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Biomedical subjects

J A Shaver

Publications and source records attributed to J A Shaver.

At least 37 records · Page 2Linked to original sources
PubMed1984

Intermittent mitral regurgitation due to Beall valve dysfunction: analysis of 13 patients with atrial fibrillation.

A unique hemodynamic event was noted in long-term survivors of mitral valve replacement with the Beall prosthesis. The event was a result of intermittent valve dysfunction and transvalvular mitral regurgitation (MR). At cycle lengths longer than 0.9 second that were preceded by shorter cycle lengths, 8 of 13 patients with Beall valve prostheses who had chronic atrial fibrillation (AF) intermittently had a marked unexpected decrease in peak left ventricular systolic pressure and a simultaneous increase in left atrial or pulmonary artery wedge "v" wave pressure. This event, which is a result of intermittent, severe MR, occurred more frequently at longer cycle lengths. In all 8 patients with the finding, severe valve disc wear was found at operation; however, 5 of these patients had only trace or 1+ MR on left ventricular angiography. In contrast, the event did not occur in 11 patients in chronic AF with organic MR or non-Beall valve MR, despite an appropriate number of sufficiently long cycles. The absence of the event in 5 Beall valve patients with significantly faster heart rates than in those with the event may in part be a result of its dependence on cycle length. This hemodynamic event, when present in a Beall valve recipient in AF, is an indication for valve replacement, even in the absence of angiographic evidence of severe MR.

Atrial Fibrillation↗
PubMed1984

The noninvasive assessment of pulmonary capillary wedge pressure in mitral regurgitation.

The interval between the aortic closure sound and the mitral opening snap (A2-OS) has been shown to have a significant inverse correlation with pulmonary capillary wedge pressure (PCW) in mitral stenosis. The present study critically examines the relationship of several noninvasively determined diastolic intervals to PCW in patients with relatively pure mitral regurgitation (MR). Fifty-seven patients with MR of diverse etiologies were studied with echocardiograms and phonocardiograms in addition to right and left heart catheterization. Noninvasive determination of the time intervals of aortic closure sound to mitral valve opening (A2-MO), mitral D point to E point (D-E), aortic closure sound to mitral E point (A2-E), the interval from the onset of the QRS to mitral closure (Q-C), and the ratio Q-C/A2-E were compared to invasive measurements of mean PCW, the height of the V wave of PCW (PCW-V), and the ratio of PCW-V to left ventricular (LV) peak systolic pressure (PCW-V/LV). Correlation between each of the five noninvasive intervals and each of the three invasive pressure measurements was then determined. Of the noninvasive intervals studied, A2-MO had the best inverse correlation with all measures of PCW. All 18 patients having a short A2-MO (less than 40 msec) had a PCW-V of greater than or equal to 40 mm Hg and all seven patients having a long A2-MO (greater than 85 msec) had a PCW-V of less than 22 mm Hg. A2-E also had a strong inverse correlation with PCW.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Isovolumic relaxation period in hypertrophic cardiomyopathy.

Previous reports have demonstrated that patients with hypertrophic cardiomyopathy have a prolonged isovolumic relaxation period as a result of a delay in mitral valve opening, reflecting a reduced rate of fall of left ventricular pressure. This period as measured from the aortic closure sound (A2 on phonocardiogram) to the opening of the mitral valve (on echocardiogram) was determined in 84 patients with hypertrophic cardiomyopathy and compared with findings in 31 normal volunteers. The duration of the isovolumic relaxation period in the 84 patients had a wide range from 0 to 160 ms (mean 71 +/- 32) that was not significantly different from that in normal subjects (63 +/- 11 ms). However, it was possible to identify a group of 15 patients with an extremely short isovolumic relaxation period, 2 standard deviations below the normal range. This shortening was due to a marked delay in aortic closure sound (A2) due to late left ventricular-aortic pressure crossover, as well as early opening of the mitral valve secondary to elevated left atrial pressure, which was confirmed by hemodynamic correlations and digitized echocardiographic data. In this subset of patients, A2 is a poor marker of the onset of rapid left ventricular pressure decline and, thus, the interval from A2 to mitral valve opening is not a valid reflection of left ventricular relaxation. It is concluded that in hypertrophic cardiomyopathy, both the timing and sequence of relaxation are abnormal, as is the rate of relaxation. Furthermore, the isovolumic relaxation period is multifactorially determined and depends not only on the rate of left ventricular pressure decline, but also on the magnitude of the pressure drop from A2 to mitral valve opening. All of these determinants must be kept in mind when the isovolumic relaxation period is used as a measure of left ventricular relaxation.

