Experimental model of chronic global left ventricular dysfunction secondary to left coronary microembolization.

A model of chronic left ventricular dysfunction characterized by left ventricular dilation, elevated filling pressures and histologic changes has been lacking. In this study the use of coronary microsphere embolization-induced ischemia was explored as a method of producing chronic left ventricular dysfunction. Acute ischemic left ventricular dysfunction was induced in 13 mongrel dogs with 50 microns plastic microspheres until the peak positive first derivative of left ventricular pressure (dP/dt) decreased by 25% and the left ventricular end-diastolic pressure increased to greater than or equal to 12 mm Hg. After 8 weeks of observation, hemodynamic and echocardiographic variables were measured in each dog. Acute left ventricular dysfunction resulted in a dilated left ventricle with systolic dysfunction (area ejection fraction 24 +/- 6% vs. 57 +/- 9% initially, p less than 0.01) and elevated left ventricular filling pressures. Isovolumetric relaxation was prolonged and the peak rapid filling/atrial filling velocity and integral ratios were reduced. Eight weeks after embolization, there was an increased left ventricular size (end-diastolic area 15.1 +/- 2.1 cm2 at 8 weeks vs. 13.5 +/- 1.4 cm2 early after microsphere injection, p less than 0.05), unchanged end-systolic area, improved area ejection fraction and increased left ventricular mass. Left ventricular end-diastolic pressure increased and, despite continued abnormal relaxation, the peak rapid filling/atrial filling velocity and integral ratios increased to above baseline values, demonstrating a "restrictive" pattern. Gross and histologic examination revealed diffuse, patchy scarring associated with perivascular fibrosis. Thus, coronary microsphere embolization resulted in a model of chronic moderate left ventricular systolic dysfunction and abnormal diastolic function characterized by a "restrictive" filling pattern.

Effect of nitroglycerin-induced reduction of left ventricular filling pressure on diastolic filling in acute dilated heart failure.

Recent information has suggested that early diastolic filling may be influenced by the left ventricular filling pressure, especially in the failing left ventricle. Acute severe left ventricular dysfunction was induced in 14 dogs by severe left ventricular global ischemia produced by left main coronary artery microsphere embolization until the left ventricular end-diastolic pressure was greater than or equal to 20 mm Hg. To assess the importance of left ventricular filling pressure on left ventricular diastolic filling, nitroglycerin was infused and titrated to reduce left ventricular end-diastolic pressure to less than 15 mm Hg in seven dogs, whereas the remaining seven dogs were observed for 1 h after acute severe left ventricular dysfunction. In both groups of dogs, severe left ventricular dysfunction resulted in left ventricular dilation and elevation of end-diastolic pressure, reduction in area ejection fraction (echocardiographically determined) and an early redistribution of diastolic filling (increased filling fractions at one-third and one-half diastole) despite prolongation of the time constant of left ventricular pressure decline. Pressure-area plots shifted upward and rightward with severe left ventricular dysfunction and were unchanged at 1 h as were all other variables. Nitroglycerin infusion reduced left ventricular size and filling pressure, redistributed diastolic filling to later in diastole as characterized by reduced filling fraction at one-third diastole (left ventricular dysfunction 48.8 +/- 9.7%, nitroglycerin 17.9 +/- 7.9%, p less than 0.001) and shifted downward left ventricular pressure-area plots. Nitroglycerin also improved the time constant of relaxation (left ventricular dysfunction 83 +/- 15 ms, nitroglycerin 52 +/- 15 ms, p less than 0.001) and lengthened the diastolic filling period.(ABSTRACT TRUNCATED AT 250 WORDS)

Diastolic filling in acute left ventricular dysfunction: role of the pericardium.

