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Biomedical subjects

J J Ferguson

Publications and source records attributed to J J Ferguson.

At least 127 records · Page 7Linked to original sources
PubMed1989

Reversal of left ventricular dysfunction after renal transplantation.

We report the cases of four patients with end-stage renal disease and New York Heart Association class III or IV heart failure of nonischemic origin as documented by coronary angiography. Because of left ventricular dysfunction (left ventricular end-diastolic pressure, 23 to 30 mm Hg; ejection fraction, 20% to 35%), all four patients were initially considered poor surgical candidates for renal transplantation. These same four patients became asymptomatic, however, with markedly improved cardiac function (ejection fraction, 43% to 69%) detected as early as 6 and 14 days after renal engraftment. Therefore, there exists a subset of patients with end-stage renal disease in whom congestive heart failure should not be considered a contraindication to renal transplantation. We conclude that some dialysis-dependent patients who manifest symptomatic heart failure of nonischemic origin have a reversible cardiomyopathy and should not be denied renal transplantation.

Adult↗
PubMed1989

Significance of nitroglycerin-induced hypotension with inferior wall acute myocardial infarction.

Up to 60% of patients with inferior wall acute myocardial infarction (AMI) develop hypotension. In many cases, profound hypotension is precipitated by the administration of nitroglycerin. To test the hypothesis that this hypotensive response to nitroglycerin may be related to right ventricular (RV) involvement, we compared 20 patients with electrocardiographic and enzyme-documented inferior wall AMI and marked hypotension (greater than 30 mm Hg decrease in systolic blood pressure, with symptoms) after nitrate administration, to 20 patients with documented inferior AMI, but without hypotension after administration of nitroglycerin. The presence of RV involvement was determined by electrocardiographic criteria of 1 mm of ST-segment elevation in at least 2 right precordial chest leads. Fifteen of the 20 patients who demonstrated a marked hypotensive response to nitroglycerin had evidence of RV involvement, while in 18 of the 20 patients without hypotension after nitrates there was no evidence of RV involvement. In a separate analysis of 28 patients with documented RV involvement in an inferior AMI, 20 developed hypotension in response to nitrates. Thus, in the setting of an inferior AMI, a marked hypotensive response to nitrates suggests the presence of RV involvement. Moreover, hypotension after nitrate administration may be anticipated in patients with known RV infarction, and in such patients, nitrates should be administered carefully.

Cardiac Output↗
PubMed1989

Assessment of right atrial pressure-volume relations in patients with and without an atrial septal defect.

Assessment of the complex relations between pressure and volume in the right atrium has been hampered in the past by difficulties in the measurement of atrial volume. Accordingly, in the present study the dynamics of right atrial pressure-volume relations were examined (with the use of an impedance catheter to measure right atrial volume) in patients with and without an atrial septal defect. Right atrial pressure and impedance volume were measured in 16 patients at the time of cardiac catheterization with the use of a multi-electrode impedance catheter to provide continuous, on-line, pressure-volume data. Eleven patients without evidence of an interatrial shunt were examined during normal respiration and during the Valsalva maneuver and contrasted with five patients with an atrial septal defect documented by oxygen saturation step-up and echocardiographic studies. Right atrial pressure-volume diagrams in patients without an atrial septal defect exhibited the normal figure eight pattern, with an A loop (atrial contraction) and a V loop (passive filling), corresponding to the A wave and V wave of right atrial pressure, respectively. During inspiration, mean right atrial pressure decreased and mean right atrial volume increased, consistent with augmented venous return. With the Valsalva maneuver, right atrial pressure increased and both right atrial stroke volume and mean right atrial volume decreased compared with baseline. Patients with an atrial septal defect demonstrated baseline pressure-volume diagrams similar to those of patients without an interatrial shunt. However, no change in mean right atrial volume occurred with either respiration or the Valsalva maneuver despite changes in right atrial pressure similar to those seen inpatients without an atrial septal defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effects of respiration and vasodilation on venous volume in animals and man, as measured with an impedance catheter.

