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Biomedical subjects

E D Wigle

Publications and source records attributed to E D Wigle.

At least 37 records · Page 2Linked to original sources
PubMed1989

Aortic regurgitation: a common complication after surgery for hypertrophic obstructive cardiomyopathy.

Surgical ventriculomyectomy and ventriculomyotomy by the aortic approach are safe and effective methods of relieving symptoms and obstruction to left ventricular outflow in patients with hypertrophic obstructive cardiomyopathy. With the addition of Doppler ultrasound to the routine follow-up assessment of these patients an unexpectedly high occurrence of aortic regurgitation was found in the postoperative patients. Because aortic regurgitation has been reported to rarely accompany this condition, 67 patients with hypertrophic obstructive cardiomyopathy were studied clinically and with Doppler echocardiography for the presence and severity of aortic regurgitation. Severity of the regurgitation was quantitated by pulsed or color Doppler echocardiography according to the length and width of the regurgitant jet in at least two views. In 37 patients with hypertrophic obstructive cardiomyopathy who did not undergo surgery, aortic regurgitation was detected in only 1 (3%) by Doppler ultrasound and in none clinically. In 52 patients who did undergo surgery and were studied a mean of 7.8 years postoperatively, aortic regurgitation of trivial to moderate degree was common, being detected in 28 (54%) by Doppler ultrasound and in 6 (12%) clinically. In a subgroup of 22 patients who were studied preoperatively and again early postoperatively (mean 6 weeks), new aortic regurgitation was found in 8 (36%) and was graded as trivial in all. Aortic regurgitation is a common complication related to ventriculomyectomy and ventriculomyotomy in patients with hypertrophic obstructive cardiomyopathy. Although initially trivial, the regurgitation may progress in severity over time. The regurgitation has been well tolerated in all patients studied to date.

Aortic Valve↗
PubMed1988

Disopyramide in hypertrophic cardiomyopathy. I. Hemodynamic assessment after intravenous administration.

The hemodynamic effects of intravenous disopyramide were determined in 43 patients with hypertrophic cardiomyopathy and pressure gradients at rest (resting obstruction). The basal subaortic pressure gradient decreased in all patients by a mean of 61 mm Hg (range 16 to 123); in 35 patients the gradient was abolished (less than 20 mm Hg). The reduction in pressure gradient was achieved through a decrease in left ventricular systolic pressure, from 178 to 135 mm Hg (p less than 0.0001), and a rise in aortic systolic pressure, from 105 to 123 mm Hg (p less than 0.0001). Left ventricular ejection time was reduced from 326 to 273 ms (p less than 0.0001). Left ventricular end-diastolic pressure decreased from 19 to 16 mm Hg (p less than 0.0001). In a subgroup of 13 patients, cardiac output was unchanged after disopyramide, despite a prolongation of the pre-ejection period from 104 to 137 ms (p less than 0.0001) indicating a decrease in contractility. The maintenance of cardiac output, despite a decrease in contractility, may reflect a decrease in mitral regurgitation resulting from the reduction of systolic anterior motion of the mitral valve by disopyramide. These results indicate that disopyramide produces predictably favorable hemodynamic effects in patients with hypertrophic cardiomyopathy and resting obstruction to left ventricular outflow.

Adolescent↗
PubMed1988

Hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic disorder of unknown cause that principally involves the left ventricle and is manifested as asymmetric or concentric hypertrophy. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the mid-ventricular level, at the apex, or rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by systolic anterior motion (SAM) of the anterior or posterior mitral leaflet(s) with mitral leaflet-septal contact. SAM occurs as the result of the Venturi forces created by the rapid ejection of blood through an outflow tract that is narrowed by upper septal hypertrophy, drawing the mitral leaflet(s) anteriorly. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. In symptomatic patients with resting obstruction this form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy currently available. The extent of hypertrophy is believed to be the principal determinant of impaired left ventricular relaxation and increased chamber stiffness that characterize diastole in hypertrophic cardiomyopathy. Diastolic dysfunction is common to most such patients irrespective of the presence or absence of outflow obstruction. Calcium entry blockers may improve the left ventricular relaxation process and relieve symptoms in patients with hypertrophic cardiomyopathy, particularly the subgroup with no obstruction to outflow. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their prevalence appears to depend on the presence of obstruction and the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole, as well as the disturbances in rhythm, appear to be related to the site and/or extent of the hypertrophic process. We have learned much about hypertrophic cardiomyopathy in the 30 years since its modern description. The vast majority of symptomatic patients can now be improved with specific medical or surgical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Arrhythmias, Cardiac↗
PubMed1987

Evidence for true obstruction to left ventricular outflow in obstructive hypertrophic cardiomyopathy (muscular or hypertrophic subaortic stenosis).

