A–C
Aase syndrome A clinical triad of congenital anaemia, triphalangeal thumbs, and VSD. The aetiology is unknown.
Adams–Stokes syncope See Stokes–Adams syndrome (p. 706).
Alfidi’s syndrome Hypertension resulting from occlusion of the coeliac axis, leading to diversion of collateral blood flow from the right renal artery. Originally described as renal-splanchnic steal syndrome.1
Andersen syndrome A triad of periodic paralysis, ventricular tachy-arrythmias, and dysmorphic features (hypertelorism, micrognathia, low-set ears, and high arched or cleft palate, short stature, scoliosis, syndactyly, and clinodactyly). The periodic paralysis can be associated with hyper-, hypo-, or normokalaemia. It is an autosomal dominant condition associated with mutations in the KCNJ2 gene encoding the inward-rectifying K+ channel Kir2.1.2
Anderson–Fabry disease A rare X-linked recessive lysosomal storage disorder involving a deficiency of the enzyme alpha galactosidase There is a resulting in accumulation of globotriasylceramide throughout the body. Cardiac manifestations include left and right ventricular hypertrophy and heart failure. Other systemic features include renal impairment, angiokeratomas, neuropathy, and corneal keratopathy. Treatment is now available in the form of enzyme-replacement therapy.
Barlow’s syndrome A familial form of mitral valve prolapse which is sometimes inherited as an autosomal dominant trait. It is a genetically heterogenous syndrome, characterized by ‘billowing’ of one or both of the mitral valve leaflets into the left atrium during systole. On auscultation there is a midsystolic click and a late or pansystolic murmur. 20% are asymptomatic. Females are twice as commonly affected.3
Barth syndrome An X-linked mutation of the TAZ gene, leading to dilated cardiomyopathy, skeletal myopathy, short stature and neutropenia. 3-methylglutaconic acid excretion in the urine has been observed in almost all reported cases.
Beemer lethal malformation syndrome A lethal syndrome of double outlet right ventricle, hydrocephalus, dense bones, thrombocytopenia, and abnormal nasal development.
Bland–Garland–White syndrome (or ALCAPA) A congenital condition featuring anomalous origin of the left coronary artery arising from the pulmonary artery (ALCAPA) resulting in myocardial ischaemia. Affected infants typically present with congestive heart failure within the first 1–2 months of life. Definitive treatment involves surgical re-implantation of the left coronary artery or bypass grafting.1
Bouillaud’s syndrome An eponym for rheumatic fever. Bouillaud was the first to emphasize the importance of cardiac involvement in the acute articular phase of rheumatic fever.2
Bourneville–Pringle disease Hamartomas of the heart and kidney associated with epilepsy, learning difficulties, cerebral cortical hamartomas (tuberose sclerosis), and adenoma sebaceum. It is inherited in an autosomal dominant manner. Renal cysts or carcinomas may occur.3
Bradbury–Egglseton syndrome An idiopathic disorder of autonomic failure characterized by orthostatic hypotension, with more widespread manifestations of thermoregulatory, bowel, bladder, and sexual function disturbance.
Brugada’s syndrome One of the principal causes of sudden cardiac death in young adults in the absence of structural heart disease, secondary to mutation of the SCN5A gene on chromosome 3, inherited in an autosomal dominant fashion. This results in malfunction of a sodium channel leading to initiation and perpetuation of ventricular arrhythmias. Clinically there is right bundle branch block, ST elevation in V1 to V3, and sudden death/syncope. The clinical phenotype may be unmasked by the administration of ajmaline (not available in the UK) or procainamide. The only effective treatment is with an implantable cardiac defibrillator.4
Carney syndrome Also known as the Carney complex. There is association of atrial myxomas with myxomas in other locations, e.g. breast or skin, spotty pigmentation, and endocrine overactivity, e.g. pituitary or testicular tumours. The inheritance is autosomal dominant, the mutation being in the PRKAR1A gene on chromosome 17. It tends to affect individuals in their third decade. They are more likely to have bilateral myxomas and develop recurrences of the myxoma after removal, in contrast to sporadic cases.
D–M
DiGeorge syndrome A disorder resulting from deletion of the TBX1 gene on chromosome 22q11.2, leading to parathyroid hypoplasia (and hypocalcaemia), thymic hypoplasia (and low T-cell counts), and outflow tract defects of the heart, including tetralogy of Fallot, truncus ateriosus, interrupted aortic arch, right-sided aortic arch, and aberrant right subclavian artery. Affected individuals typically have micrognathia, low-set ears, short philtrum, and small mouth. The Shprintzen syndrome is also caused by a disorder in the same gene.
