Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 37 records · Page 2Linked to original sources

PubMed1991

Mechanisms responsible for the heterogeneous coronary microvascular response to nitroglycerin.

Nitroglycerin dilates large (greater than or equal to 100 microns) but not small coronary arterial microvessels, and a putative metabolite of nitroglycerin, S-nitroso-L-cysteine, has been shown in vitro to dilate both large and small coronary microvessels. Based on this evidence, we tested the hypothesis that the lack of response of small coronary microvessels was due to an inability of small coronary microvessels to convert nitroglycerin into its vasoactive metabolite and examined possible explanations for this phenomenon. We studied left ventricular epicardial microvessels in vivo using video microscopy and stroboscopic epi-illumination in anesthetized, open-chest dogs. Diameters were determined while the epicardium was suffused with nitroglycerin, S-nitroso-L-cysteine, or S-nitroso-D-cysteine (all 10 microM) and nitroglycerin in the presence of L- or D-cysteine (100 microM). None of the agents affected systemic hemodynamics. Nitroglycerin dilated large arterioles (20 +/- 2%) but not small arterioles (1 +/- 1%). Both S-nitroso-L-cysteine and S-nitroso-D-cysteine were potent dilators of all size classes of microvessels. Concomitant application of L-cysteine and nitroglycerin evoked dilation in small microvessels (22 +/- 4%, p less than 0.5 versus nitroglycerin alone) and larger microvessels (27 +/- 6%, p = NS versus nitroglycerin alone). D-Cysteine did not alter the microvascular response to nitroglycerin in either small (7 +/- 4%, p = NS versus nitroglycerin alone) or large (18 +/- 3%, p = NS versus nitroglycerin alone) microvessels. Neither L-cysteine nor D-cysteine had a direct effect on microvascular diameter. These findings suggest that 1) sulfhydryl groups are required for the conversion of nitroglycerin to its vasoactive metabolite; 2) the interaction between nitroglycerin and sulfhydryl residues is a stereospecific process, indicating either an intracellular mechanism or a membrane-associated enzymatic reaction; and 3) a lack of available sulfhydryl groups may be responsible for the lack of response of small coronary arterioles to nitroglycerin.

Analysis of Variance↗

PubMed1991

The evaluation of coronary bypass graft patency: direct and indirect techniques other than coronary arteriography.

Patients having one or more coronary artery bypass graft operations constitute an important part of the practice of cardiac radiology. Bypass graft patency can be determined by indirect and direct methods. The indirect imaging methods include radionuclide ventriculography, thallium-201 scintigraphy, and positron emission tomography. The direct methods include conventional CT, ultrafast CT, MR imaging, digital subtraction angiography, and Doppler sonography. This review discusses the advantages and limitations of these methods and attempts to define the relative importance of each of these techniques in the evaluation of bypass graft patency.

Coronary Angiography↗

PubMed1991

Pathophysiology of myocardial perfusion in hypertension.

Chronic and acute hypertension have multiple untoward effects on the coronary circulation, several of which may either mimic or markedly worsen the clinical manifestations of coronary artery disease. Early after the onset of left ventricular hypertrophy secondary to hypertension, coronary vasodilator reserve is significantly impaired. During cardiac hypertrophy secondary to hypertension, the coronary arteries fail to enlarge in concert with ventricular enlargement. This failure results in a relative decrease by approximately 50% in the ratio of epicardial vessel diameter to the mass of myocardium perfused. The lower range of coronary subendocardial autoregulation is altered by chronic renovascular hypertension. A variety of vascular smooth muscle homeostatic mechanisms are abnormal in genetic models of hypertension, as is endothelium-dependent vascular relaxation. Acute hypertension may enhance constriction to serotonin, most likely through the release of potent vasoconstrictor substances from leukocytes and platelets that adhere to the endothelium as a result of endothelial damage. Finally, many of the consequences of myocardial infarction are worsened in the setting of hypertension and left ventricular hypertrophy.

Cardiomegaly↗

PubMed1991

Physiological assessment of sensitivity of noninvasive testing for coronary artery disease.

