Search PubMed⌕ Search

Biomedical subjects

J F Spann

Publications and source records attributed to J F Spann.

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

Left ventricular performance in patients with coexistent mitral stenosis and aortic insufficiency.

Isolated mitral stenosis and isolated aortic insufficiency impose unique and opposite loading conditions on the left ventricle. To assess these combined effects, hemodynamic and angiographic factors were compared among normal subjects and patients with isolated mitral stenosis, isolated aortic insufficiency or combined mitral stenosis and aortic insufficiency. Left ventricular end-diastolic volume index was lower in patients with combined lesions and severe or moderate aortic insufficiency than in patients with isolated severe or moderate aortic insufficiency (138 +/- 19 versus 206 +/- 20 cc/m2 and 87 +/- 5 versus 145 +/- 22 cc/m2, respectively) (p less than 0.05 for both). Left ventricular end-diastolic and end-systolic volume indexes were normal in two-thirds of patients with combined lesions and moderate or severe aortic insufficiency, whereas these indexes were high in all but one patient with isolated moderate or severe aortic insufficiency. Among patients with moderate or severe aortic insufficiency, 8 of 14 with isolated insufficiency had a reduced ejection fraction or circumferential fiber shortening rate compared with 5 of the 9 patients with combined lesions. Among patients with isolated aortic insufficiency, left ventricular end-systolic wall stress and end-diastolic and end-systolic volume indexes were higher (p less than 0.05) in those with reduced ejection performance than in those with normal ejection performance. These variables did not differ between patients with reduced or normal ejection performance in the group with combined lesions. The contractile index (ratio of end-systolic wall stress to end-systolic volume index) was significantly depressed in patients with severe aortic insufficiency in the groups with isolated aortic insufficiency or combined lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Differences in myocardial performance and load between patients with similar amounts of chronic aortic versus chronic mitral regurgitation.

It is not known if the favorable changes in preload and afterload that augment ejection performance in acute experimental aortic and mitral regurgitation are also present in patients with chronic regurgitation. Additionally, observations that patients with mitral versus aortic regurgitation respond differently to valve replacement suggest that differences exist preoperatively between these two types of volume overload. Therefore, ventricular mechanics were compared in nine patients with severe aortic regurgitation, eight patients with severe mitral regurgitation and seven normal subjects. The amount of volume overload was similar in both groups with regurgitation. In both aortic and mitral regurgitation, ejection performance was reduced compared with findings in normal subjects. Preload estimated as enddiastolic stress was comparably elevated above normal in both groups with regurgitation: 69 +/- 24 dynes X 10(3)/cm2 in mitral regurgitation compared with 81 +/- 34 dynes X 10(3)/cm2 in aortic regurgitation and 36 +/- 11 dynes X 10(3)/cm2 in normal subjects. However, afterload estimated as mean systolic stress was normal in mitral regurgitation (186 +/- 34 dynes X 10(3)/cm2) but markedly elevated in aortic regurgitation (260 +/- 41 dynes X 10(3)/cm2) (p less than 0.01). Contractile depression tended to be more severe in mitral regurgitation despite similar ejection performance in mitral and aortic regurgitation. Thus, in mitral regurgitation favorable loading conditions may mask contractile dysfunction, and in aortic regurgitation excessive afterload contributes to poor pump performance, possibly accounting for previously observed differences in the response to valve replacement.

Acute Disease↗
PubMed1984

Absolute left ventricular volume by an iterative build-up factor analysis of gated radionuclide images.

A method for determining absolute left ventricular (LV) volumes from radionuclide gated blood-pool (GBP) images was validated in 34 patients. The technique is nongeometric, corrects for tissue attenuation, and uses an experimentally determined set of build-up factors to account for the effects of scatter. Only four parameters are needed to determine LV volumes: the LV count rates from a left anterior oblique (LAO) and a right posterior oblique (RPO) image (180 degrees opposed to the LAO), a venous blood sample, and a patient thickness measurement. A computer algorithm is used to reach an iterative solution to two simultaneous equations that yield LV volumes. Phantom studies showed less than 4% error for volume determinations at all investigated depths. For the patients studied the correlation between volumes obtained by GBP and contrast ventriculography was 0.97 for diastole and 0.96 for systole.

