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PubMed1984

Radiation induced failures of complementary metal oxide semiconductor containing pacemakers: a potentially lethal complication.

New multi-programmable pacemakers frequently employ complementary metal oxide semiconductors (CMOS). This circuitry appears more sensitive to the effects of ionizing radiation when compared to the semiconductor circuits used in older pacemakers. A case of radiation induced runaway pacemaker in a CMOS device is described. Because of this and other recent reports of radiation therapy-induced CMOS type pacemaker failure, these pacemakers should not be irradiated. If necessary, the pacemaker can be shielded or moved to a site which can be shielded before institution of radiation therapy. This is done to prevent damage to the CMOS circuit and the life threatening arrythmias which may result from such damage.

Aged↗
PubMed1988

Neutrophils as potential participants in acute myocardial ischemia: relevance to reperfusion.

An interaction among leukocytes, platelets and endothelial cells is important in atherogenesis and in maintenance of blood flow and vascular tone. These complex cell-cell interactions are mediated by release of such metabolic substances as arachidonic acid metabolites, growth factors, oxygen free radicals and endothelium-derived relaxing factor. These substances participate in the regulation of blood flow in health and disease, and perturbation in the delicate equilibrium among various cellular elements may lead to evolution and propagation of myocardial ischemia. During reperfusion of ischemic myocardium, neutrophils together with platelets cause capillary plugging in the coronary microcirculation and exert detrimental effects on endothelial function resulting in the "no reflow" phenomenon, ventricular arrythmias, loss of coronary vascular reserve and, perhaps, extension of cellular injury. This review addresses the mechanisms of cell-cell interactions with special reference to myocardial ischemia and the potential for development of improved therapy to protect and preserve ischemic myocardium.

Arachidonic Acids↗
PubMed1991

Benefits of implantable defibrillators are overestimated by sudden death rates and better represented by the total arrhythmic death rate.

Benefits of the implantable defibrillator on survival were studied in 56 consecutive patients (concomitant coronary bypass or arrythmia surgery in 15) during an 8 year period between 1982 and 1990. During a follow-up period of 29 +/- 25 months, six patients had a sudden death and eight patients had a nonsudden cardiac death. Nonsudden cardiac deaths included three surgical deaths (death within 30 days after the surgery; two in patients without and one in a patient with concomitant cardiac surgery), one arrhythmia-related nonsudden death (death within 24 h after an arrhythmic event despite initial termination of the arrhythmia by the implantable defibrillators) and four nonarrhythmic cardiac deaths. The actuarial survival rate free of events at 1, 2 and 3 years was 96%, 96% and 92%, respectively, for sudden death, 91%, 91% and 87% for sudden death and surgical mortality and 89%, 89% and 85% for total arrhythmic death (sudden death, surgical mortality and arrhythmia-related nonsudden death). Thus, in patients treated with an implantable defibrillator, 1) the rate of sudden death is low (8% at 3 years); 2) 50% of nonsudden cardiac deaths are causally related to arrhythmia (surgical mortality or arrhythmia-related nonsudden death); 3) the total arrhythmic death rate is substantially higher than the sudden death rate; and 4) benefits of an implantable defibrillator are overestimated by reported sudden death and nonsudden cardiac death rates. The benefits may be better represented by the total arrhythmic death and nonarrhythmic cardiac death rates.

Actuarial Analysis↗
PubMed1993

Plasma atrial natriuretic peptide response to direct current cardioversion of atrial fibrillation in patients with mitral stenosis.