The sensitivity of three noninvasive tests for coronary artery disease was assessed by means of quantitative indexes of disease severity in three different groups of patients. The overall population consisted of 110 subjects with limited coronary artery disease and no myocardial infarction. Planar dipyridamole-201Tl scintigraphy was evaluated in 31 patients, computer-assisted exercise treadmill in 28, and high-dose dipyridamole echocardiography testing in 51. Sensitivity was assessed by rigorous gold standards to define disease severity, such as measurement of minimum cross-sectional area and percent area of stenosis, by quantitative computerized coronary angiography (Brown/Dodge method). On the basis of the results of previous studies, the presence of physiologically significant coronary artery disease was indicated by a stenotic minimum cross-sectional area (MCSA) of less than 2.0 mm2 or a greater than 75% area of stenosis. With MCSA as the gold standard, dipyridamole-201Tl scintigraphy, computerized exercise treadmill, and dipyridamole echocardiography testing showed sensitivities of 52%, 54%, and 61%, respectively, in the three different patient cohorts enrolled. With percent area of stenosis as the gold standard, the sensitivity figures obtained for dipyridamole-201Tl, computerized exercise treadmill, and dipyridamole echocardiography testing were 64%, 54%, and 69%, respectively. For each of the three tests, sensitivity increased with increasing lesion severity. Sensitivity was also better in patients with left anterior descending coronary (LAD) disease when compared with patients with left circumflex or right coronary artery disease. Results of these studies, which were obtained with more strict patient selection criteria and by more rigorous gold standards than previous studies, demonstrate that in patients with limited coronary artery disease none of the tests evaluated is definitely superior in sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗

PubMed1990

Effects of left ventricular hypertrophy on the coronary circulation.

Many laboratories have provided evidence to support the concept that LV hypertrophy is associated with many significant coronary perfusion abnormalities. The decreased coronary flow reserve in the presence of LV hypertrophy is implicated as the mechanism of angina in patients with aortic stenosis and normal coronary arteries. The abnormal subendocardial autoregulation found in dogs may have important implications for the abrupt treatment of hypertension in patients with LV hypertrophy. The marked increase in mortality and the wavefront of infarction in dogs with hypertension and LV hypertrophy may have striking clinical implications for the salvage of myocardium in patients with chronic hypertension and LV hypertrophy during acute myocardial infarction.

Animals↗

PubMed1990

Polymorphous ventricular tachycardia: a side effect of intracoronary papaverine.

Polymorphous ventricular tachycardia occurred in 1.3% of patients (5 of 391) who received intracoronary papaverine over a 47 month period. The arrhythmia lasted less than 1 min in all five patients, converting spontaneously in four and requiring electrical cardioversion in one. Ventricular tachycardia occurred in 4.4% of women (4 of 90) and 0.3% of men (1 of 301) (p less than 0.0025). Only one of the patients with ventricular tachycardia had coronary artery disease. To determine whether other clinical or procedural factors predispose patients to this side effect of papaverine, these 5 patients were compared with 25 control patients who were matched for gender and extent of coronary artery disease. The following variables were analyzed: age, baseline serum potassium and calcium levels, left ventricular ejection fraction, baseline heart rate, mean arterial pressure, corrected QT interval, the change in corrected QT interval produced by papaverine and the maximal dose of the drug per kilogram of body weight. Of these variables, only baseline heart rate differed significantly in the two groups of patients. Thus, polymorphous ventricular tachycardia is an infrequent, but important, side effect of papaverine that is usually self-limited. Women with a relatively slow heart rate appear to be predisposed to this side effect.

Coronary Vessels↗

PubMed1990

Effects of atherosclerosis on the coronary microcirculation.

We tested the hypothesis that atherosclerosis potentiates coronary vasoconstriction to serotonin and ergonovine. Coronary microvascular pressures and diameters were measured in the beating left ventricle in normal and atherosclerotic cynomolgus monkeys. Pressures were measured in arteries (190-350 microns diam) that were distal to atherosclerotic lesions. Microvascular pressure and simultaneous measurements of aortic pressure and myocardial blood flow were used to calculate segmental vascular resistance (large artery resistance and microvascular resistance) during serotonin, phenylephrine, and ergonovine dosages. Aortic pressure was maintained constant during all interventions. Administration of phenylephrine (50 micrograms.kg-1.min-1 iv) produced a similar increase in microvascular resistance from base line (P less than 0.05) in atherosclerotic and normal animals, 26 +/- 5 and 14 +/- 9 mmHg.min.g.ml-1, respectively. Serotonin (50 micrograms/min) did not influence coronary resistance in normal animals but produced a significant increase in both large artery (8 +/- 3 mmHg.min.g.ml-1) and microvascular resistance (21 +/- 6 mmHg.min.g.ml-1) in atherosclerotic animals (P less than 0.05). A higher dose of serotonin (200 micrograms/min) produced a modest increase in large artery resistance from base line in normal animals (3 +/- 1 mmHg.min.g.ml-1) and a greater increase in atherosclerotic animals (9 +/- 4 mmHg.min.g.ml-1) (P less than 0.05 vs. normals). Ergonovine (10 micrograms.kg-1.min-1 iv) elevated microvascular resistance in both normal and atherosclerotic animals (P less than 0.05) but increased large artery resistance only in atherosclerotic animals (10 +/- 4 mmHg.min.g.ml-1) (P less than 0.05). In summary, coronary vasoconstrictor responses to serotonin and ergonovine were potentiated by atherosclerosis. Because augmented constrictor responses to serotonin were observed in both the diseased arteries and the microcirculation of atherosclerotic animals, we speculate that the pathophysiological consequences of atherosclerosis extend into the microcirculation.

