Treatment of neurocardiogenic syncope.
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Bradycardia↗
Biomedical subjects
A P Fitzpatrick
Publications and source records attributed to A P Fitzpatrick.
Vasovagal reactions may occur after orthotopic heart transplantation.
OBJECTIVES: This study evaluated the ability of patients to manifest vasovagal reactions after orthotopic heart transplantation. BACKGROUND: Paradoxic stimulation of left ventricular baroreceptors may be the afferent limb of the vasovagal reflex in humans. Orthotopic heart transplantation causes surgical denervation of these receptors and would therefore be expected to abolish the vasovagal reflex. METHODS: To attempt to confirm this hypothesis, 10 patients with orthotopic heart transplantation underwent both head-up tilt testing while resting on a saddle support and testing for parasympathetic innervation of the donor heart before and after atropine infusion. Native and donor heart sinus rates were monitored by using an esophageal pill electrode throughout tilting and during parasympathetic testing. RESULTS: Unexpectedly, seven patients had vasovagal responses at saddle support tilt testing, during which native heart rate decreased by 25 +/- 7 beats/min and mean arterial blood pressure decreased by 55 +/- 9 mm Hg. In three of these patients, there was also a decrease in donor heart rate of 23 +/- 26 beats/min. Parasympathetic testing showed possible evidence of donor heart vagal reinnervation in these patients with donor heart bradycardia during tilt but not in those with vasovagal reactions to tilt without slowing of the donor heart rate. CONCLUSIONS: Vagal efferent reinnervation can occur after orthotopic heart transplantation in humans. However, the absence of such reinnervation in some patients with vasovagal responses to tilt calls into question the role of left ventricular receptors in inducing the vasovagal reaction.
Adolescent↗
Emergency percutaneous transluminal coronary angioplasty for intractable ventricular arrhythmias associated with acute anterior myocardial infarction.
A previously fit marathon-running 54 year old man was admitted as an emergency having collapsed with chest pain caused by an acute transmural anterior myocardial infarction. He was initially resuscitated by his general practitioner then had recurrent episodes of ventricular flutter and fibrillation requiring continuing cardiopulmonary resuscitation and repeated defibrillation. During ambulance transfer and in the hospital emergency department he received appropriate intravenous antiarrhythmic drug treatment and a total of 63 transthoracic DC shocks, with good cardiac output between shocks. After his condition failed to stabilise in intensive care, an intra-aortic balloon pump was inserted and coronary angiography showed a proximal occlusion of the left anterior descending branch. Coronary angioplasty successfully re-opened the vessel with an excellent angiographic result. The intra-aortic balloon pump was withdrawn the following day and he was well enough to be discharged 7 days later. At 4 weeks he performed a satisfactory maximal exercise test and remains in New York Heart Association functional class I.
Angioplasty, Balloon, Coronary↗
Financial audit of antitachycardia pacing for the control of recurrent supraventricular tachycardia.
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Cardiac Pacing, Artificial↗
Curing reentrant atrial arrhythmias. Targeting protected zones of slow conduction by catheter ablation.
Radiofrequency catheter ablation has become the treatment of choice for paroxysmal supraventricular tachycardia involving dual atrioventricular nodes or an accessory pathway. For reentry confined to the atrium where the arrhythmia itself or the ventricular response cannot be controlled with drugs, catheter ablation of the His bundle is a treatment option, but requires implantation of a permanent pacemaker and does not restore normal rhythm. In the atria, important anatomic obstacles, such as the great veins and the ostium of the coronary sinus, interrupt the normal arrangement of myocardial fibers. Under certain circumstances these natural obstacles, or those created during atrial surgery for congenital heart disease, may help to facilitate conditions for reentrant excitation within the atrium. The purpose of this study was to evaluate the safety and efficacy of radiofrequency ablation directed at a protected isthmus of slow conduction in patients with reentrant atrial tachycardia or flutter. Eighteen patients with drug-refractory atrial arrhythmias underwent invasive electrophysiology testing, followed in the same session by ablation using radiofrequency energy delivered between the large distal electrode of a deflectable catheter and a skin patch. In eight patients, intracardiac echocardiographic imaging was performed to compliment fluoroscopy. These 18 patients had a total of 20 atrial tachyarrhythmias: atypical atrial flutter (1 patient), typical atrial flutter (13), intraatrial reentrant tachycardia (5), and sinus node reentry (1). There were 5 women and 13 men with an age range of 8 to 81 years. Structural heart disease was present in 10 of 14 patients with atrial flutter, and 4 patients with intraatrial reentrant tachycardias had surgery for congenital heart disease. Acute success was achieved in 12 of 13 cases (92%) of typical atrial flutter and in 6 of 6 cases of other atrial reentrant tachyarrhythmias, including sinus node reentry and five arrhythmias associated with congenital heart disease surgery. One patient developed a deep venous thrombosis. Radiofrequency catheter ablation, by severing narrow corridors of slow conduction, can safely abolish reentrant atrial arrhythmias in humans. Long-term follow-up evaluation will be required since these patients generally have atrial disease and recurrence of the ablated arrhythmia or the emergence of new arrhythmias is a possibility.
