Remote monitoring of implantable cardioverter defibrillator.
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Editorial↗
Biomedical subjects
Johnson Francis
Publications and source records attributed to Johnson Francis.
Interference between cellular telephones and implantable rhythm devices: a review on recent papers.
BACKGROUND: Cardiac pacemakers and implantable defibrillators are potentially susceptible to electromagnetic interferences as they have complex circuitry for sensing and communication purposes. Cellular telephones being an important source of electromagnetic waves are likely to cause interference in the function of these devices. METHODS: A systematic analysis of studies on interaction between cellular telephones and implantable devices was done using professional databases for literature. Related articles and references of relevant articles were also searched for suitable studies. RESULTS: Fourteen studies on pacemakers and eight studies on implantable defibrillators were identified. No dangerous malfunction was found in any of the analyzed studies, but most of the studies noted interference with device function when the phone was operated very close to the device. Interference was minimally in those devices with built in feed-through filters for eliminating electromagnetic interference. Device programming and interrogation were the most susceptible phases of operation. SUMMARY: Cellular phones are likely to interfere with implantable rhythm devices if operated in close proximity or during programming of the device. Patients with implanted devices can safely use cellular phones if they are not carried close to the implanted devices or operated near them. Carrying the cellular phones in the belt position, receiving calls in the ear opposite to the side of the implanted device and keeping the phone as far away as possible while dialing can be considered a safe practice. Interrogation of the devices should take place exclusively in areas where utilization of cellular phones is strictly prohibited. Studies on pacemakers published in the current decade have shown much lesser rates of interference, possibly due to improvement in device technology.
Journal Article↗
Images in cardiovascular medicine. Ventricular tachycardia: the spectrum continues to broaden: report of Naxos disease.
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Bundle-Branch Block↗
Quality of life in patients with implantable cardioverter defibrillators.
BACKGROUND: The implantable cardioverter defibrillator (ICD) is a life saving device for individuals with life threatening ventricular arrhythmias. There is no doubt that it is a cost effective therapy in various congenital and acquired arrhythmogenic disorders. Nevertheless, shock delivery may be painful and frightening which causes psychological distress and deterioration of perceived quality of life. METHODS: A systematic meta-analysis on studies reporting quality of life in patients implanted with ICDs was done using professional databases. Related articles and references of the relevant articles were also searched for suitable studies. RESULTS: Thirty studies with a total of 3412 patients on implantable defibrillators were identified. Five of them were large randomised studies with a total of 1680 patients, while 25 were non-randomised studies. Medical Outcome Study 36-item Short Form health survey (SF -94 36) was the most common instrument used for assessment of quality of life. Only one of the 5 major randomised trial reported worsening of quality of life after implantation of a defibrillator. In the subgroup of patients receiving shocks, three out of the five trials reported worsening of quality of life. SUMMARY: Most of the randomised studies showed either neutral or better quality of life in patients on implantable defibrillators. In the subset of patients receiving shocks, worsening of quality of life was found in most randomised studies. Therefore, activation of antitachycardia pacing should be performed in every ICD-patient in order to miminze painful shocks and consequent deterioration of quality of life.
Journal Article↗
Gene therapy in cardiac arrhythmias.
Gene therapy has progressed from a dream to a bedside reality in quite a few human diseases. From its first application in adenosine deaminase deficiency, through the years, its application has evolved to vascular angiogenesis and cardiac arrhythmias. Gene based biological pacemakers using viral vectors or mesenchymal cells tested in animal models hold much promise. Induction of pacemaker activity within the left bundle branch can provide stable heart rates. Genetic modification of the AV node mimicking beta blockade can be therapeutic in the management of atrial fibrillation. G protein overexpression to modify the AV node also is experimental. Modification and expression of potassium channel genes altering the delayed rectifier potassium currents may permit better management of congenital long QT syndromes. Arrhythmias in a failing heart are due to abnormal calcium cycling. Potential targets for genetic modulation include the sarcoplasmic reticulum calcium pump, calsequestrin and sodium calcium exchanger. Lastly the ethical concerns need to be addressed.
Journal Article↗
Young male with isolated noncompaction of the ventricular myocardium presenting with atrial fibrillation and complete heart block.
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Adult↗
Biological pacemakers.
