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Biomedical subjects

R A Slutsky

Publications and source records attributed to R A Slutsky.

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

Comparative effects of ionic and nonionic contrast materials on indexes of isovolumic contraction and relaxation in humans.

The effects of contrast media on left ventricular (LV) relaxation as assessed by the time constant of isovolumic relaxation have not previously been studied. A new nonionic contrast agent (iohexol) has been shown to have fewer deleterious effects than standard ionic agents. Nineteen patients received iohexol and sodium meglumine diatrizoate (Renografin-76) in a double-blind, crossover study during left and right coronary arteriography and with simultaneous high-fidelity micromanometer measurements of LV pressure. Neither agent induced significant changes in LV end-diastolic pressure after right or left coronary arteriography. After right coronary arteriography, neither agent produced significant deterioration of peak positive dP/dt or (dP/dt)/DP40 (dP/dt at a developed pressure of 40 mm Hg). However, after right coronary arteriography both agents caused a transient deterioration in peak negative dP/dt and the time constant of isovolumic relaxation (p less than 0.05 at 20 seconds after arteriography). After left coronary arteriography, sodium meglumine diatrizoate induced deterioration of systemic blood pressure (p less than 0.05), peak positive dP/dt (p less than 0.01), (dP/dt)/DP40 (p less than 0.05), peak negative dP/dt (p less than 0.01) and the relaxation time constant (p less than 0.01). These effects were not induced by iohexol. Thus, nonionic contrast media exert negligible alterations on LV function when used for coronary arteriography. The findings are of potential clinical importance in view of the large number of patients with depressed LV function who undergo coronary arteriography.

Coronary Angiography↗
PubMed1984

Serial echocardiograms in patients with congestive cardiomyopathies: lack of evidence for thrombus formation.

We studied 90 patients with congestive myocardial disease documented at cardiac catheterization (46 idiopathic, 39 ischemic, and 5 hypertensive) who underwent M-mode and two-dimensional echocardiograms every 2-3 months for up to 7 years (mean 3.4 +/- 1.6 years, +/- 1 S.D.). All had angiographic evidence of severe left ventricular dysfunction (left ventricular ejection fraction less than 40%), and were on a variety of inotropic, diuretic, and vasodilating drugs. Only 9 were ingesting anticoagulants (5 warfarin and 4 aspirin), those on warfarin had documented pulmonary emboli or deep venous thrombosis. All but 4 patients were in normal sinus rhythm. Only one subject in this group was found to have a myocardial (left ventricular) thrombus. Postmortem examinations of 27 patients confirmed the ultrasound data. Thus, we conclude that cardiac thrombi are unusual in patients with congestive cardiomyopathies and rarely develop over the course of the illness even in the absence of chronic anticoagulation.

Adult↗
PubMed1984

The systolic arterial pressure/end-systolic volume relationship in patients with severe left ventricular dysfunction.

Performance of the intact left ventricle is well-defined by the end-systolic pressure/end-systolic volume relationship that appears independent of preload and afterload. To determine whether noninvasive measurements of this relationship could distinguish normal from abnormal subjects, we evaluated the relationship between arterial systolic pressure (determined by cuff sphygnomanometry) and radionuclide estimates of end-systolic volume in 12 normal subjects and 24 patients with severe left ventricular dysfunction. Data were acquired at rest, after atropine injection, and then during at least three increments of arterial pressure (average total increase approximately 45 mm Hg) using phenylephrine. The relationship between peak-systolic pressure (SP) and end-systolic volume (ESV) was found to be linear in all subjects (r greater than or equal to 0.91). The slope of this line was steeper in normal subjects than in myopathic patients (73 +/- 21.7 vs 20.8 +/- 8.7 mm Hg/volume unit/m2, P less than 0.001) and the zero pressure intercept also was greater (49.8 +/- 30 mm Hg vs 27.1 +/- 44.2 mm Hg, P less than 0.01). Similarly, resting ejection fraction (EF) was greater in the normals (0.71 +/- 0.88 vs 0.21 +/- 0.07% P less than 0.001) and end-diastolic volume (EDV) was smaller (4.14 +/- 0.88 vs 6.58 +/- 0.65 volume units, P less than 0.01). Systolic pressure/end-systolic volume relationship determined by these noninvasive methods was linear in both patients with severely reduced cardiac function and normal control subjects, clearly distinguishing normal from severely impaired left ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Radionuclide analysis of the forearm venous pressure-volume relationship: response to nitroglycerin.

