Novel parameters of global and regional mitral annulus geometry in man: comparison between normals and organic mitral regurgitation, before and after mitral valve repair.

AIMS: The mitral annulus (MA) saddle shape is complex but vital for a normal functioning mitral apparatus. Although conventional parameters of MA geometry such as area and height are helpful, they fall short of describing its complex regional geometry. METHODS AND RESULTS: In this prospective study, novel parameters of MA curvature and torsion were derived from three-dimensional (3D) transoesophageal echocardiography. These quantitative indices were computed in 15 patients with normal valves (age 53 ± 8 years) and in 15 patients with organic significant mitral regurgitation (MR, age 66 ± 11 years), before and after mitral valve repair (MVR). The MA was traced and modelled in mid- and end-systole. Curvature and torsion were computed at 500 points across the MA to derive regional and global indices. Overall, patients with organic MR presented the smallest global curvature and torsion; this decrease in curvature and torsion reflects a loss of tonicity of the MA tissue. These changes were largely corrected with MVR surgery, to higher values, compared with normals. The regional analysis revealed similar trends. The maximal MA curvature was found to be at the MA 'anterior horn', whereas the MA 'posterior horn' had the lowest curvature values. CONCLUSION: Novel MA parameters of curvature and torsion can be computed from 3D echocardiography and provide quantitative characteristics of dynamic regional MA geometry. In patients with organic MR, the reduced regional and global curvatures improve following surgical MVR. These quantitative parameters may help further refine the quantitative description of MA geometry in various mitral valve pathologies and after MVR.

Tissue Doppler imaging consistently detects myocardial contraction and relaxation abnormalities, irrespective of cardiac hypertrophy, in a transgenic rabbit model of human hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is diagnosed clinically by the presence of left ventricular hypertrophy (LVH). However, LVH is absent in a significant number of genotype-positive patients. Because myocyte dysfunction and disarray are the primary abnormalities in HCM, we reasoned that tissue Doppler imaging could identify contraction and relaxation abnormalities, irrespective of hypertrophy, in a transgenic rabbit model of human HCM. METHODS AND RESULTS: M-mode, 2D, Doppler echocardiography and tissue Doppler imaging were performed in nontransgenic (n=24), wild-type beta-myosin heavy chain-arginine(403) (n=14), and mutant beta-myosin heavy chain-glutamic acid(403) (n=24) transgenic rabbits. Mean septal thicknesses were 2.0+/-0.3, 2.0+/-0.25, and 2.75+/-0.3 mm in the 3 groups, respectively (P:=0.001). LVH was absent in 9 of the 24 mutant rabbits. Left ventricular dimensions, systolic function, heart rate, mitral inflow velocities, and time intervals were similar in the groups. However, the difference between atrial reversal and transmitral A wave duration was increased in the mutant rabbits (P:<0.001). More importantly, systolic and early diastolic tissue Doppler velocities were significantly lower in all mutant rabbits (7.45+/-2.2 versus 10.8+/-2.3 cm/s in nontransgenic and 9. 0+/-0.76 cm/s in wild-type; P:<0.001), including the 9 without LVH. A systolic velocity <8.5 cm/s had an 86% sensitivity and 100% specificity in identifying the mutant transgenic rabbits. CONCLUSIONS: Myocardial contraction and relaxation were reduced in the mutant beta-myosin heavy chain-glutamic acid(403) transgenic rabbit model of human HCM, irrespective of the presence or absence of LVH. In addition, tissue Doppler imaging is more sensitive than conventional echocardiography for HCM screening.

Simultaneous multisite mapping of the right and the left atrial septum in the canine intact beating heart.