OBJECTIVES: The purpose of this study was to evaluate the effect of direct current cardioversion therapy on the plasma concentration of atrial natriuretic peptide and to determine the main factors that influence the change in plasma atrial natriuretic peptide levels in patients with atrial fibrillation. BACKGROUND: In atrial arrythmias, whether the fast atrial rate itself or the associated elevation of atrial pressure, or both, contributes to the increase in atrial natriuretic peptide is a subject of debate. METHODS: In 15 patients with mild mitral stenosis, plasma atrial natriuretic peptide levels were measured and transmitral flow pattern was obtained by continuous wave Doppler echocardiography immediately before cardioversion and at 5 min, 4 h, 24 h and 5 days after direct current cardioversion. Mean mitral pressure gradient and atrial filling fraction were calculated on the basis of transmitral flow. RESULTS: In three patients who did not have a successful return to sinus rhythm, plasma atrial natriuretic peptide levels remained elevated after cardioversion. In 12 patients who maintained sinus rhythm, plasma atrial natriuretic peptide levels were significantly reduced from 79 +/- 29 to 36 +/- 11 pg/ml 4 h after cardioversion to sinus rhythm. However, the mitral pressure gradient did not change significantly during the observation period. There were progressive increases in atrial filling fraction throughout the observation period. From 4 h to 5 days after direct current cardioversion, plasma atrial natriuretic peptide levels gradually increased concomitantly with the recovery of atrial mechanical function. CONCLUSION: The reduction of plasma atrial natriuretic peptide levels after direct current cardioversion might be due to recovery from the high rate of atrial firing and not to an alteration in the mitral pressure gradient. Direct current cardioversion itself does not seem to influence atrial natriuretic peptide secretion. The increase in atrial natriuretic peptide levels from 4 h to 5 days after cardioversion concomitantly with an increase in atrial filling fraction may be due to recovery of atrial mechanical function.

Adult↗
PubMed1995

Development and validation of a claims based index for adjusting for risk of mortality: the case of acute myocardial infarction.

We developed a comorbidity index on a cohort of 162,699 Medicare beneficiaries who had an acute myocardial infarction (AMI) in 1987 and validate it on two national cohorts: (1) a cohort of 164,427 Medicare beneficiaries who had an AMI in 1988 and (2) a cohort of 10,466 patients admitted to Veterans Administration Hospitals (VAH) for AMI in 1988-1991. The impact of each sensitivity was expressed as; (1) the risk of mortality for those with the comorbidity, (2) the adjustment to the log odds for 2 year mortality and (3) the age-based likelihood of 2 year mortality. Models were validated by calculated the area under an ROC curve obtained by fitting a logistic regression model to each validation population. The two year mortality rate for 30-day survivors was approximately 30% in each of the 3 cohorts. The 5 most prevlent comorbidities coded in the developmental cohort were heart failure (34%), chronic angina (27%), minor arrythmias (25%) and uncomplicated hypertension (18%). Cancer was the most powerful predictor of 2 year mortality, impacting mortality the same as a 18.3 year age increase. Saturation (having all secondary diagnoses in the discharge summary filled) resulted in a 9.2 year age increase. Validation in the 1988 Medicare and in the Veterans Administration Hospitals cohorts resulted in areas of 73% and 72% under the respective ROC curves. Our methods can serve as a prototype for others wishing to assess comorbidity in other targeted subgroups.

Aged↗
PubMed1995

Expression in Escherichia coli of soluble and M13 phage-displayed forms of a single-chain antibody fragment specific for digoxin: assessment in a novel drug immunoassay.

A high affinity anti-digoxin single-chain Fv antibody fragment (scFv) was cloned from the mouse 2C2 hybridoma cell line and was functionally expressed both in the Escherichia coli periplasm as a soluble molecule and at the surface of the filamentous M13 bacteriophage as a fusion protein with the gene III minor coat protein. The 2C2 scFv sequence significantly differs from that of all the other anti-digoxin antibodies previously described. The 2C2 scFv shares with its parental monoclonal antibody a high specificity for digoxin, a cross-reactivity with active digoxin metabolites, but none with inactive metabolites. M13 phages displaying the 2C2 scFv at their surface have a high apparent affinity constant for digoxin (6.6 x 10(8) M-1) and were directly used to set up a novel type of immunoenzymatic assay for monitoring digoxin in sera of patients treated for either congestive heart failure or cardiac arrythmias. We thus report for the first time that phages displaying scFv may constitute a large source of important new reagents in the field of immunodiagnosis.

Animals↗
PubMed2004

Sudden unexpected death in children with a previously diagnosed cardiovascular disorder.

