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Biomedical subjects

J A Erlebacher

Publications and source records attributed to J A Erlebacher.

14 recordsLinked to original sources
PubMed1988

Comparison of mitral valve dimensions and motion in mitral valve prolapse with severe mitral regurgitation to uncomplicated mitral valve prolapse and to mitral regurgitation without mitral valve prolapse.

To determine the mitral valve abnormalities associated with hemodynamically important mitral regurgitation (MR) among patients with mitral valve prolapse (MVP), computerized 2-dimensional echocardiographic measurements of mitral leaflet and anular dimensions and motion in 26 patients with MVP and MR were compared to those in 48 subjects with uncomplicated MVP, 16 patients with MR due to etiologies other than MVP (rheumatic in 8) and 35 normal adults. Compared to both uncomplicated MVP and normal subjects, patients with MVP plus MR were older (p less than 0.05), had strikingly large mitral leaflets and anulus (p less than 0.0005) and were more likely to have systolic billowing of mitral leaflets in the parasternal long-axis view (24 of 26 [92%] vs 24 of 48 subjects with uncomplicated MVP [50%], p less than 0.001). Overlap in anular and posterior leaflet dimensions in normal and uncomplicated MVP subjects occurred in the 20 MVP plus MR patients who continue to be followed medically but not in the 6 MVP plus MR patients who underwent mitral valve surgery during 22 +/- 14 months follow-up. Patients with MR due to rheumatic or other non-MVP etiologies had enlargement of mitral leaflets and anulus virtually identical to that in MVP plus MR patients. In conclusion, patients with severe MR due to MVP are older, have striking mitral valve enlargement and more frequently exhibit leaflet billowing compared with subjects with uncomplicated MVP. Similar mitral leaflet enlargement was found in patients with non-MVP etiologies of MR, suggesting that mitral anular and leaflet enlargement may play a more general role in the pathogenesis of MR than is currently appreciated.

Adult↗
PubMed1986

Effect of magnetic resonance imaging on DDD pacemakers.

A previous study suggested the safety of exposing patients with certain pacemakers models to magnetic resonance imaging (MRI). However, the function of a variety of more advanced DDD pacemakers and the effect of higher magnetic and radio-frequency (rf) field strengths has not been reported. In the present study 4 different DDD pacemakers (Cordis 233F, Intermedic 283-01, Medtronic 7000A, and Pacesetter 283) were tested in a saline phantom under several conditions and with various imaging sequences. Pacemaker output was monitored using electrocardiographic telemetry. All units paced normally in the static magnetic field. However, during imaging, all units malfunctioned, with total inhibition of atrial and ventricular output in 3 of the pacemakers. In the fourth pacemaker, ventricular backup pacing was activated at high rf pulse repetition rates. However, the MRI scanner could trigger atrial output in this pacemaker at rates of up to 800/minute. All malfunctions were a result of rf interference, whereas gradient and static magnetic fields had no effect. Thus, despite magnetic fields had no effect. Thus, despite magnetic field strengths adequate to close pacemaker reed switches, rf interference during MRI may cause total inhibition of atrial and ventricular output in DDD pacemakers, and can also cause dangerous atrial pacing at high rates. MRI should be avoided in patients with these DDD pacemakers.

Electrocardiography↗
PubMed1986

Inappropriate ventricular blanking in a DDI pacemaker.

The DDI mode is a new pacing mode with potential advantages over DVI pacing. We describe anomalous post R wave ventricular pacing due to the presence of inappropriate ventricular blanking periods in a pacemaker programmed to the DDI mode. Although no adverse consequences were seen in our patients, potentially dangerous R-on-T pacing could occur, particularly if long atrioventricular delays are programmed. A method for eliminating this pacing anomaly is described. Patients programmed to the DDI mode with the pacemaker model described should be evaluated for post R wave ventricular pacing and corrective measures should be taken.

Aged↗
PubMed1985

Early infarct expansion: structural or functional?

With the onset of ischemia, the length of myocardial segments increases rapidly, distorting ventricular geometry. Permanent stretching and thinning of infarcted zones have been termed infarct expansion. Although these changes are noted within minutes in vivo, infarct expansion may not be seen for days in postmortem preparations. The apparent postmortem reversal of early infarct expansion suggests that early expansion may be a functional phenomenon, reversible in the early hours of infarction. Alternatively, reversal of expansion may be a postmortem artifact, concealing the importance of underlying structural abnormalities. Myocardial infarction was produced in five dogs by occluding the left anterior descending coronary artery. Ultrasound sonomicrometers were used to measure myocardial segment end-diastolic length in the infarct and normal zones. After 3 hours of ischemia, the heart was arrested in diastole and biopsy specimens were taken from the normal and infarct zones. Sarcomere length was measured from electron photomicrographs, and myofiber width was measured from light photomicrographs. After 3 hours of ischemia, infarct zone segment length had increased significantly more than normal zone length (116 +/- 11 [SD] versus 103 +/- 4% of control length, p less than 0.05), whereas 2 minutes after cardiac arrest, both the infarct and normal zones returned to preischemic segment length, demonstrating apparent reversibility of early infarct expansion. However, histologic study revealed that the infarct zone myofibers were significantly thinner than normal zone myofibers (7.9 +/- 0.3 versus 9.4 +/- 0.3 micron, p less than 0.001) and sarcomere length in the infarct zone was significantly longer than that in the normal zone (1.9 +/- 0.2 versus 1.5 +/- 0.2 micron, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Hypotension with ventricular pacing: an atria vasodepressor reflex in human beings.