Adolescent↗
PubMed1978

Cardiac tamponade: hemodynamic observations in man.

Hemodynamic studies were performed before and after pericardiocentesis in 19 patients with pericardial effusion. Right atrial pressure decreases significantly, from 16 +/- 4 mm Hg (mean +/- SD) to 7 +/- 5 mm Hg in 14 patients with cardiac tamponade. This change was accompanied by significant increases in cardiac output (3.87 +/- 1.77 to 7 +/- 2.2 l/min) and inspiratory systemic arterial pulse pressure (45 +/- 29 to 81 +/- 23 mm Hg). The remaining five patients did not demonstrate cardiac tamponade, as evidenced by lack of significant change in these hemodynamic parameters. In all patients with tamponade, right ventricular end-diastolic pressure (RVEDP) was elevated and equal to pericardial pressure; equilibration was uniformly absent in patients without tamponade. During gradual fluid withdrawal in the tamponade group, significant hemodynamic improvement was largely confined to the period when right ventricular filling pressure remained equilibrated with pericardial pressure. In 10 patients with tamponade and pulsus paradoxus, pulmonary arterial wedge pressure (PAW) was equal to pericardial pressure except during early inspiration and expiration when it was transiently less and greater, respectively; however, inspiratory right atrial pressure never fell below pericardial pressure. In these 10 patients, PAW decreased significantly following pericardiocentesis (P less than 0.001). In the remaining four patients with tamponade but without pulsus paradoxus, all of whom had chronic renal failure, PAW was consistently higher than pericardial pressure or RVEDP and did not decrease after pericardiocentesis. These data tend to confirm the hypothesis that in patients with tamponade, the venous pressure required to maintain any given cardiac volume is determined by pericardial rather than ventricular compliance. When pericardial compliance determines diastolic pressure in both ventricles, relative filling of the ventricles will be competitive and determined by their respective venous pressures (pulmonary vs systemic), which vary with respiration and alternately favor right and left ventricular filling. This results in pulsus paradoxus. However, if pulmonary arterial wedge pressure is markedly elevated before the onset of tamponade, as in patients with chronic renal failure, then pericardial compliance may only determine right ventricular filling pressure. In such cases, pulsus paradoxus may be absent.

Adult↗
PubMed1977

Pulmonary hypertension in the CREST syndrome variant of progressive systemic sclerosis (scleroderma).

Severe pulmonary hypertension without pulmonary fibrosis occurred in 10 patients with the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly, telangiectasia), reputedly a benign variant of progressive systemic sclerosis. Time from the initial symptom, Raynaud's phenomenon, to the recognition of pulmonary hypertension was as long as 40 years. Pulmonary hypertension and increased pulmonary vascular resistance was shown in all patients. Autopsy examination in three of six deaths attributable to pulmonary hypertension showed intimal proliferation with myxomatous change in the small- and medium-sized pulmonary arteries similar to changes in the digital arteries of patients with scleroderma and Raynaud's phenomenon, and interlobular renal arteries of those with "scleroderma kidney." It is concluded that the CREST syndrome is not entirely benign but may be complicated, after a long clinical course, by progressive pulmonary vascular obliteration, pulmonary hypertension, and death in the absence of significant pulmonary fibrosis.

Adult↗