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Biomedical subjects

W D Edwards

Publications and source records attributed to W D Edwards.

At least 91 records · Page 5Linked to original sources
PubMed1994

Differential neointimal response to coronary artery injury in pigs and dogs. Implications for restenosis models.

Neointimal hyperplasia occurs in the coronary arteries after percutaneous revascularization procedures and is a reparative response that frequently causes recurrent stenosis. Prior animal studies have shown that neointimal tissue thickness is proportional to the depth of arterial injury. Because animal models are increasingly used to test therapeutic strategies against restenosis, the purpose of this study was to evaluate the degree of neointimal thickening formed in the coronary arteries of pigs compared with dogs in response to severe injury. Fourteen coronary arteries in six mongrel dogs and 18 coronary arteries in nine pigs underwent severe arterial injury using tantalum metal coils delivered on oversized angioplasty balloons. Animals were killed after 4 weeks, and all coronary arteries were pressure perfusion fixed. Mean histological injury scores and neointimal thicknesses for dogs were 1.9 +/- 0.3 and 0.30 +/- 0.11, respectively, compared with 2.1 +/- 0.7 and 0.71 +/- 0.36 for pigs. Thus, there was significantly less neointimal thickening in dogs compared with pigs (P < .001) despite no differences in injury (P = NS). The neointimal thickening differences translated into significantly different percent area stenoses: 55 +/- 24% for pigs versus 27 +/- 13% for dogs (P < .001). Linear regression modeled neointimal thickness versus injury assessed by an ordinal injury score proportional to the depth of injury for each species. This analysis confirmed the differences across multiple injury levels. The slope of the regression line for dogs was small, suggesting that no relation may exist between injury and neointimal thickness in this species. The pig may be a more appropriate model for the study of the genesis of stenosing neointima.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Endothelin in human congestive heart failure.

BACKGROUND: Although recent investigations report the elevation of plasma endothelin (ET) in congestive heart failure (CHF), it remains unclear if this elevation is that of the biologically active peptide ET-1 or of its precursor big-ET. Furthermore, it is unclear if such elevation is associated with increased myocardial ET and if the molecular form from cardiac tissue is altered ET. Last, it remains to be established whether circulating ET is increased at the earliest stage of CHF in patients with asymptomatic left ventricular dysfunction and correlates with the magnitude of ventricular dysfunction. METHODS AND RESULTS: The present study was designed to investigate concentrations and molecular forms of ET in plasma and cardiac tissue in healthy subjects and CHF patients with New York Heart Association (NYHA) class I through IV using cardiac radionuclide angiogram, cardiac myocardial biopsy, radioimmunoassay, gel permeation chromatography (GPC), and immunohistochemical staining (IHCS). Plasma ET was increased only in patients with moderate (NYHA class III) or severe (NYHA class IV) CHF compared with healthy subjects and individuals with asymptomatic (NYHA class I) or mild (NYHA class II) CHF. The elevation of circulating ET in CHF showed a negative correlation with left ventricular ejection fraction and cardiac index and a positive correlation with functional class and left ventricular end-diastolic volume index. GPC demonstrated that immunoreactive plasma ET was ET-1 in healthy subjects and both mature ET-1 and its precursor big-ET in severe CHF patients, with big-ET the predominant molecular form. Cardiac tissue concentrations and IHCS revealed ET presence in healthy atrial and ventricular tissue, which were not different in severe CHF. GPC revealed that the molecular form of cardiac ET was ET-1 in both healthy and CHF hearts. CONCLUSIONS: The present study establishes for the first time that the elevation of plasma ET in severe human CHF represents principally elevation of big-ET. Second, ET is present in healthy and failing myocardia, and its activity by both immunohistochemistry and radioimmunoassay is not changed in CHF. Furthermore, the elevated plasma ET is characteristic of severe CHF and not asymptomatic or mild CHF. In addition, the degree of plasma elevation of ET correlates with the magnitude of alterations in cardiac hemodynamics and functional class. The present study confirms and extends previous investigations of ET in human CHF and establishes the evolution of circulating and local cardiac ET in the spectrum of human CHF.

