Sheila K. Heinle

Assessment of Myocardial Perfusion by Harmonic Power Doppler Imaging at Rest and During Adenosine Stress Comparison With 99mTc-Sestamibi SPECT Imaging

BACKGROUND Harmonic power Doppler imaging (HPDI) is a novel technique for assessing myocardial perfusion by contrast echocardiography in humans. The purpose of this study was to compare myocardial perfusion by HPDI with that obtained by (99m)Tc-sestamibi single photon emission computed tomography (SPECT) during rest and pharmacological stress. METHODS AND RESULTS HPDI was performed on 123 patients who were referred for SPECT imaging for known or suspected coronary artery disease. Images were obtained at baseline and during adenosine infusion (0.14 mg. kg(-)(1). min(-)(1)x6 minutes) in 3 apical views. Myocardial perfusion by HPDI was graded for each coronary territory as absent, patchy, or full. The persistence of absent or patchy myocardial perfusion by HPDI between rest and adenosine was interpreted as a fixed defect, whereas any decrease in perfusion grade was interpreted as a reversible defect. Overall concordance between HPDI and SPECT was 83 (81%) of 103 for normal versus abnormal perfusion. Agreement between the 2 methods for each of the 3 coronary territories was 81% (kappa=0.57) for the left anterior descending artery, 76% (kappa=0.52) for the right coronary artery, and 72% (kappa=0.40) for the left circumflex artery. Discrepancies between the 2 techniques were most notable in the circumflex territory, where fixed defects were observed in 33% by HPDI but in only 14% by SPECT (chi(2)=15.8, P=0.0001). CONCLUSIONS This study demonstrates that HPDI can reliably detect myocardial perfusion during pharmacological stress, although there was a significantly higher number of falsely abnormal results in the circumflex territory.

Spontaneous Variability of Left Ventricular Outflow Tract Gradient in Hypertrophic Obstructive Cardiomyopathy

BACKGROUND Improvement in the left ventricular outflow tract (LVOT) gradient has been used as a means of assessing response to therapy in patients with hypertrophic obstructive cardiomyopathy (HOCM). To our knowledge, no data exist regarding the spontaneous day-to-day variability of the LVOT gradient in patients with HOCM. Defining the magnitude of such variability is critical to properly understand how much improvement in LVOT gradient must be present to invoke a therapeutic response. METHODS AND RESULTS We studied the spontaneous variation in the continuous-wave, Doppler-derived pressure gradient on 5 consecutive days in 12 HOCM patients and 5 aortic stenosis control subjects. While in some patients the day-to-day variability in resting gradient was small, in others it varied markedly. The 95% confidence interval for attributing a change in LVOT gradient to factors other than random variation is +/-32 mm Hg for resting gradient and +/-50 mm Hg for provoked gradient. The mean coefficient of variation for gradient across 5 days for the group was 0.52+/-0.33 for resting gradient and 0.46+/-0.16 for provoked gradient. The day-to-day variability in pressure gradient could not be explained by changes in heart rate, blood pressure, or left ventricular end-diastolic dimension, each of which had a coefficient of variation <.11. Moreover, technical factors related to the performance or interpretation of the studies did not account for it because the coefficient of variation for gradient in aortic stenosis was <10% and interobserver and intraobserver agreement was excellent (r=.96 and .98, respectively). CONCLUSIONS The LVOT pressure gradient varies considerably from day to day in stable patients with HOCM. A single measurement of pressure gradient is not adequate to define the severity of dynamic LVOT obstruction in HOCM.