Dressler syndrome A myocardial infarction-associated pericarditis, usually occurring one week after the onset of infarction, but may occur several months afterwards. An autoimmune aetiology is suspected due to the delay in development of the syndrome, the presence of antibodies against the heart, evidence of altered lymphocyte subsets and complement activation, frequent recurrences, associated pleuritis and pleural effusions, and response to non-steriodal drugs and steroids. There may be a pericardial rub, fever, pericardial and pleural effusions, with PR abnormalities, as well as ST- and T-wave changes suggestive of pericarditis.
Duchenne muscular dystrophy An X-linked disorder of the dystrophin gene. There is severe skeletal muscle weakness, which may mask dilated cardiomyopathy. There is a tendency for fibrosis to affect the posterolateral and posterobasal left ventricular wall. Supraventricular arrhythmias are more common than ventricular arrhythmias and heart block, which occur as the fibrosis becomes more widespread.
Ebstein’s anomaly A malformation in which there is an abnormal attachment of the tricuspid valve leaflets leading to a downward displacement of the tricuspid valve. A portion of the right ventricle therefore lies between the atrioventricular (AV) ring and the origin of the valve, so that the proximal part of the right ventricle is ‘atrialized’, and a small right ventricular chamber exists. Tricuspid valve tissue is dysplastic. There is spectrum of severity in this condition, and it is associated with pulmonary stenosis or atresia, as well as VSD and ostium primum atrial septal defect (ASD).
Eisenmenger syndrome Any systemic-to-pulmonary circulation shunt that eventually leads to reversal or bidirectional flow of the shunt, with subsequent pulmonary hypertension and cyanosis. It was first described in a 32-year-old man with a ventricular septal defect in 1897.1
Ellis–Van Creveld syndrome An autosomal recessive condition characterized by short stature caused by metaphyseal dysplasia, poly-dactyly, dysplastic nails and teeth, and, most commonly, primum ASD. Coarctation of the aorta, hypoplastic left heart, and patent ductus arteriosus (PDA) occur in 20% of cases.
Emery–Dreifuss muscular dystrophy A clinical triad of early contractures of the elbow, Achilles tendon, and posterior cervical muscles, progressive skeletal myopathy, and cardiac manifestations. These include sinus bradycardia, atrial fibrillation and atrial flutter initially, progressing to higher levels of AV block, sustained ventricular tachycardia and ventricular fibrillation. Heart failure may also be present. Sudden death before the age of 50 years is common. It is X-linked in its transmission, with the gene responsible encoding a nuclear membrane protein called emerin.1
Fabry disease See Anderson–Fabry disease (p.438, p.698).
Fallot’s tetralogy The association of pulmonary stenosis, ventricular septal defect, over-riding aorta, and right ventricular hypertrophy, causing cyanosis in the newborn. This forms 10% of all congential heart disease, and is slightly more common in males. Fallot’s trilogy comprises pulmonary stenosis, strial septal defect, and intact ventricular septum, Fallot’s pentalogy is the addition of an atrial septum defect or patent foramen ovale to the tetralogy.2
Friedreich’s ataxia A spinocerebellar degenerative disease characterized by limb and trunk ataxia, skeletal deformities, dysarthria, and cardiomyopathy. Concentric left ventricular hypertrophy frequently occurs, as well as asymmetrical septal hypertrophy. Rarer is dilated cardio-myopathy. There may be associated atrial arrhythmias. The condition is inherited in an autosomal dominant manner, with the mutation identified as an amplified, unstable GAA trinucleotide repeat found in the first intron of the frataxin gene on chromosome 9q13.
Friedreich’s disease Sudden collapse of the cervical veins that were previously distended at each diastole, caused by an adherent pericardium. Also known as mediastinopericarditis adhesiva, or Friedreich’s sign.
Holt–Oram syndrome An autosomal dominant condition, sometimes known as heart–hand syndrome, in which there is dysplasia of the upper limbs associated most commonly with secundum ASD, but also with VSD, mitral valve prolapse, and PDA. The arm deformities may be subtle, from having distally placed or triphalangeal thumbs, to more severe forms including hypolplastic clavicles and phocomelia.