BACKGROUND: The spread of activation between the right atrium (RA) and left atrium (LA), particularly along the right and left aspects of the interatrial septum, is not clear. METHODS AND RESULTS: Basket-shaped catheters carrying 64 electrodes were deployed into both the RA and LA of 10 dogs. Position and orientation of the baskets were determined by fluoroscopy and echocardiography. Basket unipolar electrograms were simultaneously recorded in each dog during sinus rhythm, right ventricular pacing, and pacing of the right septum through the basket in the superior and inferior regions. Isochrone maps depicting all aspects of the atria, including the septum, were compared. During sinus rhythm and superior right septal pacing, wave fronts propagated predominantly from superior to inferior regions on both the right and left septum. However, activation of the left septum was delayed compared with the right septum. During right ventricular pacing and inferior right septal pacing, activation of the septum was discordant; 1 wave front propagated rapidly on the right septum from inferior to superior regions, whereas 2 opposing wave fronts originated on the left septum in both the superior and inferior regions. The left septum was activated predominantly by the superior wave front. Activation of the left septum was completed in a significantly shorter time during pacing of the right septum in the inferior region compared with the superior region. CONCLUSIONS: In dogs, activation of the right and left aspects of the interatrial septum is discordant. Electrical connections are present between the RA and LA in regions superior as well as inferior to the septum.

Desmin mutation responsible for idiopathic dilated cardiomyopathy.

BACKGROUND: Idiopathic dilated cardiomyopathy, of which approximately 20% of cases are familial (FDCM), is a primary myocardial disorder characterized by ventricular dilatation and impaired systolic function. It is a common cause of heart failure and the need for cardiac transplantation. Although 6 chromosomal loci responsible for autosomal dominant FDCM have been mapped by linkage analysis, none of these genes have been identified. By use of the candidate-gene approach, actin was identified recently as being responsible for dilated cardiomyopathy. Considerable evidence suggests desmin, a muscle-specific intermediate filament, plays a significant role in cardiac growth and development. METHODS AND RESULTS: To determine whether a defect of desmin induces dilated cardiomyopathy, 44 probands with FDCM underwent clinical evaluation and DNA analysis. Diagnostic criteria, detected by echocardiography, consisted of ventricular dimension of >/=2.7 cm/m(2) with an ejection fraction

Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy.

BACKGROUND: Conventional Doppler parameters are unreliable for estimating left ventricular (LV) filling pressures in hypertrophic cardiomyopathy (HCM). This study was undertaken to evaluate flow propagation velocity by color M-mode and early diastolic annular velocity (Ea) by tissue Doppler 2 new indices of LV relaxation, combined with mitral E velocity for estimation of filling pressures in HCM. METHODS AND RESULTS: Thirty-five HCM patients (52+/-15 years) underwent LV catheterization simultaneously with 2-dimensional and Doppler echocardiography. Pulsed Doppler echocardiography of mitral and pulmonary venous flows was obtained along with flow propagation velocity and Ea. LV preA pressure had weak or no relations with mitral, pulmonary venous velocities and atrial volumes. In contrast, preA pressure related strongly to E velocity/flow propagation velocity (r=0.67; SEE=4) and E/Ea (r=0.76; SEE=3.4). In 17 patients with repeat measurements, preA pressure changes were well detected by measuring E velocity/flow propagation velocity (r=0.68; P=0.01) or E/Ea (r=0.8; P<0.001). PreA pressure estimation with these 2 methods was tested prospectively in 17 additional HCM patients with good results (E velocity/flow propagation velocity, r=0.76; E/Ea, r=0.82). CONCLUSIONS: LV filling pressures can be estimated with reasonable accuracy in HCM patients by measuring E velocity/flow propagation velocity or E/Ea. These ratios also track changes in filling pressures.

Tissue Doppler imaging consistently detects myocardial abnormalities in patients with hypertrophic cardiomyopathy and provides a novel means for an early diagnosis before and independently of hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH), the clinical hallmark of familial hypertrophic cardiomyopathy (FHCM), is absent in a significant number of subjects with causal mutations. In transgenic rabbits that fully recapitulate the FHCM phenotype, reduced myocardial tissue Doppler (TD) velocities accurately identified the mutant rabbits, even in the absence of LVH. We tested whether humans with FHCM also consistently showed reduced myocardial TD velocities, irrespective of LVH. METHODS AND RESULTS: We performed 2D and Doppler echocardiography and TD imaging in 30 subjects with FHCM, 13 subjects who were positive for various mutations but did not have LVH, and 30 age- and sex-matched controls (all adults; 77% women). LV wall thickness and mass were significantly greater in FHCM subjects (P<0.01 versus those without LVH and controls). There were no significant differences in 2D echocardiographic, mitral, and pulmonary venous flow indices between mutation-positives without LVH and controls. In contrast, systolic and early diastolic TD velocities were significantly lower in both mutation-positives without LVH and in FHCM patients than in controls (P<0.001). Reduced TD velocities had a sensitivity of 100% and a specificity of 93% for identifying mutation-positives without LVH. CONCLUSIONS: Myocardial contraction and relaxation velocities, detected by TD imaging, are reduced in FHCM, including in those without LVH. Before and independently of LVH, TD imaging is an accurate and sensitive method for identifying subjects who are positive for FHCM mutations.

