Stokes-Adams Attacks Research Articles

Lessons from the first patient with an implanted pacemaker: 1958-2001.

On October 8, 1958 the world’s first pacemaker implantation was performed at the Karolinska Hospital in Stockholm, Sweden. The system had been developed by the surgeon A ◦ ke Senning and the physician inventor Rune Elmqvist. The patient was a 43-year-old engineer suffering from Stokes-Adams syndrome. His name was Arne H.W. Larsson (Fig. 1). At the time Senning was in charge of the experimental laboratory at the newly inaugurated Department of Thoracic Surgery at the Karolinska Hospital in Stockholm. Elmqvist was head of the Electromedical Division at Elema Schonander in Stockholm. He had studied medicine in Lund, Sweden but had not pursued a medical practice. Rather, he had become a self-taught engineer. In 1931 he had designed the first portable optical electrocardiographic (ECG) recorder and in 1948 had introduced the well-known direct writing Mingograf ink jet recorders. When Senning and Elmqvist met in 1950 they began a close cooperation in the development and testing of fibrillators and defibrillators for use in conjunction with open heart surgery, then an experimental procedure. Senning had studied and been inspired by the experimental work of Bigelow and Callaghan1,2 in stimulation for hypothermic cardiac standstill and Zoll who used external chest wall stimulation for management of Stokes-Adams attacks.3,4 During a visit to Minneapolis in 1957, Senning observed C. Walton Lillehei during open heart surgery suture stainless steel electrodes to the ventricle to manage surgically caused atrioventricular (AV) block, after closure of a ventricular septal defect. The wires were led through the thoracic wall and connected to an external pulse generator. This method avoided the discomfort and placement problems in the postoperative patient associated with Zoll’s external pacemaker. Senning considered this to be the beginning of the era of clinical pacing.5,6 On returning to Stockholm, Senning studied Lillehei’s technique experimentally and clini-

An unusual case of blackouts in insulin-treated diabetes mellitus

54-year-old man presented with a one month history of thirst and polyuria, and diabetes mellitus was confirmed by a random plasma glucose of 20 mmol/L. Dietary advice was given and gliclazide (80 mg twice-daily) prescribed. The hyperglycaemic symptoms resolved within two weeks. One year later the gliclazide dose was increased to 160 mg twice-daily because of inadequate glycaemic control and, after a further six months, metformin therapy was introduced and increased to 1 g twice-daily. Some eight months later a random plasma glucose was 26 mmol/L, and glycated haemoglobin 9.7% (n.r. 5.0‐6.2%), therefore insulin therapy was commenced with Human Mixtard 30/70 insulin twice-daily. Glycaemic control improved and four months later the glycated haemoglobin level had fallen to 7.4%. At this stage, the patient complained of intermittent dizzy spells, associated with exertion. Palpitations were not noticed. The home blood glucose monitoring showed pre-meal values of 4‐5 mmol/L, pulse rate was 80 per minute and regular, and blood pressure was 130/80 mmHg both lying and standing. No cardiac murmurs were heard on auscultation and there were no features of peripheral or autonomic neuropathy. The patient was on no medication other than insulin. It was felt hypoglycaemia might be a cause of these dizzy episodes and the insulin dose was reduced, thus the tight glycaemic control eased to allow preprandial glucose values of 7‐9 mmol/L. Nethertheless the exertional dizziness continued and on two occasions there was apparent syncope with spontaneous recovery without glucagon or intravenous glucose being required. A 24-hour cardiac monitor tape showed no heart block or arrhythmia. However, a transthoracic echocardiogram showed a large left atrial myxoma which was confirmed by transoesophageal echocardiogram which showed the left atrial myxoma was attached to the interatrial septum by a long stalk. The myxoma was successfully removed under cardiopulmonary bypass (figure 1). Some sevenyears later, the patient remains free of dizziness and syncope. His glycaemic control continues to be satisfactory with a glycated haemoglobin of 7.2%. Cardiac tumours are rare. The commonest is the myxoma which occurs most frequently in the left atrium and is usually attached, as in this case, to the atrial septum. Because its position may vary with posture, transient or complete obstruction of the mitral valve may occur leading to dizziness or syncope. Variable mitral systolic and diastolic murmurs may be heard but are not always present. The diagnosis is established readily by echocardiography. In a tightly controlled insulin-requiring diabetic subject, it is not unreasonable to suspect dizziness and light-headedness, and even blackouts may be due to hypoglycaemia with neuroglycopenia. In older subjects adrenergic ‘warning symptoms’ may not be present. However, it is important to consider the possibility of other non-hypoglycaemic causes. These might be diabetic in nature e.g. postural hypotension due to autonomic neuropathy where a systolic fall of blood pressure of 20‐30 mmHg will produce syncopal type symptoms. Alternatively, cerebrovascular or cardiovascular factors are more often seen in diabetic subjects at an earlier age. Vertebro-basilar insufficiency or abnormalities of cardiac rate or rhythm (Stokes-Adams attacks) are other possibilities. Twenty-four hour or even 48-hour continuous cardiac monitoring may be helpful in diagnosing the latter. Finally, rarer cases of cardiac syncope may need to be considered. In the case presented, the left atrial myxoma was readily diagnosed by echocardiography and the patient cured by successful cardiac surgery.