Patients with congestive heart failure and elevated left ventricular filling pressures demonstrate an abnormal pattern of diastolic filling that is characterized by a redistribution of diastolic filling to early diastole with reduced reliance on late diastolic filling. The diastolic filling pattern superficially resembles that which is seen with constrictive pericarditis. To examine potential mechanisms for these clinical findings, a model of ischemic left ventricular dysfunction was produced in seven dogs by repeated coronary microsphere embolization, producing a dilated left ventricle with reduced systolic function. Measurements of left ventricular systolic and end-diastolic pressures, rate of rise of left ventricular pressure (dP/dt) and echocardiographic end-diastolic and end-systolic areas were obtained at baseline, during intermediate embolization (moderate left ventricular systolic dysfunction, dilation and mild increases in left ventricular end-diastolic pressure), postembolization (further embolization resulting in severe left ventricular systolic dysfunction, dilation and marked increases in left ventricular end-diastolic pressure), after thoracotomy and after pericardiectomy. The filling fraction at 1/3 and 1/2 of diastole and the time constant of left ventricular pressure decline were also determined. Repetitive coronary microembolization caused progressive left ventricular dilation and decreasing systolic function, which did not change after opening the chest or pericardium. The filling fraction at 1/3 and 1/2 of diastole declined with intermediate embolization (12.0 +/- 5.6% and 23.1 +/- 10.8%, respectively) as compared with baseline values (29.0 +/- 11.9%, 42.9 +/- 15.6%, p less than 0.05). After embolization, there was an increase in the 1/3 and the 1/2 filling fraction (47.5 +/- 8.9%, 72.0 +/- 6.0%, respectively, p less than 0.01) as compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of inotropic and vasodilator therapy on left ventricular diastolic filling in dogs with severe left ventricular dysfunction.

Inotropic and vasodilator therapy for congestive heart failure improve left ventricular systolic performance by different mechanisms. However, the nature and extent to which diastolic filling is altered have not been well described. Acute severe left ventricular dysfunction was induced in 21 dogs by severe left ventricular global ischemia produced by left main coronary artery microsphere embolization until left ventricular end-diastolic pressure was greater than or equal to 18 mm Hg. Dobutamine was infused in seven dogs until the peak positive first derivative of left ventricular pressure (dP/dt) increased by greater than or equal to 33%. Nitroprusside was infused in seven dogs until left ventricular end-diastolic pressure was less than 15 mm Hg. Seven dogs were observed for 1 h after the induction of acute severe left ventricular dysfunction and served as the control group. In all groups of dogs, severe left ventricular dysfunction resulted in left ventricular dilation, reduction in area ejection fraction, elevation of left ventricular end-diastolic pressure and an early redistribution of diastolic filling (increased 1/3 and 1/2 filling fractions) despite a markedly abnormal time constant of relaxation. No changes were noted in any variable after 1 h of observation in the seven control dogs. Nitroprusside reduced left ventricular size and filling pressure, increased cardiac output, improved relaxation and redistributed diastolic filling to later in diastole as characterized by a reduced 1/3 filling fraction (19.4 +/- 7.4% versus 51.4 +/- 10%, p less than 0.001). The pressure-area curve was shifted downward and leftward.(ABSTRACT TRUNCATED AT 250 WORDS)

Venous systolic thrill and murmur in the neck: a consequence of severe tricuspid insufficiency.

A palpable venous systolic thrill and murmur at the base of the neck are described as new physical findings in five patients with severe tricuspid regurgitation. In two of these patients, the tricuspid valve had been resected as treatment for infective endocarditis related to intravenous drug abuse. The third patient had severe chronic pulmonary disease with right heart failure. The fourth patient had a complex congenital defect in which the mitral valve served as the venous atrioventricular valve and was severely incompetent. The fifth patient suffered from long-standing rheumatic mitral and tricuspid disease with pulmonary hypertension 10 years after placement of a mitral prosthesis. From these observations, it is apparent that pulsatile retrograde flow in the cervical veins resulting from severe right-sided atrioventricular valve incompetence can produce a palpable systolic thrill and murmur at the base of the neck.

The electrocardiogram in systemic sclerosis (scleroderma). Study of 102 consecutive cases with functional correlations and review of the literature.