Relation of the contractile reserve of hibernating myocardium to myocardial structure in humans.

BACKGROUND: Although dobutamine echocardiography (DE) is widely used to assess myocardial viability in humans, little is known about the relation between contractile reserve and myocardial structure. METHODS AND RESULTS: We evaluated 20 patients with coronary disease (64+/-13 years old, ejection fraction 28+/-7.5%) with DE (up to 40 micrograms . kg(-1). min(-1)), rest-redistribution (201)Tl single photon emission CT, and quantitative angiography before bypass surgery. During surgery, patients underwent transmural myocardial biopsies (n=37) guided by transesophageal echocardiography to determine the extent of interstitial fibrosis and intracellular and interstitial proteins by histopathology and immunohistochemistry. Among the 37 segments biopsied, 16 recovered function as assessed 2 to 3 months later. Segments with postoperative functional recovery had more wall thickening at low-dose DE (28% versus 3%, P<0.001), higher thallium uptake (69% versus 48%, P=0.03), and less interstitial fibrosis (2% versus 28%, P<0.001). Quantitative angiographic parameters did not predict recovery of function. Segments with DE viability (contractile reserve and/or ischemia) had less fibrosis (2.7% versus 28%, P<0.001), less vimentin and fibronectin (both P<0.01), more glycogen (P=0.016), and higher thallium uptake (64% versus 35.5%, P<0.05) than those without viability. Viable segments by both DE and thallium had less fibrosis (1%) than those viable by 1 of the 2 techniques (9%) or not viable by both (28%, P=0.005). Thickening at low-dose DE correlated well with the extent of interstitial fibrosis (r=-0.83, P<0.01). CONCLUSIONS: Contractile reserve during DE correlates inversely with the extent of interstitial fibrosis and the amount of fibronectin and vimentin and directly with rest-redistribution thallium uptake.

Deceleration time in ischemic cardiomyopathy: relation to echocardiographic and scintigraphic indices of myocardial viability and functional recovery after revascularization.

BACKGROUND: In patients with heart failure secondary to left ventricular (LV) systolic dysfunction, a short deceleration time (DT) successfully predicts clinical outcome. The impact of myocardial viability and revascularization on the mitral inflow velocities, however, is unknown. METHODS AND RESULTS: Forty patients with ischemic cardiomyopathy underwent (201)Tl scintigraphy (SPECT) and 2D, Doppler, and dobutamine echocardiography (DE, to 40 microg. kg(-1). min(-1)) 2 days before CABG. Echocardiography was repeated 3 months after revascularization to determine recovery of function. Significant correlations were present between DT and LV contractile reserve by DE (r=0.72), scar perfusion defect by SPECT (r=-0.69), and the change in ejection fraction (DeltaEF) after surgery (r=0.77) (all P:<0.01). DT >150 ms effectively identified (sensitivity 79%, specificity 81%) patients with DeltaEF >/=5%. The population was divided into 2 groups according to DT: group 1 (DT >150 ms, n=21) and group 2 (DT

Altered adrenergic receptor density in myocardial hibernation in humans: A possible mechanism of depressed myocardial function.