急性心筋梗塞に合併した完全房室ブロックによるＡｄａｍｓ‐Ｓｔｏｋｅｓ発作のために自動車事故を起こした１例

急性心筋梗塞に合併した完全房室ブロックによるＡｄａｍｓ‐Ｓｔｏｋｅｓ発作のために自動車事故を起こした１例

Internal architecture of the proximal femur--Adam's or Adams' arch? Historical mystery.

The designation 'Adam Bogen' describing the thick medial cortex of the femoral neck is an incorrect term. This arch was described by Robert Adams (1795-1871), an outstanding Irish anatomist and surgeon. He was famous mainly for his book on gout and the description of disorders of cardiac rhythm, the so-called Adams-Stokes syndrome. He published his original description in the today unfortunately almost forgotten Cyclopaedia of Anatomy and Physiology, Vol. II (London, Longman, 1836-1839). The main editor of this monumental six-volume work was the famous anatomist and surgeon R.B.Todd. This book represents a significant source of information on diseases and injuries of the great joints (shoulder, elbow, wrist, knee, ankle).

History of Heart Block

Annals of Noninvasive ElectrocardiologyVolume 7, Issue 1 p. 78-78 Free to Read History of Heart Block “Stokes-Adams Disease” Prof. William Osler M.D., F.R.S., Prof. William Osler M.D., F.R.S. Rochester, NYSearch for more papers by this authorArthur J. MOSS MD, Corresponding Author Arthur J. MOSS MD Rochester, NYAddress for Reprints: Arthur J. MOSS, M.D. Box 653, University of Rochester Medical Center, Rochester, NY 14642 Fax: (716) 273–5284.Search for more papers by this author Prof. William Osler M.D., F.R.S., Prof. William Osler M.D., F.R.S. Rochester, NYSearch for more papers by this authorArthur J. MOSS MD, Corresponding Author Arthur J. MOSS MD Rochester, NYAddress for Reprints: Arthur J. MOSS, M.D. Box 653, University of Rochester Medical Center, Rochester, NY 14642 Fax: (716) 273–5284.Search for more papers by this author First published: 27 October 2006 https://doi.org/10.1111/j.1542-474X.2001.tb00144.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume7, Issue1January 2001Pages 78-78 RelatedInformation

Stokes-Adams disease.

Stokes-Adams disease.

Illustrations of the effects of rheumatic gout or chronic rheumatic arthritis on all the articulations with descriptive and explanatory statements. 1857.

Illustrations of the effects of rheumatic gout or chronic rheumatic arthritis on all the articulations with descriptive and explanatory statements. 1857.