Chromatography, Gel↗
PubMed1994

Diffuse calcification in human coronary arteries. Association of osteopontin with atherosclerosis.

Coronary atherosclerosis is frequently associated with calcification of arterial plaque. To understand the mechanisms responsible for the formation of atherosclerotic calcification, we examined human coronary arteries for the presence and extent of mineral. In sections stained specifically for mineral, staining was diffuse and present in all atherosclerotic plaques. Hydroxyapatite was not detected in normal coronary artery sections. Distribution of hydroxyapatite coincided with a similar distribution of calcium detected by a radiodense pattern using contact microradiography of the same sections before cytochemical staining. By energy-dispersive x-ray microanalysis, the chemical composition of calcified sites was identical to hydroxyapatite (Ca10[PO4]6[OH]2), the major inorganic component of bone. Osteopontin is a phosphorylated glycoprotein with known involvement in the formation and calcification of bone and is regulated by local cytokines. Human coronary artery segments (14 normal and 34 atherosclerotic) obtained at autopsy were evaluated immunohistochemically using polyclonal antibodies generated against human osteopontin. Immunohistochemistry for osteopontin indicated intense, highly specific staining in the outer margins of all diseased segments at each calcification front; staining was evident throughout the entire plaque. Conversely, arterial segments free of atheroma and calcification and sections treated with nonimmune serum had no evidence of positive staining. Osteopontin, a protein involved in mineralization is specifically associated with calcific coronary atheroma and may play an important role in the onset and progression of this disease in human coronary arteries. The deposition of noncollagenous proteins such as osteopontin may regulate the presence or absence of calcification and ultimately alter vessel compliance.

Adult↗
PubMed1994

Long-term outcome of surgical repair of ruptured sinus of Valsalva aneurysm.

BACKGROUND: Because not much is known about the longterm results of surgical treatment of ruptured sinus of Valsalva aneurysm (RSVA), we reviewed our entire 37-year experience with this condition. METHODS AND RESULTS: From August 1956 through September 1993, 31 patients aged 3 to 54 years (median age, 29 years) underwent surgical correction of RSVA. Aneurysms originated in the right (n = 24) and noncoronary (n = 7) sinuses and entered the right ventricle in 21 patients and the right atrium in 10. Coexistence cardiac lesions included ventricular septal defect (VSD) (n = 16, 15 of which were subarterial) and aortic valve insufficiency (n = 13). There was a highly significant correlation between aortic insufficiency and the presence of an associated subarterial VSD (P < .0001). There was no hospital mortality. One patient (3.2%) died of endocarditis 9 years after subsequent aortic valve replacement; overall survival was 95% at 20 years. Two foreign patients were lost to follow-up after 11 and 13 years, respectively. Follow-up in the remaining 28 survivors extended to 37 years (mean, 25.7 years). Five patients (16.1%) underwent reoperation for aortic valve replacement (n = 3), closure of recurrent fistula (n = 1), and closure of both recurrent fistula and recurrent VSD (n = 1); all had their primary operation before 1976. All patients who had reoperation had right sinus of Valsalva-to-right ventricle fistulas, and 4 had an additional subarterial VSD. Risk of reoperation was higher with right ventricle fistulas than with right atrium fistulas, and this approached statistical significance (P = .06). Risk of reoperation in patients with right ventricle fistulas was lower when an aortotomy (with or without right ventriculotomy) was used during repair (1 of 8, 12.5%) versus right ventriculotomy only (4 of 13, 30.8%), although this did not reach statistical significance (P = .10). Need for reoperation was increased with the presence of a subarterial VSD (P = .08) but not with location of fistula or type of repair (direct suture versus patch). Of 9 patients with mild aortic insufficiency at primary operation, two developed late severe aortic insufficiency necessitating aortic valve replacement at 21 and 31 years, respectively. Twenty-five patients are in New York Heart Association class I, and 3 are in class II. CONCLUSIONS: Long-term survival after surgical treatment of RSVA is excellent. The risk for recurrent fistula or VSD is minimal in the current era. Late aortic insufficiency is still a risk, especially in right sinus of Valsalva-to-right ventricle fistula with associated subarterial VSD. Repair of RSVA through an aortotomy with or without cardiotomy permits inspection of the aortic root complex and facilitates aortic valve repair; this approach may reduce the incidence of late aortic insufficiency.