BACKGROUND: Alterations in adrenergic receptor densities can potentially contribute to myocardial dysfunction. Their relevance to myocardial hibernation in humans is unknown. METHODS AND RESULTS: Accordingly, 22 transmural myocardial biopsies were obtained in 11 patients with ischemic ventricular dysfunction during bypass surgery, guided by transesophageal echocardiography. Patients underwent dobutamine echocardiography (DE) and rest scintigraphic studies before revascularization and DE at 3 to 4 months. alpha- and ss-receptor density (ARD and BRD) and extent of fibrosis were quantified from the myocardial biopsies. Of the 22 segments, 16 had abnormal rest function and 6 were normal. Severely hypokinetic or akinetic segments showed a 2.4-fold increase in ARD with a concomitant 50% decrease in BRD compared with normal segments. An increase in ARD, a decrease in BRD to a lesser extent, and thus an increase in ARD/BRD ratio were seen in dysfunctional segments with contractile reserve compared with normal segments and were most pronounced in those without contractile reserve (P:<0.001). Similar findings were observed if recovery of function or scintigraphic uptake was analyzed as a marker for viability. No significant relation between either ARD or BRD and percent myocardial fibrosis was noted (r=0.37 and -0.39, respectively). CONCLUSIONS: Thus, graded and reciprocal changes in alpha- and ss-adrenergic receptor densities occur in viable, hibernating myocardium and may account in part for the observed depression in resting myocardial function and preserved contractile reserve in this entity.

Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a genetic disease characterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (LV) dysfunction. We have proposed that hypertrophy and fibrosis, the major determinants of mortality and morbidity, are potentially reversible. We tested this hypothesis in beta-myosin heavy chain-Q(403) transgenic rabbits. METHODS AND RESULTS: We randomized 24 beta-myosin heavy chain-Q(403) rabbits to treatment with either a placebo or simvastatin (5 mg. kg(-1). d(-1)) for 12 weeks and included 12 nontransgenic controls. We performed 2D and Doppler echocardiography and tissue Doppler imaging before and after treatment. Demographic data were similar among the groups. Baseline mean LV mass and interventricular septal thickness in nontransgenic, placebo, and simvastatin groups were 3.9+/-0.7, 6.2+/-2.0, and 7.5+/-2.1 g (P<0.001) and 2.2+/-0.2, 3.1+/-0.5, and 3.3+/-0.5 mm (P=0.002), respectively. Simvastatin reduced LV mass by 37%, interventricular septal thickness by 21%, and posterior wall thickness by 13%. Doppler indices of LV filling pressure were improved. Collagen volume fraction was reduced by 44% (P<0.001). Disarray was unchanged. Levels of activated extracellular signal-regulated kinase (ERK) 1/2 were increased in the placebo group and were less than normal in the simvastatin group. Levels of activated and total p38, Jun N-terminal kinase, p70S6 kinase, Ras, Rac, and RhoA and the membrane association of Ras, RhoA, and Rac1 were unchanged. CONCLUSIONS: Simvastatin induced the regression of hypertrophy and fibrosis, improved cardiac function, and reduced ERK1/2 activity in the beta-myosin heavy chain-Q(403) rabbits. These findings highlight the need for clinical trials to determine the effects of simvastatin on cardiac hypertrophy, fibrosis, and dysfunction in humans with hypertrophic cardiomyopathy and heart failure.

Pseudoaneurysms of the mitral-aortic intervalvular fibrosa: dynamic characterization using transesophageal echocardiographic and Doppler techniques.

OBJECTIVES: The aim of this study was to provide a detailed description of echocardiographic and Doppler features of pseudoaneurysms involving the mitral-aortic intervalvular fibrosa and to compare echocardiographic and aortographic findings. BACKGROUND: Infection of the aortic valve may spread to the aortic annulus, resulting in ring abscesses or pseudoaneurysms, or both, of the intervalvular fibrosa, which can alter patient management and prognosis. METHODS: The echocardiographic and Doppler findings of 20 patients with pseudoaneurysms or ring abscesses, or both, were reviewed and compared with surgical and aortographic results. RESULTS: A total of 23 lesions were identified, of which 16 were intervalvular pseudoaneurysms, and 7 were ring abscesses. Transthoracic echocardiography detected 43% of the lesions, whereas transesophageal echocardiography identified 90% (p < 0.01). The most distinct feature of the pseudoaneurysms was marked pulsatility, with systolic expansion and diastolic collapse (mean systolic area [+/- SD] 4.1 +/- 3.4 cm2 vs. diastolic mean area 1.8 +/- 2.2 cm2, p < 0.05). Using color Doppler, two types were identified: unruptured pseudoaneurysms (n = 9), which communicated only with the left ventricular outflow tract and had a distinct flow pattern, and ruptured pseudoaneurysms (n = 7), which, in addition, communicated with the left atrium or aorta. Compared with pseudoaneurysms, ring abscesses were smaller and nonpulsatile and showed either no flow or continuous systolic and diastolic flow, the site of paravalvular aortic insufficiency. In 10 patients who underwent aortography, three lesions were identified, and findings were concordant with echocardiography. However, in seven patients aortographic findings were normal, whereas echocardiography identified intervalvular pseudoaneurysms, all of which were documented at operation. CONCLUSIONS: Intervalvular pseudoaneurysms are more frequently detected by transesophageal echocardiography than by aortography or transthoracic examination and exhibit distinct dynamic features and Doppler patterns that can further help characterize cavitary lesions in the aortic root and guide appropriate surgical intervention.

