Biomedical subjects
Publications and source records attributed to J Snoeck.
We report a case of aortic valve endocarditis, caused by Capnocytophaga canimorsus (previously known as CDC Group DF-2) secondary to a dog bite. Vegetations were documented by cross-sectional echocardiography and bacteraemia by positive haemocultures for this unusual gram-negative bacillus.
The change of the pacing rate in response to external vibration interference was assessed in four rate responsive pacemakers with a piezoelectric crystal (Medtronic Activitrax 8403, Siemens Sensolog 3, Biotronik Ergos 01, and Medtronic Legend 8417) and one with an accelerometer (CPI Excel VR 1119). They were tested in the laboratory. External vibration was simulated in vitro by exposing the different pacemakers to a controlled sinusoidal vibration force generated by a Millar pressure vibration amplifier type MGM-30 (Millar Instruments, Inc., Houston, TX, USA). All pacemakers were programmed at standard settings. Two types of vibration forces were applied: (1) one with varying amplitude but with constant vibration frequency; and (2) one with varying frequency but with constant vibration amplitude. In this manner curves of pacing rate versus vibration forces versus vibration frequency were obtained. High vibration forces and low vibration frequencies were associated with the highest pacing rate response. In this experimental setting, the pacemaker based on the accelerometer principle apparently was the least sensitive to high frequency vibrations, which are known to be related to environmental interference. It also seemed more appropriately responsive in the lower frequency range, which is more appropriate for the detection of true physiological activity.
This study assesses the value of P wave measurements on the surface ECG at implantation, in the prediction of atrial fibrillation in VVI paced patients. From a consecutive series of 320 pacemaker implantations 172 VVI paced patients for symptomatic atrioventricular block (AVB) (n = 126; mean age 69 +/- 14) or sick sinus syndrome (SSS) (n = 56; mean age 68.6 +/- 12) and in sinus rhythm at implantation were used in this study. P wave duration in V1 is correlated with the incidence of atrial fibrillation during 5 years of follow-up. V1 at implantation was significantly longer (114.6 +/- 2.7 msec) in the patients who developed atrial fibrillation than in those who did not (91.9 +/- 2.7 msec) (P < 0.001). Although positive predictive accuracy increases progressively for higher V1 values for AVB and SSS, the negative predictive and diagnostic accuracy of V1 criteria were less in SSS. Application of the Bayes' theorem showed that in SSS the probability to develop atrial fibrillation is 33% for V1 < 110 msec and is for V1 < 90 msec still higher than that reported in DDD paced patients. In the AVB group the probability to develop atrial fibrillation is 8% for V1 < 110 msec and 6% for V1 < 100 msec. It seems, therefore, that atrial stimulation (AAI or DDD) is always indicated in SSS. In AVB with V1 < 100 msec, DDD pacing, if not needed for other indications, apparently does not offer much benefit in the prophylaxis of atrial fibrillation.
The P waves of patients with VVI pacemakers were compared with those of DDD pacemakers at implantation and then regularly for 5 years. A certain number of cardiac pathologies are known to cause P wave changes. The incidence of atrial fibrillation (AF) was much higher in VVI than in DDD patients. In the VVI group, the incidence was much greater in patients paced for sinus node disease than in patients paced for AVB. Analysis of sinus P wave characteristics in 320 patients with VVI pacemakers shows progressive abnormalities of atrial function with time. The expression of this atrial dysfunction is a statistically significant prolongation of the P wave in V1 and dII and of the terminal part of the P wave in V1. The factors responsible for this abnormality and which favours the occurrence of AF are quasi-permanent pacing, the presence of retrograde conduction and an abnormality of atrial activation at the time of implantation.
This study is an investigation of the long-term effects of VVI pacing on the atrium as derived from the evolution of P wave characteristics of 285 patients. The occurrence of left and right atrial disease is demonstrated as well as the evolution of left atrial hypertrophy in some cases. A comparison is made with DDD pacing and special attention is given to the progression to atrial fibrillation.
Bipolar pacing and sensing-recording on the same electrode is a problem during pacemaker implantation as well as during electrophysiological studies. A method is described that makes this possible. By using bipolar simultaneous sensing-pacing on the same electrode, the system can record local repolarization after a depolarization controlled by stimulation. The bipolar-paced evoked potential is useful as an indicator to drive a bipolar QT rate responsive pacemaker. Even more, during EPS it can be used to detect capture during tachycardia stimulation and to measure the exact refractory period.
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To determine the diagnostic value of R wave amplitude changes occurring during exercise testing after myocardial infarction, exercise ECG's and coronary angiograms were reviewed in 76 postinfarction patients and in 40 patients with normal coronary arteries. During exercise, an increase in R wave amplitude (mean: + 2.7 +/- 1.3 mm) was observed in the postinfarction patients, significantly different (P less than 0.001) from the decrease (mean: - 2.6 +/- 1.1 mm) observed in the group with normal coronary arteries. Although this change increased with the number of diseased coronary arteries, the difference between 1-vessel and multi- or 3-vessel disease was not significant. Extension of infarct size from one to more akinetic segments on the left ventricular angiogram was associated with a significant (P less than 0.001) increase of the R wave amplitude change during exercise (mean: + 1.6 +/- 1.1 vs 3.3 +/- 1.3 mm). It is concluded that the abnormal increase in R wave amplitude observed during exercise testing after myocardial infarction is more strongly related to infarct size then to the number of diseased coronary arteries. Furthermore exercise induced R wave amplitude changes have no diagnostic value in the prediction of multi- or 3-vessel disease in postinfarction patients.
