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Biomedical subjects

B H Bulkley

Publications and source records attributed to B H Bulkley.

At least 163 records · Page 9Linked to original sources
PubMed1976

Kartagener's syndrome with corrected transposition. Conducting system studies and coronary arterial occlusion complicating valvular replacement.

An 18-year-old man whose sister has classic Kartagener's syndrome was found to have sinusitis, bronchiectasis, and corrected transposition with normal visceral situs. Congenital complete heart block was secondary to absence of conducting-system pathways between a small posterior atrioventricular node and the transposed His bundle and bundle branches. No anterior atrioventricular node was present. Prosthetic valvular replacement of the left-sided (morphologic right) atrioventricular valve was complicated by coronary arterial occlusion by suture, with subsequent myocardial infarction. The case appears to represent an unusual variant of Kartagener's syndrome with the abnormality of laterality being expressed as corrected transposition.

Adolescent↗
PubMed1976

Systolic anterior motion of the mitral valve without asymmetric septal hypertrophy.

This report describes a patient with echocardiographic systolic anterior motion of the mitral valve causing the anterior mitral leaflet to contact the septum in systole. At necropsy a normal nonhypertrophied heart with normal-sized ventricular cavities and a normal outflow tract and mitral valve was found. Thus, asymmetric septal hypertrophy and abnormal mitral valvular placement are not requisites for systolic anterior motion of the mitral valve. During systole, a marked forward movement of the anterior mitral leaflet developed in our patient in the setting of hypovolemia and continuous intravenous administration of pressor drugs, suggesting, rather, that systolic anterior motion reflects a small, vigorously contracting ventricular cavity and that such dynamic subaortic obstruction is not pathognomonic of idiopathic hypertrophic subaortic stenosis.

Aged↗
PubMed1975

Idiopathic hypertrophic subaortic stenosis: detection by thallium 201 myocardial perfusion imaging.

To determine whether thallium 201 myocardial imaging could be used to detect hypertrophic cardiomyopathy, 10 patients with idiopathic hypertrophic subaortic stenosis were studied. Asymmetric septal hypertrophy, an anatomic marker for this disease, was evident on thallium scans in the patients with idiopathic hypertrophic subaortic stenosis, with a ratio of septum to left ventricular free wall of 1.7 cm compared to 1.0 cm in eight normal volunteers, and 1.0 cm in eight patients with concentric left ventricular hypertrophy. Patients with hypertrophic cardiomyopathy also demonstrated apical ventricular wall thickening, and a thicker posterior ventricular free wall in the obstructive in contrast to the nonobstructive form of this disease. Thallium scans of three patients with pulmonary hypertension and secondary asymmetric septal hypertrophy were distinguished from idiopathic hypertrophic subaortic stenosis by marked right ventricular wall thickening. Thus, thallium 201 myocardial perfusion imaging provides a noninvasive method for detection and evaluation of idiopathic hypertrophic subaortic stenosis.

Cardiomyopathy, Hypertrophic↗
PubMed1975

Heterografts as aortocoronary bypass conduits in human beings.

Clinical and necropsy observations are described in a man in whom two sheep carotid arterial heterografts were inserted as aortocoronary bypass conduits 30 months before death, and in whom a canine saphenous vein heterograft was inserted several hours before death. All three grafts failed. The lumens of the sheep carotid arterial heterografts had closed by the time of catheterization 6 months after operation; at necropsy both grafts were totally occluded at their coronary and aortic ends and their media and adventitia were infiltrated by granulomatous inflammatory cells. Little information is available regarding the use of heterografts as coronary bypass conduits. Examination of previous reports describing heterografts for vascular reconstruction or bypass in both man and experimental animals and observations in our patient suggest that heterografts are unsatisfactory as aortocoronary bypass conduits.

Adult↗
PubMed1975

Dilatation of the mitral anulus. A rare cause of mitral regurgitation.

To confirm or deny the thesis that mitral anular dilatation is a cause of mitral regurgitation, this anulus was measured in 102 patients, 24 of whom had normal hearts and 78 of whom had dilated left ventricles, some associated with mitral regurgitation, others not. The circumference of the mitral anulus in the 24 patients with normal hearts averaged 9 cm (range 7 to 11 cm); in 24 patients with idiopathic cardiomyopathy of the ventricular dilated type, both with (12 patients) and without (12 patients) mild to moderate regurgitation, 11 cm (range 10 to 14 cm); and in 31 patients with severe mitral regurgitation, 12 cm (range 8 to 18 cm). Among the latter 31 patients with severe mitral regurgitation, the anulus was only mildly dilated in the 15 with rheumatic disease (average 11 cm) and in the six with ruptured chordae tendinease on previously normal valves (average 10 cm); in contrast, in the 10 patients with floppy mitral valves with or without the Marfan syndrome the mitral anulus was greatly dilated (average 15.5 cm). Thus, only in patients with floppy valves with or without the Marfan syndrome or both does anular dilatation by itself appear great enough to cause mitral regurgitation. It appears, therefore, that dilatation of the mitral anulus is a rare cause of mitral regurgitation and that abnormality of the fibrous skeleton of the heart is necessary for the mitral anulus to dilate enough to cause mitral regurgitation.