BACKGROUND: It is known that children with previously diagnosed heart defects die suddenly. The causes of death are often unknown. OBJECTIVE: The aim of the study was to identify all infants and children within the Netherlands with previously diagnosed heart disease who had a sudden unexpected death (SUD), and to identify the possible cause of death. DESIGN: Retrospective, cross-sectional study. PATIENTS AND SETTING: All children (<19 years) with a previously diagnosed heart defect and SUD between January 1990 and June 2001 in seven out of eight tertiary centres in the Netherlands were identified using the hospital databases. We excluded patients receiving compassionate care. Diagnoses, clinical status and circumstances of death were sought from case notes and post mortem reports. Deaths were classified as of cardiac or non-cardiac origin. RESULTS: We identified 150 cases of SUD (89 male) at a median age of 2.3 years (range 18 days-18.9 years); 49/150 patients (33%) were </=1 year. Diagnostic categories included left to right shunts (N=34, 14 </=1 year), cyanotic lesions (N=38, 13 <==1 yar), cardiomyopathy (N=11, 2 </=1 year), univentricular heart (N=24, 10 </=1 year), obstructive lesions (N=11, 3 </=1 year), arrhythmia (N=8, 0 </=1 year), and miscellaneous defects (N=18, 5 </=1 year). 108/150 patients (72%) had been operated of whom 61 (57%) had corrective surgery. Of the infants with SUD, 32/49 (65%) had undergone surgery (11 corrective); 76/101 older children had undergone previous surgery (50 corrective). 114/150 children (76%) died of a cardiac cause. Causes of death were arryhythmia (59), heart failure (25), shunt occlusion (10), pulmonary hypertensive crisis (8) and acute myocardial infarction (4). 30/49 infants (61%) died of a cardiac cause; causes of death included arrythmia (10), heart failure (8), shunt occlusion (7), acute myocardial infarction (2). CONCLUSIONS: SUD in children with heart defects were predominantly of cardiac origin. Pumpfailure and arrhythmias were the terminal events in a significant number of patients in the entire population.

Adolescent↗
PubMed2006

Stabilization of inhomogeneous patterns in a diffusion-reaction system under structural and parametric uncertainties.

Many phenomena such as neuron firing in the brain, the travelling waves which produce the heartbeat, arrythmia and fibrillation in the heart, catalytic reactions or cellular organization activities, among others, can be described by a unifying paradigm based on a class of nonlinear reaction-diffusion mechanisms. The FitzHugh-Nagumo (FHN) model is a simplified version of such class which is known to capture most of the qualitative dynamic features found in the spatiotemporal signals. In this paper, we take advantage of the dissipative nature of diffusion-reaction systems and results in finite dimensional nonlinear control theory to develop a class of nonlinear feedback controllers which is able to ensure stabilization of moving fronts for the FHN system, despite structural or parametric uncertainty. In the context of heart or neuron activity, this class of control laws is expected to prevent cardiac or neurological disorders connected with spatiotemporal wave disruptions. In the same way, biochemical or cellular organization related with certain functional aspects of life could also be influenced or controlled by the same feedback logic. The stability and robustness properties of the controller will be proved theoretically and illustrated on simulation experiments.

Diffusion↗
PubMedDate not supplied

Carnitine-acylcarnitine translocase deficiency, clinical, biochemical and genetic aspects.

The carnitine-acylcarnitine translocase (CACT) is one of the components of the carnitine cycle. The carnitine cycle is necessary to shuttle long-chain fatty acids from the cytosol into the intramitochondrial space where mitochondrial beta-oxidation of fatty acids takes place. The oxidation of fatty acids yields acetyl-coenzyme A (CoA) units, which may either be degraded to CO(2) and H(2)O in the citric acid cycle to produce ATP or converted into ketone bodies which occurs in liver and kidneys. Metabolic consequences of a defective CACT are hypoketotic hypoglycaemia under fasting conditions, hyperammonemia, elevated creatine kinase and transaminases, dicarboxylic aciduria, very low free carnitine and an abnormal acylcarnitine profile with marked elevation of the long-chain acylcarnitines. Clinical signs and symptoms in CACT deficient patients, are a combination of energy depletion and endogenous toxicity. The predominantly affected organs are brain, heart and skeletal muscle, and liver, leading to neurological abnormalities, cardiomyopathy and arrythmias, skeletal muscle damage and liver dysfunction. Most patients become symptomatic in the neonatal period with a rapidly progressive deterioration and a high mortality rate. However, presentations at a later age with a milder phenotype have also been reported. The therapeutic approach is the same as in other long-chain fatty acid disorders and includes intravenous glucose (+/- insulin) administration to maximally inhibit lipolysis and subsequent fatty acid oxidation during the acute deterioration, along with other measures such as ammonia detoxification, depending on the clinical features. Long-term strategy consists of avoidance of fasting with frequent meals and a special diet with restriction of long-chain fatty acids. Due to the extremely low free carnitine concentrations, carnitine supplementation is often needed. Acylcarnitine profiling in plasma is the assay of choice for the diagnosis at a metabolite level. However, since the acylcarnitine profile observed in CACT-deficient patients is identical to that in CPT2-deficient patients, definitive identification of CACT-deficiency in a certain patient requires determination of the activity of CACT. Subsequently, mutational analysis of the CACT gene can be performed. So far, 9 different mutations have been identified in the CACT gene.

