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Biomedical subjects

J F Spann

Publications and source records attributed to J F Spann.

At least 55 records · Page 3Linked to original sources
PubMed1981

Point by Point Examination of the equilibrium gated radionuclide left ventricular time activity curve; validation by biplane angiography.

Examination of the time course of left ventricular ejection has been found useful in several clinical applications. Equilibrium gated radionuclide angiography provides non-invasive means to obtain the ventricular ejection curve. To evaluate the accuracy of the equilibrium gated radionuclide left ventricular volume curve we compared equilibrium gated radionuclide date with biplane cine-angiography in 16 patients examining each set of data on a point by point basis. The cine-angiographic data consisted of 60 frame per second biplane cineangiograms and the radionuclide data consisted of 28 points spanning the cardiac cycle. All data was normalized for the patient's heart rate and stroke volume. The equilibrium gated radionuclide angiographic data accurately reproduced the contrast angiographic data at each point on the curve. This result justifies using the equilibrium gated radionuclide time activity curve to evaluate parameters such as early systolic ejection rates or rates of maximum ventricular ejection.

Cardiac Output↗
PubMed1981

Synergistic relation between vasoconstriction and fixed epicardial vessel stenosis in coronary artery disease.

The clinically important hemodynamic consequences of epicardial coronary artery vasoconstriction were examined in the presence of stenosis of major vessels. For this purpose, a special isolated canine circumflex coronary artery preparation was used to provide elimination of reflex, humoral, and distal coronary vasculature resistance influences. Without stenosis, active vasoconstriction induced by either phenylephrine (10-3 M), angiotensin (10-5 M), or acetylcholine (10-5 M) had no effect on flow through the circumflex artery. Coronary arterial stenosis was created by intraluminal obstruction, which itself produced only insignificant effect on vessel flow. When the vasoconstrictor agent stimulation was superimposed on the fixed underlying vascular stenosis, there occurred dose-dependent marked flow decreases through the partially obstructed vessel accompanied by major trans-stenotic pressure gradient increases. Phenylephrine, angiotensin, and acetylcholine separately caused significant (54%, 59%, and 46%) flow decreases with 48, 54 and 50 mm Hg pressure gradient increases respectively. This study demonstrates that vasoconstriction and stenosis act synergistically to reduce flow through obstructed major vessels in coronary artery disease.

Acetylcholine↗
PubMed1981

Left ventricular regional wall motion and velocity of shortening in chronic mitral and aortic regurgitation.

Left ventricular regional wall motion (percent systolic shortening) and velocity of shortening were studied in patients with heart failure due to chronic volume overloads of mitral and aortic regurgitation. Biplane left ventriculograms were analyzed by computer and divided into four regions: anterior, inferior, posterolateral and septal. The study patients included 12 normal subjects; 21 patients with aortic regurgitation (10 asymptomatic and 11 with congestive heart failure); and 11 patients with mitral regurgitation (4 asymptomatic and 7 with congestive heart failure). No patient had coronary artery disease. With heart failure, ejection fraction was decreased (p less than 0.05) in both aortic and mitral regurgitation (normal 62 +/- 3 percent [mean +/- standard error of the mean], aortic regurgitation 48 +/- 3 and mitral regurgitation 51 +/- 5). In mitral regurgitation with heart failure, the percent segment shortening in anterior (normal 42 +/- 2, mitral regurgitation 27 +/- 5) and posterolateral (normal 23 +/- 3, mitral regurgitation 16 +/- 4) regions was significantly decreased (p less than 0.05), whereas this value in the inferior (normal 32 +/- 2, mitral regurgitation 28 +/- 6) and septal (normal 46 +/- 4, mitral regurgitation 47 +/- 5) regions was normal. In aortic regurgitation with heart failure, anterior (27 +/- 2), inferior (17 +/- 3) and septal (5 +/- 1) segment shortening was significantly decreased, whereas posterolateral segment shortening was significantly decreased, whereas posterolateral segment shortening was normal (24 +/- 3). In both groups with heart failure, mean shortening velocity showed regional variations similar to those of percent shortening, whereas peak instantaneous shortening velocity was not reduced in mitral regurgitation compared with normal values. In the asymptomatic group, shortening and mean shortening velocity were normal, whereas peak instantaneous shortening velocity was increased in mitral regurgitation. In aortic and mitral regurgitation with decreased left ventricular function demonstrated by a reduced ejection fraction, there are regional wall motion abnormalities that are not caused by coronary disease.