Adult↗
PubMed1994

Aortic dissection as complication of supravalvular aortic stenosis.

A 2-year-old patient with diffuse supravalvular aortic stenosis and the Williams-Beuren syndrome at autopsy was found to have dissection of the ascending aorta in addition to severe coronary artery disease and microfocal myocardial fibrosis. These findings emphasize the need for early surgical intervention in supravalvular aortic stenosis.

Aortic Dissection↗
PubMed1994

Pathology of coronary arteries, myocardium, and great arteries in supravalvular aortic stenosis. Report of five cases with implications for surgical treatment.

Among five patients with supravalvular aortic stenosis in whom autopsy tissues were available, all were male, 1 1/2 to 39 years old (mean 10 years, median 3 years), and the four children had Williams-Beuren syndrome (two familial, two sporadic). Medial thickening and dysplasia (disorganization) characterized the aortic sinotubular junction of three patients with discrete disease and the entire ascending aorta and arch branches of the two with diffuse disease. Medial dysplasia also involved the pulmonary arteries in each case, but less severely than the aorta. Dysplasia of coronary arteries was observed in all five hearts and was more obstructive proximally than distally, in cases with diffuse than discrete aortic disease, and in the adult than in the two children with discrete supravalvular aortic stenosis. All major epicardial arteries were involved, without predilection for any particular vessel. In contrast to the great arteries, coronary artery dysplasia involved all three layers, not just the media. To varying degrees, vessels showed intimal hyperplasia, fibrosis, and disorganization (dysplasia); disruption and loss of the internal elastic membrane, with indistinct intimal-medial junctions; medial hypertrophy and dysplasia; and adventitial fibroelastosis. In severe cases, the microscopic structure resembled that of the ductus arteriosus. Acute intramedial dissections were observed in the ascending aorta and distal right coronary artery in one patient each. Chronic microfocal ischemic fibrosis was identified in the subendocardium and papillary muscles of the left ventricle in four patients, and the adult patient also had an acute myocardial infarction. In summary, these findings emphasize the extraaortic extent of supravalvular aortic stenosis and the development of ischemic heart disease even in childhood. The presence of severe coronary obstruction in the adult with discrete aortic disease suggests that chronic high pulsatile coronary blood pressure may favor the proliferation of dysplastic tissue. Early surgical intervention may minimize the degree of proliferation, as well as allow regression of left ventricular hypertrophy, thereby lessening the risk of myocardial ischemia and aortic dissection.

Adolescent↗
PubMed1994

Mesothelial/monocytic incidental cardiac excrescences: cardiac MICE.