By means of equilibrium radionuclide forearm venous occlusion plethysmography, we studied 12 adult men without heart failure. By using stepwise increases in venous occlusion pressure (0, 10, 20, and 30 mm Hg), we found that the relationship between venous cuff pressure and forearm radionuclide volume was consistently linear (r greater than 0.985). When sublingual nitroglycerin (NTG) was administered (0.8 mg), the venous pressure-volume relationship was consistently shifted rightward (reducing the slope and increasing the intercept). This resulted in large increases in venous capacitance, as shown by other workers using alternative techniques. Increased venous distensibility due to NTG was caused by an entire shift of the venous pressure-volume relationship rather than increased capacitance at one occlusion pressure. Equilibrium radionuclide venous occlusion plethysmography is a sensitive way to characterize venous pressure-volume relations. In addition, by using radionuclide blood pool component imaging to evaluate venous compliance, concern over fluid transudation seen with standard strain gauge venous plethysmographic techniques can be ignored, particularly at higher occlusion pressures.

Aged↗
PubMed1984

Intravascular and extravascular pulmonary fluid volumes during chronic experimental left ventricular dysfunction.

To assess the effects of chronic left ventricular (LV) dysfunction on intravascular pulmonary blood volume (PBV) and extravascular lung water (EVLW) lung fluid volumes, 56 dogs were evaluated by means of double-indicator dilution techniques. PBV and EVLW were measured in seven control dogs, in eight dogs 4 hours after the production of left heart dysfunction, and then in three additional groups of dogs (n = seven in each group) 7, 14, and 30 days after the production of LV dysfunction. Twenty dogs were excluded because we were unable to produce elevations in LV end-diastolic volume greater than 25 mm Hg. EVLW was measured using heat as the diffusible indicator, and electric shock was used to create heart block and myocardial scarring in order to produce LV dysfunction. Plasma volume was calculated prior to death by means of radioiodinated albumin. In the remaining animals, electric shock acutely and chronically elevated LV end-diastolic pressure (control 2.3 +/- 1.0 mm Hg; postshock pressures greater than 25 mm Hg). PBV increased initially after cardiac failure and remained so as time progressed, although it represented a smaller fraction of the plasma volume as time passed (11.2 +/- 2.1% control, 15.9 +/- 3.4% at 4 hours after failure, and 12.6 +/- 2.0% at 7 days; the former p less than 0.005 vs control, the latter p less than 0.01 vs control). EVLW increased as time progressed, in consort with small but progressive increases in left atrial pressure. Thus, we conclude that the effects of acute and chronic LV dysfunction on pulmonary circulation are significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Sustained venous occlusion plethysmography: effects on protein osmotic pressure, intravascular volume, and capillary filtration.

In six acutely anesthetized, mechanically ventilated mongrel dogs, we evaluated sequential changes (over 30 minutes) of sustained forelimb venous occlusion (occlusion pressures 30 to 65 mm Hg) on strain gauge dimension, radionuclide blood pool emissions, and venous, subcutaneous, and intramuscular pressures (Wick technique). Forelimb intravascular volume (assessed by decay-corrected radionuclide counts/unit time) changed by a mean of only -1.2 +/- 2.8% (+/- SEM) and thus was ignored in the calculation of filtration rate. Forelimb (distal to the occlusion site) hematocrit changed insignificantly (45.3 +/- 1.4% at the control point to 48.2 +/- 1.1% at 30 minutes), colloid osmotic pressure rose slightly 19.4 +/- 1.4 mm Hg to 22.7 +/- 1.6 mm Hg, p less than 0.01), and serum osmolality remained unchanged. During sustained occlusion, venous pressure remained constant, subcutaneous pressure rose (-0.7 +/- 1.2 mm Hg control vs 0.5 +/- 1.4 mm Hg at 30 minutes, p less than 0.05), and intramuscular pressure also rose (-0.4 +/- 1.1 mm Hg to 2.6 +/- 1.6 mm Hg, p less than 0.01). Driving pressure, defined by venous pressure - oncotic pressure less the average of intramuscular and subcutaneous pressure declined slightly over the 30 minutes of the study (27.8 +/- 5.5 mm Hg to 23.3 +/- 1.3 mm Hg, p less than 0.05). The relationship between either the initial driving pressure or the initial difference between venous and protein osmotic pressure correlated (r = 0.83 for both) well with strain gauge estimates of capillary fluid flux (evaluated by the change in forelimb strain gauge dimension over time and given as cc/100 cc forelimb volume/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Intravascular and extravascular pulmonary fluid volumes during acute experimental pericardial tamponade.

