Severe Valvular Aortic Stenosis Research Articles

Aortic stenosis, angina, and coronary artery disease. Interrelations.

Sixty-nine patients over age 35 with severe valvular aortic stenosis were investigated for concomitant coronary artery disease. Forty (57.9%) had clinical angina pectoris. Sixteen (23.2%) had significant coronary occlusive disease by arteriography. Of those with angina, 13 patients (32.5) had significant coronary arterial obstruction, while in the pain-free group only (10.3%) had occlusive coronary disease. It is concluded that patients with severe aortic stenosis who are free of angina have only a small, but definite, chance of having significant coronary disease.

Cross sectional echocardiogram in assessing the severity of valvular aortic stenosis

Cross sectional echocardiogram in assessing the severity of valvular aortic stenosis

Right Aortic Arch with Coarctation of the Aorta

The first case of right aortic arch with mirror-image type branching and coarctation of the aorta is presented. The patient has Turner's syndrome. Severe valvular aortic stenosis is also present. Genetic and embryologic explanations for the unique association of these anomalies are suggested. The first case of right aortic arch with mirror-image type branching and coarctation of the aorta is presented. The patient has Turner's syndrome. Severe valvular aortic stenosis is also present. Genetic and embryologic explanations for the unique association of these anomalies are suggested.

Evaluation of severity of valvular aortic stenosis by angiocardiography and pressure gradient.

Evaluation of severity of valvular aortic stenosis by angiocardiography and pressure gradient.

Severe valvular aortic stenosis in patients over 65 years of age: A clinicopathologic study

Clinical and anatomic data are presented in 21 autopsy cases of patients over 65 years of age with severe valvular aortic stenosis. Attention is called to the unusual nature of the valvular lesion in the elderly compared to its manifestations in younger adults. The degree of aortic stenosis even in the very elderly may be extreme. The aortic valve in 2 patients was congenitally bicuspid, and in 19, tricuspid. The latter valves usually were characterized by the uniform distribution of nodular calcific deposits on the aortic aspects of the cusps and by the lack or near lack of commissural fusion. Calcification of the mitral annulus occurred in 16 of the 21 patients. Clinically, aortic stenosis in the elderly is characterized by several features that are either absent or more prominent than in younger subjects with this valvular lesion: The systemic arterial pulse pressure may be increased due to systolic hypertension; a harsh right basal systolic murmur may be relatively inconspicuous, whereas a pure musical systolic murmur may be prominent at the apex; a coexisting apical systolic murmur of mitral regurgitation may be related to mitral annular calcification and not to left ventricular failure; and systemic systolic hypertension can result in a comparatively small pressure gradient despite severe left ventricular outflow obstruction.

The structure of the aortic valve in clinically isolated aortic stenosis: an autopsy study of 162 patients over 15 years of age.

The structure of the aortic valve at autopsy is described in 162 patients over 15 years of age with clinically isolated, severe valvular aortic stenosis with or without aortic regurgitation. The valves were congenitally unicuspid, unicommissural in 17 patients, congenitally bicuspid in 67, tricuspid in 71, and in seven the structure was uncertain. Thus, in at least 84 (52%) of the patients the valve was congenitally malformed at birth. It is proposed that minor aortic valvular cuspal inequality, also present from birth, may be an underlying malformation in some of the patients with tricuspid stenotic aortic valves. Degeneration or wear-and-tear from aging almost certainly explains aortic stenosis in most of the elderly patients. Although no patient had clinical evidence of mitral valvular dysfunction, the mitral leaflets were diffusely thickened by fibrous tissue in 26 of the 162 patients. Rheumatic disease is believed to be the cause of the valve involvement in 22 of them (the other four had congenitally bicuspid aortic valves). Rheumatic disease did not appear to be the cause of the aortic stenosis in the other 136 patients with anatomically normal mitral valves.

A RARE FAMILIAL SYSTEMIC AFFECTION OF THE SKELETON: FAIRBANK'S DISEASE.