Determination of left ventricular volumes with use of a new nongeometric echocardiographic method: clinical validation and potential application.

A new nongeometric echocardiographic technique for measurement of right and left ventricular volumes was recently validated in vitro. With this method, all images are taken from one point on the chest wall as the transducer is tilted through the ventricle. This approach offers several advantages. No geometric assumptions about ventricular shape are made. All images are acquired from the best echocardiographic window. Furthermore, the digitized points can be used to make a three-dimensional reconstruction of the ventricle. The present study addresses the clinical feasibility of imaging the heart from a single pivoting point in short axis and compares the accuracy of the method in determining left ventricular volumes with that of biplane cineangiography. Twenty-four patients underwent echocardiographic studies within 2 h before angiography. At catheterization, volumes determined by the biplane area-length method ranged between 95 and 368 ml at end-diastole and between 15 and 303 ml at end-systole. A good correlation was observed between ventricular volumes by angiography and echocardiography at end-diastole and end-systole (r = 0.92 and 0.96, respectively). Correlations between volumes by the two techniques were equally good in patients with wall motion abnormalities (n = 13; r = 0.97). Ventricular ejection fraction ranged between 18% and 84% at angiography and correlated well with echocardiographic measurements (r = 0.82). Thus, the echocardiographic tilt method provides accurate determination of left ventricular volume and ejection fraction. This nongeometric method offers the potential for the determination of right ventricular volume and three-dimensional display of the heart.

Diagnosis of ischemic heart disease with adenosine echocardiography.

To assess the feasibility, safety and diagnostic accuracy of adenosine infusion combined with echocardiography, 73 patients with suspected or known coronary artery disease underwent echocardiography at baseline and during a maximal intravenous adenosine infusion of 140 micrograms/kg per min. Compared with baseline values, adenosine caused an increase in heart rate, a decrease in systolic and diastolic blood pressure and a slight but significant increase in rate-pressure product. The echocardiographic images were digitized and randomly assigned in a quad-screen format for nonbiased interpretation. An ischemic response, defined as a new or worsening wall motion abnormality, developed in 25 patients; a fixed wall motion abnormality was present in 27 and no abnormality in 21. All patients underwent coronary angiography. The sensitivity of adenosine echocardiography for greater than or equal to 75% coronary artery diameter stenosis was 85% (46 of 54), with a specificity of 92% in patients with normal coronary arteries. In the 35 patients with a normal baseline electrocardiogram the sensitivity was 60%; 9 (82%) of 11 patients with multivessel disease were correctly identified. The sensitivity for adenosine electrocardiography (greater than or equal to 1-mm ST depression) was 35% with a specificity of 100%. Side effects were transient and mild; aminophylline was used in two patients. Thus, ischemic changes can be induced in patients with coronary artery disease with intravenous adenosine that, combined with echocardiography, is sensitive for the assessment of ischemic heart disease, particularly in patients with multivessel disease.

Quantitative assessment of left ventricular wall motion by two-dimensional echocardiography: validation during reversible ischemia in the conscious dog.