Adult↗
PubMed1984

Hypertrophy without contractile dysfunction after reversal of pressure overload in the cat.

To determine whether a causal relationship exists between the myocardial hypertrophy and the deficits in myosin ATPase activity and contractile function that have been associated with chronic, experimental pressure overload, we studied contractile function, myosin ATPase, and isomyosin pattern in a model of severe pressure overload in which the pressure overload was surgically relieved but hypertrophy persisted. Severe hypertrophy, contractile dysfunction, and pump failure were produced in the cat right ventricle by tight pulmonary arterial banding. In two groups of cats banded for 2- and 7-wk periods, right ventricular mass doubled, and contractile function was severely depressed compared with controls. In another group of cats subjected to severe right ventricular pressure overload for 4 wk, pressure overload was reversed by removal of the pulmonary arterial band. After a 4-wk recovery period for this group, right ventricular mass remained markedly increased, but contractile function had returned to normal. Changes in neither isomyosin composition nor myosin ATPase activity were found regardless of contractile function. Thus, following reversal of a right ventricular pressure overload severe enough to cause pump failure and a twofold increase in right ventricular mass, muscle contractile function can return to normal even when severe hypertrophy persists. Furthermore, changes in myosin isozyme composition or ATPase activity do not explain the changes in contractile function.

Adenosine Triphosphatases↗
PubMed1984

Coagulant activities of platelets in coronary artery disease.

Platelets have been implicated in the pathogenesis of coronary artery disease, and a number of studies have examined platelet function and coagulation parameters in such patients. We have examined platelet coagulant activities, volumes, and aggregate ratios in 23 patients with chest pain, seven of whom had normal coronary angiograms (group I) and 16 of whom had angiographically proven coronary artery disease (group II). There were no significant differences in the mean values for platelet volume or platelet aggregate ratios between the two groups. The platelet coagulant activities concerned with initiation and the early stages of intrinsic coagulation were significantly increased in patients in group II as compared with those in group I. No significant differences were noted between the two groups with respect to prothrombin time, partial thromboplastin time, and plasma levels of fibrinogen and coagulation factors V and VIII. However, the mean activity in plasma of antithrombin III (but not the level of antithrombin III antigen) was significantly lower in patients of group II compared with group I. Overall, our observations provide evidence for an enhanced contribution of platelets to the intrinsic coagulation system in patients with coronary artery disease. The platelet coagulant hyperactivity noted in these patients may reflect a role of platelets in the pathogenesis of coronary artery disease or may be secondary to the underlying arterial disease.

Adult↗
PubMed1984

Coronary thrombolysis for evolving myocardial infarction.

An acute thrombus at the site of an atherosclerotic obstruction is the usual cause of myocardial infarction. Thrombolytic therapy is an exciting new therapy for reducing the extent of myocardial infarction by lysing intracoronary clots. Such therapy has now been widely applied by: prolonged intravenous infusion of streptokinase during the first 24 hours of infarction; intracoronary infusion of streptokinase, urokinase, or tissue plasminogen activator; early, high dose, brief duration intravenous infusion of streptokinase; or intravenous infusion of tissue plasminogen activator. Intracoronary streptokinase or urokinase achieves reperfusion of the coronary artery in 75% of patients and is associated with serious bleeding in 4.8% of patients. Intravenous infusion of streptokinase achieves reperfusion of the coronary artery in 50 to 80% of patients. The incidence of serious bleeding with intravenous streptokinase averaged 0.8% in 5 studies of 237 patients and was 12.8% in 1 additional study of 80 patients. Salvage of the jeopardised myocardium and improvement in left ventricular function occurred when coronary reperfusion was achieved. Mortality in streptokinase-treated patients was significantly reduced at 30 days and at 6 months after infarction in the single randomised mortality study done to date; however, more data are needed on this important question. Reocclusion after thrombolysis averages 17% in patients treated with streptokinase by either intracoronary or intravenous infusion. The newly reperfused coronary artery has been stabilised in some patients by coronary bypass surgery or percutaneous transluminal angioplasty, but further studies are needed to define criteria for appropriate patient selection for these procedures.

