Biomedical subjects
Publications and source records attributed to W G de Voogt.
A set of images in which a pacemaker lead replacement procedure was complicated by occlusion of the proximal subclavian vein is presented. However, this was not detected on venography performed before the procedure. Physicians should be aware of a more proximal occlusion of the subclavian vein while replacing pacemaker leads, even in cases with seemingly normal venography.
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This study investigated the ability to minimize pace polarization artefacts (PPA) by adjusting the post-stimulus pulse duration of a tri-phasic stimulation pulse. Adjustment of the stimulation pulse was enabled by downloading special study software into an already implanted pacemaker. Tests were performed in a total of 296 atrial leads and 311 ventricular leads. Both chronic and acute leads were included in the study. Statistically significant differences were found in the initial PPA (without any adjustment of the stimulus pulse) between atrial and ventricular leads. In addition, significant differences were observed among various lead models with respect to changes over time in the initial ventricular PPA. Successful PPA reduction was defined as a reduction of the PPA below 0.5 mV for atrial leads and below 1 mV for ventricular leads. Results show a success rate for ventricular and atrial PPA reduction of 97.8% and 98.7%, respectively. Threshold tests showed that after reduction of the PPA loss of ventricular capture can be reliably detected. However, atrial threshold tests showed many false positive evoked response detections. In addition, unexpectedly high evoked response amplitudes were observed in the atrium after reduction of the PPA. Results from additional measurements suggest that these high atrial evoked response amplitudes come from the influence of the input filter of the pacemaker.
OBJECTIVE: To evaluate whether the presence of viable myocardium, detected by low dose dobutamine echocardiography, limits the likelihood of left ventricular dilatation in patients with acute myocardial infarction. PATIENTS: 107 patients were studied by low dose dobutamine echocardiography at (mean (SD)) 3 (1) days after acute myocardial infarction. Cross sectional echocardiography was repeated three months later. Patients were divided in two groups based on the presence (n = 47) or absence (n = 60) of myocardial viability. RESULTS: Baseline characteristics were comparable between the two groups, except for infarct location. Left ventricular end diastolic volume index (EDVI) was stable in patients with viability, but end systolic volume index (ESVI) decreased significantly (p = 0.006). Patients without viability had a significant increase in both EDVI (p < 0.0001) and ESVI (p = 0.0007). Subgroup analysis in patients with small and large infarcts (peak creatine kinase < or = 1000 v > 1000 IU/l) showed that ventricular dilatation occurred only in patients with large infarcts without viability. This resulted in larger ESVI values at three months in that group compared with patients with large infarcts plus viability (p < 0.05). Multivariate regression analysis identified myocardial viability as an independent predictor of left ventricular dilatation, along with wall motion score index on low dose dobutamine echocardiography and the number of pathological Q waves. CONCLUSIONS: The presence of viability early after acute myocardial infarction is associated with preservation of left ventricular size, whereas the absence of viability results in ventricular dilatation, particularly in large infarcts.
OBJECTIVE: To evaluate the relation between changes in ejection fraction during the first three months after acute myocardial infarction and myocardial viability. PATIENTS: Myocardial viability was assessed using low dose dobutamine echocardiography in 107 patients at mean (SD) 3 (1) days after acute myocardial infarction. Cross sectional echocardiography was repeated three months later. Left ventricular volumes and ejection fraction were determined from apical views using the Simpson biplane formula. RESULTS: In patients with viability, ejection fraction increased by 4.4 (4.3)%; in patients without viability it remained unchanged (0.04 (3.6)%; p < 0.001). A > or = 5% increase in ejection fraction was present in 21 of 107 patients (20%). Receiver operating characteristic analysis showed that myocardial viability in > or = 2 segments predicted this increase in ejection fraction with a sensitivity of 81% and a specificity of 65%. Multivariate logistic regression analysis was used to define which clinical and echocardiographic variables were related to > or = 5% improvement in ejection fraction. Myocardial viability, non-Q wave infarction, and anterior infarction all emerged as independent predictors, myocardial viability being the best (chi(2) = 14.5; p = 0.0001). Using the regression equation, the probability of > or = 5% improvement in ejection fraction for patients with a non-Q wave anterior infarct with viability was 73%, and for patients with a Q wave inferior infarct without viability, only 2%. CONCLUSIONS: Myocardial viability after acute myocardial infarction is the single best predictor of improvement in ejection fraction. In combination with infarct location and Q wave presence, the probability of > or = 5% improvement can be estimated in individual patients at the bedside.