Effects of afterload reduction on vena contracta width in mitral regurgitation

OBJECTIVES We used color Doppler flow mapping to determine whether vena contracta width (VCW) is a load-independent measure of the severity of mitral regurgitation. BACKGROUND VCW has been proposed to be a relatively load-independent measure of mitral regurgitation severity in flow models using a fixed orifice. However, in patients with mitral regurgitation, VCW may not be load independent because of a dynamic regurgitant orifice. METHODS VCW, effective regurgitant orifice area and regurgitant volume were measured by quantitative Doppler mapping in 31 patients with chronic mitral regurgitation at baseline and during nitroprusside infusion. Patients with rheumatic heart disease, annular calcification or endocarditis were considered to have a fixed regurgitant orifice, whereas patients with mitral valve prolapse, dilated cardiomyopathy or ischemia were considered to have a dynamic regurgitant orifice. RESULTS Systolic blood pressure (148 +/- 27 to 115 +/- 25 mm Hg) and end-systolic wall stress (121 +/- 50 to 89 +/- 36) decreased with nitroprusside (p < 0.05). Although nitroprusside did not significantly change mean values for VCW (0.5 +/- 0.2 to 0.5 +/- 0.2 cm), regurgitant volume (69 +/- 47 to 69 +/- 56 ml) or effective regurgitant orifice area (0.5 +/- 0.4 to 0.5 +/- 0.6 cm2), individual patients exhibited marked directional variability. Specifically, VCW decreased in 16 patients (improved mitral regurgitation), remained unchanged in 7 patients and increased in 8 patients (worsened mitral regurgitation) with nitroprusside. Also, the VCW response to nitroprusside was concordant with changes in effective regurgitant orifice area and regurgitant volume, and was not different between dynamic and fixed orifice groups. CONCLUSIONS Contrary to the results from in vitro studies, VCW is not load independent in patients with mitral regurgitation caused by dynamic changes in the regurgitant orifice. The origin of mitral regurgitation does not predict accurately whether the regurgitant orifice is fixed or dynamic. Finally, short-term vasodilation with nitroprusside may significantly worsen the severity of mitral regurgitation in some patients.

Comparison of Vena Contracta Width by Multiplane Transesophageal Echocardiography With Quantitative Doppler Assessment of Mitral Regurgitation

Mitral regurgitation (MR) severity is routinely assessed by Doppler color flow mapping, which is subject to technical and hemodynamic variables. Vena contracta width may be less influenced by hemodynamic variables and has previously been shown to correlate with angiographic estimates of MR severity. This study was performed to compare mitral vena contracta width by multiplane transesophageal echocardiography (TEE) with simultaneous quantitative Doppler echocardiography in 35 patients with MR. The vena contracta width was measured at the narrowest portion of the MR jet as it emerged through the coaptation of the leaflets; it was identified in 97% of the patients. Vena contracta width correlated well with regurgitant volume (R2 = 0.81) and regurgitant orifice area (R2 = 0.81) by quantitative Doppler technique. A vena contracta width > or = 0.5 cm always predicted a regurgitant volume >60 ml and an effective regurgitant orifice area > or = 0.4 cm2 in all patients. A vena contracta width < or = 0.3 cm always predicted a regurgitant volume <45 ml and a regurgitant orifice area < or = 0.35 cm2. Thus, vena contracta width by multiplane TEE correlates well with mitral regurgitant volume and regurgitant orifice area by quantitative Doppler echocardiography and provides a simple method for the identification of patients with severe MR.

Effect of dobutamine stress echocardiography on mitral regurgitation

OBJECTIVES This study was performed to examine the effect of dobutamine stress echocardiography on mitral regurgitation and to test the hypothesis that mitral regurgitation will increase in patients with an ischemic response. BACKGROUND New or worsening mitral regurgitation during stress testing has been proposed as a marker of ischemia. However, it is unclear whether ischemia induced by dobutamine is associated with mitral regurgitation because the hemodynamic effects of dobutamine may vary with regard to mitral regurgitation, depending on left ventricular function and maximal dose attained. METHODS Dobutamine stress echocardiography was performed in 102 consecutive patients with suspected or known coronary artery disease. Color flow Doppler was used to determine the presence and change in mitral regurgitation at baseline and peak dobutamine infusion (up to 40 micrograms/kg body weight per min). The mitral regurgitation color flow Doppler area was semiquantitatively graded as mild (< 4 cm2), moderate (4 to 8 cm2) or severe (> 8 cm2). Patients were assigned to ischemic and nonischemic groups according to the dobutamine stress echocardiographic results. RESULTS The two groups achieved the same maximal dose and demonstrated similar blood pressure and heart rate responses to dobutamine infusion. Only two patients developed new mitral regurgitation during dobutamine infusion, and both had a normal dobutamine echocardiographic result. More patients without ischemia had no mitral regurgitation compared with patients with ischemia. There was an insufficient number of patients with coronary angiographic data to determine the effects of mitral regurgitation on the sensitivity and specificity of dobutamine stress echocardiography. Of 23 patients with a rest ejection fraction < 50%, 61% had an improvement in mitral regurgitation grade compared with 25% of patients with a rest ejection fraction > or = 50% (p < 0.02). CONCLUSIONS These data indicate that although dobutamine infusion often improves mitral regurgitation in patients with left ventricular dysfunction during stress echocardiography, it does not induce or worsen mitral regurgitation in those who demonstrate an ischemic response. Future studies are necessary, with large numbers of patients, to determine the effects of mitral regurgitation on the sensitivity and specificity of dobutamine stress echocardiography.