Adult↗
PubMed1981

Right ventricular performance in mitral stenosis.

Until recently, the dynamic geometry and pump function of the pressure-overloaded right ventricle in patients with mitral stenosis and pulmonary hypertension had not been well defined. With use of a recently developed method for calculating right ventricular volume in human beings, seven normal subjects and eight patients with mitral stenosis and pulmonary hypertension had right ventricular performance assessed from computer-analyzed biplane right ventriculograms. Patients with mitral stenosis has elevated values for systolic right ventricular pressure (mean +/- standard error of the mean 25 +/- 2 for normal subjects, 57 +/- 6 mm Hg for patients with mitral stenosis), but normal values for right ventricular end-diastolic volume index (normal 95 +/- 11, patients 81 +/- 9 ml/m2) and ejection fraction (normal 0.49 +/- 0.02, patients 0.58 +/- 0.04). Comparison of right ventricular function using group performance curves of stroke work versus end-diastolic volume revealed the slope of the mitral stenosis line to be significantly greater than the normal line. A plot of right ventricular stroke volume versus end-diastolic volume, which removes pressure from the performance index, revealed that the two groups have similar performance. Left ventricular function measured by ejection fraction was reduced in mitral stenosis. These data suggest that the right ventricle performs normally in patients with mitral stenosis with moderate pulmonary hypertension and maintains normal size and ejection fraction.

Blood Pressure↗
PubMed1981

Left ventricular function in chronic aortic regurgitation with reference to end-systolic pressure, volume and stress relations.

Left ventricular muscle and pump performance were evaluated in 12 normal subjects and 21 patients with aortic regurgitation (10 with minimal symptoms and 11 with congestive heart failure). A computer-based quantitative analysis of biplane left ventriculograms was used. Both patient groups had significant aortic regurgitation documented by ventriculography. Contractile function measured by peak systolic stress/end-diastolic volume and end-systolic pressure/volume curves was poorer than that in normal subjects in patients with heart failure but not in asymptomatic patients. When normalized for muscle mass, stroke work was not depressed in either asymptomatic patients (mean +/- standard error of the mean 0.008 +/- 0.001 joules/g) or patients with heart failure (0.009 +/- 0.004) by comparison with the value in normal subjects (0.010 +/- 0.001). Angiographically determined cardiac index (CI) increased with increasing volume overload even though forward cardiac index measured by the Fick method remained essentially unchanged: normal subjects (total CI 3.7 +/- 0.4 liters/min per m2, Fick CI 2.4 +/- 0.1); asymptomatic patients (total CI 7.6 +/- 0.7, Fick CI 2.3 +/- 0.2); patients with heart failure (total CI 9.1 +/- 0.82, Fick CI 2.1 +/- 0.18). Left ventricular peak stress increased significantly in patients with heart failure (511 +/- 55 dynes/cm2 x 10(-3)) compared with values in normal subjects (360 +/- 33) and asymptomatic patients (428 +/- 50). The combination of decreased muscle function and increased demands on pump function causes a significant increase in end-diastolic pressure only in patients with heart failure (23 +/- 2 mm Hg), which results in pulmonary congestive symptoms.

Adult↗
PubMed1981

Normal left ventricular emptying in coronary artery disease at rest: analysis by radiographic and equilibrium radionuclide ventriculography.