A case of dilated cardiomyopathy with AdamsStokes syndrome complicated ventricular tachycardia induced by class I c antiarrhythmic

A case of dilated cardiomyopathy with AdamsStokes syndrome complicated ventricular tachycardia induced by class I c antiarrhythmic

Colles-Stokes Contributions to the Concept of Heart Failure

“Colles fracture,” “Colles law,” “Stokes-Adams syndrome,” “Cheyne-Stokes respiration,” and “Corrigan pulse” are some of the contributions of the Irish school that are utilized for teaching purposes in medical schools and training programs, as well as in daily practice of medicine. We wish to add an important description by Drs. Colles and Stokes that personifies the considerable personal contributions of these 2 physicians in our understanding of the pathophysiologic expression of the syndrome of heart failure. The clinical–pathologic correlation of the disease that affected Dr. Colles is well described by Dr. Stokes in his treatise Diseases of the Heart and the Aorta. He recognized the cyclical nature of frequent decompensations in heart failure, the relation of clinical worsening in conjunction with reduced urine output, as well as the importance of reestablishing urinary flow to achieve a decrease in dyspnea. Dr. Colles also demonstrated a profound clinical insight when he noticed, first, that his affliction was “eventually a fatal disease and that remedies that work may lose effect over time,” illustrating an observation that has stood the test of time and, secondly, when he told Dr. Smith “… I would direct particular attention to the heart and the lungs … and the swelling in the right hypochondrium … I suspect that there is some connexion between this swelling of the hypochondrium and the diseased state of the heart.” We believe that the Colles-Stokes contributions, both in the clinical as well as the clinical–pathologic arenas, are one of the landmark descriptions that helped to evolve the concept of the syndrome of heart failure.

Adams-Stokes症候群をともなった猫の第3度房室ブロックの1例

In a one-year and three-month-old female mongrel cat with syncope, which was cardiographically diagnosed as third degree A-V block, isoproterenol administration was effective improving general condition, and no syncope (Adams-Stokes syndrome) occurred for the duration of four months.

Recurrent syncope of unknown origin: value of permanent pacemaker insertion

We studied the outcome of permanent pacing in those with a history suggestive of Stokes-Adams attacks but no electocardiographic evidence of bradyarryhthmia. Of 11 patients who fulfilled pre-defined inclusion criteria, over a mean follow-up period of 5.4 years, seven patients were free of symptoms and two were much improved following pacing. We suggest that in those with a clinical history of frequently recurrent Stokes-Adams attacks and a normal electrocardiogram, pacemaker insertion may be a reasonable course of action.

Isolated Congenital Complete Atrioventricular Block in Adult Life

The prognosis of congenital complete atrioventricular block (CCHB) is usually considered favorable in adults. This belief is based on studies comprising a limited number of patients and with rather short observation times. In the present study, the natural history of the disease was investigated by a prospective follow-up through decades of adult life of patients with a large group having well-defined CCHB without structural heart disease. The diagnostic criteria of CCHB proposed by Yater were applied. Patients registered as having CCHB in 1964, supplemented by younger patients all without symptoms during their first 15 years of life, were selected. The study was limited to patients with isolated, complete, permanent block. An interview was conducted with all patients and clinical follow-up data obtained. There were finally 102 patients, 61 women and 41 men. In November 1994, the time of observation, after the age of 15 years in survivors, was between 7 and 30 years. The mean age at follow-up or at death was 38 years, median age 37 years, and range 16 to 66 years. Stokes-Adams (SA) attacks occurred in 27 patients, in 8 with a fatal outcome. The first attack was fatal in 6 of these 8 patients. Nineteen survived and a pacemaker (PM) was implanted thereafter. Another 8 patients received a PM because of repeated fainting spells, and 27 others have had a PM implanted for other reasons such as fatigue, effort dyspnea, dizziness, ectopies during exercise tests, mitral regurgitation, and a low ventricular rate (VR). VR decreased with age, with a mean rate at 15 years of 46 beats per minute (bpm), at 16 to 20 years of 43 bpm, at 21 to 30 years of 41 bpm, at 31 to 40 years of 40 bpm, and after 40 years of age of 39 bpm. SA attacks occurred in all 7 patients with prolonged QTc time. Low VR at rest or at work, presence of bundle-branch block pattern, low working capacity, and ectopies at rest and/or during effort were not statistically significant risk factors. SA attacks occurred in 6 patients without any of these signs. Mitral regurgitation developed in 16 patients and 4 died. A PM reduced the risk of death. A change to a lower degree of block occurred in 6 patients. Prophylactic PM treatment is recommended even for symptom-free adults with CCHB because of the high incidence of unpredictable SA attacks with considerable mortality from first attacks, a gradually decreasing VR, significant morbidity, and a high incidence of "acquired" mitral insufficiency.