Hypotension during dobutamine stress echocardiography: is it related to dynamic intraventricular obstruction?

Although it has been shown that a hypotensive response during dobutamine stress echocardiography is not a marker of coronary artery disease, the mechanism of this response remains unclear. We hypothesize that hypotension during dobutamine stress echocardiography is not related to the development of dynamic intraventricular obstruction. The development of left ventricular outflow obstruction was defined as a late-peaking Doppler velocity profile that exceeded baseline outflow velocity by at least 1 m/sec in 104 consecutive patients undergoing dobutamine stress echocardiography. Left ventricular outflow obstruction was seen in 13% of 15 patients with a hypotensive response (group 1) and in 13% of 89 patients without a hypotensive response (group 2). The mean baseline systolic blood pressure was 157 +/- 21 mm Hg in group 1 compared to 139 +/- 25 mm Hg in group 2 (p = 0.008). An ischemic response to dobutamine infusion as manifested by the development of new or worsening wall motion abnormalities was seen in 40% of group 1 patients and 34% of group 2 patients (p = 0.77). These data demonstrate that a hypotensive response is not related to the development of dynamic intraventricular obstruction during dobutamine stress echocardiography. Rather, there is a significant association between a higher baseline systolic blood pressure and a hypotensive response during dobutamine infusion.

Usefulness of dobutamine echocardiography for detecting restenosis after percutaneous transluminal coronary angioplasty

To determine the usefulness of dobutamine stress echocardiography for detecting restenosis after percutaneous transluminal coronary angioplasty, the results of coronary arteriography and dobutamine stress echocardiography were compared in 103 patients 6 months after percutaneous transluminal coronary angiography. The dobutamine stress echocardiograms were obtained on the same day as the coronary arteriograms, which were analyzed by both quantitative and visual estimates of luminal narrowing. The angiographic restenosis rate was 44% by quantitative and 31% by visual estimates of stenosis. Dobutamine stress echocardiography was abnormal in 38% of previously dilated regions with restenosis and normal in 79% of previously dilated regions without restenosis by quantitative coronary angiography. Dobutamine stress echocardiography was concordant in 69% of 16 patients with multivessel disease compared with 40% of 41 patients with 1-vessel disease (p < 0.05). By quantitative coronary angiography, 64% of patients with significant disease in the left anterior descending artery were identified by dobutamine stress echocardiography compared to 12 and 24% of patients with disease in the left circumflex and right coronary arteries, respectively (p < 0.009). Concordance was seen in 79% of patients with baseline wall motion abnormalities compared with 54% of patients without baseline wall motion abnormalities. Dobutamine stress echocardiography has a low sensitivity but high specificity for detecting restenosis after coronary angioplasty, which may be explained in part by the high prevalence of 1-vessel disease in this patient population. The variables associated with significantly higher degrees of concordance were the presence of left anterior descending artery disease, multivessel disease, and baseline wall motion abnormalities.