Genetically engineered pacemakers could be a possible alternative to implantable electronic devices for the treatment of bradyarrhythmias. The strategies include upregulation of beta adrenergic receptors, conversion of myocytes into pacemaker cells and stem cell therapy. Pacemaker activity in adult ventricular myocytes is normally repressed by the inward rectifier potassium current (I(K1)). The I(K1) current is encoded by the Kir2 gene family. Use of a negative construct that suppresses current when expressed with wild-type Kir2.1 is an experimental approach for genesis of genetic pacemaker. Hyperpolarisation activated cyclic nucleotide gated (HCN) channels which generate If current, the pacemaker current of heart can be delivered to heart by using stem cell therapy approach and viral vectors. The unresolved issues include longevity and stability of pacemaker genes, limitations involved in adenoviral and stem cell therapy and creation of genetic pacemakers which can compete with the electronic units.
Editorial↗
Three major coronary artery-to-left ventricular fistula: an unusual cause of a diastolic murmur at the apex.
Coronary artery fistula involving all the 3 major coronary arteries and emptying into the left ventricle is rare. We report an asymptomatic patient with coronary artery fistula from the 3 major coronary arteries communicating with the left ventricle, who presented with a diastolic murmur at the apex.
Adult↗
Idiopathic dilatation of right atrium with atrial standstill presenting as stroke.
A 48-year-old lady presenting with stroke was found to have idiopathic dilatation of right atrium with atrial standstill.
Atrial Function↗
Atrial fibrillation and hyperthyroidism.
Atrial fibrillation occurs in 10 - 15% of patients with hyperthyroidism. Low serum thyrotropin concentration is an independent risk factor for atrial fibrillation. Thyroid hormone contributes to arrythmogenic activity by altering the electrophysiological characteristics of atrial myocytes by shortening the action potential duration, enhancing automaticity and triggered activity in the pulmonary vein cardio myocytes. Hyperthyroidism results in excess mortality from increased incidence of circulatory diseases and dysrhythmias. Incidence of cerebral embolism is more in hyperthyroid patients with atrial fibrillation, especially in the elderly and anti-coagulation is indicated in them. Treatment of hyperthyroidism results in conversion to sinus rhythm in up to two-third of patients. Beta-blockers reduce left ventricular hypertrophy and atrial and ventricular arrhythmias in patients with hyperthyroidism. Treatment of sub clinical hyperthyroidism is controversial. Optimizing dose of thyroxine treatment in those with replacement therapy and beta-blockers is useful in exogenous subclinical hyperthyroidism.
Journal Article↗
Tissue tracking imaging for identifying the origin of idiopathic ventricular arrhythmias: a new role of cardiac ultrasound in electrophysiology.
Several strategies for mapping ventricular outflow tract tachycardia have been reported as useful indices for differentiating between those originating from the right and the left side. Recently, tissue tracking imaging (TTI) has been demonstrated as a novel non-invasive modality for identifying the origin of outflow tract tachycardias. Tissue tracking imaging is an ultrasonographic technique that measures the myocardial motion amplitude towards the transducer in each region during systole, identifying regional myocardial displacement on the basis of myocardial velocities using color Doppler myocardial imaging principles. In this technique, the origin of the arrhythmia could be recognized as the site where the earliest color-coded signal (ECCS) appeared on the myocardium at the onset of the systole. In preliminary studies this modality was found to be useful in differentiating outflow tract ventricular tachycardias. ECCS was always found below or at the level of the pulmonary valve in all arrhythmias which could be ablated from the right ventricular outflow tract, while in those where the ECCS was above and close to the pulmonary valve it could be ablated from the left sinus of valsalva. These results indicate that TTI can provide detailed and accurate information on the arrhythmia origin of outflow tract tachycardia and may be useful for differentiating between an outflow tract tachycardia originating from the LV epicardium remote from the LSV and that from the LSV. Newer advances in echocardiographic technologies like high resolution, high frame rate real time three dimensional echocardiography with speckle tracking may further improve the precise localization of arrhythmias in the future.
Editorial↗
Brugada syndrome.