The volume ejected early in systole has been proposed as an indicator of abnormal left ventricular function that is present at rest in patients with coronary artery disease with a normal ejection fraction and normal wall motion. The volume ejected in systole was examined by calculating the percent change in ventricular volume using both computer-assisted analysis of biplane radiographic ventriculograms at 60 frames/s and equilibrium gated radionuclide ventriculograms. Ventricular emptying was examined with radiographic ventriculography in 33 normal patients and 23 patients with coronary artery disease and normal ejection fraction. Eight normal subjects and six patients with coronary artery disease had both radiographic ventriculography and equilibrium gated radionuclide ventriculography. In all patients, there was excellent correlation between the radiographic and radionuclide ventricular emptying curves (r = 0.971). There were no difference in the ventricular emptying curves of normal subjects and patients with coronary artery disease whether volumes were measured by radiographic or equilibrium gated radionuclide ventriculography. It is concluded that the resting ventricular emptying curves are identical in normal subjects and patients with coronary artery disease who have a normal ejection fraction and normal wall motion.

Contrast Media↗
PubMed1981

Normal rate of ventricular emptying in valvular aortic stenosis.

The delayed upstroke of the arterial pulse in valvular aortic stenosis has been attributed, in part, to prolonged left ventricular emptying. Left ventricular emptying rate, however, has not been measured in aortic stenosis. We assessed the rate of left ventricular emptying by computer analysis of biplane cineangiograms in seven normal subjects, six patients with mild to moderate aortic stenosis, and 12 patients with severe aortic stenosis. As an indicator of delayed arterial pulse rise, T time index (time to half maximum aortic pressure corrected for heart rate) was measured in each group. T time index averaged 0.07 +/- 0.01 units in normal subjects, 0.14 +/- 0.04 units in the patients with mild to moderate aortic stenosis, and 0.13 +/- 0.05 units in those with severe aortic stenosis. Patients with mild to moderate and severe aortic stenosis differed significantly from normal subjects. Relative emptying rates were defined as the percentage of initial systolic volume ejected divided by the percentage of systole elapsed. These relative emptying rates were determined during the first, second, and third thirds of systole in all three groups. No significant decrease in the relative rate of left ventricular emptying was noted when each group of patients with aortic stenosis was compared with the normal subjects. Neither was there slowing in the actual rate of ejection of blood in ml per second throughout systole. We conclude that the rate of ventricular emptying is normal in aortic stenosis and does not explain the arterial pulse delay in this disease.

Adult↗
PubMed1981

Resting potential changes associated with Na-K pump in failing heart muscle.

Microelectrode and single sucrose gap techniques were used to measure transmembrane potentials in normal and failing papillary muscles. Six muscles from control animals and 10 from banded animals were cooled (2-4 degrees C) and subsequently rewarmed to 37 degrees C. Normal muscles demonstrated significantly greater increases in maximum diastolic potential (--Emax) on rewarming than those from failing animals. In muscles subjected to transient periods of rapid stimulation, --Emax depolarized initially on stimulation but eventually plateaued at a depolarized level and then hyperpolarized beyond prestimulation levels. These changes in --Emax were altered in failing muscles. The initial rate of depolarization (delta -- Emax/delta t) on stimulation and the magnitude of this depolarization (delta -- Emax) was decreased at all rates studied. The time necessary to arrive at the plateau (time to delta -- Emax) was significantly lengthened in failing muscles. The hyperpolarization seen on rewarming cooled preparations and the changes in --Emax during stimulation have both been related to an activation of an electrogenic Na-K pump suggesting that this ion-transport system is altered in failing heart muscle. The decrease in delta -- Emax/delta t and delta -- Emax seen in failing muscles indicates that K efflux may be lower or that the volume of confined intercellular spaces is greater in failing heart muscle.

Animals↗
PubMed1981

Effect of thyroid hormone on canine cardiac Purkinje fiber transmembrane potential.