Does hypotension during dobutamine stress echocardiography correlate with anatomic or functional cardiac impairment

The development of hypotension during various exercise stress tests has been correlated with the presence of multivessel coronary artery disease and impaired left ventricular contractility. Hypotension may also occur during dobutamine stress echocardiography; however, its anatomic and functional significance remains unknown. As part of an ongoing study of restenosis, dobutamine stress echocardiography and diagnostic cardiac catheterization were performed on the same day in 105 outpatients approximately 6 months after percutaneous coronary revascularization (balloon angioplasty or directional coronary atherectomy) to determine the anatomic and functional significance of dobutamine-induced hypotension. Dobutamine was infused in stepwise increments to a maximum rate of 30 micrograms/kg/min. Hypotension was defined as a reduction in systolic blood pressure of > or = 15 mm Hg. Anatomic abnormalities were defined by quantitative coronary angiography and functional abnormalities by digitized two-dimensional stress echocardiography. Clinical, angiographic, hemodynamic, and electrocardiographic data underwent multivariable regression analysis to determine their ability to predict independently the development of dobutamine-induced hypotension. Dobutamine-induced hypotension was not associated with the presence of severity of coronary artery disease or with echocardiographic wall motion abnormalities. Univariable predictors of stress-induced hypotension included high baseline systolic blood pressure, advanced age, and high left ventricular ejection fraction. Only a high baseline systolic blood pressure contributed independent predictive information in multivariable stepwise logistic regression analysis. Therefore, the development of hypotension during dobutamine stress echocardiography, unlike that during traditional exercise stress tests, is not associated with the presence of significant coronary artery disease or left ventricular dysfunction.

Transesophageal echocardiographic assessment of reversal of systolic pulmonary venous flow in mitral stenosis

Transesophageal echocardiography and diagnostic cardiac catheterization were performed in 36 patients with symptomatic mitral stenosis to assess the incidence and significance of systolic flow reversal in the pulmonary veins. Mitral regurgitation was graded by contrast ventriculography, and left atrial pressure was directly measured after transseptal puncture. Pulmonary venous flow was recorded with transesophageal Doppler imaging from the left upper pulmonary vein. Early systolic flow reversal was identified in 11 patients (31%) and began an average of 58 +/- 13 ms after QRS onset. This pattern correlated strongly with the presence of atrial fibrillation or flutter. Late systolic flow reversal was identified in 8 patients (22%), beginning an average of 245 +/- 46 ms after the QRS complex. These patients had higher left atrial V-wave pressure (36 +/- 10 vs 29 +/- 8 mm Hg; p < 0.05) and V-wave peak-X-descent trough (18 +/- 7 vs 11 +/- 5 mm Hg; p < 0.01) than patients without systolic flow reversal. Neither pattern of pulmonary venous flow reversal was related to the severity of angiographic mitral regurgitation. Systolic reversal of pulmonary venous flow is not specific for angiographically severe mitral regurgitation in patients with mitral stenosis. Similar limitations to pulmonary venous flow analysis likely apply to other patient groups with elevated left atrial pressure and poor left atrial compliance.

Correlation of adenosine echocardiography and thallium scintigraphy.

Echocardiography and thallium-201 imaging with coronary vasodilators such as dipyridamole have been shown to be useful in detecting the presence and prognostic significance of coronary artery disease. Adenosine, a potent and direct coronary vasodilator, has a shorter physiologic half-life than dipyridamole, which exerts its effect by blocking the cellular uptake of adenosine. Because of the potential advantage of dipyridamole, we undertook this study to determine the correlation of adenosine echocardiography with thallium scintigraphy. Forty-two patients (18 men and 24 women; mean age 64) who were unable to undergo treadmill exercise and were known or suspected to have coronary artery disease were studied. A baseline echocardiogram was obtained in four standard views followed by adenosine infusion at a rate of 140 micrograms/kg/min for 6 minutes. Thallium-201 was administered 3 minutes into the infusion while a second echocardiogram was performed. Thallium-201 imaging was begun immediately after the infusion of adenosine and repeated 4 hours later. Sixteen patients underwent coronary angiography within 1 month of the adenosine echocardiogram and thallium-201 study. At the peak infused dose of adenosine there was a significant increase in heart rate (12 beats/min; p = 0.0001) and rate-pressure product (1.3 x 10(3) beats/min x mm Hg; p = 0.02) and statistically insignificant decreases in systolic and diastolic blood pressures. Sixty-two percent of patients experienced side effects during the adenosine infusion, with chest pain, shortness of breath, and flushing occurring most frequently. These side effects resolved within 1 to 2 minutes after the infusion was stopped. Ischemic electrocardiographic changes occurred in 19% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)