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Biomedical subjects

J Wynne

Publications and source records attributed to J Wynne.

At least 73 records · Page 4Linked to original sources
PubMed1983

Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation?

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.

Adolescent↗
PubMed1983

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

The left ventricular diastolic pressure-volume relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and M-mode echocardiography before and during angina induced by pacing tachycardia. All patients had two- or three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development of angina and a postpacing rise in left ventricular end-diastolic pressure (15 +/- 3 to 31 +/- 6 mm Hg, p less than 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 +/- 2.1 to 9.2 +/- 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 +/- 37 to 48 +/- 27 mm/sec, p less than 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 +/- 5 to 58 +/- 7 msec, p less than 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (sigma R = -PR). A radial stiffness modulus (ER) was determined by the slope of the PR vs log h plots before and after pacing. Over the same range of residual radial stress (sigma R), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.

Adult↗
PubMed1983

Effect of timolol on exercise-induced reduction in regional ejection fraction in patients with coronary artery disease.

In order to evaluate the effects of timolol, a new beta-adrenergic blocking agent, on exercise-induced left ventricular wall motion abnormalities, we studied nine patients with chronic, angiographically-documented coronary artery disease. A computerized technique for determining apical, anteroseptal and inferoposterior regional ejection fractions during gated radionuclide ventriculography was used to assess left ventricular dysfunction. During exercise prior to the administration of timolol, the apical regional ejection fraction fell from 0.62 +/- 0.08 to 0.51 +/- 0.08 (p less than .01). The anteroseptal ejection fraction fell from 0.50 +/- 0.08 to 0.41 +/- 0.05 (p less than .05), and the inferoposterior ejection fraction fell from 0.75 +/- 0.10 to 0.59 +/- 0.06 (p less than .05). Three days after beginning therapy with 10-30 mg of timolol, this reduction was markedly attenuated. The apical ejection fraction fell from 0.59 +/- 0.09 to 0.54 +/- 0.08 (p = NS), the anteroseptal ejection fraction fell from 0.49 +/- 0.07 to 0.47 +/- 0.18 (p = NS) and the inferoposterior ejection fraction fell from 0.62 +/- 0.06 to 0.59 +/- 0.07 (p = NS). Furthermore, several individual regions showed increases in ejection fraction. This study demonstrates a previously unreported and beneficial anti-ischemic effect of timolol.

Cardiac Output↗
PubMed1982

Use of radionuclide ventriculography for assessment of changes in myocardial performance induced by disopyramide phosphate.

Disopyramide phosphate may precipitate heart failure in susceptible patients with cardiomegaly. To identify those at risk, gated radionuclide ventriculography (RVG) was performed in two groups. Eleven patients without evidence of structural heart disease constituted group 1, and 12 with impaired ventricular function made up group 2. RVG was carried out before and 2 hours after administration of a single 300-mg dose of disopyramide orally. After disopyramide mean left ventricular ejection fraction (EF) decreased in the 12 patients in group 2 (35% to 26%) (p less than 0.01); depression of function was most pronounced in regions with the poorest baseline value. Of the 11 patients in group 1 (mean EF 60%), EF was reduced after disopyramide in only one. Serum levels of drugs were comparable in patients in both groups (3.1 vs. 3.7 micrograms/ml). We conclude that (1) patients with left ventricular dysfunction are particularly susceptible to the depressant effects of disopyramide; (2) RVG is a sensitive technique for detecting disopyramide-induced changes in ventricular performance; and (3) RVG before and shortly after a dose of disopyramide orally may help to identify those patients at high risk.

Adolescent↗
PubMed1982

Inotropic contractile reserve: a useful predictor of increased 5 year survival and improved postoperative left ventricular function in patients with coronary artery disease and reduced ejection fraction.

The increase in left ventricular ejection fraction produced by postextrasystolic potentiation or epinephrine infusion has been used to demonstrate inotropic contractile reserve in patients with coronary artery disease and a depressed ejection fraction (less than 0.50). Prior studies have shown that a change in ejection fraction of 0.10 or more after postextrasystolic potentiation or epinephrine infusion is helpful in discriminating those patients with a better short-term (1 year) prognosis whether treated medically or surgically. This study related inotropic contractile reserve to 5 year prognosis in 54 patients receiving postextrasystolic potentiation or epinephrine infusion between 1971 and 1974. Current left ventricular function in surviving patients was assessed with radionuclide ventriculograms whenever possible. Five year survival was significantly better in patients with an initial change in ejection fraction greater than 0.10 in both the surgically treated group (16 of 20 versus 5 of 15, p less than 0.01) and the medically treated group (6 of 8 versus 1 of 11, p less than 0.01). Furthermore, among the surviving patients in the surgical group, current ejection fraction in the radionuclide ventriculogram was significantly greater in patients who demonstrated inotropic contractile reserve in their 1971 to 1974 contrast left ventriculogram. These findings support the concept that coronary revascularization enhances function of ischemic but viable myocardium.