In obstructive hypertrophic cardiomyopathy (muscular or hypertrophic subaortic stenosis), there is rapid early systolic ejection through an outflow tract that is narrowed by ventricular septal hypertrophy. This results in Venturi forces acting on the mitral leaflets, which cause mitral leaflet systolic anterior motion. Subsequent mitral leaflet-septal contact results in obstruction to left ventricular outflow and concomitant mitral regurgitation. Evidence is provided that the subaortic pressure gradient in obstructive hypertrophic cardiomyopathy reflects true obstruction to left ventricular outflow. It is important to distinguish this truly obstructive subaortic pressure gradient, due to mitral leaflet-septal contact, from an early systolic impulse gradient, as well as from the intraventricular pressure difference that may be encountered in midventricular obstruction or cavity obliteration.

Aortic Valve Stenosis↗
PubMed1987

Results of surgery for hypertrophic obstructive cardiomyopathy.

Between 1971 and March 1986, 61 patients underwent surgery for hypertrophic obstructive cardiomyopathy. Age at operation varied from 3.5 to 76 years (mean 38). The standard approach was a generous transaortic myectomy. One-quarter of the patients underwent concomitant repair of associated lesions. There was one operative and two late deaths, for an actuarial 5 years survival 93% (+/- 8%). Average follow-up is 3 years per patient. Sixty-four percent of these patients are asymptomatic and another 30% were in New York Heart Association class II. Persistent symptoms were usually related to arrhythmias. Early atrioventricular block did not occur, but two patients were paced for complex arrhythmias 3 and 4 years after surgery. Hemodynamic studies (n = 22), two-dimensional echocardiographic (n = 47), and Doppler assessments (n = 23) demonstrated a left ventricular outflow tract pressure gradient of 70 and 14 mm Hg before and after surgery, respectively, left ventricular diastolic pressure of 18 and 14 mm Hg, percent of patients with mitral regurgitation of 70% and 30%, percent of patients with systolic anterior motion of 100% and 35%, and percent of patients with aortic insufficiency of 9% and 49%. Eight-six percent of the patients catheterized had no resting obstruction. Subaortic myectomy produces symptomatic improvement by reducing the left ventricular outflow tract pressure gradient, mitral regurgitation, and left ventricular end-diastolic pressure, and probably improves longevity.

Adolescent↗
PubMed1986

Randomised controlled trial of computer assisted management of hypertension in primary care.

The hypothesis that general practitioners would obtain better outcomes for patients with hypertension using a computer than doctors not using a computer was tested. Sixty family physicians were randomised to two treatment strategies. "Test" physicians completed a data collection form after each visit from a patient with hypertension and mailed the forms to the test centre for processing. Computer feedback on management was mailed to the doctors. This encouraged doctors to apply the "stepped care" protocol, supplied charts of diastolic blood pressure v time, and ranked patients' diastolic blood pressures by percentile. Letters were mailed to patients to remind them of appointments. "Control" doctors filled out the same data collection forms as test physicians, but neither doctors nor patients received computer feedback. Physicians who used the computer saw more patients per practice than control doctors (test 50 patients, control 40). For all patients the length of follow up was significantly longer in test practices (test 199 days, control 167), and a smaller percentage dropped out of active treatment in test practices (test 37.5%, control 42.1%). For patients with "moderate" hypertension of a baseline diastolic pressure of greater than 104 mm Hg the mean score of the last recorded pressure was below the goal of 90 mm Hg in test practices (88.5 mm Hg), but it failed to reach this goal in control practices (93.3 mm Hg). A greater average reduction of diastolic pressure was achieved in test practices (test 21.7 mm Hg, control 16.7 mm Hg). Though patients with "moderate" hypertension were better controlled in test practices than in control practices, the patients in test practices visited their doctors less often (test 13.3 visits per patient-year, control 17.4 visits). Among patients with newly detected hypertension test practices achieved a greater reduction in diastolic pressure than control practices (test 15.1 mm Hg v control 11.3 mm Hg) and more sustained control of hypertension (test 323 days per patient-year with a diastolic pressure of 90 mm Hg or less v control 259 days).

Blood Pressure↗
PubMed1986

Muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy): the evidence for true obstruction to left ventricular outflow.