Adenosine↗

PubMed1990

Effects of acute coronary artery occlusion on the coronary microcirculation.

The exact microvascular site of coronary vasodilation after coronary artery occlusion has not been clearly established. We sought to determine 1) the microvascular site of recruitable vasodilator reserve after a critical stenosis as assessed by adenosine and EDTA, 2) the coronary microvascular site responsible for vasodilatation after total coronary artery occlusion, and 3) the microvascular site for recruitable vasodilator reserve after coronary artery occlusion as assessed by adenosine and EDTA. Hemodynamics and coronary epicardial microvascular diameter were measured in 33 dogs by means of intravital epiillumination microscopy at control conditions, during a critical stenosis, or 30, 60, and 120 min following coronary artery occlusion. To evaluate the site of pharmacologically recruitable vasodilator reserve, EDTA or adenosine was suffused onto the epicardial surface. After a critical stenosis EDTA dilated all sizes of microvessels, whereas adenosine only dilated small microvessels (less than 150 microns). After coronary artery occlusion there was vasodilation that was inversely proportional to the control microvascular diameter. Coronary microvascular diameter did not change during 2 h after coronary artery occlusion. In addition, intravenous or topically applied adenosine or topically applied EDTA had no additional effect on the coronary arteriolar diameter. We concluded that in response to sudden coronary artery occlusion, the coronary microvascular dilation was inversely related to the control microvascular diameter, and in contrast to the response after a critical stenosis, there was no pharmacologically recruitable vasodilator reserve to adenosine or EDTA following acute coronary artery occlusion.

Acute Disease↗

PubMed1990

Connections between hypothalamus and medullary reticular formation mediate coronary vasoconstriction.

We have recently identified discrete sites within the lateral hypothalamus and medullary reticular formation that, when stimulated electrically, produce neurally mediated coronary vasoconstriction. This study examined whether these sites are part of the same coronary vasomotor pathway. The neuronal tracing dye fast blue was injected in cats into the coronary vasoconstrictor site within medullary reticular formation. Fluorescence microscopy revealed major afferent projections originating from within the same region of midbrain ventrolateral periaqueductal gray that receives projections from lateral hypothalamus. To determine the functional importance of the proposed connections between the hypothalamic and medullary sites, anesthetized cats were prepared for continuous hemodynamic measurements. Constant current electrical stimulation within lateral hypothalamus produced significant increases in heart rate (21 +/- 6%), arterial pressure (11 +/- 3%), and femoral (36 +/- 18%) and coronary resistances (14 +/- 9%) with no change in coronary flow velocity (-1.1 +/- 2.5%). After beta-adrenoreceptor blockade, significantly greater increases in arterial pressure (35 +/- 8%) and coronary resistance (39 +/- 5%) with transient decreases in coronary flow velocity (21 +/- 6%) were seen. Microinjections of lidocaine into the medullary site blocked coronary constriction produced by lateral hypothalamic stimulation (39 +/- 5% increase in coronary resistance to electrical stimulation before and 2.4 +/- 2% increase after lidocaine in medullary reticular formation). These data provide evidence that specific regions of lateral hypothalamus and medullary reticular formation are part of a common central vasomotor projection that mediates coronary vasoconstriction in addition to other hemodynamic effects.

Amidines↗

PubMed1990

Understanding the coronary circulation through studies at the microvascular level.