Coronary Disease↗
PubMed1984

Assessment of systolic ventricular muscle function in man: the end systolic index.

Accurate assessment of ventricular muscle contractile function in patients with heart disease is impaired by alterations in afterload, preload and wall thickness which often accompany the disease. The relationship between pressure and volume at end systole is considered to provide a contractile index which is independent of preload and which accounts for afterload. Use of the index prerequisites determinations of the left ventricular end systolic pressure, wall thickness as well as the dimensions or volumes, respectively, which may be assessed with either invasive or noninvasive methods. In patients with aortic stenosis and congestive heart failure, there was a significantly reduced slope (0.9 +/- 0.5) of the end systolic stress-volume relationship as compared with healthy subjects (5.8 +/- 1.3) or patients with aortic stenosis without congestive heart failure (3.9 +/- 1.3), while the ejection fraction showed no significant differences. In patients with mitral regurgitation with no or only minimal symptoms postoperatively, preoperatively the end systolic index (ESS/ESVI) was higher (3.3 +/- 0.4) than in patients with marked symptoms postoperatively or those who died perioperatively (2.2 +/- 0.2) and the values of both patient groups were lower than those of normals. In contrast, the values for ejection fraction among the normals and both groups of patients showed substantial overlap. In patients with aortic insufficiency and congestive heart failure, as opposed to patients with aortic insufficiency and only slight symptoms, there was a significantly compromised ejection fraction as well as diminished end systolic index (ESS/ESVI). Patients with hypertension accompanied by congestive heart failure had a significantly diminished slope of the relationship between end systolic left ventricular stress and volume while the values for hypertensive patients without congestive heart failure were within normal limits; in both groups of patients, the ejection fraction was normal. In patients with mitral stenosis, the end systolic index at 5.28 +/- 0.53 did not differ significantly from that of healthy subjects at 4.87 +/- 0.53, while the velocity of circumferential fiber shortening was diminished. Patients with large atrial septal defects and symptoms of congestive heart failure did not differ with respect to end systolic index or ejection fraction as compared with atrial septum defect patients without symptoms. In children with aortic stenosis and high pressure gradients, there was an increased ejection fraction together with a normal end systolic index.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia, Sickle Cell↗
PubMed1983

Left ventricular wall stress in compensated aortic stenosis in children.

It is known that children with aortic stenosis (AS) frequently have supernormal indexes of left ventricular (LV) pump function and remain compensated for many years. Factors causing this increase in pump performance have not been elucidated. A study was done on LV mechanics in 11 children with AS (aortic valve area 0.5 +/- 0.3 cm2/m2) and 10 normal subjects. The ejection fraction in the AS group (0.88 +/- 0.08) was significantly higher than in normal subjects (0.64 +/- 0.08, p less than 0.001). The mean velocity of fiber shortening was also higher in AS patients (1.80 +/- 0.35 circ/s) than in normal subjects (1.22 +/- 0.21 circ/s, p less than 0.001). The end-systolic volume index in patients with AS (9 +/- 8 ml/m2) was much lower than in normal subjects (27 +/- 8 ml/m2). LV mass in patients with AS was 180 +/- 58 g/m2 compared with 96 +/- 9 in normal subjects. LV wall stress was reduced throughout the cardiac cycle in patients with AS. Peak stress in patients with AS was 238 +/- 51 dynes/cm2 X 10(3) versus 439 +/- 85 in normal subjects. The end-systolic stress-end-systolic volume index ratio, an indicator of contractile state, was not elevated in patients with AS. It is suggested that diminished wall stress in concert with normal contractile function permits the supernormal pump function seen at rest in children with AS.

Adolescent↗
PubMed1983

Absolute left ventricular volume from gated blood pool imaging with use of esophageal transmission measurement.