The Brugada syndrome is an autosomal dominant disease with incomplete penetrance that may cause syncope and sudden cardiac death in young individuals with a normal heart. It is characterized by an electrocardiographic pattern of complete or incomplete right bundle branch block and ST segment elevation in leads V1-V3. One of the genes linked to this syndrome is SCN5A, the gene encoding for the cardiac sodium channel. Mutations in SCN5A cause a functional reduction in the availability of cardiac sodium current in Brugada syndrome. However, only 20-25% of patients affected by this syndrome have mutations on this gene. A novel gene locus on chromosome 3, distinct from SCN5A, has been identified recently. The relative male preponderance of the phenotype, despite equal inheritance of the gene in males and females, has led to the speculation of a role for testosterone in the phenotype. The disease could manifest at first time as cardiac arrest without any previous symptom, and the electrocardiographic pattern could be intermittent, requiring a pharmacological challenge with Class I antiarrhythmic drugs to unmask ST elevation. Several conditions producing Brugada-like electrocardiographic patterns should be borne in mind and excluded while making a diagnosis of the Brugada syndrome. The management is difficult as pharmacological agents are not universally effective. The mode of treatment recommended by the majority of cardiac electrophysiologists is the implantation of a cardioverter defibrillator. Symptomatic patients with inducible ventricular arrhythmias and a positive family history should be considered for prophylactic implantation of a cardioverter defibrillator.
Bundle-Branch Block↗
Role of implantable cardioverter defibrillators in the treatment of hypertrophic cardiomyopathy.
Hypertrophic cardiomyopathy (HCM) is an important cardiovascular disease with sudden cardiac death as the most devastating presentation. Implantable cardioverter defibrillators (ICD) are the optimal therapy for prevention of sudden death from ventricular tachycardia or fibrillation of any cause. While there is no controversy with implanting ICDs in patients who have already survived a cardiac arrest, identifying high-risk patients for primary prevention in this disease remains a challenge. Implanting ICDs in patients with HCM is an important clinical consideration since many individuals could achieve normal or near-normal lifespans with this protection.
Editorial↗
Role of catheter ablation in arrhythmogenic right ventricular dysplasia.
Arrhythmogenic right ventricular dysplasia/cardiomyopathy is a disorder characterized by frequent ventricular tachycardia originating from the right ventricle and fibro-fatty replacement of right ventricular myocardium. Though the disorder was originally described during surgical ablation of refractory ventricular tachycardia, catheter ablation of tachycardia is one of the options for patients not responding to anti arrhythmic agents. Direct current fulguration was used in the initial phase followed by radiofrequency catheter ablation. In the present day scenario, all patients with risk for sudden cardiac death should receive an implantable cardioverter defibrillator. Radiofrequency catheter ablation remarkably reduces the frequency of defibrillator therapies. Direct current fulguration can still be considered in cases when radiofrequency ablation fails, though it requires higher expertise, general anesthesia and carries a higher morbidity. Newer mapping techniques have helped in identification of the site of ablation. In general, the success rate of ablation in arrhythmogenic right ventricular dysplasia is less than in other forms of right ventricular tachycardias like right ventricular outflow tract tachycardia.
Journal Article↗
Catecholaminergic polymorphic ventricular tachycardia.
Catecholaminergic polymorphic ventricular tachycardia (VT) is a rare arrhythmogenic disease characterized by exercise- or stress-induced ventricular tachyarrhythmias, syncope, or sudden death, usually in the pediatric age group. Familial occurrence has been noted in about 30% of cases. Inheritance can be autosomal dominant or recessive, usually with high penetrance. The causative genes have been mapped to chromosome 1. Mutations of the cardiac ryanodine receptor gene (RyR2) have been identified in autosomal dominant pedigrees, while calsequestrin gene (CASQ2) mutations are seen in recessive cases. Ankyrin-B mutations may also be implicated in catecholaminergic polymorphic VT: mutations in this gene were previously linked to the long-QT 4 phenotype. Ventricular ectopy, bidirectional VT, and polymorphic VT occur in a predictable and progressive manner with increasing heart rate during exercise or isoproterenol infusion. Estimated mortality of untreated cases ranges from 30% to 50% before the age of 20-30 years according to family studies. Although beta-blocker therapy was considered to be effective in preventing clinical recurrence in the initial series, recent data show low efficacy. As there is a chance for sudden cardiac death if even a single dose of beta-blocker is missed, there is a trend toward implantation of defibrillators in more and more patients.
Calsequestrin↗
Comparison of proximal isovelocity surface area method and pressure half time method for evaluation of mitral valve area in patients undergoing balloon mitral valvotomy.