Congenital AV Block

Congenital complete atrioventricular block (CCAVB) has been recognized for almost 100 years. First described by Morquio1 in 1901, it has been of interest in the past primarily because of the risk of Stokes-Adams attacks or sudden cardiac death in these patients.2 3 4 5 6 As a result of some of these studies4 5 6 and others,7 8 the Committee on Pacemaker Implantation published the American College of Cardiology/American Heart Association Task Force Report in 19919 with specific indications for implantation of a pacemaker in the presence of CCAVB. Although this syndrome is not diagnosed solely in children, the section under which these guidelines appear is “Indications for Permanent Pacing in Children.” This certainly makes sense from the perspective that this disease is congenital in nature and initially recognized in childhood. With the advent of fetal echocardiography, in utero diagnosis of CCAVB has resulted in earlier intervention in newborns. Heightened suspicion of the possibility of CCAVB in children born to mothers with connective tissue disease, especially systemic lupus erythematosis, has had the same consequence. To those faced with making the difficult decision of when to implant a pacemaker in an infant or child, arbitrary guidelines can be of concern. Should an asymptomatic newborn be referred for a pacemaker if the average heart rate when awake is found to be 58 beats per minute, or must this be done only if it is less than the recommended value of 55 beats per minute? What is the best plan for a 6-year-old referred to the clinic because of a murmur recognized during a school physical examination in whom complete AV block incidentally happens to be found on the ECG? The child’s parents give a history that the child seems “normal” to them in terms of keeping up …

Clinical and Electrophysiological Characteristics of Atrial Standstill

To clarify the clinical and electrophysiological characteristics of atrial standstill (AS) we studied 11 patients (7 males and 4 females), whose average age was 62 years and who were followed over a period of 4-179 months. Underlying heart disease was present in nine patients and two cases were idiopathic. Major clinical symptoms in the 11 cases included Adams-Stokes attacks, and dyspnea on exertion. In the standard 12-lead ECGs obtained on admission, the P wave was absent in six cases. Atrial flutter (AF) was noted in 3, atrial fibrillation (Af) in 1, and multifocal atrial tachycardia in 1. In some cases, the ECG initially showed AF or Af, and was transformed after several years into ectopic atrial tachycardia or an ectopic atrial rhythm with a markedly decreased amplitude of the P wave. Finally, the P wave disappeared over a prolonged period. When intracardiac mapping was performed, the atrial electrograms tended to diminish at the site of high, mid-lateral right atrium (RA). Electrograms were remained present in the vicinity of the tricuspid valve (TV) annulus. A repeated mapping and pacing study conducted in two patients revealed that the "silent" area spread toward the lower site of RA. During the average follow-up period of 64 months, four patients died. The interval until death in one patient with myocarditis was 6 months, and in another with dilated cardiomyopathy (DCM) it was 8 months. It appears that the atrial muscular lesion starts in the high lateral RA and progresses toward the lower RA, then to the vicinity of the TV annulus. A diffuse and progressive disturbance may occur not only in the atrial muscle, but also in the atrioventricular conduction system in patients with AS who had progressive myocarditis or DCM.

A pill for old people.

On Being a Doctor1 November 1994A Pill for Old PeopleRoger M. Cass, MDRoger M. Cass, MDUniversity of Rochester; Rochester, NY 14620Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-121-9-199411010-00015 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail She was coming up on her 92d birthday. After two lens implants, her eyesight was good and her hearing was, well, selective. She had had a few Stokes-Adams attacks, a bit of angina, and mild hypertension treated with diltiazem, but her mind and her Irish wit, every bit of it, were all there.She had told me when I was a boy, “When people get old they ought to give them a pill”. This went right by me, as did her casual remark 50 years later that she was never going to Hebron Hall, the skilled nursing home in her ... Author, Article, and Disclosure InformationAffiliations: University of Rochester; Rochester, NY 14620 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByFrance 1 November 1994Volume 121, Issue 9Page: 717KeywordsFatigueHearingHematologic testsHypertensionMyocardial infarctionNursesNursing homesOilsRespirationStroke Issue Published: 1 November 1994 CopyrightCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...