Angina Pectoris↗
PubMed1982

Measurement of infarct size using single photon emission computed tomography and technetium-99m pyrophosphate: a description of the method and comparison with patient prognosis.

The application of dual tracer transaxial emission computed tomography of the heart was studied with use of technetium-99m pyrophosphate and technetium-99m-labeled red blood cells for measuring infarct size in 20 patients with acute myocardial infarction and 10 without infarction. Imaging was performed with a standard gamma camera and with a multidetector transaxial emission computed tomographic body scanner 3 hours after injection of technetium-99m pyrophosphate. Immediately after the scanning procedure, technetium-99m pertechnetate was injected to label red blood cells, and the scanning protocol was repeated. Technetium-99m pyrophosphate was detected in the anterior wall with involvement of the interventricular septum or lateral wall in patients with electrocardiographic criteria for anterior infarction, whereas uptake was detected in the diaphragmatic left ventricular wall with involvement of the posterior, posteroseptal or posterolateral left ventricle or of the right ventricle in patients with electrocardiographic criteria for inferior or posterior infarction. Infarct size measured from transaxial images ranged from 14.0 to 117.0 g in weight. There was a direct relation between infarct size and patient prognosis in that, of the 13 patients with infarct greater than 40 g, 11 (85 percent) had complications, whereas only 2 (29 percent) of 7 patients with an infarct less than 40 g had complications during a follow-up period averaging 17.8 months (p less than 0.05).

Aged↗
PubMed1982

Scintigraphic diagnosis of tricuspid regurgitation.

The authors describe a simple technique for diagnosis of tricuspid regurgitation. Red blood cells were labeled in vivo with 99mTc and 22 patients were studied with ECG-gated blood-pool imaging of the liver. A single region of interest was manually drawn around the liver and a time-activity curve obtained. The per cent change in liver counts during the cardiac cycle was found to be significantly higher in the 12 patients with tricuspid regurgitation (Group I) (mean, 4.04 +/- 1.6%; range, 1.3-21.4%) compared with the 10 controls (Group II) (mean, 0.35 +/- 0.16%; range, 0.013-1.3%) (p less than 0.05). Using a 1% change in liver counts as the criterion of a positive study, all 12 cases in Group I were diagnosed correctly, but there was one false positive in Group II; thus the sensitivity was 100% and the specificity 90%.

Cardiac Catheterization↗
PubMed1982

Modification of abnormal left ventricular diastolic properties by nifedipine in patients with hypertrophic cardiomyopathy.

The effect of nifedipine on left ventricular isovolumic relaxation and diastolic filling properties and systemic and left ventricular hemodynamics was studied in 15 patients with hypertrophic cardiomyopathy. After nidefipine (10 mg sublingually), the prolonged left ventricular isovolumic relaxation time assessed by echocardiography decreased from 112 +/- 26 to 83 +/- 23 msec (p less than 0.0001), and the left ventricular pressure decay as measured by time constant T improved from 63 +/- 20 to 49 +/- 11 msec (p less than 0.05). Left ventricular filling dynamics also improved as assessed by a return toward normal in the depressed peak rate of left ventricular diastolic filling (dimension change 72 +/- 37 to 101 +/- 39 mm/sec, p less than 0.01) and the peak rate of posterior wall thinning (47 +/- 31 to 68 +/- 36 mm/sec, p less than 0.001). These changes were accompanied by hemodynamic evidence of improved diastolic function shown as a decrease in left ventricular end-diastolic pressure and a downward shift in the left ventricular diastolic pressure-dimension relationship, suggesting improved left ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic arterial blood pressure, and no depression of the left ventricular percent fractional shortening or cardiac index. These data indicate that abnormal left ventricular relaxation and diastolic filling rates in hypertrophic cardiomyopathy are dynamic and favorably modified by nifedipine, and that this effect is not related to a depression of left ventricular systolic function.

Adolescent↗
PubMed1982

Sensitivity of end-systolic pressure-dimension and pressure-volume relations to the inotropic state in humans.

