Search PubMed⌕ Search

Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 289 records · Page 16Linked to original sources
PubMed1987

Mechanisms of severe mitral regurgitation in mitral valve prolapse determined from analysis of operatively excised valves.

Certain clinical and mitral valvular morphologic findings are described in 83 patients (age 26 to 79 years [mean, 60]; 26 women [31%] and 57 men [69%]) with mitral valve prolapse (MVP) and mitral regurgitation (MR) severe enough to warrant mitral valve replacement. All 83 operatively excised valves were examined by the same person, and all excised valves had been purely regurgitant (no element of stenosis). No patients had hemodynamic evidence of dysfunction of the aortic valve. In each valve a portion of the posterior mitral leaflet was elongated such that the distance from the distal margin to basal attachment of this leaflet was similar to the distance from the distal margin of the anterior leaflet to its basal attachment to the left atrial wall. Two major mechanisms for the severe MR were found: dilatation of the mitral anulus with or without rupture of chordae tendineae and rupture of chordae tendineae with or without dilatation of the mitral anulus. Of the 83 patients, 48 (58%) had both dilated anuli (greater than 11 cm in circumference) and ruptured chordae tendineae; 16 (19%) had dilated anuli without ruptured chordae, and 16 (19%) had ruptured chordae without significant anular dilatation. In three patients the anulus was not dilated, nor were chordae ruptured, and therefore the mechanism of the MR is uncertain. Mitral chordal rupture was nearly as frequent in the 64 patients with clearly dilated anular circumferences as in the 19 patients with normal or insignificantly dilated anular circumferences (less than or equal to 11 cm).

Adult↗
PubMed1987

Some realities of present-day cardiologic journal publishing in the USA.

The types and quantities of cardiological publications in the USA have changed drastically in recent years. The small, independent medical publisher in the USA is vanishing. Medical publishers in the USA today primarily are parts of larger, nonmedical publishing corporations, and the nonmedical publications are affecting the medical publications. The 'throw-away' journals are increasing and their existence is diminishing the reading time available and advertising support provided to the peer-review subscription journals. The publication of symposia proceedings supported entirely by grants from single pharmaceutical or medical device companies in otherwise peer-review journals is increasing. It is better, in my view, for physicians not to exert efforts to discontinue this practice, which is here to stay, but to exert their influence to reduce excess bias and overstatement. The peer-review subscription journals, most of which are published by for-profit corporations, are the sources of our new medical information and the 'storehouse' of our knowledge. They need our strong support. They need to be published on acid-free paper which will not deteriorate, for they are the permanent record of our information. We need more editorial pages in the peer-review subscription journals so that more review and experimental-type articles can be published, and less pages in the 'throw-away' journals which diminish support available to the peer-review subscription journals.

Cardiology↗
PubMed1987

Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy.

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.

Adult↗
PubMed1986

Clinical and necropsy observations early after simultaneous replacement of the mitral and aortic valves.

Clinical and necropsy findings are described in 54 patients, aged 25 to 83 years (mean 53), who died within 60 days of simultaneous replacements of both mitral and aortic valves. The patients were separated into 4 groups on the basis of the presence of stenosis (with or without associated regurgitation) or pure regurgitation of each valve: 30 patients (56%) had combined mitral and aortic valve stenosis; 12 patients (22%) had mitral stenosis and pure aortic regurgitation; 8 patients (15%) had pure regurgitation of both valves; and 4 patients (7%) had pure aortic regurgitation and mitral stenosis. Necropsy examination in the 54 patients disclosed a high frequency (48%) of anatomic evidence of interference to poppet or disc movement in either the mitral or aortic valve position or both. Anatomic evidence of interference to movement of a poppet or disc in the aortic valve position was twice as common as anatomic evidence of interference to poppet or disc movement in the mitral position. Interference to poppet movement is attributable to the prosthesis's being too large for the ascending aorta or left ventricular cavity in which it resided. The ascending aorta is infrequently enlarged in patients with combined mitral and aortic valve dysfunction irrespective of whether the aortic valve is stenotic or purely regurgitant. Likewise, the left ventricular cavity is usually not dilated in patients with combined mitral and aortic valve stenosis, the most common indication for replacement of both left-sided cardiac valves. Of the 54 patients, 12 (22%) had 1 mechanical and 1 bioprosthesis inserted. It is recommended that both substitute valves should be mechanical prostheses or both should be bioprostheses.

Adult↗