The electrocardiographic findings in 102 consecutive patients with scleroderma were reviewed to determine the frequency and nature of the electrocardiographic abnormalities associated with this disease. Septal infarction pattern unassociated with QRS prolongation was present in 10 percent, compared with none of 96 control subjects (p less than 0.001). Ventricular conduction abnormalities were present in 17 percent. A normal electrocardiogram was obtained in 49 percent. A subset of 48 patients underwent detailed cardiopulmonary evaluation including exercise thallium scintigraphy, rest and exercise radionuclide ventriculography, pulmonary function tests, and chest roentgenography. Functional correlations of the electrocardiographic findings were examined in this subset. Septal infarction pattern (five of 48) and ventricular conduction abnormalities (10 of 48) were both associated with septal or anteroseptal thallium perfusion abnormalities (10 of 15 versus six of 33 of the remainder, p less than 0.005), which were present despite normal coronary angiographic results. Thallium defect scores were greater in patients with septal infarction pattern or ventricular conduction abnormalities compared with the remainder (defect scores 3.0 +/- 2.6 versus 1.4 +/- 2.2, respectively, p less than 0.025). In patients with ventricular conduction abnormalities, both left bundle branch block and right bundle branch block with left anterior fascicular block were associated with abnormal left ventricular function, whereas isolated right bundle branch block or left anterior fascicular block was associated with normal left ventricular function. A normal electrocardiographic finding (19 of 48) was associated with normal left ventricular function at rest (19 of 19). However, 11 of 19 (58 percent) had thallium perfusion defects and four of 19 (21 percent) had an abnormal response to exercise, although in none was the peak ejection fraction less than 50 percent. It is concluded that both septal infarction pattern and ventricular conduction abnormalities are electrocardiographic abnormalities associated with scleroderma heart disease; they appear to be a result of myocardial fibrosis. Some degree of myocardial fibrosis may be present with a normal electrocardiographic result, but significant left ventricular dysfunction is unlikely. Septal infarction pattern and ventricular conduction abnormalities, when present, are indicators of more advanced fibrosis.

Redistribution on the thallium scan in myocardial sarcoidosis: concise communication.

Resting and redistribution thallium studies were performed in four young patients with sarcoidosis to evaluate the possibility of myocardial involvement. In each case the resting scan showed marked defects that resolved on the redistribution studies. In a different patient population, these results would have implied significant coronary artery disease.

Effect of mitral regurgitation on diastolic filling with left ventricular hypertrophy.

Earlier studies have suggested that mitral regurgitation (MR) augments early left ventricular (LV) diastolic filling. To determine whether MR affects early diastolic filling in patients with abnormal diastolic filling, transmitral pulsed-wave Doppler recordings were used to study 32 normal subjects, 21 patients with LV hypertrophy, 23 with LV hypertrophy and MR and 15 patients with MR. Patients with MR had increased peak early filling velocities (MR 108 +/- 27 cm/s, normal 80 +/- 16 cm/s, p less than 0.01), peak atrial filling velocities (MR 72 +/- 18 cm/s, normal 55 +/- 12 cm/s, p less than 0.05) and increased deceleration rates (MR 5.0 +/- 1.9 m/s2, normal 3.5 +/- 1.2 m/s2, p less than 0.05). Patients with LV hypertrophy had reduced peak early filling velocities (69 +/- 14 cm/s, p less than 0.05) and increased peak atrial filling velocities (83 +/- 16 cm/s, p less than 0.001). There was also an increase in the atrial filling fraction and reduction in the rapid filling fraction as compared with normal patients. Patients with LV hypertrophy and MR had increased peak early filling velocities (98 +/- 26 cm/s, p less than 0.01 vs normal, p less than 0.001 vs LV hypertrophy patients), increased atrial filling velocities (84 +/- 27 cm/s, p less than 0.001 vs normal), increased deceleration rates (4.4 +/- 2.4 m/s2, p less than 0.05 vs normal) and a normal distribution of diastolic filling. Within the LV hypertrophy and MR group, diastolic filling parameters were similar when patients were subgrouped on the basis of auscultability of MR. MR augments early diastolic filling and may tend to normalize diastolic filling patterns in LV hypertrophy patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Importance of the left ventricular filling pressure on diastolic filling in idiopathic dilated cardiomyopathy.