Adolescent↗
A new statistical appraisal of baseline ECG features for localization of accessory pathways.
In order to develop a better approach to accessory pathway localization, the authors analyzed 18 separate electrocardiographic characteristics in 93 consecutive patients. All patients had successful radiofrequency catheter ablation of a single accessory pathway causing preexcitation, prolonging QRS duration to > 100 ms, with 56 pathways ablated on the right side of the heart and 37 ablated on the left side. Eight individual locations were specified at the time of ablation, five right sided and three left sided. Initially, a simple statistical approach was used, with group mean statistical comparison for both delta-wave frontal axis and QRS horizontal transition lead being compared between adjacent locations by Student's t-test. Overlap between individual values was assessed by calculating the percentage of total pathway numbers in each of the two adjacent locations being compared that lay within an arc of 2 SDs in the direction of the location being compared. The statistical significance of all 18 variables was tested using univariate analysis and oneway analysis of variance for continuous variables and the chi-square test for categorical data. Post hoc tests performed were Scheffe's test for the analysis of variance and Bonferroni's test for the chi-square test. All electrocardiographic characteristics were then reanalyzed in a stepwise linear discriminant analysis using BMDP statistical software. A jack-knifed classification was made to assess the accuracy of classification. The statistical level for a characteristic to enter the model was set at P < .05 and the statistical level for a characteristic to be removed from the model was set at P > .10. Six linear discriminant analyses were performed: (1) right side versus left side, (2) right free wall versus right septum, (3) right anterior free wall versus right posterior free wall, (4) right anterior septum versus, right midseptum versus right posterior septum, (5) left anterior pathway versus left posterior pathways, and (6) left posteroseptal versus left posterior free walls.(ABSTRACT TRUNCATED AT 250 WORDS)
Algorithms↗
Methodology of head-up tilt testing in patients with unexplained syncope.
Prolonged 60 degree head-up tilt has been shown to be valuable in the investigation of unexplained syncope, diagnosing neurally mediated bradycardia/hypotension or malignant vasovagal syndrome. To evaluate the methodology of tilt testing, the following were examined: reproducibility of results, tilt duration, angle of tilt, method of tilt support and effect of age in patients and control subjects. Seventy-one patients with recurrent unexplained syncope underwent 60 min of 60 degree tilt; 53 (75%) had an abnormal test with vasovagal syncope at 24 +/- 10 min (mean +/- SD). Tilting to 60 degrees resulted in an abnormal test in only 2 (7%) of 27 control subjects without cardiovascular symptoms (p less than 0.001); and 5 (15%) of 34 patients with syncope and documented conduction tissue disease (p less than 0.001). Of 15 youthful fainters, 3 (20%) had vasovagal reactions as did 1 (8%) of 12 asymptomatic youthful control subjects. These 12 control subjects also underwent tilting with a saddle support and 7 (67%) had vasovagal reactions. It is concluded that the duration of tilting at 60 degrees should be 45 min (mean time to syncope +2 x SD in the 53 patients with abnormal results). Twenty percent of patients with an abnormal tilt test may not demonstrate syncope with repeat tilting. Saddle tilt testing in unexplained syncope may result in a loss of specificity. Tilting at less than 60 degrees results in a loss of sensitivity. Head-up tilt may be less useful in youthful subjects with vasovagal syncope than in other subjects.
