Exercise echocardiography: detection of coronary artery disease in patients with normal left ventricular wall motion at rest

Most studies investigating the ability of exercise two-dimensional echocardiography to identify patients with coronary artery disease have included patients with left ventricular wall motion abnormalities at rest. This has the effect of increasing sensitivity because patients with only abnormalities at rest are detected. To determine the diagnostic utility of exercise echocardiography in patients with normal wall motion at rest, 64 patients were studied with exercise echocardiography in conjunction with routine treadmill exercise testing before coronary cineangiography. All 24 patients who had no angiographic evidence of coronary artery disease had a negative exercise echocardiogram (100% specificity). Nine of 40 patients with coronary artery disease (defined as greater than or equal to 50% narrowing of at least one major vessel) also had a negative exercise echocardiogram (78% sensitivity). Of the nine patients with a false negative exercise echocardiographic study, six had single vessel disease. Among 25 patients with single vessel disease, exercise echocardiography was significantly more sensitive (p = 0.01) than treadmill exercise testing alone (76 versus 36%, respectively). Among 15 patients with multivessel disease, the two tests demonstrated similar sensitivity (80%). In conclusion, exercise echocardiography is highly specific and moderately sensitive for the detection of coronary artery disease in patients with normal wall motion at rest. Although exercise echocardiography is significantly more sensitive than treadmill exercise electrocardiographic testing alone in patients with single vessel disease, the two tests are similar in their ability to detect coronary artery disease in patients with multivessel disease and normal wall motion at rest.     

Left ventricular wall motion in patients with Chagas's disease.

The effect of early chronic Chagas's disease on the timing and extent of regional left ventricular wall motion was studied with a frame by frame analysis of left ventriculograms in nine patients and compared with those in 19 normal subjects. In all the patients there was hypokinesis or akinesis in the anteroapical region together with delay in the onset of inward movement. Hypokinesis of the proximal inferior segment was also present, but the time of onset of inward motion here was normal. These differences can be explained on the basis of regional asynchrony within the normal left ventricle, where anteroapical wall motion is delayed with respect to that elsewhere. Thus contraction of the diseased anteroapical segment starts against an appreciable pressure and so may be isometric, whereas the affected proximal inferior segment starts contracting earlier against a lower pressure and so is able to shorten. No abnormalities of wall motion were seen during isovolumic relaxation despite segmental involvement, which is a distinctly different finding from that in patients with coronary artery disease. This may be due partly to the absence of incoordinate relaxation in Chagas's disease and partly to myocardial involvement by Chagas's disease in the mid-anterior segment. This is the site of rapid early diastolic wall thinning, which has been put forward as a major mechanism of normal rapid ventricular filling and whose premature activity causes disturbances in regional wall motion before mitral valve opening when relaxation is incoordinate. Thus quantitative analysis of both the timing and amplitude of wall motion indicates fundamental differences between Chagas's disease and coronary artery disease, when a less complex analysis would have shown a similar pattern of segmental dysfunction in both. Since the effect of the same pathological process on wall motion varies with the site of ventricular involvement, the importance of the disturbances seen in Chagas's disease becomes apparent only when the non-uniformity of normal left ventricular structure and function is taken into account.     

Left ventricular filling and early diastolic function at rest and during angina in patients with coronary artery disease.

Left ventricular diastolic function was studied in 11 patients with coronary artery disease. Single plane ventriculography (30 degrees right anterior oblique projection) was performed at rest and during an episode of angina immediately after a period of rapid atrial pacing. Left ventricular pressure was recorded simultaneously by a micromanometer tipped catheter. The ventriculograms were digitised frame by frame to derive continuous plots of left ventricular shape, volume, and rate of change of volume. The time constant (tau) of the fall in left ventricular pressure was determined from the exponential portion of pressure decay during isovolumic relaxation. Ventricular pressure-volume loops were constructed to study the left ventricular diastolic pressure-volume relation. The time of minimum left ventricular pressure was used to divide diastole into an early phase and a late phase. Angina was associated with an increase in end systolic volume and a fall in ejection fraction with no significant change in end diastolic volume. Peak left ventricular pressure was unchanged but left ventricular minimum and end diastolic pressures were both increased and the diastolic pressure-volume relation was moved upwards. The time constant of left ventricular pressure fall was prolonged. At rest more than 50% of the stroke volume entered the left ventricle during the period of early diastole. This proportion was significantly reduced during angina and as a consequence a significantly greater proportion of the stroke volume entered the ventricle during late diastole. Despite this, and although the left ventricular diastolic pressure-volume relation was moved upwards with angina, the mean slope of the relation during late diastole--that is, chamber stiffness--was not significantly altered. The upward shift of the left ventricular diastolic pressure-volume relation seen during angina is thus already apparent in early diastole, and its extent does not change during the later phase of diastole, which alone shows the property of passive stiffness. A primary increase in the passive stiffness of the ventricle cannot therefore be the cause of the upward shift of the diastolic pressure-volume relation, and events occurring in early diastole have to be looked to for an explanation. The study findings show that left ventricular function in early diastole is profoundly disturbed during angina pectoris and it is suggested that loss of elastic recoil and dissipation of this restoring force by asynchronous onset of relaxation and abnormal changes in shape are important factors contributing to this disturbance of function.     