The prognostic value of myocardial viability early after acute myocardial infarction (AMI) is still controversial, depending on the patient under study and the outcome end point considered. Furthermore, the relative prognostic importance of viability compared with indicators of systolic left ventricular (LV) dysfunction is not known. One hundred thirty-eight patients were studied with low-dose dobutamine echocardiography 3 +/- 1 days after AMI. Patients were divided in 2 groups based on presence (n = 55) or absence (n = 83) of myocardial viability and followed up for in-hospital and late cardiac events. During hospitalization, myocardial viability was the only independent predictor for recurrent ischemic events (chi-square 5.0, p = 0.025). End-systolic volume index and ejection fraction were both independent predictors of the occurrence of heart failure, whereas gender and end-systolic volume index emerged as independent predictors of hard cardiac events (death and sustained ventricular tachycardia). After hospital discharge, patients were followed for 19 +/- 7 months. Again, myocardial viability emerged as the only independent predictor of unstable angina (chi-square 7.7, p = 0.005). Age, hypertension, and ejection fraction were the most important independent predictors of hospitalization for heart failure, whereas ejection fraction was the only independent predictor of hard cardiac events. Presence of myocardial viability early after AMI is the single best predictor of recurrent in-hospital ischemic events and unstable angina after discharge. With respect to hard cardiac events and occurrence of heart failure, indicators of LV systolic dysfunction have a higher prognostic value than presence of myocardial viability.
Duchenne and Becker muscular dystrophy are caused by a mutation in the dystrophin gene, located on the short arm of the X chromosome. Three so called dystrophinopathy patients, a women aged 54 and two men aged 23 and 21 years, suffered from a severe dilated cardiomyopathy. Such a cardiomyopathy can develop in both carriers and patients. In addition, it is often more important for prognosis than muscle weakness. For these two reasons it is important to screen both groups for (early) cardiological abnormalities. If these are present, regular follow-up is necessary to start timely therapy. When cardiological investigations yield normal results, it is advised to screen carriers with a five-year interval. Dystrophinopathy patients should be checked every year, because the cardiomyopathy sometimes develops and deteriorates over a short period of time. Patients with dilated cardiomyopathy and with a positive family history for dilated cardiomyopathy, muscle weakness or high serum creatine kinase activity should be screened for a mutation in the dystrophin gene.
Pacing leads remain the "weaker link" of the permanent pacing system. Lead failure has been an issue since the beginning of implantable pacemaker therapy. Modern electronics have brought about considerable progress in pacing technology, but lead design has been slower to evolve and problems persist. IS-1 standardization must be considered a significant advance, but some issues regarding IS-1 standardization persist and have been the cause of some compatibility problems. With respect to lead insulation, silicone has proved to offer total reliability for > 30 years. In the search for better handling characteristics, polyurethane 80A was employed for bipolar leads, but it failed to demonstrate satisfactory insulating properties. New insulation materials, such as ethylene-fluoro-ethylene (ETFE), and coated wire technology look promising, having shown 99.32% survival at 5-year follow-up. Reliability is the main objective in lead design, but leads should provide low battery consumption as well. Low coil resistance, with high electrode impedance in steroid-eluting leads, is the standard at present. Low polarization is a desirable property for 2 main reasons: (1) in conjunction with low-threshold leads, it decreases battery consumption; and (2) it allows capture detection and, therefore, safer pacing at low battery consumption. Lead tip design as well as pacing pulse configuration can influence polarization.
OBJECTIVE: To assess the frequency, nature, and severity of cardiac abnormalities in limb girdle muscular dystrophy, and its relation to age and weakness in various genotypes. DESIGN: In 26 autosomal dominant, 38 autosomal recessive, and 33 sporadic strictly defined patients with limb girdle muscular dystrophy, cardiac evaluation included history, physical examination, chest x ray, electrocardiography, 24 hour ECG Holter monitoring, and echocardiography. In 35 of the 71 autosomal recessive and sporadic cases muscle biopsies were available for sarcoglycan analysis. MAIN RESULTS: Dilated cardiomyopathy was present in one autosomal dominant case and in three advanced autosomal recessive or sporadic patients, of whom two were found to have alpha sarcoglycan deficiency. Two of these three patients and three other cases showed ECG abnormalities known to be characteristic of the dystrophinopathies. A strong association between the absence of alpha sarcoglycan and the presence of dilated cardiomyopathy was found (p = 0.04). In six autosomal dominant cases there were atrioventricular (AV) conduction disturbances, increasing in severity with age and in concomitant presence of muscle weakness. Pacemaker implantation was necessary in four. CONCLUSIONS: 10% of these patients had clinically relevant cardiac abnormalities. In autosomal dominant limb girdle muscular dystrophy one subtype characterised by muscle weakness and AV conduction disturbances is recognised. In the course of autosomal recessive/sporadic limb girdle muscular dystrophy, dilated cardiomyopathy may develop, probably related to deficiency of dystrophin associated proteins.