Aged↗
Recurrent symptoms after ventricular pacing in unexplained syncope.
We report clinical and hemodynamic data in two cases of recurrent syncope. Both patients received permanent demand ventricular pacing (VVI) for unexplained syncope. Both patients experienced recurrent syncope after pacemaker implantation. They later underwent 60 degrees head-up tilt testing, initially noninvasively and then with hemodynamic profile. A vasovagal response to tilt occurred with bradycardia and was complicated by the onset of ventricular pacing and retrograde atrioventricular conduction (RAVC) with hemodynamic deterioration and rapid reproduction of syncope. Limited intracardiac electrophysiological study (EPS) excluded atrioventricular (AV) conduction disease, sinus node disease, and carotid sinus syndrome, and confirmed RAVC. Both patients were upgraded to dual chamber pacing, DDI mode, with 50/80 rate hysteresis. One patient was asymptomatic at repeat tilt testing; the other experienced continued symptoms due to the vasodepressor component of vasovagal syncope. Cardiac pacing alone is ineffective treatment for this phenomenon, and no proven therapy is presently available. Ventricular pacing applied to patients with unexplained syncope may lead to an increase in or continuation of symptoms rather than an amelioration. There is a need for full investigation of such patients, which must include tilt testing, to allow for the most accurate diagnosis possible and guide the most appropriate therapy.
Aged↗
Familial restrictive cardiomyopathy with atrioventricular block and skeletal myopathy.
Five generations of an Italian family with an autosomal dominant restrictive cardiomyopathy are described. Members of four generations were examined. Symptoms usually developed in the third or fourth decade but the disease did occur in childhood. Initially the condition was characterised by normal ventricular size and systolic function with increased diastolic filling pressures in both ventricles and consequent bi-atrial enlargement. Cardiac catheterisation showed a left ventricular filling pattern of "dip and plateau". The electrocardiogram typically showed non-specific changes in the ST segment and T wave and changes indicating considerable atrial enlargement, which were confirmed by echocardiography. Light microscopy of two endocardial biopsy specimens showed no specific features but excluded the endomyocardial fibrosis of eosinophilic heart disease, amyloid, and specific heart muscle diseases. At necropsy in one case examined under light microscopy extensive patchy fibrosis was found throughout the endocardium, myocardium, and subepicardium, but there were no features typical of eosinophilic heart disease. Histopathological and biochemical examination of skeletal muscle identified no abnormality. The disease often had an insidious course over five to ten years after presentation. Bundle branch blocks, leading to complete atrioventricular block, however, often occurred and may be the first manifestation. Some individuals who survived into the fifth decade developed a progressive, non-wasting skeletal myopathy.
Adolescent↗
Familial neurofibromatosis and hypertrophic cardiomyopathy.
Two siblings from a family in which neurofibromatosis was inherited as an autosomal dominant had hypertrophic cardiomyopathy and neurofibromatosis. Idiopathic hypertrophic cardiomyopathy may have occurred by chance in two first degree relatives with neurofibromatosis. An alternative explantation is that these diseases are both manifestations of a common hereditary defect of neural crest tissue. Another possibility is that abnormalities of catecholamine metabolism and nerve growth factor in neurofibromatosis can cause secondary ventricular hypertrophy with septal involvement.
Adult↗
Cardiac tumours simulating collagen vascular disease.
Cardiac tumours can mimic collagen vascular disease and they are often accompanied by profound systemic upset. Both benign and malignant tumours may present in this way. Three cases of cardiac tumour, two malignant and one benign, are reported with just such a presentation. A review of fifteen similar case reports showed that a spectrum of different collagen vascular diseases was diagnosed and treated before the true diagnosis emerged. In half of these cases the cardiac tumour was only diagnosed at necropsy. The diagnosis of collagen vascular disease should not be made in the absence of corroborative laboratory data. In cases of malignant cardiac tumour, and less commonly with atrial myxoma, M mode and cross sectional echocardiography may not exclude the diagnosis. There may be a good response to steroid treatment in cases of suspected but not confirmed collagen vascular disease in which the true diagnosis is cardiac tumour.
Adolescent↗