The value for the slope of the left ventricular (LV) end-systolic pressure-dimension and pressure-volume relations has been proposed as a quantitative measure of the LV inotropic state. This measure of LV inotropic state is attractive because it is independent of preload and incorporates afterload. To investigate the sensitivity of the slope of these relations to alterations in contractile state, 10 normal subjects were studied using M-mode echocardiographic, phonocardiographic and indirect carotid pulse recordings during infusion of methoxamine to alter end-systolic pressure and during infusion of dobutamine (5 micrograms/kg/min) to increase LV inotropic state. Heart rate was maintained within a narrow range for each subject. End-systolic volume was calculated from end-systolic echocardiographic dimension by standard methods. End-systolic pressure was estimated from the dicrotic notch pressure determined from a calibrated carotid pulse recording; peak systolic pressure was also measured. Regardless of the method of approximating end-systolic pressure, the positive inotropic intervention caused a leftward shift in the end-systolic pressure-dimension and pressure-volume lines. With the dobutamine infusion, the value for the slope of the end-systolic pressure-dimension relation increased by 25% (range 16-46%, p less than 0.001), while the slope of the end-systolic pressure-volume relation increased by 55% (range 37-85%, p less than 0.001). In all cases, the curves were linear and became steeper with the positive inotropic intervention. In contrast, the value of the slope of the peak systolic pressure-end-systolic dimension relation showed a variable response to the dobutamine infusion (mean change 13%, range -77% to 73%; NS). Although the position of the peak systolic pressure-end-systolic dimension curve is consistently shifted with an alteration in inotropic state, the values of the slope of these curves are not reliable indicators of change in LV contractility. The values for the slope of the line relating end-systolic pressure (estimated by dicrotic notch pressure) to end-systolic dimension or volume, however, are highly sensitive to a change in inotropic state in human subjects.

Adult↗
PubMed1982

Effect of exercise on erythrocyte count and blood activity concentration after technetium-99m in vivo red blood cell labeling.

We studied the effect of exercise on blood radiotracer concentration after technetium-99m in vivo red blood cell labeling. After red blood cell labeling, 13 subjects underwent maximal supine bicycle exercise. Radioactivity, analyzed with a well counter, was measured in heparinized venous blood samples drawn at rest and during peak exercise. Changes in activity were compared with changes in erythrocyte count. Activity and erythrocyte counts increased during exercise in all 13 subjects. Percent increase in activity correlated with percent increase in erythrocyte count (r = -0.78), but did not correlate with either duration of exercise or maximal heart rate. Twenty minutes after termination of exercise, activity and erythrocyte count had decreased from peak exercise values but remained higher than preexercise values. In nine nonexercised control subjects, samples drawn 20 minutes apart showed no change in activity or in erythrocyte count. We conclude that exercise increases blood activity, primarily because of an increase in erythrocyte count. During radionuclide ventriculography, blood activity must be measured before and after any intervention, particularly exercise, before a change in left ventricular activity can be attributed to a change in left ventricular volume.

Adult↗
PubMed1981

Decreased lymphocyte beta-adrenergic-receptor density in patients with heart failure and tolerance to the beta-adrenergic agonist pirbuterol.

We compared the initial and long-term effects of the beta-adrenergic agonist pirbuterol in 12 patients with chronic congestive heart failure. The drug's initial effect was a 35 per cent increase in cardiac index, but there was no significant change in heart rate or mean arterial pressure. After one month of therapy, the mean cardiac index and ejection fraction had returned to base-line values, and no clinical effect was evident in most patients. This apparent tolerance was not accompanied by changes in heart rate, blood pressure, or body weight, and it occurred in the presence of therapeutic drug levels during long-term therapy. The density of beta-adrenergic receptors on lymphocytes from patients treated with pirbuterol was significantly depressed as compared with that of patients with heart failure of comparable severity but not treated with pirbuterol. We conclude that tolerance to the hemodynamic and clinical effects of pirbuterol develops during long-term administration; this tolerance may be related to a decrease in myocardial or vascular beta-adrenergic receptors or both.

Adrenergic beta-Agonists↗
PubMed1981

Tricuspid stenosis masquerading as right ventricular failure in a patient with a prosthetic mitral valve.

Echocardiographic, phonocardiographic, and pulse tracing recordings demonstrated clinically unsuspected tricuspid stenosis in a 53-year-old man with a prosthetic mitral valve and signs of right heart failure. Physiologic correlates of the patient's heart sounds and diastolic murmur were studied by simultaneous M-mode echocardiograms and phonocardiograms. Cardiac catheterization and subsequent valve surgery confirmed the presence of tricuspid stenosis. It is important to consider the diagnosis of tricuspid stenosis in all patients with a history of rheumatic mitral valve disease who develop findings suggestive of right ventricular failure.

Cardiac Catheterization↗
PubMed1981

Problems in assessment of new pharmacologic agents for the heart failure patient.