A new method for determining absolute left ventricular (LV) volume from equilibrium gated blood pool images was validated in 36 patients by comparing gated blood pool (GBP) imaging with contrast ventriculography (CV) using both Simpson's rule (SR) and area-length (AL) calculations. The technique is geometry-independent and is the first to correct for tissue attenuation with use of an in vivo point source. An orally administered capsule containing 1 to 2 mCi of technetium-99m (Tc-99m) sulfur colloid is used for this purpose. Left ventricular volumes are determined by dividing attenuation and background-corrected count rates obtained from semiautomated LV regions of interest by the count rate per milliliter from a blood sample. The correlation between GBP and CV (SR) was 0.96 (CV [SR] = 0.99 GBP + 1.32 ml; standard error of the estimate [SEE] = 21.2 ml) for diastole and 0.97 (CV [SR] = 0.93 GBP - 0.03 ml; SEE = 11.9 ml) for systole. The correlation between GBP and CV (AL) was 0.92 (CV [AL] = 0.90 GBP + 16.72 ml; SEE = 27.8 ml) for diastole and 0.95 (CV [AL] = 0.87 GBP + 4.56 ml; SEE = 14.4 ml) for systole. The method is noninvasive and can be performed easily as part of routine gated blood pool imaging and analysis.

Adult↗
PubMed1983

Coexistent mitral stenosis and dynamic left ventricular outflow obstruction.

A 66-year-old female with known mitral stenosis presented with symptoms of progressive pulmonary congestion. Concomitantly, subvalvular left ventricular outflow obstruction was suspected clinically and both lesions were confirmed at cardiac catheterization. At operation, marked septal hypertrophy and rheumatic mitral stenosis were observed, the mitral valve was replaced, and a septal myomectomy was performed.

Aged↗
PubMed1983

Cardiac function in sickle cell anemia.

Although ventricular dysfunction is suspected to underlie congestive heart failure in sickle cell anemia (SCA), ejection indexes of left ventricular (LV) pump performance have been found to be normal. The increased preload and decreased afterload of SCA increases the ejection phase indexes and might obscure true LV dysfunction. Therefore, the preload and afterload independent end-systolic stress-volume index was compared in 11 patients with SCA and in 11 normal volunteers. End-systolic pressure and echocardiographic LV dimensions were determined during rest, leg raise, hand-grip and amyl nitrite inhalation. Systemic vascular resistance (afterload) was decreased to 1,033 +/- 314 dynes s cm-5 (mean +/- standard deviation) in SCA from 1,701 +/- 314 dynes s cm-5 in normal subjects. End-diastolic volume index (preload) was increased to 102 +/- 24 ml/m2 in SCA from 66 +/- 10 ml/m2 in normal subjects. Cardiac index was increased to 4.7 +/- 1.1 liters/min/m2 in SCA from 2.8 +/- 0.8 liters/min/m2 in normal subjects. Ejection fractions were similar: 0.59 +/- 0.09 in SCA versus 0.62 +/- 0.07 in normal subjects. However, in patients with SCA, the ratio of resting end-systolic stress-volume index was decreased (1.5 +/- 0.5 in SCA versus 2.8 +/- 0.6 in normal subjects) and the slope of the end-systolic stress versus end-systolic volume index relation was decreased (2.7 +/- 1.3 in SCA versus 4.4 +/- 1.8 in normal subjects), suggesting LV dysfunction in those patients. Thus, LV muscle contractile performance is depressed in SCA. Increased preload and decreased afterload compensate for the LV dysfunction and maintain a normal ejection fraction and high cardiac output.

Adolescent↗
PubMed1983

Multiple scintigraphic findings in a patient with a primary myocardial sarcoma.

Primary myocardial sarcomas are rare. We report the scintigraphic findings observed with TI-201, Ga-67, Tc-99m pyrophosphate, and Tc-99m pertechnetate labeled red cell gated cardiac imaging in a patient with this tumor. We found that thallium and gated blood pool imaging can be used both in the diagnosis of these tumors and the assessment of the effects of chemotherapy on the tumor and normal myocardium. The thallium study was particularly helpful in identifying the malignant nature of the tumor by showing extensive infiltration into surrounding areas.