This study was designed to test the accuracy of echocardiographic radial shortening measurements during variable degrees of regional dysfunction produced by 14 transient (less than or equal to 10 min) coronary occlusions (8 left anterior descending coronary artery, 6 left circumflex coronary artery) followed by up to 24 h of reperfusion in chronically instrumented conscious dogs. Independent measurement of regional myocardial thickening was obtained using epicardial pulsed Doppler probes and served as a standard for comparison. Radial shortening fraction was derived from two-dimensional short-axis views along 12 equidistant radii. Six reference systems from the epicardial and endocardial centers of geometry (centroids) in a fixed or a floating position were explored. In the ischemic zone, percent thickening fraction averaged 22 +/- 5% at baseline, decreased to -4 +/- 4% during occlusion and gradually returned to baseline values after reperfusion. Percent change in radial shortening correlated significantly with percent change in thickening fraction in the ischemic zone. The worst correlation was seen with the floating endocardial centroid (r = 0.68), and the best was observed with the epicardial floating reference (r = 0.91). Moreover, the epicardial floating reference provided narrower 95% confidence limits of radial shortening and less heterogeneity among radii than did fixed reference systems. Thus, compared with an independent standard, echocardiographic measurement of radial shortening from the short axis provided recognition of discrete grades of regional dysfunction induced by transient reversible ischemia. This technique may be amenable for serial assessment of regional function after interventions on the ischemic myocardium.

Estimation of left ventricular end-diastolic pressure from Doppler transmitral flow velocity in cardiac patients independent of systolic performance.

In patients with heart disease, changes in left ventricular filling pressures produce alterations in the Doppler transmitral flow velocity and isovolumetric relaxation time. This investigation explored the hypothesis that combining isovolumetric relaxation time with measurements derived from the transmitral flow velocity can be used to estimate left ventricular end-diastolic pressure. Simultaneous Doppler and left ventricular pressure recordings were obtained in 33 patients (24 men with a mean age of 58 +/- 11 years) and an ejection fraction ranging from 15% to 74% (mean 55 +/- 15%). The following Doppler measurements correlated significantly with left ventricular end-diastolic pressure (range 4 to 36 mm Hg): isovolumetric relaxation time (IVRT; r = -0.73), atrial filling fraction (AFF; r = -0.66), deceleration time (DT; r = -0.59), ratio of early transmitral flow velocity to atrial flow velocity (E/A ratio; r = -0.53) and time from termination of mitral flow to the electrocardiographic R wave (MAR; r = 0.37). Combining these measurements into a multilinear regression equation provided a more accurate estimate of end-diastolic pressure (LVEDP; r = 0.80; SEE = 7.4). The equation LVEDP = 46 -0.22 IVRT -0.10 AFF -0.03 DT -(2 divided by E/A) + 0.05 MAR was tested prospectively in 26 additional patients (mean age 55 +/- 11 years; ejection fraction 41 +/- 23%) with simultaneous Doppler and hemodynamic recordings but with the two measurements made independently, in blinded fashion, by additional observers. Estimated and measured end-diastolic pressures correlated well with each other (r = 0.86).(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of regional myocardial perfusion by contrast echocardiography. II. Detection of changes in transmural and subendocardial perfusion during dipyridamole-induced hyperemia in a model of critical coronary stenosis.

Measurements of myocardial contrast (sonicated meglumine diatrizoate) intensity were compared with myocardial flow by radioactive microspheres before and after administration of dipyridamole (0.5 mg/kg body weight intravenously) in 10 open chest dogs with a critical stenosis in the left circumflex coronary artery. Computer measurements of contrast time-intensity curves corrected for background myocardial intensity were made along 12 transmural segments of the left ventricle at mid-papillary level and for the subendocardial and subepicardial half of each segment. After administration of dipyridamole, transmural flow in the control region increased significantly (p less than 0.001), resulting in a dipyridamole/baseline flow ratio (i.e., coronary reserve ratio) of 2.54 +/- 0.95. Similar changes (p less than 0.001) were seen by contrast echocardiography; the coronary reserve ratio was 2.10 +/- 0.60 with use of peak intensity and 3.48 +/- 1.58 with use of area under the time-intensity curve. In contrast, no significant changes were observed in myocardial flow, peak contrast intensity or area under the curve in the ischemic region after dipyridamole. In the control region the ratio of subendocardial to subepicardial flow was similar at baseline and after dipyridamole administration as assessed by microspheres (1.08 +/- 0.24 versus 1.17 +/- 0.25) or by area under the time-intensity curve (1.11 +/- 0.45 versus 1.11 +/- 0.56). In the ischemic region, the subendocardial/subepicardial flow ratio decreased significantly after dipyridamole administration as measured by microspheres (1.15 +/- 0.19 to 0.82 +/- 0.25; p less than 0.001) or by area under the curve (1.10 +/- 0.28 to 0.70 +/- 0.47; p less than 0.01). Thus, myocardial contrast echocardiography appears to be a sensitive technique with which to detect changes in myocardial flow induced by dipyridamole in the various myocardial layers of normal segments as well as of segments supplied by a critically stenotic coronary artery.