Studies of the coronary circulation have divided vascular resistances into three large components: large vessels, small resistance vessels, and veins. Studies of the epicardial microcirculation in the beating heart using stroboscopic illumination have suggested that resistance is more precisely controlled in different segments of the circulation. Measurements of coronary pressure in different sized arteries and arterioles have indicated that under normal conditions, 45-50% of total coronary vascular resistance resides in vessels larger than 100 microns. This distribution of vascular resistance can be altered in a nonuniform manner by a variety of physiological (autoregulation, increases in myocardial oxygen consumption, sympathetic stimulation) and pharmacological stimuli (norepinephrine, papaverine, dipyridamole, serotonin, vasopressin, nitroglycerin, adenosine, and endothelin). Studies of exchange of macromolecules in the microcirculation using fluorescent-labeled dextrans have also identified the size of the small pore (35-50 A) in coronary microvessels that can be altered by myocardial ischemia. Studies of the coronary microcirculation have demonstrated that the control of vascular resistance is extremely complex, and mechanisms responsible for these heterogeneous responses need further examination.

Animals↗

PubMed1990

Determination of right ventricular mass in humans and dogs with ultrafast cardiac computed tomography.

There is currently no clinical approach to precisely measure right ventricular (RV) mass. We postulated that the radiological mode of ultrafast computed tomography (CT) of 3-mm-thick slices with 0.7-mm resolution would allow sufficient resolution to accurately estimate RV mass. Using this radiological mode, we serially imaged the entire right ventricle from apex to base, gated to end diastole, and applied Simpson's rule to calculate mass of the RV free wall. Thirteen mongrel dogs (weight, 6-30 kg) were studied. The free wall mass of the right ventricle was in the range of 12.0-47.5 g and averaged 35.4 +/- 3.7 g (mean +/- SEE). The correlation between RV mass estimated by ultrafast CT and actual RV mass was r equaling 0.85, SEE equaling 5.5 g, slope equaling 0.99, and gamma intercept equaling -1.8. Intraobserver and interobserver variability (r = 0.99 and r = 0.99, respectively) was excellent with a standard deviation (SD) equal to 1.5 and 1.8, respectively. The effect of variable RV preload (right atrial pressure, -5 to +20 mm Hg) on accuracy of RV mass measurements produced minimal error (SD = 3.6 g) in RV mass measurements. Seven normal young healthy men were also studied. The free wall mass of the right ventricle was in the range of 48.3-67.4 g and averaged 54.6 +/- 2.8 g (mean +/- SEE). The left ventricular to right ventricular (LV:RV) ratio averaged 3.2 +/- 0.2:1. These results are in agreement with human autopsy data in healthy males reporting mean RV mass equal to 46 g and an LV:RV ratio equal to 3.4:1. Because imaging every 3-mm slice from apex to base requires two contrast injections, we determined the accuracy of RV mass measurements if only every fourth 3-mm slice with interpolation was used. RV mass measurements using every slice or every fourth slice with interpolation were excellent (dogs, r = 0.99; humans, r = 0.97). It is concluded that high resolution CT imaging (3-mm tomograms) allows accurate measurements of RV mass. It is possible to add this stop-action mode of ultrafast CT, to previous CT studies, using every fourth tomographic slice for mass determinations and only one additional contrast injection of 40-60 ml. This should permit the study of progression and regression of RV mass in patients with various diseases.

Animals↗

PubMed1990

Incidence of sudden cardiac death associated with coronary artery occlusion in dogs with hypertension and left ventricular hypertrophy is reduced by chronic beta-adrenergic blockade.

Because beta-adrenergic blockade has as one of its many effects altered electrophysiological abnormalities after dogs with left ventricular hypertrophy have been subjected to coronary occlusion, we tested the hypothesis that metoprolol (200-400 mg/day) would reduce mortality rates in dogs with one-kidney, one clip left ventricular hypertrophy while a similar reduction in arterial pressure with enalapril (20-40 mg/day) would not. Dogs with left ventricular hypertrophy were given metoprolol or enalapril for 5-7 days before a 3-hour coronary occlusion. Infarct size and risk area were measured with triphenyltetrazolium chloride stain and barium angiography, respectively. For control (n = 15), left ventricular hypertrophy (n = 17), left ventricular hypertrophy plus metoprolol (n = 12), and left ventricular hypertrophy plus enalapril (n = 15) groups, mean arterial pressure, ratio of infarct size to risk area, and dogs experiencing sudden death were 110 +/- 4, 142 +/- 4, 121 +/- 7, and 120 +/- 3 mm Hg; 44 +/- 5%, 65 +/- 5%, 44 +/- 7%, and 30 +/- 4%; and 27%, 65%, 17%, and 53%, respectively. Thus, the excessive increase in early mortality occurring when dogs with hypertension and left ventricular hypertrophy undergo coronary occlusion is interrupted with beta-blockade, possibly via electrophysiological effects rather than by changes in arterial pressure or infarct size.