We have identified four new cases of the cardiac lesion resembling a histiocytoid (epithelioid) hemangioma from the consultation and surgical pathology files of the Mayo Clinic from 1979 to 1992. The lesions occurred in two men and two women, mean age 60 yr (range, 55 to 63), three of whom had undergone previous cardiac catheterization. All were found incidentally, two as separate tissue fragments obtained by right ventricular endomyocardial biopsy during investigations for dilated cardiomyopathy, and two during mitral valve replacement (one free floating in the left atrium and the other attached to the mitral valve). The latter two lesions measured 1.0 and 0.8 cm. All were composed of histiocytes (macrophages) focally admixed with cuboidal cells which formed strips and tubular arrays in three cases. Immunohistochemistry (two cases) confirmed their biphasic nature with cytokeratin positivity of the cuboidal cells and CD68 (KP-1) positivity (macrophage-myeloid lineage) of the histiocytes. Carcinoembryonic antigen and Leu-M1 were negative for both cell types. Transmission electron microscopy (two cases) showed macrophage-like cells and cuboidal cells with intracytoplasmic intermediate filaments, desmosome-like cellular junctions, and rough endoplasmic reticulum consistent with mesothelial cells. All four patients had a benign clinical course (range, 2 mo to 13 yr). This mesothelial and monocytic (histiocytic) process is postulated to relate to previous cardiac catheterization (applicable in three of our patients). The importance of these nodules, which are likely reactive, is their potential confusion with metastatic adenocarcinoma. We propose the name mesothelial/monocytic incidental cardiac excresences (cardiac MICE) for these lesions.

Antigens, CD↗
PubMed1994

Supravalvular aortic stenosis. Long-term results of surgical treatment.

To determine long-term outcome after operation for supravalvular aortic stenosis, we reviewed the case histories of 80 patients who had repair of the localized form (group A) (n = 67) or diffuse form (group B) (n = 13) from 1956 to 1992, including 31 patients with the Williams-Beuren syndrome. Ages ranged from 7 months to 54 years (mean = 12.6 years). Forty-six patients had one or more associated cardiovascular anomalies; the most common was aortic valve stenosis (33.8%). Eighteen patients had 22 previous cardiovascular operations, and 28 patients had one or more additional anomalies repaired during their initial procedure at our institution. In group A, the aortic root was enlarged with a teardrop-shaped patch (n = 61) or a pantaloon-shaped patch (n = 6). In group B, patch enlargement of the aorta was confined to the root (n = 4) or extended into the ascending aorta or aortic arch (n = 7); one patient had a graft placed between the ascending and descending thoracic aorta and one patient had a left ventricular-aortic conduit. There were no deaths in group A; two patients in group B in whom patch enlargement was confined to the aortic root died during the operation (2.5%). Follow-up extended to 33.4 years (mean = 14.2 years); there were five late deaths in group A and one in group B. Survival excluding operative mortality was 94% at 10 years and 91% at 20 years. All patients were in functional class I or II. There was no significant difference between patients with a teardrop-shaped or pantaloon-shaped patch in terms of late gradient, survival, or aortic insufficiency. By Cox multivariate model, the only independent predictor of late death for all patients was associated aortic valve disease (p = 0.02), which was also a risk factor for late reoperation (p = 0.02). In group B, overall survival was better in patients who received an extended patch versus aortic root patch only (p = 0.02). We reached the following conclusions: (1) Associated aortic valve disease was strongly correlated with late death and need for reoperation. (2) Both the teardrop-shaped and pantaloon-shaped patch techniques provide excellent long-term relief of localized supravalvular gradients and preservation of aortic valve competence. (3) In diffuse supravalvular aortic stenosis, aortic enlargement should be extended into the ascending aorta or beyond as required to relieve the gradient; some patients may require a graft or conduit.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1993

Coronary embolization after balloon angioplasty or thrombolytic therapy: an autopsy study of 32 cases.