Both mitral regurgitation and elevated left ventricular (LV) filling pressures may normalize or enhance rapid filling in patients with idiopathic dilated cardiomyopathy. To assess the individual effects of the LV filling pressure and mitral regurgitation, 33 normal subjects, 14 patients with cardiomyopathy and normal LV filling pressures (measured as mean pulmonary capillary pressure) and 26 patients with elevated LV filling pressures (greater than 15 mm Hg) were studied with transmitral spectral tracings derived from pulsed Doppler echocardiography. Both cardiomyopathy groups demonstrated similarly dilated left ventricles with reduced systolic dysfunction. Patients with cardiomyopathy and normal LV filling pressures had prolonged isovolumic relaxation periods and a reduced ratio of the rapid filling to atrial filling integrals. Patients with cardiomyopathy and elevated LV pressures demonstrated an increased peak rapid filling velocity (97 +/- 21 cm/s) and rapid filling fraction (74.8 +/- 16.2%) compared with normal subjects (80 +/- 16 cm/s, p less than 0.01; 62.4 +/- 12.5%, p less than 0.05) and patients with cardiomyopathy and normal LV filling pressures (81 +/- 27 cm/s, p less than 0.05; 59.3 +/- 8.8%, p less than 0.05). Conversely, the atrial filling fraction was decreased in the cardiomyopathy group with elevated LV filling pressures compared with normal subjects and patients with cardiomyopathy and normal LV filling pressures. Mitral regurgitation increased the peak rapid filling velocity in both cardiomyopathy groups without altering the distribution of diastolic filling. In conclusion, elevated LV filling pressures appear to affect the distribution of diastolic filling, whereas mitral regurgitation affects the peak rate of rapid filling.

Pattern of left ventricular diastolic filling associated with right ventricular enlargement.

Right ventricular (RV) dilatation associated with pressure overload may alter left ventricular (LV) geometry resulting in abnormal diastolic function as demonstrated by a smaller LV diastolic volume for a given LV diastolic pressure. To determine whether abnormalities in LV geometry due to RV dilatation result in abnormalities in the LV diastolic filling pattern, we obtained pulsed Doppler transmitral recordings from 23 patients with RV dilatation with RV systolic pressure estimated to be less than 40 mm Hg (group 1), 18 patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg (group 2) and 33 normal patients. RV systolic pressures were estimated from continuous wave Doppler peak tricuspid regurgitation velocities using the modified Bernoulli equation. Diastolic filling parameters in group 1 patients were similar to normals. In group 2 patient, increased peak atrial filling velocity (76 +/- 14 vs 57 +/- 12 cm/s, p less than 0.001), decreased peak rapid filling velocity/peak atrial filling velocity (1.1 +/- 0.4 vs 1.5 +/- 0.4, p less than 0.01), increased atrial filling fraction (41 +/- 14 vs 30 +/- 10%, p less than 0.01) and prolongation of the atrial filling period (171 +/- 47 vs 152 +/- 39 ms, p less than 0.05) were noted compared with the normal group. RV end-diastolic size and LV end-systolic shape were significantly correlated with the atrial filling fraction in group 2 patients. In patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg, there is increased reliance on atrial systolic contribution to the LV filling volume.

Left ventricular diastolic filling in valvular aortic stenosis.

The pattern of left ventricular diastolic filling in patients with valvular aortic stenosis (AS) as assessed by gated blood pool scintigraphy has received little attention. Twenty-one normal persons (group 1), 24 patients with significant AS and ejection fractions of 50% or more (group 2) and 15 patients with significant AS and ejection fractions less than 50% (group 3) were studied. From the time-activity curve, the peak filling rate and mean filling rate (as end-diastolic volumes [EDV]/s) and percent stroke volume filled at first third of diastole and at the end of the rapid filling period were determined. Group 2 had a reduced peak filling rate (2.58 +/- 0.65 EDV/s, p less than 0.05) compared with group 1 (3.11 +/- 0.65 EDV/s). Similarly, the percent stroke volume filled at the end of the rapid filling period was reduced in group 2. Group 3 patients had a lower peak filling rate and mean filling rate than group 1 patients. However, percent stroke volume filled at first third of diastole and percent stroke volume filled at the end of the rapid filling period were greater in group 3 than in group 1. Two distinct patterns of diastolic filling were noted in patients with AS. Group 2 patients had reduced peak filling rates with less diastolic filling during the rapid filling period. Although the peak filling rate was reduced in group 3, more complete filling occurred during the rapid filling period.

Effect of heart rate alterations produced by atrial pacing on the pattern of diastolic filling in normal subjects.