Venous return determines cardiac preload and is in turn affected by respiration and vasodilation. The purpose of the present study was to examine the dynamics of venous return and venous volume, using impedance volume measurements in the venous system. In order to develop a methodology for the assessment of venous volume and venous return in man, we first studied 17 endotracheally intubated and ventilated anesthetized closed-chest dogs. We measured central venous and inferior vena cava (IVC) pressure (micromanometer) and volume (impedance catheter). Studies were done above and below the diaphragm with normal ventilation, with positive end-expiratory pressure (PEEP), and with beta-adrenergic blockade and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with lung inflation, while PEEP raised extrathoracic IVC volume and lowered intrathoracic IVC volume. Nitroglycerin lowered intrathoracic IVC volume. Beta blockade did not affect IVC volume, ventilatory variation, or response to PEEP and nitroglycerin. We performed similar studies in 14 human subjects during normal quiet respiration, with measurements above and below the diaphragm, and with interventions including Valsalva maneuver and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with expiration and Valsalva maneuver. Nitroglycerin again lowered intrathoracic IVC volume. We conclude that venous volume and the dynamics of venous return can be assessed in animals and man with an impedance catheter. Specifically, we show the divergent effects of respiration, ventilation, PEEP, and nitroglycerin on IVC volumes above and below the diaphragm. Beta-adrenergic blockage does not appear to play a role in altering any of these effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1989

Effect of balloon aortic valvuloplasty on the dynamics of left ventricular ejection.

To evaluate the effect of balloon aortic valvuloplasty on left ventricular ejection dynamics, simultaneous left ventricular and aortic pressures were obtained by use of a micromanometer catheter in nine patients before and after the procedure. Ejection times, stroke volumes (thermodilution), ejection rates, and pressure gradients were measured. For each parameter, ejection was then divided into two components: accelerative (onset systole to peak gradient) and decelerative (peak gradient to end systole). After valvuloplasty, there was 1) a decrease in overall ejection time and in mean and peak pressure gradients; 2) an increase in overall ejection rate; 3) no change in stroke volume or heart rate; 4) an increase in both accelerative and decelerative ejection rates and a decrease in the decelerative ejection time (expressed as a percentage of the R-R interval); and 5) a decrease in the time for the ejection of the final 25% of stroke volume (P less than 0.01) and time occupied by the final 25% of the gradient. Immediately following balloon aortic valvuloplasty, there is a decrease in ejection time and in increase in ejection rate. Balloon aortic valvuloplasty has a significant effect on the dynamics of left ventricle ejection, with changes primarily expressed in late systole. By improving the mobility of calcified leaflets, balloon aortic valvuloplasty may reduce the forces opposing forward blood movement during the decelerative phase of ejection.

Aortic Valve Stenosis↗
PubMed1989

Doppler echocardiographic assessment of the effect of balloon aortic valvuloplasty on left ventricular systolic function.

In order to evaluate the effects of balloon aortic valvuloplasty on left ventricular systolic function and ejection dynamics, Doppler echocardiographic studies were performed on 29 patients before and following valvuloplasty. Continuous wave aortic velocity signals were digitized and (with catheterization laboratory before and after valvuloplasty valve areas) were used to calculate: stroke volume; ejection time; ejection rate; time to 25%, 50%, and 75% ejection; accelerative (onset systole to peak velocity) ejection volume, time, and rate; and decelerative (peak velocity to end systole) ejection volume, time, and rate. Following valvuloplasty, there were no significant changes in heart rate; time to 25%, 50%, and 75% ejection; accelerative ejection time; and decelerative ejection time. There were significant increases in stroke volume, total ejection rate, accelerative ejection volume, decelerative ejection volume, accelerative ejection rate, and decelerative ejection rate, and a significant decrease in total ejection time. Balloon aortic valvuloplasty has a significant effect on the dynamics of left ventricular ejection. There is an increase in stroke volume and a decrease in ejection time, with relatively little effect on early systole, and a more pronounced effect in late systole. There are significant increases in accelerative and decelerative ejection volumes and rates, and a decrease in the time required for the last 25% of ejection. By improving the mobility of calcified leaflets, balloon aortic valvuloplasty may reduce the forces opposing forward blood movement during the decelerative phase of aortic ejection.