We evaluated the course of cardiac involvement in 27 previously reported patients with Becker muscular dystrophy (BMD) originating from nine kindreds. Since almost all affected individuals of each kindred were included, intrafamilial variability could be studied. We also attempted to identify associations between cardiac involvement, functional ability and mutations at DNA level. The mean follow-up period was 12.5 years. The number of patients with electrocardiographic abnormalities progressed from 44% to 71%. Dilated cardiomyopathy (DCM) with or without congestive heart failure was now present in 33% as compared with 15% in the previous study. In addition, 22% developed borderline echocardiographic abnormalities. Six patients (22%) became symptomatic and four patients died of congestive heart failure. In all families cardiac abnormalities were found. There was no association between DCM and mutation type. Despite equal functional motor ability, there was a considerable intrafamilial variation in cardiac involvement, even in brother pairs. We conclude that cardiac abnormalities are the rule and not the exception in BMD and are progressive over time. Left ventricular dilatation may begin at any moment in the course of BMD and the rate of progression is unpredictable. A substantial proportion of patients will develop an incapacitating and life-threatening DCM.
Sixty-five members of three families with limb girdle muscular dystrophy (LGMD) underwent neurological, cardiological, and ancillary investigations. Thirty-five individuals were diagnosed as having slowly progressive autosomal dominant LGMD. Symmetrical weakness started in the proximal lower limb muscles, and gradually upper limb muscles also became affected. Early contractures of the spine were absent. Contractures of elbows and Achilles tendons were either minimal or late. Serum creatine kinase activity was normal to moderately elevated. Electromyogram and muscle biopsy were consistent with a mild muscular dystrophy. Cardiological abnormalities, found in more than one-half the patients, included dysrhythmias and atrioventricular (AV) conduction disturbances presenting as bradycardia, syncopal attacks necessitating pacemaker implantation, and sudden cardiac death. There was a significant relation between the severity of AV conduction disturbances and age. In nearly all patients, neuromuscular symptomatology preceded cardiological involvement. The early recognition of this previously not described, autosomal dominant LGMD with life-threatening cardiac involvement offers an opportunity for therapeutic intervention.
In order to compare ibopamine (IBO), a dopamine congener, with isosorbide mononitrate (ISMN) and to study their interaction in effects on the capacitance vasculature in congestive heart failure (CHF), a prospective, randomized, placebo-controlled, double-blind clinical trial was performed in 32 patients with New York Heart Association class II-IV CHF, randomly assigned to receive single oral doses of placebo, 200 mg IBO, 20 mg ISMN, or both IBO and ISMN. After labelling of red cells with 99mTc, changes in regional radioactivity, indicative of changes in blood volume, were recorded using a gamma-camera before and at 30, 60 and 120 min after drug administration. At 30 and 60 min, arterial systolic and pulse pressures were higher with IBO than with ISMN and placebo (for pulse pressure by mean 13.7 mmHg, 95% confidence interval 4.5-23.0 mmHg, at 30 min), probably reflecting an IBO-induced rise in stroke volume at unchanged heart rate and mean arterial pressure. IBO did not change regional radioactivity except for a transient increase of 4.4% (0.5-7.6%) in the thorax at 30 min. This was attenuated by concomitant ISMN treatment since, starting at 30 min, the drug increased radioactivity in the legs, compared with patients not receiving the drug, by 8.0% (95% confidence interval 0.2-15.8%), leading to a fall in thoracic and left ventricular radioactivity at 30 min of 3.4% (0.3-7.0%) and 6.4% (0.8-11.9%), respectively, and a fall of 5.5% (0.5-10.5%) in hepatic radioactivity at 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a study, assessing involvement of the heart in 33 familial cases of Becker muscular dystrophy (BMD), 31 familiar cases of facioscapulohumeral (FSH) dystrophy, and 27 familial cases of Bethlem myopathy. In the patients with BMD, correlations of myocardial involvement with age and extent of musculoskeletal involvement were made. We performed physical examination, chest x-ray, electrocardiographic (EKG), and echocardiographic examination on all patients, and continuous EKG Holter-monitoring in the patients with FSH dystrophy. Thirteen patients with BMD (45%) showed EKG changes similar to those found in Duchenne muscular dystrophy. Only 1 of the 13 individuals with cardiac involvement was wheelchair-bound. We found no evidence of cardiac changes in the patients with FSH dystrophy. In Bethlem myopathy, only 1 patient had a form of hypertrophic cardiomyopathy (asymmetrical septal hypertrophy).
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Explore the source record for details and available documents.