmHg. Late evolution was good until the age of 26, remaining without symptoms and without medication. Physical examination: Good general condition, eupneic, acyanotic, normal pulses. Weight: 74 kg; height: 183 cm; BP = 105/70 mmHg; HR: 86 bpm. Aorta discreetly palpated with mild systolic murmur at the suprasternal notch. In the precordium, apical impulse was not palpable and there were no systolic impulses. The heart sounds were normal and moderate systolic murmur of ++ intensity was harsh across the left sternal border (LSB), not accompanied by fremitus. Diastolic murmur was mild, +/++, at the LSB. The liver was not palpable and the lungs were clear.

Anorexia nervosa artefacta

A 14 year old girl presented with an 8 month history of increasing weight loss, peaking at approximately 10%; and disordered eating, increasing pallor, intermittent fevers and lethargy on the background of a complex social situation, anxiety issues and known congenital heart disease. This occurred on the background of known previous issues regarding desire for thinness in her mother. An outpatient referral had already been made by the GP for concerns of weight loss and food restriction. At presentation she was a pale, sick, emaciated and frail looking adolescent girl. She was afebrile with tachycardia (140 bpm), tachypnoiec (RR 40 breath per min), normotensive with no significant postural drop. Further careful physical examination revealed a cardiac murmur with hyperkinetic apex beat, tender hepatosplenomegaly, red splinter haemorrhages and red macular lesions on her neck, arms and abdomen. Echocardiogram confirmed extensive vegetative lesions consistent with infective endocarditis and she was transferred for cardiac surgery. As her acute issues were being managed, the aetiology of her weight loss was explored and the possible co-existence of an eating disorder was thoroughly assessed but found not to be implicated in this case.

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