Adult↗
PubMed1982

High-dose, brief intravenous streptokinase early in acute myocardial infarction.

An acute thrombus at the proximal border of a high-grade atherosclerotic obstruction is the usual cause of myocardial infarction. Although intracoronary thrombolysis is potentially an exciting new therapy for reducing the extent of myocardial infarction by lysing coronary clot, a number of major difficulties limit its widespread application. It is a complex procedure requiring intracoronary visualization and infusion within a few hours of onset of symptoms. Since intravenous streptokinase could be widely applied if effective, we and others have wondered whether high-dose, brief-duration intravenous streptokinase infusion given early in myocardial infarction would lyse coronary clots without bleeding. To date we have treated 13 patients within 6 hours of onset of symptoms and with ECG and angiographic evidence of typical myocardial infarction caused by coronary clot. Clot lysis and angiographically proved coronary reperfusion were achieved in 6 patients within 1 hour of starting a systemic intravenous infusion of 850,000 IU of streptokinase. Schroeder et al., in Berlin, West Germany, achieved angiographically proved coronary reperfusion in 11 of 21 patients with acute myocardial infarction following a 30-minute intravenous streptokinase infusion of 500,000 IU. Neuhaus et al., in Göttinen, West Germany, achieved angiographically proved coronary reperfusion in 24 of 39 similar patients within 48 minutes by intravenous infusion of 1,700,000 IU of streptokinase. In these three studies, no serious bleeding occured; left ventricular function was improved in patients who achieved coronary reperfusion. We conclude that rapid intracoronary clot lysis and coronary reperfusion can be achieved early in myocardial infarction by brief-duration systemic intravenous infusion of high-dose streptokinase without a high incidence of serious bleeding.

Clinical Trials as Topic↗
PubMed1982

Normal left ventricular systolic function in adults with atrial septal defect and left heart failure.

Systolic left ventricular contractile function has not been extensively evaluated in patients with atrial septal defect who have symptoms of left-sided congestive heart failure. This study examined left ventricular systolic function hemodynamically and angiographically in 6 such adult patients (Group A), 12 adult patients with atrial septal defect without heart failure (Group B) and 20 normal subjects. The mean ( +/- standard error of the mean) left ventricular end-diastolic pressure was higher in patients in Group A (17 +/- 0.8 mm Hg) than in patients in group B (6.9 +/- 0.6 mm Hg) (p less than 0.001). Both right atrial pressure ( 11 +/- 1.3 versus 4.9 +/- 0.5 mm Hg) (p less than 0.001) and mean pulmonary arterial pressure (30 +/- 1.8 versus 15 +/- 1 mm Hg) were also higher in Group A than in Group B. Left ventricular cardiac index and stroke work index did not differ in the two groups. Variables of left ventricular systolic function were similar in both groups of patients and in normal subjects: Ejection fraction was 0.71 +/- 0.05 in Group A, 0.74 +/- 0.02 in Group B and 0.74 +/- 0.01 in normal subjects. Velocity of circumferential shortening was 1.38 +/- 0.14 circumferences/s in Group A, 1.38 +/- 0.07 circumferences/s in Group B and 1.27 +/-0.04 circumferences/s in normal subjects. There was no difference in left ventricular contractile function as indicated by the ratio of end-systolic wall stress to end-systolic volume index among the three groups: normal subjects, average 5.6 +/- 0.19 versus 6.1 +/- 0.5 in Group B and 6.0 +/- 0.6 dynes X 10(3)/cm(2)/(ml/m(2) in Group A. This study of patients with atrial septal defect and left heart failure indicates that abnormal left ventricular systolic contractile function is probably not the cause of the symptoms and elevated left heart filling pressures observed in this group. An abnormality in left ventricular diastolic filling, perhaps related to the volume loaded right ventricle, may explain these changes.

Adolescent↗