Animals↗
PubMed2006

Sleep and vascular disorders.

It is not surprising that cardiovascular diseases such as congestive heart failure and coronary insufficiency can give rise to varying degrees of sleep impairment; it is less readily appreciated that certain physiologic events occurring during sleep-as well as long-term unsatisfactory sleep-may cause or increase the risk of cardiovascular conditions such as hypertension, atherosclerosis, stroke, and cardiac arrythmias. Heart rate abnormalities during sleep in normotensive subjects predict later cardiovascular disease, and their early identification alerts the physician to undertake preventive measures. Maneuvers, such as induction of hypoxia, can elicit abnormal blood pressure responses during sleep, and such responses have been used to identify impending cardiovascular problems that could become therapeutic targets. The spontaneously hypertensive rat has been used to examine the effect of sympathetic nervous system (SNS) activity on the heart under a variety of experimental conditions, including quiet and paradoxical sleep. The results have disclosed significant differences between the responses of spontaneously hypertensive rats and normal rats to SNS stimulation. Exploration of other pathophysiologic pathways affected by exposure to light and dark, including those responsive to the cyclic production of melatonin, will improve our understanding of the effect of disruptions of the circadian cycle on cardiovascular function. There is growing evidence that melatonin can influence important processes such as fluid, nitrogen, and acid-base balance. Human subjects whose nocturnal arterial blood pressure fails to show the "normal" decrement during sleep ("nondippers") are also prone to sleep poorly, exhibit increased SNS activity during sleep, and have an increased risk of total and cardiovascular disease mortality. Chronic sleep deficit is now known to be a risk factor for obesity and may contribute to the visceral form of obesity that underlies the metabolic syndrome. The rising prevalence of obstructive sleep apnea and central sleep apnea is linked to the modern-day epidemic of obesity. Obstructive sleep apnea is associated with an enhanced risk of having a new stroke or a transient ischemic attack.

Animals↗
PubMed2005

Cardiovascular interventional MR imaging: a new road for therapy and repair in the heart.

Over the last 5 years, interventional MR imaging has been fertile ground for research. Real-time MR imaging, combined with recent advances in other MR imaging modalities such as perfusion imaging and intravascular imaging, has opened up new paths for cardiac therapy. The recent reports on cardiac stem cell therapy guided and monitored by MR imaging suggest that we are already seeing the establishment of an important role for cardiac MR imaging in cardiac restoration. The collaborative effort from a multidisciplinary team of basic biologists, engineers, and clinicians will refine stem cell incubation and labeling for MR-guided transcatheter endomyocardial injections, and this in turn may facilitate new studies in humans. Several groups have demonstrated in animal studies the feasibility of MR-guided catheter interventions for the treatment of congenital heart disease and arrythmia therapy. Hence, applications in humans remain the challenge for the next years. Although there have been first reports of cardiac catheterizations in humans by combined use of x-ray fluoroscopy and MR imaging, there are no reports in the literature suggesting that active tracking methods by MR imaging have been applied to humans. Safety issues (namely, heating of catheters and wires) hamper clinical use, particularly in infants and children. Current reports are promising that these limitations will be overcome in the near future and will eventually reduce x-ray usage during catheterization. In its current state, cardiac MR imaging offers a unique opportunity to investigate new therapeutic strategies for the treatment of congenital and acquired heart disease.