Heyde’s syndrome The association of gastrointestinal bleeding and calcific aortic stenosis. Since Heyde’s original description in 1958, the bleeding has been shown to be due to an acquired von Willebrands disease type 2a caused by high shear stress around the aortic valve, leading to haemorrhage from arteriovenous malformations in the gut. The bleeding abnormality ceases after replacement of the valve.1,2
Hurler’s syndrome An autosomal recessive mucopolysaccharide storage disorder resulting from deficiency of the lysosomal enzyme alpha-L-iduronate. It is also designated mucopolysaccharidosis type IH (MPSIH). Clinical features include coarse facial characteristics, corneal clouding, hepatosplenomegaly, thickened skin, mental retardation, and cardiac problems. These consist of restrictive cardiomyopathy due to endomyocardial fibroelastosis, coronary artery stenosis, and valvular thickening (left side more than right side) and regurgitation. Most die in the first decade. Hunter’s syndrome is MPS II, and pursues a slower course. Scheie syndrome is MPS IS, and has the most benign course of the mucopolysaccharidoses.3
Jervell–Lange–Nielsen syndrome An autosomal recessive condition associated with deafness caused by mutation in the KVLQT1 gene, or the KCNE1 gene, both encoding components of the delayed rectifier potassium channel involved in the action potential. As a result, the QT interval is prolonged and affected individuals have a variable risk of developing torsade de pointes and sudden cardiac death (SCD).
Kartagener’s syndrome A clinical triad of situs inversus, abnormal frontal sinuses, and immotile cilia. The patient has recurrent respiratory infections, sinusitis, bronchiectasis, and infertility. Some may have anosmia, or low levels of immunoglobulin A (IgA). Inheritance is autosomal recessive. The defect lies in the genes encoding the dynein protein that contributes to the structure of cilia. Also known as the Siewert syndrome.4
Kawasaki disease An acute vasculitis that affects children, which manifests with fever, cervical lymphadenopathy, bilateral conjunctivitis, erythema or desquamation of the palms and soles, and coronary artery aneurysms or ectasia. These may lead to myocardial infarction and sudden death. The aetiology is unknown.5
Kearns–Sayre syndrome A clinical triad of AV block, pigmentary retinopathy, and progressive external ophthalmoplegia. It is caused by the deletion of several mitochondrial genes. In most cases it occurs sporadically and is not inheritable.1
Leber hereditary optic neuropathy A mitochondrial encephalomyopathy characterized by painless loss of vision in a young man. There may be an associated short PR interval and pre-excitation.2
Lenegre–Lev disease Also known as progressive familial heart block type I (PFHBI). An autosomal dominant disorder mapped to chromosome 19, defined by evidence of bundle branch block with wide QRS complexes that may progress to complete heart block. This is distinct from progressive familial heart block type II (PFHBII), which has narrow QRS complexes. There is an accelerated degenerative process that primarily affects the conduction tissue.
Løffler’s syndrome A rare form of endocarditis associated with high levels of circulating eosinophils. The underlying cause may be helminthic infection or leukaemia, but in most it is unknown. Typically, the lungs are involved with diffuse reticular nodular shadowing on the chest X-ray. The acute form is characterized by an eosinophilic vasculitis that leads to dilated cardiac chambers, whereas the chronic form leads to fibrosis of myocardium leading to a clinical syndrome of restrictive cardiomyopathy, resulting in reduced effort tolerance, wheezing, hepatomegaly, heart block, mitral and tricuspid regurgitation, and systemic embolization.