The clinical and haemodynamic significance of the subaortic pressure gradient in patients with muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy) has long been debated. In this report we summarize the evidence which indicates that true obstruction to left ventricular outflow exists in these patients. Rapid left ventricular ejection, through an outflow tract narrowed by ventricular septal hypertrophy, results in Venturi forces causing systolic anterior motion of the anterior (or posterior) mitral leaflets. Mitral leaflet-septal contact results in obstruction to outflow and the accompanying mitral regurgitation. The time of onset of mitral leaflet-septal contact determines the magnitude of the pressure gradient and the severity of the mitral regurgitation, as well as the degree of prolongation of left ventricular ejection time and the percentage of left ventricular stroke volume that is ejected in the presence of an obstructive pressure gradient. Early and prolonged mitral leaflet-septal contact results in a large pressure gradient, significant mitral regurgitation, as well as dramatic prolongation of the ejection time and a large percentage of left ventricular stroke volume being obstructed. Late and short mitral leaflet-septal contact results in little haemodynamic perturbation. Hypertrophic cardiomyopathy patients with obstructive pressure gradients are significantly more symptomatic than those without. Thus the obstructive pressure gradients in hypertrophic cardiomyopathy are of clinical as well as haemodynamic significance. To deny the existence of obstruction to outflow in patients with muscular subaortic stenosis is to deny these patients appropriate medical and surgical therapy.

Blood Pressure↗
PubMed1986

The role of echocardiography in the assessment of hypertrophic cardiomyopathy.

Echocardiography has greatly simplified the diagnosis of hypertrophic cardiomyopathy and routine haemodynamic studies are usually only required in patients being considered for myectomy or the assessment of coexistent coronary disease. A complete echo Doppler study should be performed in all patients with hypertrophic cardiomyopathy to define the degree of obstruction, the degree of asymmetric hypertrophy and abnormalities of diastolic function. In this manner the patient can be classified according to haemodynamic subgroup, thus influencing the choice of treatment and helping to determine prognosis. These studies also provide a simple quantitative method of assessing the beneficial effects of medical or surgical therapy.

Cardiomyopathy, Hypertrophic↗
PubMed1984

Muscular subaortic stenosis: the quantitative relationship between systolic anterior motion and the pressure gradient.

We performed simultaneous echocardiographic and hemodynamic studies in 11 patients with muscular subaortic stenosis to determine whether systolic anterior motion (SAM) of the anterior mitral leaflet and the pressure gradient are related quantitatively. SAM without septal contact was associated with either no gradient or a small impulse gradient of less than 10 mm Hg. SAM with septal contact was always associated with a pressure gradient of more than 10 mm Hg. The size of the pressure gradient correlated inversely with the time periods: (1) onset of SAM-septal contact (r = .79, p less than .001) and (2) onset of aortic ejection to onset of SAM-septal contact (r = -.89, p less than .001). Size also correlated directly with the time period: (3) duration of SAM-septal contact (r = .80, p less than .001). Thus when the time from the onset of SAM to the onset of SAM-septal contact was long, SAM-septal contact developed late in systole, the duration of SAM-septal contact was brief and the pressure gradient was low. When SAM-septal contact developed in early systole, the duration of SAM-septal contact was long and the pressure gradient was high. With the index of time period (3) divided by time period (1), a regression equation was devised to predict the size of the pressure gradient (pressure gradient [mm Hg] = 25 [ratio] + 25; r = .90, p less than .001; SE +/- 15 mm Hg). The echocardiographic time period index was validated prospectively in nine other patients and the significant correlation with the hemodynamically determined gradient persisted (r = .89, p less than .01). We conclude that SAM and the pressure gradient are related quantitatively in muscular subaortic stenosis. These observations have implications regarding the mechanism and significance of the pressure gradient in muscular subaortic stenosis.

Adult↗
PubMed1982

Carcinoid heart disease: diagnosis by two-dimensional echocardiography.

We prospectively studied 14 patients with the carcinoid syndrome to determine if two-dimensional echocardiography could detect the nature and extent of valvular abnormalities. Eight of the 14 patients had definite abnormalities of the right-sided cardiac valves. The tricuspid valve had a characteristic appearance, similar to previously described pathologic findings. The leaflets appeared diffusely thickened, shortened and stiff without evidence of commissural fusion. Saline contrast studies demonstrated tricuspid regurgitation, which corresponded to the severity of the tricuspid valve involvement. The pulmonary valve could only be adequately assessed in seven of 14 patients, and morphologic abnormalities similar to those in the tricuspid valve were found. Follow-up studies have shown progression of cardiac disease in six of eight patients. We conclude that two-dimensional echocardiography can detect the characteristic cardiac abnormalities in the carcinoid syndrome and may be a useful tool for following their progression.

Adult↗
PubMed1981

Prinzmetal's angina with documented coronary artery spasm. Treatment and follow-up.

