Search PubMed⌕ Search

Biomedical subjects

J M Riddle

Publications and source records attributed to J M Riddle.

At least 55 records · Page 3Linked to original sources
PubMed1986

Broncholith removal using the YAG laser.

An 85-year-old woman presented with a broncholith in the intermediate bronchus that could not be extracted with either flexible or rigid bronchoscopes. A YAG laser was used to fragment this broncholith so that it could be removed in pieces through a bronchoscope. Chemical composition and morphology of the broncholith were determined. Fragmentation of the large, impacted broncholith with the laser eliminated the necessity for a thoracotomy in this elderly woman.

Aged↗
PubMed1986

The fate of intraarticular loose bodies of meniscus origin in canine species.

A potential risk of arthroscopic meniscectomy is the retention of debris of meniscus origin in the knee joint. This prospective study analyzes the fate of loose bodies of meniscus origin placed into the canine knee joint. At 12 weeks, 16.7% of the free fragments were completely degraded, 16.7% were absorbed by the synovium, and 66.6% were loose, located between synovial folds. At 12 weeks, 93.3% of the fragments had disappeared, and the remaining fragments had decreased 70% in length and 50% in width. A focus of calcification was present in one fragment at 12 weeks. By three weeks, all loose bodies had a pseudocapsule composed of cells with intense fibroblastic activity, occasional mitoses, and a loss of connective tissue matrix at the periphery. A mononuclear leucocytic response was present in the synovium at 12 weeks in four of the five dogs. Free fragments of meniscus origin are most commonly degraded completely by 12 weeks. Enzymatic digestion, mechanical abrasion, and synovial phagocytosis are processes that may contribute to this phenomenon.

Animals↗
PubMed1985

Relation of calcification to torn leaflets of spontaneously degenerated porcine bioprosthetic valves.

The gross appearance of 54 spontaneously degenerated porcine bioprosthetic valves was evaluated to determine the relation of calcium deposition to cusp disruption. Tears or perforations were shown in 89% (48) of the degenerated valves. The most common site of tears or perforations was near the commissural attachment (60% of all tears). Grossly visible deposits of calcium salts that ruptured to the surface of the cusps or caused changes in the topography were observed in 70% (38) of the 54 valves. Calcification was adjacent to tears or perforations in 56% (27) of the 48 valves with torn cusps. Among the valves that showed calcification, the deposits of calcium salts were adjacent to tears or perforations in 71% (27 of 38). The location of deposits of calcium did not relate to the age or sex of the patient or to the position of the valve, but valves with calcium were inserted longer than valves with no calcium (87 +/- 4 versus 58 +/- 7 months; p less than 0.001). The outflow surfaces showed more calcification than the inflow surfaces, irrespective of whether the valves were in the aortic or mitral position. Among the 38 valves with calcification, 92% (35) showed calcification at the commissural attachments, 53% (20) showed calcification in the body of 1 or more cusps, 11% (4) near the base, and 8% (3) near the free edge. In conclusion, most patients with spontaneous porcine valve degeneration showed calcification. The calcification was associated with tears or perforations of the cusps in 50% of all degenerated valves, in 56% of valves with torn cusps, and in 71% of valves that showed gross calcification.

Adult↗
PubMed1985

Effect of warfarin on calcification of spontaneously degenerated porcine bioprosthetic valves.

Synthesis of a calcium-binding amino acid, gamma-carboxyglutamic acid, is a vitamin K-dependent enzymatic process. Warfarin inhibits gamma-carboxyglutamic acid synthesis and, therefore, might diminish the calcification of porcine bioprosthetic valves. To evaluate this, we studied 40 porcine bioprosthetic valves removed because of spontaneous degeneration; 17 patients were treated with warfarin (prothrombin time greater than or equal to 1.5 control) and 23 were untreated. Gross visualization of calcification corresponded closely to x-ray visualization of calcification in explanted valves. No grossly visible calcification or only a single localized nodule was shown in 11 of 17 valves (65%) in treated patients and in only five of 23 valves (22%) in untreated patients (p less than 0.02). Histologic examination showed no calcium or only fine specks of calcium in nine of 13 valves (69%) among warfarin-treated patients and three of 19 valves (16%) from untreated patients. Warfarin, therefore, administered in usual clinical doses, appeared to diminish calcification in spontaneously degenerated porcine bioprosthetic valves.

1-Carboxyglutamic Acid↗
PubMed1984

Platelet adherence to bioprosthetic cardiac valves.

