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Biomedical subjects

B G Firth

Publications and source records attributed to B G Firth.

65 records · Page 4Linked to original sources
PubMed1982

Radionuclide techniques for valvular regurgitant index: comparison in patients with normal and depressed ventricular function.

We compared contrast angiography with three techniques of quantitating valvular regurgitation from radionuclide ventriculograms in 70 patients: 45 with documented regurgitation graded 1-4+, and 25 without regurgitation. The radionuclide "regurgitant index" (ratio of L to R ventricular stroke counts) was measured from fixed end-diastolic regions of interest (method A), from separate end-diastolic and end-systolic regions of interest (method B), and from a "stroke-volume image" (method C). Sensitivities for detecting 1+ or more regurgitation were: method A = 57.8%, method B = 37.8% and method C = 62.2%. Sensitivities for detecting 2+ or more regurgitation were: method A = 74.2%, method B = 54.8%, and method C = 77.4%. All methods are greater than 97% specific. Interobserver coefficients of variability were: method A = 9.1%, method B = 19.2%, and method C = 5.4%. The sensitivity of each method was improved when left-ventricular ejection fractions were greater than 0.35. No method consistently differentiated between 2+, 3+, and 4+ valvular regurgitation.

Angiography↗
PubMed1981

Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease.

Endogenous modulators of platelet aggregability and vascular tone may play a part in coronary-artery disease. We therefore measured the release of prostaglandins and thromboxane into the coronary circulation in patients with various kinds of cardiac disease. Simultaneous coronary-sinus (CS) and ascending-aortic (AO) blood samples were obtained from 60 patients for measurement of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha, a prostaglandin I2 metabolite) and of thromboxane B2 (TxB2). Samples from 45 of these patients were also tested for prostaglandin E2 (PGE2) and lactate. Patients with unstable angina pectoris who reported chest pain within 24 hours of study had higher TxB2 CS/AO ratios (5.8 +/- 2.8, mean +/- S.D.) than patients whose most recent anginal pain was more than 96 hours before study (1.3 +/- 0.6; P less than 0.05), than those with nonischemic chest pain (1.2 +/- 0.4; P less than 0.05), or with valvular or congenital nonischemic heart disease (1.2 +/- 0.6; P less than 0.05). Those whose most recent anginal pain occurred 24 to 96 hours before study were distributed bimodally: the majority had low TxB2 CS/AO ratios (range, 0.5 to 2.1) like the patients in the three aforementioned groups, whereas a few had markedly elevated values (range, 10.5 to 46.6). The 6-keto-PGF1 alpha and PGE2 CS/AO ratios and myocardial lactate extraction were not significantly different among the five groups. These data suggest that local thromboxane release is associated with recent episodes of angina in patients with unstable angina pectoris, but whether this release is a cause or an effect is not yet known.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Evaluation of postextrasystolic T wave alterations in identification of patients with coronary artery disease or left ventricular dysfunction.

This study was performed (1) to assess the value of postextrasystolic T wave alterations in identification of patients with cardiac disease and (2) to determine if their frequency depends on length of compensatory pause. In 52 patients a pacing catheter was placed in the right ventricular (RV) apex, and premature beats were programmed to occur 30 msec beyond RV refractory period. Postextrasystolic T wave alterations occurred in 32 patients, 13 with an 19 without coronary artery disease (CAD) (NS). Such alterations were also not related to presence of abnormal left ventricular (LV) ejection fraction (less than 0.55) or end-diastolic pressure (greater than 12 mm Hg). In 33 patients, premature beats were also introduced 330 msec beyond the RV refractory period to compare effects of long and short compensatory pauses on frequency of postextrasystolic T wave alterations. When the pause was near maximal, 18 patients had alterations in 60 ECG leads; when it was shorter, seven patients had alterations in 10 leads (p less than 0.001). Thus, judging from provoked postextrasystolic T wave alterations, such spontaneous changes appear neither sensitive nor specific in the identification of patients with cardiac disease. The frequency of postextrasystolic T wave changes depends on the length of the compensatory pause.