Lown–Ganong–Levine syndrome A ventricular pre-excitation phenomenon characterized by a short PR interval (<120 ms) and normal QRS duration, in association with paroxysms of supraventricular tachycardia but not atrial flutter or fibrillation. Patients without a history of tachycardia may be described as having accelerated AV nodal conduction. Although first described by Clerc in 1938, the eponymous individuals reported this syndrome in 1952. No single structural abnormality has been found to be the cause of this syndrome. It may be due to intranodal or paranodal fibres that bypass the AV node. Most patients at electrophysiological study have been found to have a reason other than a bypass tract for their paroxysmal tachycardia, such as atrioventricular node re-entrant tachycardia (AVNRT). Therefore, this is a syndrome of a pre-electrophysiological study era that describes a clinical phenomenon of paroxysmal tachycardia with a short PR interval that may be at one end of the normal range (2–4% of adults have PR<120 ms).3
Libman–Sacks syndrome A cardiac manifestation of systemic lupus erythematosus, which occurs late in the disease process, and is found in 50% of patients with fatal lupus at post-mortem. It characterized by sterile, verrucous lesions on valve leaflets and chordae consisting of fibrin, neutrophils, lymphocytes, and histiocytes. The mitral and aortic valves are most commonly affected, although most cases are clinically silent. Valvular regurgitation is more common than stenosis. Similar lesions may occur in association with the antiphospholipid syndrome. Women are more commonly affected.1
Lutembacher’s syndrome The combination of mitral stenosis (congenital or acquired) and ASD (congenital or iatrogenic), with left-to-right shunt. If the ASD is large, pulmonary hypertension is avoided, but with the consequence of progressive right heart dilatation.2
Marfan syndrome A disorder resulting from mutations in the FBN1 gene on chromosome 15q21.1 encoding fibrillin-1, which constitutes the microfibrils that make up the extracellular matrix. Features include tall stature, kyphosis, scoliosis, pectus excavatum, upwards lens dislocation, dural ectasia, retinal detachment, and a variety of cardiac abnormalities. These include mitral valve prolapse and regurgitation, dilated sinuses of Valsalva, aortic root dilatation with aortic regurgitation and increased risk of dissection, and arrhythmias. Patients may be at increased risk of endocarditis secondary to the valve abnormalities. 75% are inherited as autosomal dominant; the remainder occur sporadically.3
Morquio’s syndrome One of the mucopolysaccharide storage disorders, designated mucopolysaccharidosis IVB (MPSIVB), inherited in an autosomal recessive manner. Two types are recognized. Type A is caused by deficiency of galactosamine-6-sulphatase, whereas type B is caused by deficiency in beta galactosidase. Clinical features include short stature, skeletal and joint abnormalities, cloudy corneas, hepatomegaly, and aortic and mitral regurgitation. Heart failure may result from either an infiltrative cardiomyopahthy or valvular regurgitation.4
N–W
Noonan’s syndrome A dysmorphic syndrome characterized by cardiac anomalies, short stature, low-set ears, hypertelorism, deafness, and bleeding diathesis. It is inherited in an autosomal dominant manner. Cardiac problems include valvular pulmonary stenosis. This syndrome has sometimes been called ‘male Turner’s syndrome’, although it affects both sexes, and, in contrast, has no chromosomal abnormalities.1
Ortner’s syndrome First described as compression of the recurrent laryngeal nerve by a dilated left atrium in mitral valve stenosis, giving rise to a hoarse voice from vocal cord paresis. Sometimes used to describe any non-malignant cardiac or intrathoracic process that damages the recurrent laryngeal nerve. The left nerve is more commonly affected than the right, due to its longer course around the aortic arch.
Pompe disease An autosomal recessive metabolic disorder caused by an accumulation of glycogen within lysosomes due to deficiency of the enzyme alpha-glucosidase. Cardiac manifestations include left ventricular hypertrophy, outflow tract obstruction, and heart failure. The disease can present in infants, juveniles, or adults. Treatment is available in the form of enzyme-replacement therapy.2
Prinzmetal’s (variant) angina Angina resulting from spasm of a coronary artery, which may lead to heart block and myocardial infarction. It may be prevented by long-acting calcium antagonists.3
Romano–Ward syndrome An autosomal dominant condition caused by mutation in genes on chromosomes 3, 4, 7, 11, and 21 encoding different components of both sodium and potassium channels. The QT interval is prolonged and there is a high risk of developing torsades de pointes and sudden cardiac death (SCD). It not associated with deafness and is therefore distinct from Jervell–Lange–Nielson syndrome.
Shprintzen syndrome A disorder caused by mutation in the TBX1 gene, which is also responsible for the DiGeorge syndrome. The characteristic features are cardiac anomalies (most commonly VSD), cleft palate, learning difficulties, and typical facies including prominent nose, narrow palpebral fissures, and micrognathia. Also known as the velocardiofacial syndrome.
Stokes–Adams syndrome Syncope caused by cardiac arrhythmia. Also known as Spens syndrome and Morgagni’s syndrome.4,5
Sydenham’s chorea A delayed manifestation of rheumatic fever, due to an inflammatory reaction caused by autoantibodies in the basal ganglia and caudate nuclei, following group A streptococcal infection. It usually occurs three months after the initial infection and symptoms may last for up to two weeks. It is characterized by involuntary movements, muscle incoordination, and emotional lability.