Tissue from porcine aortic bioprosthetic valves (Hancock) and bovine pericardial valves (Ionescu-Shiley) were incubated with platelets tagged with chromium-51. There was a significantly decreased platelet-collagen adhesion reaction in both porcine and bovine glutaraldehyde-treated valves compared with reactions in fresh porcine aortic valve and fresh bovine pericardium (p less than 0.001). There was no significant difference in the platelet-collagen reaction between porcine aortic valve and bovine pericardium, whether treated with glutaraldehyde or in the fresh state (p greater than 0.05). The addition of aspirin did not significantly decrease the platelet-collagen reaction on glutaraldehyde-treated or fresh valves (p greater than 0.05). Rinsing fresh valves in plasma appeared to offer more protection against platelet adhesion than rinsing them in saline solution (p less than 0.01). It is concluded that there is no difference in platelet adherence to porcine aortic valve or bovine pericardium and that glutaraldehyde, and perhaps plasma, offers a protective effect against platelet adhesion.

Animals↗
PubMed1984

A morphologic overview of the porcine bioprosthetic valve--before and after its degeneration.

Patients with valvular heart disease have had their diseased, natural heart valves replaced with the porcine aortic bioprosthetic valve (Hancock type) at Henry Ford Hospital since 1971. This commercially available valvular bioprosthesis is characterized by 1) loss of endothelium from both surfaces of the leaflets, 2) modification in the organization of the fibrous connective tissue of the leaflet, and 3) a reduction in the macromolecular complexes (proteoglycan) of the extracellular matrix. Subendothelial components are therefore exposed to the circulating blood. This bioprosthetic heart valve undergoes degeneration after it is inserted into patients for various lengths of time. Prominent features of the degenerated porcine bioprosthetic valve include 1) penetration of plasma proteins into the interior of the leaflet, 2) adhesion of various types of leukocytes (mononuclear cells and granulocytes) to the surfaces of the leaflets, 3) deposition of single platelets, platelet aggregates and microthrombi onto the leaflet's surface, 4) destruction of collagen fibers, and 5) pathologic deposition of calcium salts. The mechanisms responsible for the degeneration of the porcine aortic bioprosthetic valve are incompletely understood at this time.

Animals↗
PubMed1983

Evaluation of platelet reactivity in patients with valvular heart disease.

Transmission electron microscopy with a standardized in vitro method was used to evaluate the degree of blood platelet reactivity in 72 normal subjects and 72 patients with valvular heart disease. Among the patients with abnormal natural heart valves, 51 had either aortic insufficiency or aortic stenosis, and 21 patients showed either mitral insufficiency or mitral stenosis. For normal subjects, the platelet differential counts were dominated by the dendritic type platelet, and only a few platelets showed cytoplasmic spreading between adjacent pseudopodia (spread type). A hyperactive response was defined as greater than 20% of the spread type platelet or more than 93 aggregates per 100 single platelets counted, or both. Only 6 (8%) of the 72 normal subjects showed hyperactive platelets. In contrast, 45 (62%) of the 72 patients with valvular heart disease had hyperactive platelets (p less than 0.01). For patients with abnormal valves, the mean percent of the spread type platelet was 35% with a mean value of 105 platelet aggregates. The increased level of platelet reactivity was independent of both the position of the valve (aortic versus mitral) and its functional status (insufficient versus stenotic). Disturbed flow and the exposure of subendothelial thrombus-producing materials are features associated with abnormal heart valves. These factors, which usually occur in combination, may explain the hyperactive platelet response found in these patients.

Adolescent↗
PubMed1981

A comparative study of platelet reactivity in arthritis.

We utilized a standardized in vitro method which employs transmission electron microscopy to monitor the degree of surface activation (cytoplasmic spreading) and amount of aggregation displayed by platelet populations from 314 patients with one of five distinct rheumatic diseases and from 72 normal subjects. The percentage of patients in each group whose platelet populations were hyperactive was as follows: polymyalgia rheumatica, 75 percent; scleroderma, 65 percent; primary gout, 61 percent; rheumatoid arthritis, 57 percent; and degenerative joint disease, 40 percent. Pair-wise contrasts performed after an analysis of variance suggest the following differences and similarities: (1) the mean differential platelet count of the normal subjects differed from that in each disease state; (2) the platelet responsivity in patients with degenerative joint disease most closely resembled that in normal subjects; (3) the platelet response in polymyalgia rheumatica plus temporal arteritis was the most abnormal; and (4) platelet response in scleroderma, rheumatoid arthritis, and gout closely resembled each other. The increased platelet response in vitro may reflect the in vivo presence of disease-related "risk factors" (hyperuricemia, immune complexes, and atherosclerosis). Those patients with "triggered" platelet populations may be appropriate candidates for antiplatelet therapy.

Adult↗