Pulmonary congestion is usually absent in cardiac tamponade. To examine the effects of experimental pericardial tamponade on pulmonary fluid volumes, we studied 14 anesthetized dogs with indicator-dilution techniques to measure extravascular (EVLW) and intravascular (PBV) pulmonary fluid volumes. Seven dogs were studied at two levels of tamponade and seven were studied during two levels of left atrial (LA) hypertension produced with an LA balloon. EVLW and PBV were measured in both groups at control state and then at two levels of elevated LA pressure (P). When LAP was raised by the balloon, PBV rose with the increase in LAP (4.9 +/- 2 cc/kg control at LAP 1.2 +/- 1.0 mm Hg versus 6.8 +/- 2.1 cc/kg at LAP 8.4 +/- 1.4 mm Hg and 6.8 +/- 2.1 cc/kg at LAP 14.7 +/- 2.0 mm Hg; both intervention PBV values p less than 0.01 vs control). During tamponade, PBV did not change (4.1 +/- 1.1 cc/kg at LAP 1.3 +/- 2.2 mm Hg control versus 4.4 +/- 1.0 cc/kg at LAP 7.4 +/- 1.4 mm Hg and 4.8 +/- 1.3 cc/kg at LAP 12.7 +/- 2.8 mm Hg). EVLW changes were similar during elevation of LAP in both groups (tamponade dogs 7.1 +/- 2.6 cc/kg, 7.1 +/- 1.6 cc/kg and 8.9 +/- 2.1 cc/kg, respectively; and LA hypertension dogs 6.9 +/- 2.5 cc/kg, 7.3 +/- 2.0 cc/kg, and 8.0 +/- 2.0 cc/kg, respectively. We conclude that during cardiac tamponade there is little change in PBV in response to rises in LAP. This is significantly different from the changes seen when increasing LAP by inflating an LA balloon, where fluid is shifted from the peripheral to the central circulation. EVLW changes were similar for the two methods during elevation of LAP.

Animals↗
PubMed1984

Usefulness of the chest x-ray for predicting abnormal left ventricular function after acute myocardial infarction.

We evaluated 229 patients discharged after a definite acute myocardial infarction. Pulmonary venous congestion determined from chest x-ray films during the hospitalization and at discharge and the cardiothoracic ratio at discharge were compared to the left ventricular ejection fraction measured at discharge by a gated radionuclide technique. During hospitalization, pulmonary venous congestion was found on at least one x-ray frame in 94 patients (41%). At discharge 134 patients (59%) had abnormal ejection fraction (less than 0.51) and 35 had pulmonary venous congestion (15%). The sensitivity of the x-ray for detecting an abnormal ejection fraction was 20% when pulmonary venous congestion was observed on the discharge x-ray film (specificity 92% and predictive value 77%), 52% if pulmonary venous congestion was present on any x-ray film during the hospitalization (specificity 74% and predictive value 73%), and 47% if the cardiothoracic ratio was abnormal (greater than or equal to 0.50) on the discharge x-ray film (specificity and predictive value 66%). We conclude that an abnormal x-ray film at discharge or during the hospitalization will identify approximately one-half of the abnormal ejection fractions at the time of hospital discharge. Therefore, to reliably assess left ventricular function, either for prognostic or therapeutic purposes in the individual patient, a more direct measure of left ventricular function such as radionuclide angiography must be obtained.

Adult↗
PubMed1984

Nuclear magnetic resonance analysis of acute and chronic myocardial infarction in dogs: alterations in spin-lattice relaxation times.