To determine the effect of heart rate alterations on diastolic timing intervals and filling parameters, 10 normal patients were paced from the right atrium at 30 and 50 beats/min above their baseline rates. M-mode echocardiograms of the aortic valve, mitral valve and left ventricle were obtained and digitized at baseline and with each pacing rate. With increased atrial pacing, left ventricular systolic time became an increasingly greater proportion of cycle length while the diastolic filling period occupied a lesser proportion of the cycle length. The time to peak filling rate and the rapid filling period occupied a greater proportion of the diastolic filling period. The peak filling rate increased progressively with increased atrial pacing (baseline 128 +/- 19 mm/s, first paced rate 146 +/- 27 mm/s, p less than 0.05 vs baseline; second paced rate 167 +/- 23 mm/s, p less than 0.01 vs baseline and first paced rate). The early diastolic filling fraction and rapid filling fraction also increased with pacing. Increasing the heart rate resulted in an alteration of the time course of diastolic filling and extent of diastolic filling during the rapid filling period. Interventions that improve diastolic filling and increase heart rate may in part be due to heart rate changes.

Pattern of left ventricular diastolic filling in chronic aortic regurgitation: a gated blood pool assessment.

Limited information exists regarding the pattern of left ventricular diastolic filling in moderate to severe chronic aortic regurgitation (AR). The left ventricular diastolic filling curve derived from gated blood pool scans was evaluated in 24 normal subjects and 29 patients with AR. The peak filling rate (PFR), mean filling rate (MFR), peak ejection rate (PER), PFR/MFR, PFR/PER, and the time of the rapid filling period divided by the diastolic time were determined. PFR, MFR and PER were calculated as end-diastolic volumes per second (EDV/s). PFR was lower in the AR group than in the normal subjects (2.24 +/- 0.70 vs 3.09 +/- 0.71 EDV/s, p less than 0.001). Similarly, MFR was lower in the AR group (1.31 +/- 0.40 vs 1.63 +/- 0.29 EDV/s, p less than 0.01). PER was also reduced in the AR group. Both PFR/MFR and PFR/PER were reduced, while the ratio of rapid filling period to diastolic time was longer in the AR group than in normal subjects. Clinical evidence of congestive heart failure occurred in 8 patients in the AR group. Diastolic filling variables were not significantly different from the asymptomatic subgroup of patients with AR, but were abnormal when compared with those of normal subjects. In patients with AR, an abnormal pattern of diastolic filling was noted, consisting of a reduced PFR, MFR and PFR/ with a more linear pattern of filling (reduced PFR/MFR) during a longer rapid filling period.

Left ventricular diastolic filling in patients with left ventricular dysfunction.

The pattern of abnormal left ventricular diastolic filling and its specificity in coronary disease patients with severe left ventricular dysfunction has received little attention. We evaluated the left ventricular diastolic filling curve derived from gated blood pool scans in 21 normals, 61 coronary disease patients with ejection fractions less than or equal to 30%, and 51 congestive cardiomyopathy patients with ejection fraction less than or equal to 30%. The peak filling rate (PFR), peak ejection rate (PER), PFR/PER and the % stroke volume filled at 1/3 of diastole (%SV-1/3 DT) and at the end of the rapid filling period (%SV-RFP) were determined for each group. The PFR and PER were reduced in both coronary disease and congestive cardiomyopathy groups. The PFR/PER was increased in the coronary disease group (1.19 +/- 0.28) and congestive cardiomyopathy group (1.21 +/- 0.32) as compared to normals (0.93 +/- 0.20, P less than 0.001). A greater %SV-1/3 DT and %SV-RFP were noted in both coronary disease and congestive cardiomyopathy groups. Coronary disease and congestive cardiomyopathy patients with a mean pulmonary capillary pressure (PCP) greater than or equal to 18 mm Hg had a greater PFR/PER, %SV-1/3 DT, and %SV-RFP than patients with a PCP less than 18 mm Hg. An abnormal and nonspecific pattern of left ventricular diastolic filling is present in both coronary disease and congestive cardiomyopathy patients and is characterized by an increased PFR/PER, a greater %SV-1/3 DT, and a greater %SV-RFP. This pattern may be related to elevated PCPs.

Simplified count-based estimates of left ventricular volume.