Aged↗
PubMed1989

Pulsed Doppler echocardiographic determination of the time course of left ventricular filling: validation with cineangiography.

Several noninvasive techniques are used to evaluate left ventricular diastolic function, but none has optimally characterized the time course of left ventricular filling. We have developed a method to characterize left ventricular filling, by integrating Doppler measurements of flow velocity across the mitral valve. The purpose of the present study was to compare this new method with contrast left ventriculographic assessment of left ventricular filling. Pulsed Doppler studies were obtained within 24 hours of left ventriculography in 15 patients: three normal subjects, seven with coronary disease, two with mitral stenosis, and three with dilated cardiomyopathy. Patients with myocardial infarction, regional wall movement abnormalities, or aortic regurgitation were excluded. Doppler-derived relative left ventricular filling was compared to filling from right anterior oblique left ventriculograms. Doppler and angiographic filling curves were qualitatively different in normal subjects and in patients with mitral stenosis and cardiomyopathy. For individual patients, however, the Doppler and angiographic filling curves were qualitatively similar, with a strong correlation between Doppler and angiographic estimates of percent filling (r = 0.95; p less than 0.001). These preliminary observations suggest that Doppler echocardiography may provide a reliable assessment of the time course of left ventricular diastolic filling. Further studies are warranted and should include more patients with diverse cardiac abnormalities.

Adult↗
PubMed1989

The use of nitroprusside to characterize aortic pressure-diameter relationships.

The viscoelastic properties of the wall of the ascending aorta can be determined by calculating the relationship between pressure and diameter of the vessel. Because of potential nonlinearities in aortic pressure-diameter relationships, however, pressure-diameter curves are more accurate than compliance expressed as a single value in measuring aortic viscoelastic properties. To determine whether nitroprusside could be used to obtain aortic pressure-diameter curves over a wide range, we measured simultaneous aortic pressure and diameter in anesthetized dogs. The inferior vena cava (IVC) of each animal was briefly occluded to generate a baseline series of pressure-diameter points over a wide range of pressure and diameter. We found that moderate lowering of systolic arterial pressure (30 mmHg) with nitroprusside did not significantly affect the aortic pressure-diameter relationship in comparison with control measurements during brief IVC occlusions at similar pressures and diameters. Prolonged inferior vena caval occlusion and a more profound lowering of arterial pressure with nitroprusside or IVC occlusion resulted in a leftward and upward shift of the aortic pressure-diameter relationship, with higher pressures at comparable diameters and lower diameters at comparable pressures. However, with more profound changes in arterial pressure, possible reflex-mediated mechanisms that alter the baseline aortic pressure-diameter relationship may be activated. We conclude that nitroprusside can be used to obtain aortic pressure-diameter data over a wider range than that possible from a single cardiac cycle.

Journal Article↗
PubMed1989

Indications for thrombolytic therapy in acute pulmonary embolism.

Pulmonary thromboembolism is commonly misdiagnosed and is associated with significant morbidity and mortality both in the early and late stages. A major cause of late morbidity is chronic pulmonary hypertension. Although the incidence of chronic thromboembolic pulmonary hypertension is unknown, there is anatomic and physiologic evidence that it is responsible for a significant degree of the late morbidity and mortality following acute pulmonary embolism. In the absence of underlying cardiopulmonary disease, pulmonary artery pressure is a useful indicator of the severity of acute pulmonary embolism and of the patient's prognosis. Thrombolytic agents accelerate the lysis of the thromboemboli, offer an excellent alternative to emergency embolectomy, and are likely to decrease the incidence of chronic pulmonary hypertension. All currently available agents have been shown to be effective and have similar bleeding-complication profiles. In this review, we discuss the natural history and pathophysiology of pulmonary thromboembolic disease, as well as applications of thrombolytic therapy in the treatment of acute pulmonary embolism.

Journal Article↗
PubMed1988

Assessment of aortic pressure-volume relationships with an impedance catheter.