BACKGROUND: The pressure half time (PHT) method is unreliable for measurement of mitral valve area (MVA) immediately after valvotomy. The proximal isovelocity surface area (PISA) method has been used to derive mitral valve area in patients with mitral stenosis. The aim of our study was to compare PISA method and PHT method in patients undergoing percutaneous balloon mitral valvotomy (BMV). METHODS: The PISA was recorded from the apex and MVA was calculated using continuity equation by the formula 2pir(2) Vr/Vm, where 2pir(2) is the hemispheric isovelocity area, Vr is the velocity at the radial distance "r" from the orifice, and Vm is the peak velocity. A plain angle correction factor (theta)/180 was used to correct the inlet angle subtended by leaflet tunnel as a result of leaflet doming. RESULTS: MVA calculated using PISA method (r = 0.5217, P < 0.0001, SE = 0.016) and PHT (r = 0.6652, P < 0.0001, SE = 0.017) correlated well with 2D method in patients with mitral stenosis before BMV. After BMV, MVA by PISA method correlated well with 2D planimetry (r = 0.5803, P < 0.0001, SE = 0.053) but PHT showed poor correlation (r = 0.1334, P = 0.199, SE = 0.036). The variability of measurement of MVA was most marked with PHT method in the post-BMV period. CONCLUSION: The PISA method correlates well with 2D planimetry in patients with mitral stenosis before and after BMV and is superior to the PHT method in the post-BMV period where the latter may be unreliable.
Adult↗
Brief review of the recently described short QT syndrome and other cardiac channelopathies.
There are many diseases related to ion-channel disorders, so-called "channelopathies." Hereditary short QT syndrome is a clinical-electrocardiographic entity with autosomal-dominant mode of transmission and it is the most recently described channelopathy. The syndrome may affect infants, children, or young adults with strong positive family background of sudden cardiac death. Short QT syndrome is characterized by short QT and heart-rate-corrected QTc intervals. It is frequently associated with tall-, peaked-, and narrow-based T waves that are reminiscent of the typical "desert tent" T waves of hyperkalemia. There is a high tendency for paroxysmal atrial fibrillation due to the heterogeneous abbreviation of action potential duration and refractoriness of atrial myocytes. The arrhythmia can also be induced by programmed electrical stimulation. The safest treatment suggested is an implantable cardioverter defibrillator, though the possibilities of inappropriate shocks have caused some concern, especially in teenagers. The ability of quinidine to prolong the QT interval has the potential to be an effective therapy for patients with short QT syndrome. This is particularly important in developing countries, where the implantable cardioverter-defibrillator therapy is not always available. Since these patients are at risk of sudden cardiac death from birth, and implantable cardioverter-defibrillator implantation has a lot of limitations in very young children, the utility of quinidine has to be evaluated further. Clinicians need to be aware of this deadly electrocardiographic (ECG) pattern as it portends a high risk of sudden cardiac death in otherwise healthy subjects with structurally normal hearts.
Arrhythmias, Cardiac↗
Heart rate turbulence: a new predictor for risk of sudden cardiac death.
Initial acceleration and a subsequent deceleration of sinus rhythm following a ventricular ectopic beat with a compensatory pause has been termed heart rate turbulence (HRT). The changes in sinus rhythm are thought to be mediated by a baroreflex response to the lower stroke volume of the ectopic beat. HRT is vagally mediated and abolished by atropine, whereas beta-blockers have no effect. HRT has been shown to be an independent and powerful predictor of mortality after myocardial infarction. In patients on beta-blockers, it scores better than left ventricular ejection fraction (LVEF) in its predictive value. Two common measures of HRT are turbulence onset and turbulence slope. When both these measures are abnormal, it is as powerful a predictor of mortality as LVEF. HRT correlates with other indices of cardiac autonomic functions like baroreflex sensitivity and heart rate variability. A composite autonomic index including all these three has been shown to be a powerful predictor of mortality. In patients undergoing direct percutaneous intervention for myocardial infarction, HRT improves in those attaining successful reperfusion. Abnormal values for HRT have been noted in patients with dilated cardiomyopathy and Chagas disease. Diabetic and elderly individuals are more likely to have blunted HRT. HRT cannot be measured in patients lacking ventricular ectopic beats and in patients presenting with atrial fibrillation.
Arrhythmias, Cardiac↗