Two patients with prosthetic valve endocarditis due to methicillin-resistant Gram-positive cocci (Staphylococcus epidermidis and Micrococcus spp.) are described. They were successfully treated with rifampicin combined first with an aminoglycoside and later with co-trimoxazole or co-trimoxazole plus vancomycin. The addition of rifampicin to these antibiotics resulted in enhanced serum bactericidal activity. High doses of rifampicin (1200-1800 mg) for 7-8 weeks did not cause any serious side-effect. Surgery was not required. During surveillance for more than 2 years endocarditis did not recur.
The results of prospective noninvasive cardiologic investigations, including echocardiography and Holter monitoring are described in 2 siblings with juvenile ceroid lipofuscinosis of the Spielmeyer-Vogt-Sjögren type. In the elder patient, echocardiography revealed ventricular hypertrophy with slowed ventricular relaxation. Holter monitoring showed not only bradycardia but also slow and fast ectopic atrial rhythms, sinus arrests and complex ventricular ectopic activity including ventricular tachycardia. In the younger patient the findings were less severe. These functional disturbances due to cardiac involvement, never reported before in this disease, are discussed.
The prognosis of patients after an acute myocardial infarction depends on the extent of the myocardial damage, its resulting left ventricular dysfunction and on the number and degree of narrowing of diseased coronary arteries. Patients with a severe multivessel disease constitute a high-risk group with an important morbidity and mortality during the first few months after hospitalization for a myocardial infarction. They could benefit from early revascularization therapy, whether by coronary artery bypass surgery, whether by percutaneous transluminal coronary angioplasty. Although early coronary revascularization is still controversial, management of patients after a myocardial infarction certainly will improve from a more accurate risk profiling by a careful diagnostic evaluation--including coronary arteriography in some subsets of patients--during the in-hospital period.
Clinical and biologic features of adult Still's disease developed in a patient who had high antibody titers against Yersinia enterocolitica during his illness. Immunocomplexes containing antibodies against Yersinia antigens were isolated at the beginning of the disease. Yersinia was not isolated from blood or stool specimens probably because we observed the patient during the secondary phase of the disease.
The electro-, phonomechano- and echocardiographic manifestations observed in a family with documented X-linked Becker-type muscular dystrophy (BMD) are described. Important myocardial dystrophic lesions may occur in young patients with BMD. They are associated with typical electrocardiological findings which were described as a distinctive pattern in Duchenne-type muscular dystrophy. Myocardial involvement is seldom observed in heterozygotes for BMD.
To determine the occurrence of inhibition of pacing by sensing of myopotentials, forty-five patients with predominant pacemaker driven heart rhythm were studied. In eleven patients with a bipolar lead system myopotential inhibition was never observed. In the remaining group (34 patients) with unipolar pacemakers myopotential inhibition was demonstrated in fifteen patients. Three of them were symptomatic, two severely. In forty new implants a silicone-rubber insulating sheath was placed against the muscular side of the pacemaker. In none of these patients myopotential inhibition could be demonstrated. The authors conclude that myopotential inhibition occurs frequently in unipolar ventricular inhibited pacemakers, and can be prevented by insulating the muscular side of the anodal surface.
The antihypertensive and clinical effects of two centrally acting drugs, guanabenz and clonidine, were compared in a double-blind trial in 29 patients with established hypertension. After a 1-week baseline period and 2 weeks on placebo, patients received treatment with either guanabenz (mean dose 24 mg daily) or clonidine (mean dose 0.45 mg daily) alone for 8 weeks. Both drugs produced equivalent and highly significant (p < 0.001) reduction in systolic and diastolic blood pressures in the standing and supine positions. They also reduced significantly the standing and supine pulse rates. Normal orthostatic responses were maintained with both regimens. All but 1 patient in each group reported side-effects during active treatment, the most frequent being dry mouth and sedation with each drug. No laboratory or ECG abnormalities related to treatment were observed.
The present publication reviews actual knowledge of the electrophysiological properties of low doses of digitalis in perspective of its use in patients with ventricular dysrhythmia. Both animal experiments and observations in humans have demonstrated that increased adrenergic and decreased cholinergic tone predispose to ventricular arrhythmia. An increased cholinergic tone on the other hand has been shown to protect against increased ventricular vulnerability, especially in situations of increased adrenergic tone. Therefore the combination of the cholinergic and anti-adrenergic actions of digitalis may help to control situations of increased ventricular vulnerability. This principle is especially attractive because digitalis, in contrast to classical anti-arrhythmics is devoid of any cardiodepressive effects. The clinical experience with digitalis in ventricular dysrhythmia as documented by the group of Lown is discussed in detail. The studies presently available do not yet allow digitalis to be accepted as a drug of first choice in this indication, but its careful use is not longer to be rejected for patients with non-digitalis induced ventricular dysrhythmia.
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