Eighteen patients with Prinzmetal's angina were studied angiographically and 17 were followed for an average of 27 months. The were 12 men and six women, with a mean age of 46.3 years. The mean duration of symptoms before clinical diagnosis was 4.1 weeks. Four had had a previous myocardial infarction. Six patients had spontaneous cardiac arrests within 48 hours of diagnosis and hospital admission. At coronary arteriography, 10 patients had significant coronary artery disease; two of these had coronary artery spasm. The remaining eight patients had normal cornary arteries with significant coronary artery spasm at arteriography. Angiographic mitral valve prolapse was found in eight patients; seven of these had inferior ST segment elevation with pain. Six of the 10 patients with significant coronary artery disease had aortocoronary bypasses performed with good results. Ten of the remaining 11 patients who were treated medically had their symptoms controlled with oral isosorbide dinitrate alone or in combination with propranolol, nifedipine or perhexiline but propranolol may have an adverse effect. Though the initial clinical course in untreated patients was unfavourable, progress after starting treatment was good, with no further cardiac arrests, myocardial infarctions, or deaths.

Angina Pectoris↗
PubMed1981

Effect of negative intrathoracic pressure on left ventricular outflow tract obstruction in muscular subaortic stenosis.

To study the effect of respiration and negative intrathoracic pressure on the left ventricular outflow tract gradient in patients with muscular subaortic stenosis, we studied nine patients using various respiratory maneuvers at the time of cardiac catheterization. Deep inspiration decreased the left ventricular outflow tract gradient from 60 +/- 11 to 34 +/- 6 mm Hg (p less than 0.01) and decreased the left ventricular ejection time (corrected for heart rate) from 0.42 +/- 0.01 to 0.38 +/- 0.01 second (p less than 0.001). The Müller maneuver decreased the left ventricular outflow tract gradient from 69 +/- 13 to 7 +/- 3 mm Hg (p less than 0.001) and decreased the corrected left ventricular ejection time from 0.42 +/- 0.02 to 0.24 +/- 0.01 second (p less than 0.01). In keeping with this amelioration of left ventricular outflow tract obstruction, echocardiography showed a reduction or abolition of the systolic anterior motion of the anterior mitral leaflet, and auscultatory and phonocardiographic studies revealed a decrease or abolition of the apical systolic murmur. These findings indicate that negative intrathoracic pressure reduced the left ventricular outflow tract gradient in muscular subaortic stenosis. We believe that negative intrathoracic pressure produced these changes by increasing left ventricular afterload through an increase in left ventricular transmural pressure, resulting in a decrease in the left ventricular outflow tract obstruction. These observations provide an explanation for the decrease in pressure gradient that occurs on inspiration in patients with muscular subaortic stenosis.

Adolescent↗
PubMed1980

Computer-assisted reporting system for the follow-up patients with cardiac pacemakers.

The implantation of large numbers of permanent cardiac pacemakers carries with it the responsibility for continual reassessment of all aspects of patient management. Experience with more than 4,000 pacemaker implants and replacements since 1963 has led to the development of a comprehensive computer-assisted data collection, management, and reporting system for the follow-up of patients with cardiac pacemakers. Over a seven-year period, data forms have been developed for the detailed documentation of pre-operative, intraoperative and follow-up information. These were designed in the form of checklists suitable for direct computer entry using mark-sense document readers. Special emphasis has been placed on pre-operative indications, selection of appropriate pacing systems, reliable follow-up methodology, and monitoring the performance of various pulse-generators. This system makes possible the rapid computer production of hospital records and reports to involved physicians and can be used to schedule follow-up assessments as required. The information also can be used for hospital statistics, billing, research, and pacemaker registration at the provincial, state of federal level. Experience has shown that a computer-assisted methodology is the only practical means of providing adequate follow-up for a large group of patients. In addition, direct access to relevant information helps to create an environment in which essential research can be carried out in the face of demanding clinical practice.

Computers↗
PubMed1980

Electrophoretic profiles of nonhistone nuclear proteins of human hearts with muscular subaortic stenosis.

Muscular subaortic stenosis (MSS) is a genetically determined cardiomyopathy, whereas right ventricular infundibular hypertrophy (IH) apparently is an acquired condition. Since genetic expression in eukaryotic cells may be regulated primarily by DNA-associated proteins, we isolated and characterized the proteins of heart nuclei from nine patients with MSS, eight with IH, and two with normal (N) hearts. More than 150 proteins could be identified by two-dimensional polyacrylamide gel electrophoresis. Proteins in the entire region from pH 7.0 to 9.0 with molecular weights (Mr) ranging from 35,000 to 41,000 and a protein focusing from pH 5.2 to 5.3 with Mr of 55,000 were strikingly reduced in MSS. Again the electrophoretic patterns of N and IH were similar. The electrophoretic patterns of nonhistone nuclear protein (NHNP) in MSS relative to N showed a striking resemblance to those demonstrated previously for the early stage (myolytic phase) of hamster cardiomyopathy relative to the matched control. Since NHNP interacting with DNA appears to play a major role in genetic expression, it is possible that some of the manifestations of MSS could be due to different components of NHNP in the affected hearts.

Animals↗