The electrophysiological effects of chronic 3,5,3'-triiodo-L-thyronine (T3) administration on cardiac Purkinje fibers were studied using intracellular recording techniques. Adult mongrel dogs receiving T3 injections (1 mg/kg sc) three times daily for 7-12 days demonstrated elevated resting heart rates and serum total T3 content, atrophied thyroid glands, and a small body weight loss when compared with controls. Isolated Purkinje fibers from control and T3-treated animals were superfused with an oxygenated Tyrode solution containing 4 mM K+ at 35 degrees C. Preparations were stimulated externally at 1.0, 2.0, and 3.1 Hz for 2-3 min while measurements of action potentials were made. At 1.0 Hz, action potential duration (APD) of T3-treated Purkinje fibers was significantly (P less than 0.01) greater than controls at both 20% (APD20) and 80% (APD80) of repolarization to the maximum diastolic potential (Emax). The overshoot, plateau height, and Emax were not different. Raising the stimulus frequency to 2.0 and 3.1 Hz produced a slight increase in the overshoot and a rate-dependent shortening of the action potential duration until it resembled controls. APD20 shortened proportionately more than APD80, giving the action potential a triangular appearance. The K+ selectivity of the resting membrane was not affected as evidenced by Nernst plots, which were identical in normal and T3-treated fibers. These results demonstrate that thyroid hormone influences the action potential of isolated cardiac Purkinje fibers.

Action Potentials↗
PubMed1981

The direct myocardial energetic response to nitroglycerin in the rabbit heart.

The coronary resistance, total heat production, oxygen consumption and isovolumic mechanical performance were measured simultaneously in the isolated beating rabbit heart. The direct effects of nitroglycerin (0.12 mg/l) were determined. The expected coronary dilatation occurred; coronary resistance fell by 21.5% independent of mechanical performance. There was a 14% fall in mechanical performance at the apex of the Frank-Starling curve and lesser reductions at less-than-apical diastolic volumes. Oxidative metabolism was not affected; there was no change in the calorific equivalent of oxygen (20.97 mJ/mul:O2) nor was there any significant anerobic metabolism. The ergonic cost of the force-independent metabolism which includes calcium activation energy was reduced by 17.7%. The unit metabolic cost of mechanical performance, or the performance-dependent metabolism, was unchanged resulting in a net increase in overall mechanical economy. It is concluded that it is against a background of a more metabolically efficient but less mechanically active myocardium that nitroglycerin exhibits its well known peripheral and reflex in the intact organism.

Animals↗
PubMed1980

The effects of vasoconstriction on experimental coronary artery stenosis.

In summary, we have examined the response to arterial vasoconstriction in an in vitro coronary artery preparation. Without a preexisting stenosis, arterial vasoconstriction had minimal hemodynamic effects. Similarly, with a stenosis created by a circumferential snare, arterial vasoconstriction had minimal hemodynamic effects. In striking contrast, with a stenosis created by intraluminal obstruction, arterial vasoconstriction dramatically increased the hemodyamic severity of the stenosis. The use of an intraluminal obstruction provides a useful animal model for examining hemodynamics in coronary artery disease and had provided some insight into the effects of vasoconstriction on coronary artery hemodynamics. Obviously, this is an experimental study, and care must be taken in extrapolating these results to diseased human coronary arteries.

Angina Pectoris↗
PubMed1980

Myocardial blood flow and capillary density in chronic pressure overload of the feline left ventricle.

The effects of chronic pressure overload hypertrophy on myocardial blood flow and capillary density was measured in the feline left ventricle. Myocardial hypertrophy was produced by and 84% banding constriction of the ascending aorta 2.8 +/- 1.2 months before the experiments. In seven cats with aortic constriction, cardiac hypertrophy produced a 40% increase in left ventricular mass. Seven cats served as normals. Our findings show that, in chronic pressure overload hypertrophy, coronary blood flow at control (resting) levels is increased compared with normals. In both normal and hypertrophy cats endocardial/epicardial flow ratios were equal at the control level. In the hypertrophied hearts, coronary reserve, measured as the percentage increase in myocardial blood flow from control to near maximal flow during adenosine infusion, was reduced. In the hypertrophy group a shift in the transmural distribution of blood flow in the left ventricle was noticed, as indicated by a reduced endo/epi flow ratio, during adenosine infusion. A decreased capillary density in hypertrophy, most marked in endocardial tissue regions, was demonstrated by this study. These findings indicate that capillary growth does not parallel myofibre growth in the endocardium of pressure overload hypertrophied left ventricles. The resultant anatomical imbalance causes a compromise of flow reserve in the endocardium, making this region vulnerable to ischaemia.

Adenosine↗