Takotsubo cardiomyopathy A syndrome that mimics acute coronary syndrome, with chest pain, ischaemic electrocardiogram (ECG) changes, and elevated cardiac enzymes. It is typically triggered by emotional or physical stress. Angiography usually demonstrates unobstructed coronary arteries, and characteristic echocardiography findings include ballooning of the left ventricular apex with a hypercontractile base, which earned the syndrome its name, meaning ‘octopus trap’ in Japanese. Treatment is supportive and patients usually recover completely.1
Taussig–Bing syndrome A congenital anomaly in which the aorta arises from the right ventricle, the pulmonary artery arises from both ventricles, and there is an associated VSD.2
Tietze’s syndrome Inflammation of the costochondral cartilages of unknown aetiology. There is characteristic swelling of the cartilages, which distinguishes the syndrome from other types of costochondritis, and the swelling may persist after the pain has resolved. Mostly men in their third decade are affected.3
Townes–Brocks syndrome An autosomal dominant condition describing the association of imperforate anus, and abnormalities of the kidneys, hand, foot, and ear, sporadically associated with cardiac malformations including VSD and ASD.
Turner’s syndrome A disorder resulting from the absence of one of the X chromosomes, XO. Features include coarctation of the aorta, short stature, absence of secondary sexual characteristics, webbing of the neck, cubitus valgus, and lymphoedema. It is one of the most common chromosomal abnormalities.4
Twiddler’s syndrome Not strictly an eponym. The phenomenon of permanent malfunction of a pacemaker due to the patient’s manipulation of the pulse generator.1
Wenkebach’s heart A description of a heart located in the midline which is smaller than normal. Also known as mesocardia, or the ‘hanging heart’.
Wenkebach’s phenomenon A form of second degree atrioventri-cular heart block characterized by progressive lengthening of the PR interval on the ECG until a P wave is not conducted to the ventricles.2
Williams syndrome A congenital supravalvular aortic stenosis associated with peripheral pulmonary artery stenosis, hypercalcaemia, elfin facies, outgoing personality, learning difficulties, strabismus, and dental anomalies. The left ventricle may be hypertrophied, and the sinuses of Valsalva may be dilated. In addition, the coronary arteries may be dilated or tortuous, and demonstrate accelerated atherosclerosis. The patient is at higher risk of endocarditis and sudden death than unaffected individuals. Autosomal dominant transmission is observed if this syndrome is inherited.
Wolff–Parkinson–White syndrome Tachyarrhythmias that occur as a result of an accessory atrioventricular pathway, typified by the ECG features in sinus rhythm of a PR interval less than 120 ms and QRS duration greater than 120 ms caused by a delta wave, representing antegrade conduction through the accessory pathway. Patients can have intermittent conduction via this pathway, leading to variable ECG patterns.3
1 Alfidi RJ, Filson EJ, Frohlich ED, Gifford RW Jr, Meaney TF (1967). Renal-splanchnic steal. Report of a case. Cleveland Clin Q 34: 43–54.
2 Donaldson MR, Jensen JL, Tristani-Firouzi, M, et al. (2003). PIP2 binding residues of Kir2.1 are common targets of mutations causing Andersen syndrome. Neurology 60(11): 1811–16.
3 Barlow J, Marchand BP, Pocock WA, Denny D (1963). The significance of late systolic murmurs. Am Heart J 66: 443.
1 Bland EF (1933). Congenital anomalies of the coronary arteries: report of an unusual case associated with cardiac hypertrophy. Am Heart J 8: 787–801.
2 Bouillaud B (1832). Traité clinique du rheumatisme articulaire. Paris.
3 Bourneville DM (1880). Sclérose tubéreuse des circonvolution cérébrales: Idiotie et épilepsie hemiplégique. Archives de neurologie Paris 1: 81–91.
4 Brugada P, Brugada J (1992). Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol 20(6): 1391–6.
1 Eisenmenger, V (1897). Die angeborenen Defekte der Kammerscheidewände des Herzens. Zeitschrift für klinische Medizin 32(suppl): 1–28.
1 Muntoni F (2003). Cardiomyopathy in muscular dystrophies. Curr Opin Neurol 16(5): 577–83.
2 Fallot ELA (1888). Contribution à l’Anatomie Pathologique de la Maladie Bleue (Cyanose Cardiaque). Marseille: Marseille Médical.