Modern management of congestive heart failure (CHF) employs inotropic drugs, vasodilators, and diuretics. Although pharmacologic classification of drugs is possible in animals, identification of predominant hemodynamic mechanisms in humans is more complex, because many effects of vasodilators and inotropic drugs are similar. We compared the effects of a vasodilator, prazosin, and two agents with both inotropic and vasodilatory properties, amrinone and pirbuterol, on cardiac index (CI), mean aortic pressure, left ventricular stroke work index (LVSWI), LV filling pressure (LVFP), systemic vascular resistance, LV ejection fraction (LVEF), and myocardial O2 consumption (MVO2) in 34 patients with advanced CHF. We concluded that (1) a rise in CI and LVEF, together with a fall in LVFP, does not necessarily indicate an inotropic effect; (2)both CI and LVEF may be increased by an inotropic mechanism in advanced CHF without a rise in MVO2; and (3) a drug-induced rise in LVSWI with stable or lower LVFP suggests an inotropic mechanism of action.

Aminopyridines↗
PubMed1981

Improved right ventricular function and reduced pulmonary vascular resistance during prazosin therapy of congestive heart failure.

Although the effect of systemic vasodilator therapy on left ventricular function in congestive heart failure has been extensively evaluated, little is known about its effect on pulmonary vascular resistance and right ventricular function. Since pulmonary vascular resistance is mediated in part by alpha-adrenergic receptors, we studied the effects of the alpha-adrenergic antagonist prazosin on right ventricular function as determined by a radionuclide ventriculographic technique which assessed right and left ventricular ejection fractions simultaneously. In 11 patients treated for two months with prazosin, right ventricular ejection fraction increased from 0.28 +/- 0.04 to 0.44 +/- 0.07 (p less than 0.01). In 10 patients who received a single dose of prazosin 48 hours after withdrawal of prior prazosin therapy, right ventricular ejection fraction increased from 0.29 to 0.05 to 0.38 +/- 0.06 (p less than 0.02). In nine patients who received a single dose of prazosin during right sided heart catheterization, pulmonary vascular resistance decreased from 358 +/- 70 to 236 +/- 60 dyne-sec-cm -5 (p less than 0.01). These studies suggest that prazosin has beneficial effects on right ventricular function both immediately and long-term in patients with severe congestive heart failure. Although the mechanism of this effect is not known, possibilities include a direct effect of prazosin on the pulmonary vasculature, a secondary reduction in right ventricular afterload due to improved left ventricular performance and a withdrawal of reflex-mediated pulmonary vasoconstriction due to improved left ventricular performance.

Adrenergic alpha-Antagonists↗
PubMed1981

A simplified technique for measuring right ventricular ejection fraction using the equilibrium radionuclide angiocardiogram and the slant-hole collimator.

The authors developed and tested a simplified technique for measuring the right ventricular ejection fraction (RVEF). Following in vivo 99mTc red cell labeling, equilibrium (ECG-gated) radionuclide angiocardiography was performed in the modified left-anterior-oblique projection using a 30 degree slant-hold collimator. A single region-of-interest was defined from the ejection fraction image, and background was corrected. In 11 normal patients, the mean RVEF was 0.59 +/- 0.08 (SD). In 20 patients with suspected disease, who had RVEF measured by both equilibrium and first-pass techniques, the correlation between the two methods was excellent (r = 0.95; RVEF [first-pass] = 0.74 RVEF [equilibrium] + 0.03; Sy,x = 0.05). Interobserver correlation was also excellent (r = 0.98; Sy,x = 0.03), as was the correlation between RVEFs measured at least 60 minutes apart (r = 0.98; Sy,x = 0.03). This method was more accurate than alternative techniques, using either a background region-of-interest adjacent to the right ventricle or a fixed right ventricular region-of-interest which included the infundibulum. This simplified technique provides a reproducible method for the sequential quantitative assessment of right ventricular performance.

Cardiac Output↗
PubMed1981

Use of equilibrium (gated) radionuclide ventriculography to quantitate left ventricular output in patients with and without left-sided valvular regurgitation.

We examined the accuracy with which left ventricular output can be estimated by equilibrium radionuclide ventriculography. After red blood cells were labeled in vivo, we measured left ventricular end-diastolic and end-systolic count rates and the count rate in 5 ml of the patient's blood. After estimating the average ratio of counting efficiency for the left ventricle to counting efficiency for the blood sample (Elv/Es) in six patients, we calculated left ventricular output in 26 other patients as (left ventricular activity ejected per minute divided by activity per liter of blood) divided by the previously estimated Elv/Es. Radionuclide left ventricular output closely approximated Fick cardiac output (r = 0.94) in patients without mitral or aortic regurgitation and exceeded Fick cardiac output in all patients with valvular regurgitation. Regurgitant fraction, calculated as the difference between the radionuclide and Fick outputs divided by the radionuclide output, correlated with the severity of of regurgitation as assessed angiographically. The equilibrium radionuclide ventriculogram is an excellent means for noninvasive estimation of left ventricular output.

Adult↗