Adult↗
PubMed1981

Direct measurement of cardiac output by gated equilibrium blood pool scintigraphy: validation of scintigraphic volume measurements by a nongeometric technique.

A nongeometric technique for the determination of left ventricular volumes from the count data derived from gated equilibrium blood pool scans was previously described and validated by the demonstration of an excellent correlation between the derived data and angiographically determined left ventricular volumes. To provide a further prospective evaluation of this method and to validate its ability to determine stroke volume and cardiac output by a technique that is itself independent of geometric assumptions, simultaneous measurements of cardiac output by the thermodilution technique and gated scintigraphy were performed in 21 patients without valve regurgitation or intracardiac shunts. To substantiate the reliability of scintigraphic measurements at high levels of cardiac output, seven patients had multiple measurements of cardiac output at rest and during an infusion of isoproterenol. There was an excellent correlation between thermodilution and scintigraphic values for cardiac output (scan cardiac output = 0.99 thermodilution cardiac output - 0.005 liters/min; n = 31, standard error of the estimate [SEE] = 0.175 liters/min, r = 0.97) as well as between thermodilution and scintigraphic stroke volumes (scan stroke volume = 1.03 thermodilution stroke volume - 2.8 ml; n = 31, SEE = 2.5 ml, r = 0.95). In addition, the relation between scintigraphic and angiographic measurements of left ventricular volumes continued to be excellent: In 15 patients with technically adequate angiograms, scintigraphic left ventricular volume = 0.90 angiographic left ventricular volume + 7 ml (n = 30, SEE = 10 ml, r = 0.91). Thus, this study further validates the nongeometric method of measuring left ventricular volumes with gated scintigraphy and demonstrates its ability to measure left ventricular stroke volume and cardiac output reliably.

Adult↗
PubMed1981

Assessment of myocardial performance in ischaemic heart disease: from changes in left ventricular power output produced by graded-dose isoprenaline infusion.

Current clinical indices of myocardial contractility derive from concepts of muscle mechanics developed from isolated muscle experiments. Numerous simplifying assumptions are needed to apply these concepts to contractility studies in the whole heart. An alternative is to consider the heart as a pump which generates both pressure (P) and flow (Q) and to estimate its performance from the power output of its ventricles (P X Q). A method is described for measuring peak left ventricular power output in patients during routine cardiac catheterisation. The measurements have been made at rest and following inotropic challenge with gradient infusions of isoprenaline intravenously. Results from 13 patients with coronary artery disease and severe angina pectoris, who were clinically indistinguishable from one another, are reported. The patients could be grouped according to their left ventricular peak power responses to isoprenaline, although no difference could be demonstrated between them at rest. The patients who showed no increase in left ventricular power response to isoprenaline had a poor prognosis.

Adult↗
PubMed1980

Effect of selective coronary arteriography on left ventricular volumes and ejection fraction in man.

This study was performed to assess the influence of selective coronary arteriography on left ventricular volumes and ejection fraction in man. In 30 patients with assorted cardiac diseases, left ventricular end-diastolic and end-systolic volumes and ejection fraction were quantitated immediately before and after selective coronary arteriography. In 19 patients (Group A), contrast left ventriculography was performed immediately before and after selective coronary arteriography. In the remaining 11 patients (Group B), multigated equilibrium blood pool imaging was performed just before and after coronary arteriography. In both groups, mean systemic arterial pressure and heart rate did not change from just before the first to immediately before the second assessment of left ventricular volumes and ejection fraction, but left ventricular end-diastolic pressure increased. End-diastolic and end-systolic volume indexes, and ejection fraction did not change from just before to immediately after selective coronary arteriography. Therefore, selective coronary arteriography (1) consistently causes an increase in left ventricular end-diastolic pressure but (2) exerts no effect on left ventricular volumes and ejection fraction, even in patients with severely compromised left ventricular function.

Adult↗