Adrenergic beta-Antagonists↗

PubMed1990

Heterogeneous changes in epimyocardial microvascular size during graded coronary stenosis. Evidence of the microvascular site for autoregulation.

The purpose of this study was to determine the coronary microvascular sites of autoregulation. The epimyocardial coronary microcirculation was observed through an intravital microscope by stroboscopic epi-illumination in anesthetized open-chest dogs (n = 20). Aortic pressure and heart rate were held constant by an aortic snare and atrial pacing, respectively. Distal pressure of the left anterior descending coronary artery was controlled by a screw occluder on the proximal left anterior descending coronary artery and monitored with a 24-gauge plastic cannula inserted into the branch or distal portion of the left anterior descending coronary artery. Distal pressure of the left anterior descending coronary artery was stepwisely reduced to 59 +/- 1 mm Hg (mild stenosis, n = 20) and 38 +/- 1 mm Hg (severe stenosis, n = 16). In the left circumflex coronary artery area, myocardial blood flow measured with radioactive microspheres to subepicardium, midmyocardium, and subendocardium did not change with the mild and severe stenosis from control. In the left anterior descending coronary artery area, myocardial blood flow to each layer remained at nearly control level with the mild stenosis but was reduced in midmyocardium and subendocardium with the severe stenosis. With the mild stenosis, diameters of coronary arterial microvessels less than 100 microns in diameter dilated, and those larger than 100 microns in diameter did not change. The magnitude of vasodilation in small arterial microvessels was inversely related to control diameter. With the severe stenosis, small arterial microvessels dilated, and simultaneously, large arterial microvessels constricted. Again, the magnitude of vasodilation in small arterial microvessels was inversely related to control diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Chronic hypertension and left ventricular hypertrophy facilitate induction of sustained ventricular tachycardia in dogs 3 hours after left circumflex coronary artery occlusion.

The purpose of this study was to investigate the electrophysiology of acute ischemia in hypertrophic as compared with nonhypertrophic myocardium. Left circumflex coronary artery occlusion was produced in anesthetized open chest dogs. Of 40 dogs studied, 22 were normotensive and 18 had chronic hypertension produced by a single kidney renal clamp procedure. Recordings of electrograms and extrastimulus testing were performed in endocardial and epicardial sites in both normal and ischemically damaged zones documented by triphenyltetrazolium chloride. In the hypertrophy group, there was greater endocardial to epicardial conduction delay in ischemic zones, mean +/- SEM 57 +/- 4 ms versus 31 +/- 2 ms in the normotensive group (p less than 0.05). Also, sustained monomorphic ventricular tachycardia was inducible in seven of eight dogs with hypertrophy and in none of eight normotensive dogs surviving to 3 h. Entrainment and several observations during induction were consistent with reentrant ventricular tachycardia. To exclude hypertension alone as an etiology of tachycardia, five normotensive dogs without inducible monomorphic tachycardia remained unchanged during hypertension produced with low doses of phenylephrine or descending aortic occlusion. Thus, the electrophysiologic response to ischemia is altered in hypertrophied myocardium, which predisposes to rapid sustained monomorphic ventricular tachycardia.

Animals↗

PubMed1989

Ultrafast computed tomography in the diagnosis of cardiac disease.