Incidence of exertional right ventricular wall motion abnormalities in patients with coronary artery disease

To evaluate the role of analysis of right ventricular function with exercise in patients with presumed coronary artery disease referred for radionuclide ventriculography, the records of 55 patients referred to our laboratory over a 19-month period were reviewed. All underwent rest and exercise first-pass radionuclide stress testing and cardiac catheterization within a period of four months. Three groups were identified: (1) patients with normal exercise right ventricular function (n = 24); (2) patients with exercise-induced right ventricular regional wall motion abnormalities (n = 15); and, (3) patients with abnormal resting right ventricular function without new exercise abnormalities (n = 16). Patients in each group were similar in age, sex, baseline left ventricular function, medication usage, and indication for study. The incidence of right coronary artery disease was identical in the three groups, as was the incidence of left ventricular functional abnormalities with exercise. Patients with proximal right coronary artery disease were more likely to have reduced left ventricular ejection fraction and more extensive coronary artery disease than those without disease at this site. We conclude that: (1) analysis of rest and exercise right ventricular function does not allow prediction of coronary anatomy in an unselected group of patients; (2) normal right ventricular function with exercise is compatible with extensive coronary artery disease, including proximal right coronary artery disease; and (3) abnormal exercise right ventricular function may be due to exertional left ventricular dysfunction in the absence of proximal right coronary artery disease.     

Left ventricular opacification: improved detection of global and regional wall motion at rest

Contrast echocardiography is officially validated for improvement of endocardial visualization in patients with poor acoustic window. In fact, and due to its cost, contrast injection is nowadays limited to few cases in standard echocardiography: LV volume measurement, LV thrombi, wall motion analysis.     

Ejection fraction and regional wall motion at rest and during stress in the diagnosis of coronary artery disease

Stress radio nuclide ventriculography is used to determine ejection fraction and changes in regional wall motion for the detection of ischemia-induced left ventricular dysfunction in patients with coronary artery disease. We have evaluated the relative sensitivity of regional wall motion and of ejection fraction during hand-grip and cold pressor test, in 21 patients with angina pectoris and documented coronary artery disease at angiography. Regional wall motion appeared a more sensitive index than global ejection fraction producing only two false negative cases. Ejection fraction showed great variability among the patients during both hand-grip and cold pressor test. This might be explained by the fact that both tests do not produce a sufficient degree of ischemic stress on the left ventricle. Hand-grip and cold pressor tests appear useful alternative to dynamic exercise in the diagnosis of coronary artery disease being also safe and simple to perform.     

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.     

Left ventricular diastolic filling in patients with coronary artery disease without myocardial infarction

Left ventricular diastolic dysfunction at rest was studied in 24 patients with coronary artery disease but no evidence of previous myocardial infarction. Seven patients with normal coronary arteries were studied as control. Diastolic filling was analyzed by the serial left ventricular volume and 14 radial axes from the gravity point of the left ventricle with cine left ventriculography. There were no differences in the systolic function between coronary artery disease and the normal control. Peak filling rate was decreased significantly in the groups with left anterior descending artery disease (LAD, p less than 0.05) and multivessel disease (MVD, p less than 0.05), but not in the group with right coronary artery disease (RCA). Time to peak filling rate was prolonged in each group of LAD (p less than 0.05), RCA (p less than 0.05), and MVD (p less than 0.001), compared with controls. The time-volume curve showed disturbed rapid filling in the LAD and RCA groups, and also both depressed rapid and slow filling in the MVD group. In the LAD group, the filling fraction was decreased significantly at the time of 25% of the diastolic period (p less than 0.001) and radial distension to the anterior wall was decreased at the time of 25%, 50%, and 75% of the diastolic period, compared with controls. In the RCA group, the filling fraction (p less than 0.001) and radial distension to the posterior wall were decreased only at the time of 25% of the diastolic period. In the MVD group, filling fraction and radial distension to the most wall were decreased at 25%, 50%, and 75% of the diastolic period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular function before and after diltiazem in patients with coronary artery disease