1 Heyde EC (1958). Gastrointestinal bleeding in aortic stenosis. N Engl J Med 259: 196.
2 Batur P (2000). Increased prevalence of aortic stenosis in patients with arteriovenous malformations of the gastrointestinal tract in Heyde Syndrome. Arch Intern Med 163: 1821–4.
3 Hurler G (1919). Über einen Typ multipler Abartungen, vorwiegend am Skelettsystem. Zeitschrift für Kinderheilkunde, Berlin 24: 220–234.
4 Kartagener M (1933). Zur Pathogenese der Bronchiektasien: Bronchiektasien bei Situs viscerum inversus. Beiträge zum Klinik der Tuberkulose 83: 489–501.
5 Kawasaki T (1967). Acute febrile mucocutaneous syndrome with mucoid involvement with specific desquamation of the fingers and toes in children. Jpn J Allergy 116: 178.
1 Schmitz K, Lins H, Behrens-Baumann W (2003). Bilateral spontaneous corneal perforation associated with complete external ophthalmoplegia in mitochondrial myopathy (Kearns–Sayre syndrome). Cornea 22(3): 267–270.
2 Leber (1868). Beiträge zur Kenntniss der atrophischen Veränderungen des Sehnerven nebst Bemerkungen über normale Structur des Nerven. Archiv für Ophthalmologie, Berlin 14: 164–76.
3 Lown B, Ganong WF, Levine SA (1952). The syndrome of short PR interval, normal QRS complex, and paroxysmal rapid heart action. Circulation 5: 693–706.
1 Libman E, Sacks B (1924). A hitherto undescribed form of valvular and mural endocarditis. Arch Intern Med Chicago 33: 701–37.
2 Lutembacher R (1916). De la sténose mitrale avec communication interauriculaire. Archives des Maladies du Coeur et des Vaisseaux Paris 9: 237–60.
3 Marfan AB (1896). Un cas de déformation congénitale des quatre membres, plus prononcée aux extrémités, caracterisée par l’allongement des os avec un certain degré d’aminicissement. Bulletins et Memoires de la Société Medicale des Hôpitaux de Paris 13: 220–6.
4 Morquio L (1929). Sur une forme de dystrophie osseuse familiale. Archives de Médecine des Enfants, Paris 32: 129–35.
1 Noonan A, Ehmke DA (1963). Associated noncardiac malformations in children with congenital heart disease. J Pediatr St Louis 63: 468–70.
2 Pompe JC (1932). Over idiopathische hypertrophie van het hart. Ned Tijdschr Geneeskd 76: 304–12.
3 Prinzmetal M, Massumi RA (1955). The anterior chest wall syndrome-chest pain resembling pain or cardiac origin. JAMA 159: 177–84.
4 Adams R (1827). Cases of diseases of the heart, accompanied with pathological observations. Dublin Hospital Reports 4: 353–453.
5 Stokes W (1846). Observations on some cases of permanently slow pulse. Dublin Q J Med Sci 2: 73–85.
1 Sato H, Tateishi H, Uchida T, Dote K, Ishihara M, Sasaki K et al (1990). Tako-tsubo-like left ventricular dysfunction due to multivessel coronary spasm. In: Kodama K, Haze K, Hori M, eds. Clinical Aspect of Myocardial Injury: from ischaemia to heart failure. Tokyo: Kagakuhyouronsya: pp. 56–64.
2 Taussig HB, Bing RJ (1949). Complete transposition of the aorta and levoposition of the pulmonary artery: clinical, physiological, and pathological findings. Am Heart J, St Louis 37: 551–9.
3 Tietze A (1921). Über eine eigenartige Häufung von Fällen mit Dystrophie der Rippenknorpel. Berliner klinische Wochenschrift 58: 829–31.
4 Turner HH (1938). A syndrome of infantilism, congenital webbed neck, and cubitus valgus. Endocrinology 23: 566–74.
1 Bayliss CE, Turner HH (1968). The pacemaker-twiddler’s syndrome: a new complication of implantable transvenous pacemakers. Can Med Assoc J 99(8): 371–3.
2 Wenckeback KF (1898). De Analyse van den onregelmatigen Pols. III. Over eenige Vormen van Allorythmie en Bradykardie. Nederlandsch Tijdschrift voor Geneeskunde, Amsterdam 2: 1132.
3 Wolff L, Parkinson J, White PD (1930). Bundle-branch block with short P–R interval in healthy young people prone to paroxysmal tachyardia. Am Heart J St Louis 5: 685.
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