Volume measurements obtained with an impedance catheter (impedance volume measurements) have been used previously in determining pressure-volume relationships in the right and left ventricles and in the right atrium. The purpose of the present study was to determine the utility of impedance volume techniques in the assessment of aortic pressure-volume relationships in animals and humans. Experiments to develop this methodology were first performed in ten anesthetized dogs, with simultaneous measurements of aortic pressure (micromanometer), diameter (ultrasonic crystals), and impedance volume. Transient (20 sec) inferior vena cava (IVC) occlusion and nitroprusside infusion resulted in a reproducible series of aortic pressure-volume and pressure-diameter points. In each case changes in impedance volume closely paralleled changes in diameter. From the wide range of pressure-volume points, it was possible to construct pressure-volume plots for a single cardiac cycle, as well as longer loops over a 20-40 mm Hg pressure range. End-systolic and end-diastolic pressure-volume points could subsequently be identified, which outlined a more precise pressure-volume relationship that was linear in six cases and curvilinear in four cases, depending on the level of aortic pressure. We extended these techniques to human subjects undergoing diagnostic cardiac catheterization. Studies using the impedance catheter in the aorta were performed in 11 patients. Aortic pressure-volume curves were elicited during Valsalva maneuver to obtain data over a range wider than that of a single cardiac cycle. Measurements of relative volume were calibrated with simultaneous M-mode echocardiography in three patients. We conclude that pressure-volume relationships in the aorta can be assessed with impedance volume techniques, making possible in vivo measurements of arterial compliance. Potential nonlinearities in aortic P-V relationships require that the assessment of aortic compliance encompass as much as possible of the physiologic range of pressure and volume.

Animals↗
PubMed1988

Diastolic function in patients with aortic stenosis: influence of left ventricular load reduction.

Pressure overload hypertrophy of the left ventricle due to aortic stenosis is associated with abnormalities of left ventricular isovolumic relaxation and early diastolic filling. The relative contribution of the hemodynamic load on the left ventricle to the impairment of diastolic function observed in this disorder remains poorly understood. To study this relation, the vasodilator nitroprusside was administered to eight patients with aortic stenosis and normal systolic function. The effect of a short-term reduction in left ventricular preload and afterload on left ventricular isovolumic relaxation and early diastolic filling was assessed by analysis of simultaneous micromanometer left ventricular pressure and radionuclide angiographic volume measurements. At baseline, left ventricular systolic and end-diastolic pressures were markedly elevated, and associated with prolongation of the time constant of left ventricular relaxation and depression of the left ventricular peak filling rate. Infusion of nitroprusside resulted in reduction of left ventricular systolic (204 +/- 31 to 176 +/- 31 mm Hg, p less than 0.05) and end-diastolic (31 +/- 8 to 18 +/- 6 mm Hg, p less than 0.05) pressures, with no associated improvement in time constant of left ventricular pressure decay (T) (68 +/- 25 to 80 +/- 37 ms, p = NS), T 1/2 (34 +/- 8 to 34 +/- 14 ms, p = NS), left ventricular peak filling rate (2.3 +/- 0.5 to 2.3 +/- 0.8 end-diastolic volume/s, p = NS) or time to left ventricular peak filling rate (150 +/- 50 to 144 +/- 37 ms, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy.

Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19 +/- 0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69 +/- 0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressure-volume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values. We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.

Cardiac Output↗
PubMed1987

Age-related disappearance of Mayer-like heart rate waves.

Healthy elderly subjects (greater than or equal to 65 years) did not show the prominent low frequency (0.07-0.09 Hz) heart rate oscillations (Mayer waves) recorded in young adults immediately following passive upright tilt. This difference may be related to altered autonomic function with physiologic aging.

Adult↗
PubMed1986

Hemodynamic correlates of arterial compliance.

There is at present no good understanding of the exact clinical correlates of arterial compliance. The purpose of this study was to establish which hemodynamic variables are most strongly associated with compliance. Hemodynamic measurements were performed on 41 patients undergoing diagnostic cardiac catheterization. Cardiac outputs were determined by thermodilution, and pressures were measured in the ascending aorta with a catheter-tip manometer. Compliance was calculated from a mono-exponential fit of diastolic decay pressures. Pulse pressure(PP), stroke volume(SV), age, systolic blood pressure(SBP), and cardiac output(CO) were significantly related to compliance. The quotient SV/PP was a good estimate of compliance, as was a first-order function of both SV and PP. There appear to be specific clinical correlates of arterial compliance, as well as ways to estimate arterial compliance on the basis of conventional hemodynamic measurements when direct calculations are not possible.