Left ventricular contraction, relaxation and diastolic mechanics were investigated before and after intravenous administration of 15 mg of diltiazem in 15 patients with coronary artery disease. High fidelity left ventricular pressure measurements were performed in all 15 patients, with simultaneous biplane cineangiography in 13. The time constant of left ventricular isovolumic pressure decay was calculated from the linear relation of left ventricular pressure and its rate of change with time (negative dP/dt). Frame by frame volume analysis through one cardiac cycle was completed to construct volume-time and pressure-volume curves before and after the administration of diltiazem. After diltiazem, left ventricular peak systolic pressure decreased from 124 to 113 mm Hg (p less than 0.001), while left ventricular end-diastolic pressure and heart rate were not altered. Maximal positive dP/dt also remained unchanged. End-diastolic volume was not changed after diltiazem, but end-systolic volume increased from 48 to 52 ml/m2 (p less than 0.025); as a result, ejection fraction decreased slightly from 57 to 55% (p less than 0.025). The time constant of left ventricular pressure decay and maximal negative dP/dt decreased from 58 to 54 ms (p less than 0.025) and from -1,404 to -1,321 mm Hg/s (p less than 0.025), respectively. Peak early diastolic filling rate increased from 621 to 752 ml/s (p less than 0.01) in association with an increase in filling volume during the first half of diastole from 60 to 68% (p less than 0.005). No consistent displacement of the diastolic pressure-volume curve was observed after diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular mechanical efficiency in coronary artery disease

The effect of coronary artery disease and prior myocardial infarction on cardiac energetics was determined by measuring left ventricular myocardial blood flow, oxygen consumption (MVO2), efficiency and ejection phase indexes in 36 patients undergoing coronary arteriography. Eight control patients with normal coronary arteriograms and normal left ventricular function, 15 patients with coronary artery disease without prior myocardial infarction and 13 patients with coronary disease and prior myocardial infarction (greater than 6 months) were studied. Left ventricular efficiency was calculated from left ventricular work, myocardial blood flow (measured by clearance of intracoronary xenon-133), and aortic and coronary sinus oxygen content. Left ventricular volumes, mass and ejection phase indexes were measured by quantitative left ventriculography. Left ventricular myocardial blood flow per 100 g/min was reduced in patients with coronary artery disease (49.0 +/- 8; p less than 0.01) and in patients with myocardial infarction (51.6 +/- 10; p less than 0.05) compared with control subjects (62.4 +/- 16), but total left ventricular flow was not reduced because of increased left ventricular mass. As a result, MVO2 did not differ significantly for the three patient groups (control 13.3, coronary artery disease 14.0 and myocardial infarction 14.3 ml/min). In the patients with myocardial infarction, left ventricular work index was reduced (2.4 versus 4.0 kg X m/m2 per min in the control group; p less than 0.001), causing efficiency to be reduced (15.9 versus 28.8% in the control group; p less than 0.001). Decreased efficiency correlated with ejection fraction (r = 0.54), mean velocity of circumferential fiber shortening (MVcf) (r = 0.45) and mean percent chordal shortening (r = 0.43) (all p less than 0.01). These data indicate that in control patients with normal coronary arteriograms, left ventricular myocardial efficiency averages 29%; in patients with coronary disease without myocardial infarction, left ventricular MVO2 and efficiency are in the normal range; in patients with prior myocardial infarction, left ventricular efficiency is significantly reduced as a result of diminished left ventricular work and normal MVO2; and reduced efficiency after myocardial infarction correlates with reduced ejection phase indexes.     