Diagnostic dilemma: ‘nocturnal fits‘

Dear Sir, Doctors face diagnostic dilemmas when managing elderly patients with multiple pathology. A 70-year-old man was seen in outpatients with the following history. About 1 week previously he had gone to bed feeling well but had woken his wife early in the morning with what looked like a bad dream. His eyes were rolling, the body was rigid and in spasm, shaking uncontrollably. During the next 20 minutes his wife could not evoke any response: there was froth at the comers of his mouth but he was not incontinent. His wife said that over the past 18 months he had been getting attacks in which he would ‘go off momentarily for two or three seconds, as if he was going to pass out‘, but had always recovered immediately and completely. He has a past history of pulmonary tuberculosis, and had to retire from the army. He suffers from bronchitis and uses ipratropium bromide and salbutamol inhalers. He has arthritis affecting the cervical and lumbar spine, with poor mobility. On examination his blood pressure was 130/80 mmHg, pulse 70/min and regular, there was no cardiac murmur or carotid bruit, and the chest was clear. Fundi showed grade 1 changes only. There was no neurological deficit. ECG showed basic sinus rhythm and grade 1 heart block. At times the heart rate slowed to 42/min, showing marked bradycardia. Routine investigations, including skull and chest x-rays, were reported normal. With the history and ECG findings, we thought the patient might have had a Stokes-Adams attack during the night, and admitted him for further investigation. On 24-hour ambulatory monitoring he showed a heart rate varying between 42 and 121/min. There were two recordings of asystolic events in the early hours of the morning, and grade 1 heart block. His EEG was reported normal. He was referred to the cardiologist at Hull Royal Infirmary, where he had further tests carried out and was fitted with a permanent pacemaker. However, after 6 weeks he had another nocturnal episode, witnessed by his wife. His rhythm strips showed occasional pacing as well as sensing failure. The faulty electrode was removed and a new permanent, screw-in type biotronic lead placed. A 24-hour rhythm tape showed this to be working satisfactorily. He was reviewed regularly in our clinic and in Hull. After about 2 months the patient had another nocturnal ‘fit‘. His minor episodes of passing out had not recurred. He was again admitted to cardiology 4 months after we had first seen him, where about 10 days later he had an epileptic fit lasting 6–7 minutes at 4.30am. When he returned to consciousness there was no neurological deficit. Repeat EEG was normal. CT scan of the skull showed two quite well-defined high-density lesions in the right temporal region, with some calcification. These were suggestive of a large right middle cerebral artery aneurysm (perhaps multiloculated and bleeding). He was seen by the neurosurgeon, and 4-vessel angiography showed a long, irregular aneurysm, extending from the posterior communicating origin on the right, extending laterally. There was a small aneurysm arising from the origin of one of the striate vessels on the same side. A diagnosis of bleeding aneurysm was made. The epileptic fits were thought to be related to the aneurysm but not to the cardiac problem, which was stable with the pacemaker. He was operated on in spite of his age, as the risk of leaving the bleeding aneurysm was thought to be greater than that of surgery. The posterior communicating artery aneurysm was clipped, clots were removed, and the patient made a good recovery. This case, with its interesting clinical problems, has made us aware of the danger of multiple pathology, and we have learned to maintain an open-minded approach. Thanks are due to Mrs P Gillham for her secretarial services.