OBJECTIVES: This study was undertaken to examine the nature, extent and clinical relevance of coronary embolism after balloon angioplasty or thrombolytic therapy, or both. BACKGROUND: Histopathologic documentation of postinterventional coronary embolization has been reported in only 10 patients from five studies. METHODS: This retrospective autopsy-based study included 32 patients, treated with balloon angioplasty or thrombolysis, or both, who died within 3 weeks of the procedure and underwent autopsy at the Mayo Clinic. Clinical variables included patient age and gender, artery treated, site and type of obstruction, type of intervention, success of the procedure, and postprocedural changes in the electrocardiogram (ECG), cardiac enzymes and hemodynamic status. Histopathologic variables included characteristics of treated plaques, acutely infarcted myocardium and coronary microemboli. Associations between microemboli and clinical and microscopic factors were evaluated by t tests and simple and multiple linear regression. RESULTS: Emboli were observed in 26 (81%) of the 32 patients. Among 83 emboli, 95% were thrombotic or atheromatous. The presence of microemboli was associated statistically with the development of postprocedural infarct extension, new myocardial infarction or new ECG abnormalities. Moreover, the greatest number of microemboli were associated with intervention in the left anterior descending coronary artery, multiple interventional sites, postprocedural medial dissection and plaque rupture or extrusion. CONCLUSIONS: Among patients undergoing balloon angioplasty or thrombolytic therapy who die and undergo autopsy, coronary microemboli occur in a substantial percent. The frequency in survivors is unknown. However, in living patients who develop acute myocardial ischemia or new ECG abnormalities after these interventions, coronary microembolization should be considered a potential cause.

Adult↗
PubMed1993

Cloning and sequencing of a full length cDNA encoding ovine lipoprotein lipase.

A cDNA clone encoding lipoprotein lipase has been isolated from an ovine adipocyte library. Sequencing of this clone has revealed a single open reading frame encoding a 450 amino acid protein. Comparison with known LPL sequences from other species shows a high degree of conservation in the sequence of the protein and in the 5' untranslated region of the DNA sequence.

Adipose Tissue↗
PubMed1993

Effects of angiotensin converting enzyme inhibition on neointimal proliferation in a porcine coronary injury model.

To assess the effectiveness of angiotensin converting enzyme inhibition in a proliferative porcine coronary restenosis model, 35 animals received orally administered trandolapril (10 mg) or captopril (200 mg) or no drug (control group) for 6 days before and 28 days after injury by oversized metallic coils in one or more coronary arteries. Twenty arterial lesions in the trandolapril group, 17 in the captopril group, and 18 in the control group were evaluated. There was no significant difference in neointimal thickness or percentage luminal area stenosis for the groups as a whole. However, in quantitative comparisons in which vessel injury score was used as a covariate, the fractional increase in mean neointimal thickness per unit of injury was significantly less for the trandolapril group (p = 0.019) but not for the captopril group when compared with control animals. In this model, neointimal proliferation from arterial injury was inhibited by angiotensin converting enzyme inhibition with trandolapril but only modestly. Such an effect may not be clinically significant.

Angioplasty, Balloon, Coronary↗
PubMed1993

Evaluation of surgically excised mitral valves: revised recommendations based on changing operative procedures in the 1990s.

In 1990, 95 mitral valves from 54 women and 41 men (mean age, 61 years; age range, 8 to 85 years) were replaced (76%) or repaired (24%) at the Mayo Clinic. Functionally, 58% of the valves were purely regurgitant (MR), 25% were stenotic and regurgitant (MS-MR), and 17% were purely stenotic (MS). Postinflammatory (presumably rheumatic) disease accounted for 100% of MS cases, 92% of MS-MR cases, and 16% of MR cases. Other causes of pure MR included floppy valves (49%), ischemic heart disease (13%), infective endocarditis (9%), miscellaneous (9%), and indeterminate (4%). Thus, postinflammatory disease represented the major cause of both mitral stenosis (MS and MS-MR) and overall mitral valve disease in our surgical population. In contrast, floppy valves were the most commonly observed cause of pure MR. Among postinflammatory valves, 55% were completely excised and 45% had only the anterior leaflet removed; all were replaced. In contrast, floppy valves were incompletely excised in 96%; 67% were repaired and only 33% were replaced. Because mitral valves frequently are incompletely excised, rendering an accurate etiologic diagnosis requires not only a morphologic assessment of resected tissues but also a knowledge of the clinical history, operative details, and functional state of the valve.