Cardiac Catheterization↗
PubMed2005

Seizures, syncope, or breath-holding presenting to the pediatric neurologist--when is the etiology a life-threatening arrhythmia?

Using case reports from their own experience and in the literature the authors illustrate the difficulty in distinguishing non-life threatening causes, including epilepsy, from a serious cardiac arrythmia when evaluating children with paroxysmal events. Focusing on long QT syndrome, they suggest an approach for the pediatric neurologist that utilizes the electrocardiogram recorded during the electroencephalogram--direct measurement of the corrected QT interval. This approach requires knowledge of the distribution of the corrected QT interval in long QT syndrome.

Adolescent↗
PubMed1976

The effect of coronary bypass surgery on exercise-induced ventricular arrhythmias.

Ninety-one patients with angiographically proved coronary artery disease and stable angina were randomly assigned into surgical and medical therapy. Graded exercise tests were performed on entry into the study and repeated in 1 year. Ventricular arrhythmias during exercise and 8 minutes of recovery were studied. Arrhythmias were graded on a scale of 0 to 7 by their presumed severity. On entry, both groups were similar in the severity of coronary disease, exercise capacity, and frequency and severity of exercise-induced ventricular arrhythmias. At 1 year, the frequency and severity of arrhythmias remained unchanged in both groups, whereas the surgically treated patients showed a marked improvement in their exercise capacity (p less than 0.005). The medically treated patients had a slight deterioration in their work capacity which, however, did not achieve statistical significance (p = 0.08). Twelve patients died suddenly. In seven medically treated patients who died suddenly, the frequency and severity of ventricular arrythmias on exercise were not different from those of the rest of the medical patients. In the five surgically treated patients who died suddenly, one had multiform premature ventricular beats, a second developed ventricular fibrillation (2 years before dying suddenly), and a third had no arrhythmias during exercise. Two died before the 1 year evaluation. Successful coronary surgery improves exercise capacity without decreasing associated ventricular arrhythmias. Exercise-induced ventricular arrhythmias, with the exception of ventricular fibrillation, may not be closely associated with the risk of sudden death.

Arrhythmias, Cardiac↗
PubMed2003

Relations among heart failure severity, left ventricular loading conditions, and repolarization length in advanced heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

In patients with heart failure (HF), low peak oxygen consumption (VO(2)) and prolonged QT interval or enhanced QT variability are associated with poor prognosis. Whether HF severity or left ventricular (LV) loading conditions can influence repolarization length is unknown. Survival, QTc interval, peak VO(2), clinical, laboratory, echocardiographic, and invasive hemodynamic data were analyzed in 154 transplant candidates; mortality was examined after a mean follow-up of 4.3 +/- 1.8 years. The relation between the QTc interval and other variables was examined using multivariate analysis and multiple correlation coefficients. Patients were stratified by peak VO(2) to study its relation with peak VO(2), mortality, loading conditions, and QTc intervals. Mean ejection fraction was 10 +/- 9%; mean cardiac index was 2.06 +/- 0.7 L/min/m(2). Seventy-one patients (47%) were dead at the end of study. Mortality and nonfatal ventricular arrythmias were higher (p <0.01) in patients with lower peak VO(2) and longer QTc intervals (p <0.001). An inverse correlation was found between QTc interval length and peak VO(2) (r = -0.790, p <0.0001). No correlation was found between QTc interval and LV loading conditions or the other analyzed variables. Thus, repolarization length measured by the QTc interval is inversely correlated with HF severity measured by peak VO(2) and is independent of LV loading conditions in patients with severe HF.

Cardiomyopathies↗
PubMed1996

The results of atrial flutter ablation in patients with and without a history of atrial fibrillation.

To determine the impact of atrial flutter radiofrequency catheter ablation on recurrence of atrial flutter and atrial fibrillation, 32 patients with atrial flutter (18 with a history of atrial fibrillation) were followed for a mean of 8.6 months; atrial flutter has not recurred after 1 (26 patients) or 2 (5 patients) successful ablation procedures. Atrial flutter did not appear proarrhythmic for atrial fibrillation, with only 1 of 15 patients without a history of atrial fibrillation developing the arrythmia in the absence of an alcohol binge or cocaine use.