Nocturnal Enuresis Secondary to Heart Block: Report of Cure by Cardiac Pacemaker Implantation

This report describes an unusual case of secondary nocturnal enuresis presumptively secondary to progressive bradycardia from complete heart block. Congenital complete heart block occurs in approximately 1 of 22,000 livebirths and is typically associated with structural congenital heart disease or maternal collagen vascular diseases. It can be entirely asymptomatic during infancy and childhood, depending in part on the escape rate and rhythm and other hemodynamic variables. The case described above was not diagnosed until the patient coincidentally underwent cardiac monitoring. The picture was confusing initially, as a tricyclic antidepressant medication had been ingested. Heart block is one of the known cardiovascular effects of tricyclic antidepressant overdose. However, the conduction disturbance should have resolved as the drug was excreted from the body. As children with congenital complete heart block get older, the ventricular escape rate typically decreases. In addition, as activity increases with age, more demand is placed for cardiac output. The resting end-diastolic volume is increased to elevate stroke volume in compensation for lower heart rate. As the escape rate decreases and the metabolic demand increases, patients with congenital complete heart block then may begin to develop symptoms. Typical symptoms in children include dizziness, Stokes-Adams syncopal attacks, fatigue, daytime somnolence, and other somatic complaints. Bedwetting has not been reported as an initial symptom, but in this case is likely secondary to the excessive somnolence and difficulty with arousal.(ABSTRACT TRUNCATED AT 250 WORDS)

Feasibility of Long‐Term Electrocardiographic Monitoring with an Implanted Device for Syncope Diagnosis

Patients with infrequent recurrent syncope undiagnosed after extensive noninvasive and invasive testing pose a diagnostic and therapeutic dilemma. The purpose of this pilot study was to assess the feasibility of using an implanted, long-term monitor as an aid to diagnosis in these patients. This was done using commercially available pacemakers with monitoring functions. Sixteen patients (eight males and eight females), aged 59.7 +/- 17 years who had unexplained syncope despite a 12-lead electrocardiogram, repeated Holter monitoring, exercise testing, echocardiography, an electrophysiological study, and a tilt test (n = 6), were entered into the study. Patients had experienced a mean of 3.1 +/- 1 episodes of syncope in the 12 months prior to the study. All provided a history suggestive of Stokes-Adams attacks and were referred for consideration of pacemaker implantation. Two patients had ischemic heart disease and one patient had a long QT interval. Patients had an Intermedics Nova II or Medtronic Quintech DPG pulse generator capable of recording sensed and paced events implanted with a single right ventricular lead. Syncope or presyncope occurred in ten patients (62%) 4.9 +/- 4.2 months after pacemaker implantation. Bradycardia was detected in six patients and four patients had no arrhythmia. In addition to bradycardia, one patient also had tachycardia detected. Pacing therapy resulted in symptom relief in all six patients with syncope or presyncope due to bradycardia. Complications of pacemaker implantation (lead insulation failure) occurred in two patients. One of these patients subsequently had an infection of the generator pocket with associated systemic sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)

Management of Stokes-Adams Syndrome

Stokes-Adams attacks are related to paroxysmal or chronic atrioventricular (AV) block (50-60%), sinoatrial (SA) block (30-40%) or paroxysmal tachycardia or fibrillation (0-5%). In between attacks most patients present with sinus rhythm, a large part with widened QRS complex. A minor proportion of patients present with chronic AV block. ECG is very rarely normal. Diagnosis is based on ECG recording during fainting. In patients with sinus rhythm and bundle-branch block or AV block, ECG monitoring should be performed in hospital, since Stokes-Adams syndrome in these patients is a potentially life-threatening disease. In sick sinus syndrome where the suspected arrhythmia is not life-threatening, ambulatory ECG by Holter monitoring can be performed to establish the diagnosis. In cases where ECG monitoring leaves doubt, an electrophysiologic study including His bundle electrography and sinus node recovery time may support the diagnosis, although normal findings do not preclude the diagnosis. Pacemaker implantation should be performed in Stokes-Adams syndrome, as oral drug treatment is ineffective. The dual-chamber pacemaker presents the advantages of both physiological heart rate and AV synchrony, but has troublesome side effects. Most patients with tachycardia/bradycardia syndromes require supplementary anti-arrhythmic treatment, and in some patients additional long-term anticoagulation should be considered.

Malignant Lymphoma with Adams-Stokes Syndrome as the First Manifestation

Malignant Lymphoma with Adams-Stokes Syndrome as the First Manifestation