Left ventricular wall motion abnormalities in 80 patients with systemic sclerosis

Summary Segmental analysis of left ventricular wall motion was performed in 80 patients with systemic sclerosis by echocardiography. Half of the cases showed normal wall motion. Eighteen of the 57 patients with limited cutaneous systemic sclerosis (31.6%) exhibited hypokinetic wall motion abnormalities, while five of the 23 cases with diffuse cutaneous systemic sclerosis (21.7%) had similar findings. The three cases showing akinesis also belonged to the limited scleroderma subgroup. Our findings show that hypokinetic wall motion abnormalities can be detected in a remarkably high proportion of cases with limited cutaneous systemic sclerosis.     

Improvement in regional wall motion and left ventricular relaxation after administration of diltiazem in patients with coronary artery disease

To assess the effect of diltiazem on left ventricular systolic regional wall motion and diastolic function in patients with coronary artery disease (CAD), 22 patients underwent biplane left ventricular cineangiography before and after intravenous diltiazem (plasma concentration 154 +/- 12 ng/ml). Left ventricular and right ventricular pressures were measured by micromanometer-tipped catheters. Regional wall motion was assessed quantitatively with an area ejection fraction technique. Diltiazem decreased mean arterial pressure 11.5% (p less than .0001) and heart rate 6.8% (p less than .005); it increased cardiac index 8.8% (p less than .025) and global ejection fraction 9.1% (p less than .0001). However, left ventricular end-diastolic pressure increased 14.2% (p less than .001) and the left ventricular end-systolic pressure-volume (P-V) ratio decreased 8.8% (p less than .02). Diltiazem decreased the time constant of left ventricular relaxation by 14.3% (p less than .002), despite lack of change in the left ventricular diastolic P-V relationship, in 16 patients. Diltiazem caused a significant increase in area ejection fraction in 53% of hypokinetic areas supplied by diseased arteries compared with 13% of normokinetic areas supplied by diseased arteries (p less than .0001). Response of ejection fraction to diltiazem in areas supplied by normal coronary arteries was less (p less than .05) than that in hypokinetic areas supplied by arteries affected by disease. In conclusion, diltiazem improves regional wall motion abnormalities in patients with CAD and the improvement is associated with better left ventricular relaxation but not with a change in the diastolic P-V relationship. Global indexes of left ventricular systolic performance are favorably influenced by diltiazem, despite a mild negative inotropic effect.     

Left ventriculography induced coronary artery spasm

Angiographic contrast material is generally considered a vasodilator, although in vitro experiments have documented a spasmogenic effect. In this report we describe a patient with exercise and rest angina who developed spasm of the right coronary artery immediately following left ventricular angiography. The patient was treated successfully with calcium channel blockers. This is the first reported case of left ventricular angiography-induced coronary artery spasm.     

Effect of intravenous and intracoronary nitroglycerin on left ventricular wall motion and perfusion in patients with coronary artery disease

Left ventricular anterior wall motion and distribution of coronary perfusion were assessed by contrast cineangiography and the dual isotope-labeled intracoronary microsphere technique before and after intravenous or intracoronary administration of nitroglycerin in 30 patients with significant left anterior descending coronary artery disease and resting anterior wall asynergy. Perfusion was measured in 11 additional control patients before and after administration of saline solution. Reversible asynergy was observed in 6 (43 percent) of 14 patients after systemic (intravenous) nitroglycerin and in 7 (44 percent) of 16 patients after intracoronary nitroglycerin. Significant reductions of blood pressure and improved wall motion were noted in both groups receiving nitroglycerin, suggesting afterload reduction as the common mechanism. There was also a small increase in end-diastolic volume index in patients with reversible asynergy after intracoronary administration of nitroglycerin, but no significant trends in preload change after intravenous administration. Ejection fraction increased significantly in patients with reversible asynergy after both intravenous and intracoronary nitroglycerin. Both intravenous and intracoronary nitroglycerin resulted in significant increases and decreases in distribution of coronary perfusion to the anterior wall. However, these changes were randomly distributed and improved perfusion did not consistently occur with improved wall motion.In conclusion, both intravenous and intracoronary nitroglycerin may reverse wall motion asynergy and produce both favorable and unfavorable changes in perfusion in patients with coronary disease. The common mechanism in improving wall motion with either intravenous or intracoronary nitroglycerin was afterload reduction, suggesting that the systemic effects of nitroglycerin are the most important in reversing asynergy.