The purpose of this study was to evaluate the effects of acute and chronic ischemic injury on myocardial spin-lattice relaxation times (T1) in dogs. Ligation of the left anterior descending coronary artery was performed on 23 dogs which were divided into four experimental groups and killed at 3 hours (n = 6), 4 days (n = 6), 21 days (n = 5), and 56 days (n = 6) after coronary occlusion. T1 was measured in vitro with a 2.5 kg nuclear magnetic resonance (NMR) spectrometer using tissue from ischemic and control areas of the myocardium. Both the 3-hour and 4-day groups showed prolongations in T1 (p less than 0.01) for tissue from the ischemic area. In the 21-day group, two infarcts showed an increase in T1, two showed a decrease in T1, and one showed no significant change. The 56-day old infarcts had a lower mean value for T1 than control myocardium (p less than 0.01). The differences in myocardial water content between control and infarcted myocardium were found to parallel changes in T1 values in each experimental group. Pathologic examination of the myocardial scar from 21- and 56-day-old infarcts revealed extensive fibrosis in the infarcts with lower T1 values and tissue water contents than control myocardium. We conclude that myocardial edema in 3-hour and 4-day-old infarcts results in association with prolongations in T1. Twenty-one-day-old infarcts may be edematous (with increased T1) or fibrotic (with T1 values lower than normal myocardium), while 56-day-old infarcts are fibrotic and have shorter T1 values than normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Right ventricular mural thrombus caused by myocardial infarction diagnosed by computed tomography.

Thrombi of the left ventricle are common sequelae to acute anterior myocardial infarctions that involve the apex of the heart and produce akinetic or dyskinetic wall thickening patterns. While infarctions of the right ventricle are being increasingly recognized in the setting of inferior myocardial infarcts, little data on in vivo clot formation in the right ventricle of the heart are available in these patients. In the current study we were able to demonstrate a right ventricular mural thrombus using gated computed tomography of the heart. Although an abnormality in the right ventricle extending from the septal margin of the ventricle into the outflow tract could be identified with standard blood pool computed tomographic images and from cross sectional echocardiograms, only with cardiac gating could the relationship between the mass (thrombus) and the noncontractile section of the right ventricular myocardium be clearly identified. We conclude that cardiac gating may help in the evaluation of cardiac masses, and in particular cardiac thrombi. This will be particular valuable in the setting of recent or remote infarction, as the relationship between wall-motion abnormalities and thrombus formation has been well documented.

Adult↗
PubMed1984

Nuclear magnetic resonance tissue analysis of acute renal artery and renal vein occlusion: the effect of a paramagnetic contrast agent.

In order to assess the potential sensitivity of nuclear magnetic resonance for the assessment and detection of renal vascular insufficiency, nuclear magnetic resonance spectroscopy was performed on rabbit renal cortices following 45 minutes of unilateral renal artery or vein occlusion with and without the injection of a paramagnetic contrast material (manganese chloride). Renal vein occlusions produced a marked increase in T1 and T2 relaxation times when compared to the contralateral control kidney (mean increase of 18 per cent in T1 and 27 per cent in T2). Renal artery occlusions produced no change in T1 and only a slight increase in T2 (mean increase of 5 per cent). After the intravenous injection of 0.03 mM/kg. of manganese chloride, T1 of the control kidneys was reduced by almost 50 per cent. Relaxation parameters from the kidneys undergoing arterial occlusion did not change after manganese injection when compared to the occluded kidneys without contrast. In the kidneys undergoing venous occlusion, a moderate decrease in T1 resulted from manganese chloride. We conclude that in the absence of a paramagnetic contrast material, nuclear magnetic resonance discriminates well between normal and (venous occlusion) congested kidneys, but not between normal and acutely ischemic (arterial occlusion) kidneys. In the presence of a renal paramagnetic contrast material, NMR aids in the differentiation of acute unilateral arterial insufficiency, as relaxation times from the normal kidney decline while the ischemic kidney does not change.

Animals↗
PubMed1984

Effects of transient coronary ischemia and reperfusion on myocardial edema formation and in vitro magnetic relaxation times.