Adult↗
PubMed1975

Mitral valve disease of systemic lupus erythematosus. A cause of severe congestive heart failure reversed by valve replacement.

Libman-Sacks endocarditis caused progressive life-threatening mitral regurgitation necessitating mitral valve replacement in an 18 year old woman with systemic lupus erythematosus (SLE). Although Libman-Sacks endocarditis is frequently seen at autopsy in patients with SLE, hemodynamically significant valvular disease due to that lesion is quite rare. We found no previous reports describing mitral regurgitation in a patient with SLE which has necessitated surgical intervention.

Adolescent↗
PubMed1975

The heart in systemic lupus erythematosus and the changes induced in it by corticosteroid therapy. A study of 36 necropsy patients.

The natural history of the cardiovascular manifestations of systemic lupus erythematosus (SLE) have been altered by corticosteroids which exert their own cardiovascular effects. This study describes clinical and necropsy observations in 36 corticosteroid-treated patients with SLE and compares them to necropsy observations in patients with SLE reported before the use of corticosteroid therapy. The 36 patients averaged 32 years of age, and 33 were women. Systemic hypertension was present in 25 (69 per cent) and left ventricular hypertrophy in 23 (64 per cent) patients. Hypertension was twice as common in the 19 patients who received this drug for more than 12 months (average 38 months) than in the 17 patients who received this drug for less than 12 months (average 6 months), and was almost five times more common among our patients than in patients with SLE in the presteroid era. Congestive cardiac failure occurred in 15 patients (43 per cent), eight times more frequent than that reported in noncorticosteroid-treated patients with SLE. Subepicardial and myocardial fat was increased in all 36 patients. Lupus carditis was similar in frequency but differed morphologically in our patients compared to those not treated with corticosteroids. Libman-Sacks-type endocardial lesions, present in 18 (50 per cent) of our patients, were smaller, fewer in number, univalvular rather than multivalvular, and mainly left-sided. Most verrucae were either partly or completely healed, and some were calcified. Pericarditis, present in 19 (53 per cent) patients, was predominantly of the fibrous type. Myocarditis was present in three patients, each of whom also had endocarditis and pericarditis. The lumen of at least one of the three major coronary arteries was narrowed more than 50 per cent by atherosclerotic plaques in 42 per cent of the 18 patients who received corticosteroids for more than 1 year, but in none of the 17 patients who received corticosteroids for less than 1 year. Four of the eight patients with narrowed coronary arteries had myocardial infarcts. Although vital to the management of SLE, corticosteroids have an over-all deleterious effect on the heart. Systemic hypertension and left ventricular hypertrophy appear or, when present, worsen; congestive cardiac failure increases; epicardial apartment of Me

Adipose Tissue↗
PubMed1975

Aortic sinus of Valsalva aneurysms simulating primary right-sided valvular heart disease.

While acute regurgitation is the most common valvular lesion associated with aortic sinus of Valsalva aneurysms, this report describes the pathological findings in five patients in whom primary right-sided valve dysfunction was simulated by sinus of Valsalva aneurysms. In two patients aneurysms of the noncoronary sinus projected into the right atrium at the level of the tricuspid valve and caused tricuspid incomptence. In three patients aneurysms of the right sinus of Valsalva projected into the right ventricle immediately below the pulmonic valve and caused pulmonary outflow tract obstruction. In only one of these patients was the aneurysm perforated at necropsy. Although valvular dysfunction was evident clinically, in none was there a clinical suspicion of a sinus of Valsalva aneurysm. In addition to valvular dysfunction, two patients had conduction disturbances and two, right coronary arterial occlusions found to be the result of aneurysms. The risks of valve dysfunction, arrythmias, aneurysm rupture, and sudden death and the ability to correct this lesion surgically make it especially important to consider aortic sinus of Valsalva aneurysm as a cause of obscure right-sided valvular disease.

Adolescent↗
PubMed1975

Tuberous xanthoma in homozygous type II hyperlipoproteinemia. A histologic, histochemical, and electron microscopical study.

Histologic, histochemical, and ultrastructural studies of a tuberous xanthoma from a patient with homozygous type II hyperlipoproteinemia showed that all of the lipid was within histiocytic foam cells; no lipid was identified in interstitial regions or in blood vessels. Primitive mesenchymal cells, elongated perivascular and fibroblast-like cells, and lysosome-filled macrophages also were present within the xanthoma, indicating possible stages in the evolution of dermal mesenchymal cells into mature, cholesterol-rich foam cells. Morphologically, the lipid was in four different forms: large droplets, which were the dominant form, and membrane-bound crystals, concentric lamellar bodies, and ceroid. The paucity of membrane-bound lipid forms, relative to the abundant free lipid droplets, indicated that lysosomal digestion was a minor metabolic pathway for the intracellular metabolism of lipid in the xanthoma. Thus, nonlysosomal lipid storage in foam cells is a characteristic tissue response to the underlying metabolic defect in type II hyperlipoproteinemia.

Adolescent↗