The case to be presented in this paper belongs to a large group of sclerotic affections involving the skeletal system. Many articles clearly defining these various entities have been written since the early days of radiology, though little has actually been added to their descriptions in that time. Some of these abnormalities are seen not uncommonly in the general practice of radiology, while others are represented by only single case reports. The present report includes information covering four generations. The patient's father suffered the same disease process and a chest film demonstrated the same findings; he died of severe aortic valvular stenosis. The disease process is also well documented in the patient's grandfather, though films were unavailable for demonstration purposes. A child six years of age has been studied, but without evidence of skeletal abnormality. The case presented falls into a group of skeletal affections described in 1943 by Uehlinger (3), whose name they now bear. They are known also as hyperostosis generalisata with pachyderma, acromeg-aloid osteosis, familial acromegaloid disease of the skeleton, osteodermopathic hypertrophiante, idiopathic familial generalized osteophytosis, chronic idiopathic hypertrophic osteoarthropathy, and meg-alia ossium cutis (2). Uehlinger's disease usually starts during puberty and is progressive until death. The patients are grotesque in appearance and because of their skin involvement appear acromegalic. None, however, have been found to have pituitary tumors. The bony changes as described by Uehlinger are very similar to changes demonstrated in the case to be reported here. So far as we know the only similar case in the literature is described by Sir Thomas Fair-bank in his book An Atlas of General Affections of the Skeleton (1). This case was called hyperostosis generalisata with striations, or “Fairbank's disease.” We shall use the same terminology in our report. Along with the two cases in the patient's family, one documented by a chest film and one with no films, this makes a total of 3 new cases. The radiographic picture and pathology of Fairbank's disease and Uehlinger's disease are almost identical, with the exception of striae and skin changes. The bone lesions are assumed to be the same. The long bones in Fairbank's disease demonstrate marked widening and increased sclerosis of the diaphyses. Multiple heavy trabeculae traverse the areas of stress, being more pronounced in the diaphyses. The medullary cavity is obliterated by the marked overgrowth of bone. A sclerotic thick cortex involves the long bones in their entirety, including the epiphyses. New bone is deposited subperiosteally, replacing the original compact cortical bone, and heavy trabeculae are formed. The ribs, clavicles, and pelvis are involved and are very sclerotic.

INTRAMURAL DEPOSITION OF CONTRAST AGENT DURING SELECTIVE ANGIOCARDIOGRAPHY.

Intramyocardial injection of contrast agent is a unique complication of selective angiocardiography and has been recognized with increasing frequency in recent years. Its potential gravity prompted us to investigate its cause, effects, and possible prevention, and this report comprises the results of this study. Bjöork et al. (2) report 3 intramyocardial injections with 1 death in a series of 142 transthoracic needle punctures. In a review article, Greenberg and Knox (5) cite 19 instances of intramural injection in a total of 437 percutaneous ventriculographies, with 3 fatalities. From experience with the catheter approach, Keith et al. (6) mention 3 cases of subintimal injection, all in infants, apparently producing no significant clinical manifestations. Also in reference to catheter studies, Bagger et al. (1) found 4 right ventricular intramural injections in a series of 1,375 angiocardiograms, with no late sequelae. Dotter et al. (4) report 1 case in which the intramural injection through a catheter was held responsible for the patient's death eight hours later. Davidsen et al. (3), in a series of 500 selective studies, and Kjellberg et al. (7), in a series of 728 angiocardiograms (the number of selective studies is not stated), do not refer to this complication. Clinical Material and Methods During the past five years, the present authors have recognized 16 intramural injections. Of 248 selective catheter angiocardiographic studies made between June 1957 and September 1962, 13 gave evidence of partial intramural injection. Of 4 transthoracic needle injections into the left ventricle during this same period, 3 were partially intramural. Side-hole catheters were either #5 or #6 Eppendorf or NIH aortographic. End-side-hole catheters were #8 Teflon except for one #6 woven nylon. All catheter injections were performed at pressures between 525 and 675 lb. per square inch. The contrast agent was usually Ditriokon, but in some of the earlier studies, 70 per cent Urokon or 75 per cent Hypaque was used. Clinical Manifestations: Clinical manifestations were apparent in only 2 of the 16 cases of intramural injection. These will be briefly reported. Case I: In B. S., a four-year-old boy with severe aortic valvular stenosis, retrograde left ventricular catheterization revealed a 90 mm. gradient across the aortic valve. A selective left ventricular angiocardiogram was planned. Prior to the high-pressure injection of contrast medium, several hand injections of saline failed to provoke ectopic ventricular systoles, and the catheter tip was thought to lie freely within the left ventricular cavity. Accordingly, 20 c.c. of Ditriokon was injected at a pressure of 675 lb. per square inch through a #6 side-hole catheter.