Adult↗
PubMed1986

Assessment of left ventricular end-systolic pressure-volume relations with an impedance catheter and transient inferior vena cava occlusion: use of this system in the evaluation of the cardiotonic effects of dobutamine, milrinone, Posicor and epinephrine.

The end-systolic pressure-volume relation has been postulated as a load-independent measure of cardiac contractility, but has been difficult to measure because of technical problems associated with the serial measurement of intracardiac volume over a physiologic range of ventricular loading conditions. Utilizing a multielectrode impedance catheter to assess continuous, on-line left ventricular relative volume during transient inferior vena cava occlusion, a method is described for determining the end-systolic pressure-volume relation and for assessing changes in this relation secondary to inotropic modulation. In particular, using this method, the relative inotropic properties were determined of four drugs: dobutamine, milrinone, epinephrine and an experimental cardiotonic agent (Ro 13-6438, Posicor). Left ventricular micromanometer pressure and impedance catheter volume were measured continuously in 10 open chest, anesthetized dogs and 14 pigs. Arterial pressure was altered over a range of 20 to 60 mm Hg by brief inferior vena cava constriction. A linear end-systolic pressure-volume relation was observed in pressure-volume diagrams constructed from on-line pressure and impedance catheter recordings. Administration of dobutamine, milrinone and epinephrine resulted in a leftward shift and an increase in the slope of the end-systolic pressure-volume relation as compared with baseline; Posicor did not alter the slope over a range of doses, despite an increase in the cardiac output secondary to arterial vasodilation. Volume changes as measured by the impedance method closely paralleled simultaneous changes in the ultrasonic crystal-determined segment length, and the impedance end-systolic pressure-volume relation slope was reproducible with repeated load-altering maneuvers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Right atrial pressure-volume relationships in tricuspid regurgitation.

Pressure-volume relationships in the right atrium were examined before and after the creation of acute experimental tricuspid regurgitation in pigs. A 1.3 kHz multielectrode impedance catheter with a measuring current of 4 mA was used to determine instantaneous right atrial pressure and relative blood volume; right atrial dimension was assessed simultaneously with ultrasonic crystals attached to the atrial walls. Impedance volume waveforms and ultrasonic crystal dimensions closely paralleled each other at baseline and after the induction of tricuspid regurgitation. The normal right atrial pressure-volume plot exhibited a figure-of-eight configuration, with an "a-loop" and a "v-loop" corresponding to the a-wave and v-wave of the right atrial pressure tracing. With severe tricuspid regurgitation, atrial pump function was abolished, and the pressure-volume plot exhibited a single clockwise loop, consistent with complete ventricularization of the right atrium. Intermediate degrees of tricuspid regurgitation preserved the figure-of-eight loop, but the size of both the a-loop and the v-loop were increased, consistent with a Starling-type load imposed on the atrium by the regurgitant blood volume. Increased right ventricular afterload mediated by constriction of the pulmonary artery and infusion of methoxamine reversibly converted the right atrial pressure-volume loop from that of mild to that of severe tricuspid regurgitation. Alternatively, constriction of the inferior vena cava and infusion of nitroprusside changed the right atrial pressure-volume loop from that of a severe pattern of tricuspid regurgitation to a less severe type of pattern. Infusion of dobutamine increased the size of the a-loop relative to the v-loop both at baseline and after induction of tricuspid regurgitation. We conclude that tricuspid regurgitation induces changes in right atrial mechanics that can be detected and quantified with an impedance catheter.

Animals↗
PubMed1986

Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion.

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p less than .01), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p less than .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p less than .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p less than .05) and significant increases in angiographic cardiac index (p less than .01) and LVESV index (p less than .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akinetic-dyskinetic segments and volume-overload hypertrophy of noninfarcted segments.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