Pathologic correlates of aortic plaques, thrombi and mobile "aortic debris" imaged in vivo with transesophageal echocardiography.

OBJECTIVES: This study sought to evaluate the pathologic correlates of aortic atheromas, thrombi and mobile "aortic debris" imaged in vivo by transesophageal echocardiography (TEE). BACKGROUND: Atherosclerotic plaques with various complexity, thrombi and debris are frequently identified by TEE during imaging of the aorta. However, pathologic data to characterize these lesions imaged in vivo are lacking. METHODS: Intraoperative TEE was performed prospectively in 31 patients undergoing repair of aortic aneurysm or dissection. TEE was used to guide the surgeon to mark aortic areas of interest that were sent for pathologic examination. A four-point scoring system was used for both TEE and pathologic evaluation to grade the degree of involvement of the aortic wall with atheroma. Ultrasound video intensity of the aortic wall lesions was measured and compared with quantitative measures of wall composition at pathologic examination. The presence of thrombi and mobile aortic debris by TEE was noted and compared with pathologic findings. RESULTS: Histologic-TEE correlations were possible in 62 aortic segments. There was 73% exact agreement between TEE and pathologic grading. Discrepancies were mostly in the inability of TEE to detect superficial ulcerations. However, separation of normal aorta and minimal intimal thickening (grades I and II) from more complex atheromas (grades III and IV) was observed in 93%. For identification of thrombus, TEE had a sensitivity of 91% (29 of 32 segments) and a specificity of 90% (27 of 30 segments). Mobile aortic debris were identified in six aortic segments and were confirmed at pathologic examination to be thrombi. Ultrasound video intensity increased with worsening complexity of atheroma and related significantly to aortic plaque composition at pathologic evaluation (r = 0.80, p < 0.0001). Ultrasound intensity of thrombi and mobile debris was similar and was lower than that of complex atheromas. CONCLUSIONS: Thus, in the evaluation of aortic pathologic segments, TEE can assess aortic plaque complexity and identify thrombus formation, findings that may have important therapeutic implications.

Serial changes in response of hibernating myocardium to inotropic stimulation after revascularization: a dobutamine echocardiographic study.

OBJECTIVES: We sought to evaluate the serial changes in the response of the hibernating myocardium to dobutamine stimulation after revascularization. BACKGROUND: An improvement in myocardial contraction during dobutamine stress echocardiography (DSE), particularly a biphasic response, predicts recovery of rest function. However, little is known about the changes in the response of the myocardium to dobutamine after revascularization. METHODS: Thirty-four patients with stable coronary artery disease and regional left ventricular dysfunction underwent DSE before, early (within 1 week) and late (>6 weeks) after coronary angioplasty. Dobutamine was given in incremental doses from 2.5 to 40 microg/kg body weight per min. RESULTS: Of 180 revascularized segments with severe rest dysfunction, recovery of rest function was seen in 56 segments (31%) late after angioplasty, 80% of which had early recovery. Ventricular function during DSE was similar early and late after revascularization. Patients who showed a biphasic response to DSE before revascularization (n = 12) had the most improvement in function at rest (mean [+/-SD] wall motion score index [WMSI] 1.98 +/- 0.75 vs. 1.35 +/- 0.54, p < 0.05) and during DSE (2.11 +/- 0.67 vs. 1.21 +/- 0.41, p < 0.05) late after revascularization. Patients with sustained improvement during DSE before revascularization had no significant change in wall motion during DSE after angioplasty. However, patients without improvement in function at low dose DSE, who demonstrated worsening of function at a high dose, had significant augmentation in wall motion during DSE after revascularization (WMSI 2.16 +/- 0.50 vs. 1.60 +/- 0.57, p < 0.05). Patients who had no recovery of rest function had significant improvement in wall motion response to DSE, particularly when ischemia was inducible before revascularization. CONCLUSIONS: In myocardial hibernation, the majority of recovery of rest function occurs early after revascularization. Although patients who recover rest function show the most marked improvement in wall motion during DSE, those without recovery of rest function also have improved function during DSE, particularly when there is evidence of ischemia before revascularization.

