Biomedical subjects
Publications and source records attributed to E D Wigle.
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To better understand the pathophysiology of obstruction of left ventricular outflow in hypertrophic cardiomyopathy and to determine the value of intraoperative transesophageal Doppler echocardiography in decision making, 32 consecutive patients undergoing ventriculomyectomy were assessed. The mean preoperative left ventricular outflow gradient was 83 +/- 39 mm Hg and the mean basal septal width was 24 +/- 6 mm. Compared with transesophageal findings in 10 normal control subjects, the mitral leaflets were longer and the coaptation point was abnormal in the patients with obstructive hypertrophic cardiomyopathy (anterior and posterior leaflet lengths in the patients were 31 +/- 4 vs. 22 +/- 3 mm in the control group [p less than 0.00001] and 20 +/- 2 vs. 15 +/- 3 mm in the control group [p less than 0.00001]). The coaptation point in the patient group was in the body of the leaflets at a mean of 9 +/- 2 mm from the anterior leaflet tip, whereas it was at or within 3 mm of the leaflet tip in the normal group. During early systole, the distal third to half of the anterior mitral leaflet angled sharply anteriorly and superiorly (systolic anterior motion), resulting in leaflet-septal contact and incomplete mitral leaflet coaptation in mid-systole. This caused the formation of a funnel, composed of the distal parts of both leaflets, that allowed a jet of posteriorly directed mitral regurgitation to occur in mid- and late systole. The sequence of events in systole was eject/obstruct/leak. Transesophageal echocardiography was also helpful in planning the extent of the resection, assessing the immediate result and excluding important complications. In successful cases, the post-myectomy study showed 1) a dramatic thinning of the septum, with widening of the left ventricular outflow tract to a width similar to that in the normal subjects, 2) resolution of systolic anterior motion and the left ventricular outflow tract color mosaic, and marked reduction or abolition of mitral regurgitation despite persistence of abnormal mitral leaflet length and an abnormal mitral leaflet coaptation point. The routine use of transesophageal echocardiography in patients undergoing surgical myectomy for the treatment of obstructive hypertrophic cardiomyopathy is recommended.
To evaluate scar-type and matrix connective tissue and to assess their role in the diastolic dysfunction of hypertrophic cardiomyopathy, surgically resected subaortic myectomy specimens and several autopsy hearts from patients with hypertrophic cardiomyopathy were studied. Eighteen specimens were differentially stained by a newly developed method that precisely determines relative collagen content; these tissues were compared with postmortem hypertrophied and normal control subaortic specimens. Quantitation revealed a 72% higher level (36.5 vs. 22.1 micrograms collagen/mg protein) of stainable collagen in the hearts with hypertrophic cardiomyopathy than in hypertrophied control hearts. The endocardial plaque was quantitated morphometrically, and it constituted only 4.6 +/- 1.7% of the total increased collagen content in the cardiomyopathy specimens. For the matrix studies, the cardiomyopathy specimens were stained by a silver impregnation technique that identifies connective tissue elements not normally visible with routine histologic methods. There was a marked increase in content of all matrix components, both in areas of pathologic scarring and in "normal" zones. Whorls of matrix connective tissue were noted in regions of myocyte whorls, as well as independent of them. Thus, these studies revealed a striking increase of both scar-type and matrix connective tissue in hypertrophic cardiomyopathy. The extensive scarring and the pronounced interstitial and intercellular matrix connective tissue may contribute to the increased ventricular chamber stiffness and impaired relaxation in this disease.
The pathology of a case of idiopathic calcification affecting the ascending aorta in a young woman is presented. A varying width of media throughout the aorta and extending into its proximaques of calcium, found in the acellular media, were confined to the ascending aorta. No inflammatory or reparative reaction was seen in the vessel wall. Electron microscopically, the calcium seemed to have an affinity for elastic tissue elements of all sizes and the mode of deposition appeared to be by 'avenues' of the microfibrillar component. Possible pathogenetic mechanisms are discussed.