Accurate count-based radionuclide estimates of left ventricular volume without the use of a blood sample have not been well described. Resting gated blood pool scans were obtained within 24 hours of catheterization in 31 patients (group 1), and simultaneously with thermodilution cardiac outputs in 29 other patients (group 2) at rest and during an induced-volume change (intervention). End-diastolic and end-systolic volumes were calculated from the single-plane angiogram in Group 1 and from the combination of thermodilution stroke volume and radionuclide ejection fraction in group 2. Excellent correlations were noted between scintigraphic counts and angiographic volumes (r = 0.964), between scintigraphic counts and thermodilution-derived volumes (r = 0.979), and between interventional scintigraphic counts and interventional thermodilution-derived volumes (r = 0.941). Thermodilution and scintigraphic volume changes during the intervention were well correlated (r = 0.85). Accurate count based estimates of left ventricular volume without a blood sample are feasible at rest and during an intervention.

Racial differences in drug response: isoproterenol effects before and after propranolol.

The aim of this study was to determine in young, healthy men the relative contribution of pharmacodynamic factors inherent between two groups known to respond differently to hypertensive therapy. Black (n = 10) and white (n = 10) men received an isoproterenol sensitivity test before and after propranolol (0.1 mg/kg, then 50 micrograms/min). There were greater increases (twofold) in systolic BP following the 1.0- and 1.5-microgram isoproterenol dose (P less than 0.05) in the black group. During propranolol there were no differences in free (1)-propranolol concentrations between the groups; however, propranolol decreased resting heart rate in the white group more than in the black group (P less than 0.05). Cardiac index decreased less in the black group compared to the white group (P less than 0.05). Following the second isoproterenol challenge, there again were greater increases in systolic BP in the black group at both the 10- and the 20-micrograms isoproterenol dose (P less than 0.05). Our study has highlighted the importance of cross-racial studies in evaluating drug effects.

Left ventricular diastolic filling abnormalities in left anterior descending disease.

Reduced left ventricular diastolic filling (DF) has been noted in coronary disease (CD) patients with normal left ventricular systolic function (NLVF). However, previous studies have included patients with regional wall disease, hypertension, or left ventricular hypertrophy. In the absence of these factors, only a subgroup of patients who had greater than 75% luminal obstruction of the left anterior descending artery (LAD) demonstrated DF abnormalities. Using 60 frames/sec biplane contrast ventriculography, we evaluated the left ventricular filling curve and its derivative in 21 patients with normal coronary arteries and NLVF (group 1), 17 CD patients with NLVF and no LAD disease (group 2), and 18 patients with LAD disease and NLVF (group 3). The peak filling rate (PFR) as end diastolic volumes/sec (EDV/S) was reduced in group 3 patients (group 3: 3.00 +/- 0.51 EDV/S vs group 1: 3.59 +/- 0.84 EDV/S, p less than .05; and group 2: 3.61 +/- 0.91 EDV/S, p less than .05). There was marked overlap in the PFR's between the normal and LAD group. DF may be normal in CD patients with NLVF in the absence of LAD disease. LAD patients have abnormal DF, but these abnormalities lack predictive valve.

Left ventricular diastolic filling in patients with coronary artery disease and normal left ventricular function.

Abnormal left ventricular diastolic filling (DF) has been noted in coronary disease (CD) patients with normal left ventricular function (NLVF). Inclusion of patients with regional wall disease, hypertension, and left ventricular hypertrophy may be responsible for abnormal DF. We evaluated left ventricular DF curves derived from gated blood pool scans in 21 normals (group 1), in 38 CD patients with NLVF specifically defined (group 2), and in 28 CD patients with ejection fractions greater than 50% and regional disease (group 3). The peak filling rate (PFR), mean filling rate (MFR), the percentage of stroke volume filled at one third of diastole (%SV-1/3 DT) and at the end of the rapid filling period (%SV-RFP) were determined. Groups 1 and 2 had similar DF parameters. Group 2 patients with 75% obstructive left anterior descending disease (LAD) had a reduced %SV-RFP and PFR (2.56 +/- 0.56 end-diastolic volumes/sec [EDV/S]) as compared to normals (3.11 +/- 0.65 EDV/S, p less than 0.01). Group 3 patients had a reduced PFR (2.14 +/- 0.53 EDV/S, p less than 0.001), MFR, %SV-1/3 DT, and %SV-RFP. DF in CD patients with NLVF was similar to normals in a select group of patients but was abnormal in patients with regional disease and greater than 75% LAD disease with NLVF.