Differentiating thrombus from pannus formation in obstructed mechanical prosthetic valves: an evaluation of clinical, transthoracic and transesophageal echocardiographic parameters.

OBJECTIVES: We sought to determine the clinical and echocardiographic parameters that differentiate thrombus from pannus formation as the etiology of obstructed mechanical prosthetic valves. BACKGROUND: Distinction of thrombus from pannus on obstructed prosthetic valves is essential because thrombolytic therapy has emerged as an alternative to reoperation. METHODS: We analyzed clinical, transthoracic and transesophageal echocardiography (TEE) data in 23 patients presenting with 24 obstructed prosthetic valves and compared the findings to pathology at surgery. RESULTS: Fourteen valves had thrombus and 10 had pannus formation. Patients with thrombus had a shorter duration from time of valve insertion to malfunction, shorter duration of symptoms, but similar New York Heart Association functional class at the time of operation. Patients with thrombus had a lower rate of adequate anticoagulation (21% vs. 89%; p=0.0028). Pannus formation was more common in the aortic position (70% vs. 21%; p=0.035). Abnormal prosthetic valve motion was detected by TEE in all cases with thrombus formation but in 60% with pannus (p=0.0198). Thrombi were larger than pannuses (total length 2.8+/-2.47 cm vs. 1.17+/-0.43 cm; p=0.038). This was mostly due to extension of thrombi into the left atrium in prosthetic mitral valves. Thrombi appeared as a soft mass on the valve in 92% of cases, whereas 29% of pannuses had a soft echo density (p= 0.007). Ultrasound video intensity ratio, derived as the videointensity of the mass to that of the prosthetic valve, was lower in the thrombus group (0.46+/-0.14 vs. 0.71+/-0.17, p=0.006). A videointensity ratio of <0.70 had a positive predictive value of 87% and a negative predictive value of 89% for thrombus. Duration from onset of symptoms to reoperation of <1 month separated thrombus from pannus formation. The best objective clinical parameter for prediction of thrombus was inadequate anticoagulation, whereas the best TEE parameters were qualitative and quantitative ultrasound intensity of the mass. The presence of either inadequate anticoagulation or a soft mass by TEE improved the predictive power of either parameter alone and was similar to that of ultrasound videointensity ratio. CONCLUSIONS: Duration of symptoms, anticoagulation status and qualitative and quantitative ultrasound intensity of the mass obstructing a mechanical prosthetic valve can help differentiate pannus formation from thrombus and may therefore be of value in refining the selection of patients for thrombolytic therapy of prosthetic valve obstruction.

Myocardial viability during dobutamine echocardiography predicts survival in patients with coronary artery disease and severe left ventricular systolic dysfunction.

OBJECTIVES: The purpose of this study was to assess whether the presence or absence of myocardial viability during dobutamine echocardiography (DE) predicts survival in patients with coronary artery disease (CAD) and severe left ventricular (LV) dysfunction. BACKGROUND: In patients with CAD, the presence of myocardial viability during DE identifies viable myocardium and predicts recovery of LV systolic function after revascularization. However, there is little data on the relation between myocardial viability and clinical outcome in patients with CAD and severe LV dysfunction. METHODS: We studied 318 patients with CAD and a LV ejection fraction (EF) < or =35% who underwent DE and were followed for 18+/-10 months. Patients were classified into four groups. Group I (n=85) consisted of patients who had evidence of myocardial viability and subsequently underwent revascularization. Group II (n=119) consisted of patients with myocardial viability who did not undergo revascularization. Group III (n=30) consisted of patients who did not have myocardial viability and underwent revascularization. Finally, group IV (n=84) patients lacked myocardial viability and did not undergo revascularization. RESULTS: The four groups had similar baseline characteristics and rest LVEF. During follow-up there were 51 deaths (16%). The mortality rate was 6% in group I, 20% in group II, 17% in group III and 20% in group TV (p=0.01, group I vs. other groups). CONCLUSIONS: In patients with CAD and severe LV dysfunction who demonstrated myocardial viability during DE, revascularization improved survival compared with medical therapy.