Hypotension with ventricular pacing has generally been attributed to loss of atrial transport, but it has been suggested that atrial vasodepressor reflexes may play a role. To study this, constant rate atrial and ventricular pacing was performed in 20 supine patients 24 to 36 hours after surgical coronary artery bypass or aortic valve replacement. The pulmonary capillary wedge tracing was examined for the presence or absence of cannon A waves during ventricular pacing in each patient. Thirteen patients had cannon A waves (group I) and seven did not (group II). Ten of the 13 patients with cannon A waves had ventriculoatrial conduction compared with only 2 of 7 patients without cannon A waves. There was a nonsignificant trend toward an association between cannon A waves and ventriculoatrial conduction (p = 0.1). Stroke volume index decreased in both groups when patients were changed from atrial to ventricular pacing. In the patients with cannon A waves, stroke volume index decreased from 31.2 to 26.3 cc/min per m2 (p less than 0.001) and from 31.2 to 25.0 cc/min per m2 (p less than 0.001) in those without cannon A waves (group I versus group II, p = NS). However, mean systemic blood pressure decreased only in patients with cannon A waves (99.4 to 85.9 mm Hg [p less than 0.001] versus 101.8 to 100.9 mm Hg [p = NS]) in those without cannon A waves (group I versus group II, p less than 0.001). Hypotension in patients with cannon A waves was caused by inhibition of the normal reflex increase in systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Early dilation of the infarcted segment in acute transmural myocardial infarction: role of infarct expansion in acute left ventricular enlargement.

Left ventricular enlargement after myocardial infarction is a poor prognostic sign, the mechanism of which has not been well defined. Early left ventricular dilation may be due to the Frank-Starling effect, which results in an increase in the length of uninfarcted segments in response to a reduction in contractile muscle mass. In contrast to this adaptive physiologic mechanism, left ventricular dilation may alternatively be caused by a pathologic process that stretches and thins the infarcted myocardial segment (that is, infarct expansion). To determine the relative contributions of these two mechanisms to left ventricular dilation after an initial transmural anterior myocardial infarction, two-dimensional echocardiograms were obtained from 27 patients within 72 hours of the onset of symptoms of myocardial infarction and from 13 healthy control subjects. In the minor-axis echocardiographic view at the level of the papillary muscles, anterior and posterior endocardial segment lengths at end-diastole were measured with a microprocessor-based graphic system. The papillary muscles were used as internal landmarks to demarcate the anterior and posterior segments. Anterior (infarcted) segment length in patients with myocardial infarction was 11.6 +/- 2.2 cm (mean +/- SD), whereas in control subjects, anterior segment length was 8.6 +/- 1.2 cm (p less than 0.001). Posterior (uninfarcted) segment length in the patients was not significantly different from posterior segment length in the control subjects (5.4 +/- 1.2 versus 5.3 +/- 1.0 cm, respectively). Measurable left ventricular dilation during the first 3 days after transmural anterior myocardial infarction is due to dilation of the infarcted segment and not of the normal uninfarcted segment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1981

Clinical recognition of giant left ventricular aneurysm.

The noninvasive diagnosis of left ventricular aneurysm has markedly improved with gated blood pool scintigraphy. However, in patients with giant anterior ventricular aneurysms, the gated blood pool scintigram performed in two standard views (anterior and 40 degree left anterior oblique) may incorrectly suggest ischemic cardiomyopathy. We retrospectively identified five patients who underwent resection of a ventricular aneurysm over a 2 1/2 year period and who had preoperative scintigraphic studies that appeared to show severe diffuse left ventricular dysfunction. contrast ventriculography demonstrated preserved wall motion in septal, inferior and lateral segments not seen by gated blood pool scintigraphy and showed extraordinarily large anterior aneurysms. M-mode or two-dimensional echocardiograms showed intact posterior wall function in all patients, suggesting severe regional myocardial disease rather than global dysfunction. Two-dimensional echocardiography showed additional segments with preserved function as well as discrete aneurysms in all patients. We conclude that gated blood pool scintigraphy, when performed in two standard views, may fail to correctly diagnose some patients with very large anterior wall aneurysms. M-mode echocardiography, two-dimensional echocardiography and additional scintigraphic views that visualize the posterior portions of the left ventricle improve noninvasive diagnosis of patients with resectable giant left ventricular aneurysms.

Aged↗