Ultrafast computer tomography (CT) is one of the major new imaging modalities that has become available for the evaluation of patients with heart disease. With cine CT it is possible to obtain high resolution images of the heart at 58-ms intervals. The inplane resolution is 0.7 to 1.5 mm, and the slice thickness is 3 to 9 mm. Images require the intravenous injection of nonionic contrast agents to obtain quantitative information about cardiac function. Cine CT has thus far been used in 3 general areas that relate to the evaluation of patients with heart disease: evaluation of cardiac structure and function, evaluation of vein bypass graft patency and flow reserve, and measurements of regional myocardial perfusion. Because of the outstanding spatial resolution of the images, it is possible to obtain very precise information about cardiac structure and function. The weight of the left ventricle and right ventricular walls can be measured to +/- 5%, and the stroke volumes and end-diastolic volumes of all 4 cardiac chambers can also be measured with an accuracy of +/- 5%. With this technology it is possible to determine the magnitude of aortic regurgitation within +/- 5 to 8%. This modality has also proved useful in the diagnosis of surgically resectable left ventricular aneurysm and a multitude of other cardiac disorders that involve abnormalities in cardiac structure, including congenital heart defects, aortic aneurysms and constrictive pericarditis. These diagnostic procedures use the peripheral injection of usually about 100 ml of contrast media and can ordinarily be completed in less than 15 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗

PubMed1989

Importance of abnormalities in coronary flow reserve to the pathophysiology of left ventricular hypertrophy secondary to hypertension.

Left ventricular hypertrophy (LVH) appears to be a critically important risk factor for the prediction of coronary events. This is probably related to the fact that cardiac hypertrophy causes a profound decrease in coronary reserve and various electrophysiological abnormalities in hypertrophied myocytes that contribute to the pathogenesis of lethal ventricular arrhythmias. Physicians involved in the care of patients with cardiac hypertrophy need to be aware of the importance of LVH in modifying the pathophysiology of the two prevalent cardiac diseases in our society: obstructive coronary disease and systemic hypertension.

Blood Flow Velocity↗

PubMed1989

What have we learned about coronary artery disease from high-frequency epicardial echocardiography?

We have used a high frequency epicardial echocardiographic technique to visualize and measure coronary artery lumens and walls in patients undergoing cardiac surgery. A 12 MHz probe (Surgiscan, Biosound Corp.) is sterilized and placed on the exposed epicardial coronary arteries. Transverse cross-sectional views are obtained from the arteries on the anterior surface of the heart: the right coronary artery to the cardiac margin and the left anterior descending coronary artery to the cardiac apex. Numerous echocardiographic-angiographic-pathological correlations have been obtained from this work. We have validated the echocardiographic lumen and wall measurements by comparing the echo measurements to histological material from pressure-distended coronary arterial segments (from animals and fresh human autopsy specimens). We have shown by comparison with angiography that coronary arteries which appear normal or only minimally diseased by angiograms are often diffusely and severely atherosclerotic. We have also evaluated the shape of atherosclerotic lesions and demonstrated a wide range of lumen shapes (oval, circular, complex) and location within the residual coronary lumen (eccentric vs. concentric). Highly eccentric lesions are characterized by relative preservation of portions of the arterial wall, and this may preserve vasoreactivity of the atherosclerotic vessel. We have also demonstrated remodeling of atherosclerotic lesions: enlargement of the total arterial area (wall plus lumen) as a compensatory mechanism to preserve the arterial lumen in the face of encroaching atherosclerosis. High frequency epicardial echocardiography offers an accurate, real-time, in-vivo method for the anatomic and functional evaluation of coronary atherosclerosis. This dynamic, in-vivo technique supports and extends information previously obtainable only from pathologic studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗

PubMed1989

Patterns of regional diastolic function in the normal human left ventricle: an ultrafast computed tomographic study.

The detailed evaluation of regional diastolic filling at multiple ventricular levels in the normal human left ventricle has not previously been reported. Ultrafast computed tomography was used to characterize global and regional early diastolic filling in the left ventricle of 11 normal male volunteers. Regional early diastolic filling data from six distinct ventricular levels (apex to base) were fit to a third-order polynomial curve, and the peak rate of diastolic filling and time of peak filling were determined. Peak filling rate was 259 +/- 17 ml/s (+/- SEM) as a global average, where peak filling rate referenced to end-diastolic volume and stroke volume across the levels examined was 3.78 +/- 0.17 s-1 and 4.83 +/- 0.20 s-1, respectively. Average filling fraction was 39 +/- 1%, and time to peak filling from end-systole was 145 +/- 5 ms. Regional (tomographic) peak filling rates, except for the most apical level examined, were not statistically different across the ventricle. Filling fraction and time to peak filling were remarkably constant from one level to another. However, reference of regional peak filling rate to regional end-diastolic volume demonstrated significant nonuniformity from apex (120% of average for all levels) to base (87% of average for all levels). Peak filling rate referenced to tomographic stroke volume was less variable and not statistically different across the ventricle as a whole.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