Adolescent↗
PubMed1993

New observations on the etiology of aortic valve disease: a surgical pathologic study of 236 cases from 1990.

Among 236 aortic valves surgically excised at the Mayo Clinic in 1990 (mean patient age, 66 years; age range, 10 to 92 years), 154 (65%) were stenotic, 58 (25%) were insufficient, and 24 (10%) were both stenotic and insufficient. Pure stenosis was related to calcification, and causes included degenerative (51%), bicuspid (36%), post-inflammatory (9%), and other (4%) reasons. Fourteen (9%) valves with pure stenosis also underwent ventricular septal myectomy, 12 for hypertrophy and two for co-existent hypertrophic cardiomyopathy. Pure insufficiency was not related to calcification, and causes included aortic root dilatation (50%), bicuspid valve (14%), post-inflammatory (14%), post-therapeutic (14%), and other (8%) reasons. Combined stenosis and insufficiency was secondary to degenerative calcification (46%), bicuspid and post-inflammatory etiologies (17% each), post-therapeutic (13%), and indeterminate (8%) causes. New observations include the following findings: (1) degenerative (senile) disease is the most common cause of aortic stenosis and combined stenosis and insufficiency at the Mayo Clinic, (2) aortic root dilatation is the most common cause of pure aortic insufficiency, (3) post-therapeutic aortic valve disease now leads to valve replacement in a substantial percentage of patients, particularly among those with insufficiency, (4) post-inflammatory (presumably rheumatic) disease is relatively uncommon in all three functional categories, (5) septal myectomy may be performed for hypertrophic states other than hypertrophic cardiomyopathy, and (6) adults with operated congenital heart disease are undergoing valve replacement for annular dilatation with insufficiency. Because of the increasing age of the general population, the prominence of age-related degenerative aortic valve calcification and aortic root dilatation may have important implications concerning future health care costs.

Adolescent↗
PubMed1993

Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations.

OBJECTIVE: To test the hypothesis that certain clinical events may precede free wall myocardial rupture and allow its prediction, we conducted a retrospective and prospective study of 70 patients with rupture. BACKGROUND: Rupture of the left ventricular free wall develops in approximately 10% of patients with fatal acute transmural myocardial infarction. Clinically, its occurrence has been considered precipitous and unexpected. Pathologically, however, rupture appears to be a stuttering, progressive process characterized in many instances by an infiltrating intramural hemorrhage and a thrombus within the tear of > or = 1 day's duration. METHODS: The clinical course and evolutionary electrocardiographic (ECG) changes in 70 consecutive patients with rupture and 100 comparison patients with acute myocardial infarction but without rupture were reviewed to ascertain whether certain clinical symptoms, signs and ECG alterations occur in patients prone to develop rupture, allowing its anticipation. In addition, a correlation was established between the site of infarction indicated by the ECG and the site of rupture determined at autopsy or surgery. RESULTS: Patients with rupture had a significantly greater incidence of pericarditis, repetitive emesis and restlessness and agitation than did patients without rupture. More than 80% of patients with rupture had two or more symptoms compared with 3% of patients without rupture (p < 0.002). A deviation from the expected evolutionary T wave pattern occurred in 94% of patients with rupture and 34% of control patients (p < or = 0.02). An abrupt transient episode of hypotension and bradycardia, probably due to the initial tearing of the epicardium with a resultant small hemopericardium, was observed in 21% of patients with rupture. Rupture of the midlateral wall was most common (32%) and usually occurred in the setting of an inferoposterolateral infarction related to an acute left circumflex artery occlusion. On the basis of these clinical and ECG changes, rupture was confirmed by echocardiography and pericardiocentesis in the two most recent patients, and the defect was successfully repaired. CONCLUSIONS: Rupture is often preceded by particular symptoms, signs--namely, one or more episodes of abrupt, transient hypotension and bradycardia and unexpected alterations of the T waves, especially directional changes of the latter. Patients displaying these symptoms, signs and ECG changes require a bedside echocardiogram and echocardiographically guided pericardiocentesis if fluid is visualized. If the pericardiocentesis identifies the fluid as blood, immediate surgery is indicated.