The effects of transient ischemia and reperfusion on regional myocardial function, salvage and swelling have been systematically analyzed in experimental canine preparations. The results of these interventions on myocardial in vitro measurements of magnetic relaxation times (T1 = magnetization recovery, T2 = spin echo) are of significant importance with respect to future nuclear magnetic resonance tomographic imaging. Thus, using a pulsed magnetic resonance spectrometer (10.7 MHz), myocardial tissue samples from two groups of dogs were evaluated. In group 1 (n = six dogs), the left anterior descending artery was occluded for 3 hours before sacrifice; in group 2 (six dogs), 3 hours of occlusion was followed by 1 hour of reperfusion. Multiple tissue samples from normal and ischemic (or ischemic and reperfused) myocardium were obtained for measurement of T1, T2 and % water content (wet weight--dry weight/wet weight). Water content increased with ischemia (78 +/- 4%) and reperfusion (81 +/- 4%) (both p less than 0.01 versus control values). Values for T1 increased with ischemia (598 +/- 39 versus 487 +/- 23 ms in normal tissue from the same heart, p less than 0.01). Even greater T1 changes occurred in the animals with reperfusion (654 +/- 52 ms, p less than 0.01 versus the intra-animal control values). Changes in T2 were similar but less marked (ischemic zone 43.9 +/- 1.0 versus 41.2 +/- 1.0 ms in nonischemic tissue in the corresponding heart, p less than 0.05; reperfusion zone 48.3 +/- 3.5 versus 41.9 +/- 2.3 ms in the normal zone, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Myocardial infarct size determined by computed transmission tomography in canine infarcts of various ages and in the presence of coronary reperfusion.

Thirty-one dogs underwent in vivo scanning with computed transmission tomography; 15 dogs were studied within 7 days (mean 4) after coronary occlusion, 10 dogs 21 to 25 days (mean 28) after occlusion and 6 dogs 4 days after coronary reperfusion of a 2 to 3 hour coronary ligation. Ungated scans (1 cm in depth) of the left ventricle were obtained from apex to base to determine infarct size. In all animals with documented (postmortem) infarction (n = 26), contrast medium caused delayed enhancement of the entire infarct or the periphery of the infarct. Infarct size was calculated from scans showing contrast enhancement of the infarct. Infarct size was also determined from the postmortem heart using histochemical morphometry (nitroblue tetrazolium) and then compared with infarct size derived from tomography using the outer margin of the contrast-enhanced periphery of the infarct as the border of the infarct. Infarct size calculated by the tomographic technique (excluding the animals without an infarct) correlated well with infarct size determined at autopsy (r = 0.90, p less than 0.001). The tomographic estimate (18.2 +/- 11.3 g) of infarct size was similar to autopsy values (18.6 +/- 11.8 g, p = NS). Thus, ungated computed transmission tomographic imaging of the heart can reliably estimate infarct size in a variety of potential clinical circumstances, particularly when the area of rim enhancement of the infarct is included within the presumed infarct region.

Animals↗
PubMed1984

Perfluoroctylbromide as a blood pool contrast agent for liver, spleen, and vascular imaging in computed tomography.

Perfluoroctylbromide (PFOB) in emulsion form was tested as a blood pool imaging agent for computed tomography (CT) in five animals (three dogs and two pigs). Computed tomography of the kidneys, liver, spleen, and mediastinum was performed in the control state and at various time intervals after the end of PFOB infusion. The attenuation coefficient of the vascular space increased by 117 Hounsfield units (HU) (range 105-128 HU), the liver by 54 HU (range 43-70 HU), and the spleen by 77 HU (range 69-86 HU) 30 to 50 min after the end of PFOB infusion, 5 ml/kg. The vascular space enhanced by 25 HU for every g of PFOB/100 ml of blood and remained at almost a constant level for hours after the end of infusion. In conclusion, PFOB emulsion, in addition to hepatosplenic enhancement, produces prolonged and substantial opacification of the vascular space, allowing CT imaging of the heart and vascular structures minutes to hours after the end of infusion.

Angiography↗
PubMed1984

Experimental pericardial inflammation evaluated by computed tomography.

Experimental pericardial inflammation was evaluated with ungated and cardiac gated computed tomography (CT) in 12 dogs, including 2 controls. All were studied during and after contrast infusion; in addition, several were sequentially imaged for up to six weeks after inducing inflammation by instilling toxic materials into the pericardial space. All dogs with inflammation had contrast enhancement of the parietal and visceral pericardium; this could be demonstrated within one week of the pericardial insult and for up to six weeks and was frequently associated with effusion. Increased pericardial density was not seen in controls or animals with pericarditis prior to contrast infusion. This technique may be useful in evaluating acute pericardial inflammation.

Animals↗