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The implantation of large numbers of prosthetic heart valves carries with it the responsibility for continual reassessment of all aspects of patient management. Experience with more than 2,000 prosthetic valve operations since 1963 led to the development of a comprehensive computer-assisted data collection, management and reporting system. Over a 5 year period, data forms were developed for the detailed documentation of preoperative, intraoperative and postoperative information. These were designed in the form of checklists suitable for direct computer entry with use of mark-sense document readers. Special emphasis was placed on preoperative assessment of ventricular function, valve selection, intraoperative myocardial preservation, postoperative rehabilitation and prosthetic valve-related complications. This system makes possible rapid computer generation of a variety of reports to the referring physician regarding the individual patient and to the clinical investigator in relation to patient group statistics. Also, questionnaires to patients of physicians, or both, to update patient data can be produced by the computer at appropriate intervals after valve surgery. Experience indicated that a computer-assisted methodology is the only practical way to provide adequate follow-up of large groups of patients. Additionally direct access to relevant information helps to create an environment in which essential research can be carried out in the face of a demanding clinical practice.
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Explore the source record for details and available documents.
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Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
Although aortocoronary bypass (ACB) for patients with stable angina carries a low mortality, some unexpected deaths do occur. Since in patients with normal coronary arteries the endocardial viability ratio (EVR) can be correlated with subendocardial perfusion, with a ratio of 0.7 or less indicating ischemia of the left ventricular subendocardium, and since the EVR postoperatively is useful in determining the need for intra-aortic balloon pump assist (IABPA), it was decided to ascertain whether the EVR might have prognostic value in patients with stable angina scheduled for standard ACB. Three groups of patients were studied: 50 with stable angina, 24 who had died after ACB, and 18 who required IABPA for cardiogenic shock after surgery for stable angina. No significant differences were found for cardiac index, left ventricular end-diastolic pressure, left ventricular ejection fraction and pre- and postoperative artery scores, but there were significant differences in the EVR between the first and second groups and between the first and third groups (P less than 0.01 in each instance). These findings suggest that the left ventricular EVR may indeed be of prognostic value in patients scheduled to undergo ACB and that use of IABPA, which produces an increase in EVR, may be useful in patients with EVRs of less than 0.7, even if other parameters of cardiac function are normal.
The association of prolapse of the posterior leaflet of the mitral valve with secundum atrial septal defect has recently been reported but the prevalence and features of this association have not been defined. Analysis of left ventricular cineangiograms in 54 patients have secundum atrial septal defect revealed evidence of prolapse of the posterior leaflet of the mitral valve in 20 (37 percent). In 11 patients (20 percent) there was clinical evidence of a mitral valve lesion (pansystolic murmur in 9 patients and mid-systolic click in 2 patients, 1 of whom also had a late systolic murmur); the remaining 9 patients had no auscultatory evidence of a mitral valve lesion. Thus, the incidence of clinically silent prolapse in association with secundum atrial septal defect was 17 percent (9 of 54 patients). Analysis of the angiographic findings revealed that the prolapse was triscalloped in 4 patients, biscalloped in 11 and uniscalloped in 5. Mitral regurgitation was present in 12, including the 11 patients with clinical signs of a mitral lesion. Three patients with moderate or severe mitral regurgitation had triscalloped prolapse. The association of prolapse of the posterior leaflet of the mitral valve with secundum atrial septal defect is common and may be present in the absence of any clinical evidence of a mitral valve lesion.
During one six-month period 11 patients were referred with a diagnosis of coronary artery disease, because of recurrent episodes of severe, prolonged retrosternal chest pain necessitating from one to seven hospital admissions per patient for "suspect myocardial infarction". In no instance was this diagnosis proved by electrocardiogram or serum enzyme changes, but 7 of the 11 patients had abnormal resting electrocardiograms. Selective coronary arteriograms were normal in 10 patients and revealed nonobstructive coronary artery disease in the 11th patient. Esophageal studies revealed hiatus hernia in 9 and mild to severe disordered motored activity of the esophagus in all 11. Acid perfusion into the esophagus reproduced the chest pain in nine patients and in the other two, the hiatus hernia was incarcerated. On direct questioning, all patients indicated that the pain was worsened by lying down and bending over, and in eight patients there was a history of pharyngoesophageal or gastroesophageal dysphagia. In this day when the problem of chest pain with normal coronary arteries is very topical, our report emphasizes the need to consider symptomatic esophageal disease in the differential diagnosis of this problem.