Aged↗
PubMed1993

Coronary restenosis: prospects for solution and new perspectives from a porcine model.

Coronary restenosis, a major unresolved problem for percutaneous coronary revascularization procedures, has thus far been resistant to all therapeutic strategies. In part, ineffective treatment or prevention of coronary restenosis may be due to reliance on a conceptualization of the restenosis process that incompletely reflects the pathophysiologic factors associated with neointimal formation after arterial injury. In a porcine coronary restenosis model, three stages of neointimal growth after arterial injury have been identified: an early thrombotic stage, with platelets, fibrin, and erythrocytes; a cellular recruitment stage, with endothelialization and an infiltration by lymphocytes and monocytes; and a proliferative stage, in which smooth muscle cells migrate into and proliferate within the fibrin-rich degenerating thrombus. Evaluation of basic mechanisms responsible for neointimal formation has been possible with this model. In particular, a direct relationship exists between the depth of arterial injury and subsequent neointimal thickness. This relationship can be used for investigating the efficacy of new therapies. Treatment strategies for restenosis should be directed toward interference with the cellular or humoral events that lead to neointimal formation, with the specific goal of decreasing the neointimal volume. These strategies may include delivery of drugs to the site of arterial injury to limit the amount of early mural thrombus or decreasing subsequent cellular recruitment and proliferation as well as synthesis of extracellular matrix.

Animals↗
PubMed1993

Multiplane transesophageal echocardiography: image orientation, examination technique, anatomic correlations, and clinical applications.

Multiplane transesophageal echocardiography (TEE) consists of a single ultrasound array or imaging sector that can be rotated around the long axis of the ultrasound beam typically in a 180 degrees arc. This capability produces a circular (conical) continuum of tomographic two-dimensional images. The principal advantage of multiple TEE is that the transducer can be rotated to an image-specific orientation and critically optimized. Thus, manipulation of the transducer is less complex than with the biplane technique, and user adaptation is considerably enhanced. The logical image notation (that is, degrees of rotation) and orientation are described in this report. A step-by-step approach to the multiplane TEE examination, which evolved from our initial experience with 400 consecutive patients, is correlated with accompanying tomographic anatomic corroboration. The unique clinical applications are discussed and related to the amplification of diagnostic information. Although the multiplanar TEE transducer is relatively large, all adult patients who weigh 40 kg or more can be examined. No major complications occurred in our initial experience with this promising new technology.

Adolescent↗
PubMed1993

Clinical features and differential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990).

Acute aortic dissection is the most common fatal condition that involves the aorta; nevertheless, despite major advances in noninvasive diagnosis, the correct antemortem diagnosis is made in less than half the cases. To promote continued improvement in the prompt recognition of aortic dissection, we present a review of the Mayo Clinic experience with 235 patients who had 236 substantiated aortic dissections. At the time of initial assessment, 158 patients (67%) had acute and 78 patients (33%) had chronic aortic dissection. Hypertension was the most common predisposing factor (78% of patients overall). The acute onset of severe chest pain was the most common initial complaint (74%), but 33 patients (15%) had painless aortic dissection and abnormal chest roentgenographic findings. Less common manifestations included congestive heart failure, syncope, cerebrovascular accident, shock, paraplegia, and lower extremity ischemia. The initial clinical impression was aortic dissection in 62% of patients overall. In 17 patients (28%), the correct diagnosis was not made before postmortem examination. Although the clinical features of aortic dissection have gained wider appreciation, the diagnosis still remains unsuspected in a substantial number of patients. In a patient who has a catastrophic illness and unexplained symptoms that could be of vascular origin, especially in the presence of chest pain, aortic dissection should always be included in the differential diagnosis.

Acute Disease↗