Atrial Fibrillation↗
PubMed1988

Sleep apnea and hypothyroidism: mechanisms and management.

PURPOSE: There is a high incidence of sleep apnea in patients with untreated hypothyroidism. Thyroxine treatment is said to significantly reduce the apnea index and length and sleep apnea symptoms. We undertook a review of 10 consecutive hypothyroid patients with sleep apnea to investigate mechanisms and management of these two disorders. PATIENTS AND METHODS: Polysomnograms were obtained in 10 consecutive hypothyroid patients referred to our sleep disorders unit. All patients were studied while hypothyroid. Eight patients were restudied later when euthyroid. Lung function, blood gas values, and awake supraglottic resistance were also assessed in each patient. RESULTS: All 10 patients had sleep apnea and were treated with thyroxine. In one patient, hypothyroid myopathy involving the upper airway was demonstrated to be a potential mechanism of sleep apnea in hypothyroidism. Nocturnal angina and ventricular arrhythmias developed in two patients, despite the use of low thyroxine doses. Nasal continuous positive airways pressure (CPAP) was begun in eight patients. Initiation of CPAP prevented further angina or arrythmia in the patients with these cardiac complications. Six of the eight patients who were available for follow-up studies had persistent sleep apnea despite an euthyroid status (apnea index before thyroxine, 51 +/- 6; apnea index after thyroxine, 45 +/- 8), and CPAP therapy was continued in these patients. CONCLUSION: Our experience suggests that the apnea index does not decrease significantly in all patients with hypothyroidism and sleep apnea when euthyroidism is achieved. Treatment of hypothyroidism in the presence of sleep apnea is potentially hazardous and may lead to cardiovascular complications. Management by a combination of CPAP and low-dose thyroxine is helpful in this situation.

Aged↗
PubMed2001

Modulation of chagasic cardiomyopathy by interleukin-4: dissociation between inflammation and tissue parasitism.

Chronic chagasic cardiomyopathy (CChC) is characterized by an inflammatory reaction which may eventually lead to heart enlargement, arrythmia, and death. As described herein, interleukin-4-deficient mice mount increased specific T helper (Th) 1 immune responses when infected with Trypanosoma cruzi, as compared to wild-type mice. Interestingly, these mice had reduced parasitism and mortality and exacerbated inflammation in their hearts, demonstrating a clear dissociation between inflammation and parasite load. The modulation of these phenomena so as to maximize host and parasite survivals may depend on a fine balance between Th responses, in which a Th1 response will, on one hand, control parasitism and, on the other hand, enhance heart inflammation throughout the course of the infection.

Animals↗
PubMed2000

The complication rate of edrophonium testing for suspected myasthenia gravis.

BACKGROUND: The incidence of life-threatening complications from edrophonium chloride (Tensilon) testing for suspected myasthenia gravis is thought to be extremely low. We carried out a survey to determine the rate of serious complications from such testing. METHODS: In April 1998, 357 physicians listed in the 1998 roster of the North American Neuro-ophthalmology Society were mailed a questionnaire for anonymous completion. Questions asked included the number of years the clinician had practised neuro-ophthalmology, the estimated number of edrophonium tests performed since completion of training, the number and nature of major complications from edrophonium, and whether the clinician preferred the sleep test or ice test to edrophonium testing. RESULTS: The response rate was 56% (199/357). Of the 199 respondents, 105 (53%) had practised neuro-ophthalmology for at least 10 years. The group estimated that they had performed at least 23,111 edrophonium tests, of which 37 (0.16%) were associated with a serious complication, mostly attributed to brady-arrythmias and syncope. Respiratory failure, seizure, severe vomiting and transient ischemic attack were also reported. Thirty-one respondents (16%) preferred the sleep test or ice test to the edrophonium test; one-third of this group reported a serious complication with edrophonium. INTERPRETATION: The rate of significant complications of edrophonium testing is low, but the complications can be potentially life threatening. Clinicians should know the nature and incidence of these complications when obtaining informed consent for edrophonium testing.

Cholinesterase Inhibitors↗