Loss of contrast intensity during systole in the left ventricular cavity with the use of the contrast agent Albunex. An analysis of its correlation with pressure and velocity.

RATIONALE AND OBJECTIVES: Several investigators have observed a decrease in video intensity in the left ventricular cavity during systole when using contrast echocardiography. It has been suggested that this phenomenon is related to microbubble instability. The authors propose that this phenomenon is, in part, related to the effects of pressure and velocity on the acoustic reflectance of ultrasound contrast agents. METHODS: Using an in vitro flow tube model and varying concentrations of Albunex contrast agent, the effects of pressure and velocity on microbubble video intensity were investigated. Velocity and pressure were varied independently and the imaging tube was scanned using three transducer frequencies at different concentrations of Albunex. Contrast video intensity was analyzed using high and low velocities (at constant pressure) and high and low pressures (at constant velocity). In addition, the fluid from the system was collected and imaged in a nonflowing reservoir tank to investigate the video intensity of the microbubbles when exposed to variable velocity and pressure. RESULTS: The video-intensity measurements were inversely and irreversibly related to ambient pressure changes (independent of velocity) in a tube model. However, video intensity varied inversely but reversibly with velocity (independent of pressure). This observation could not be explained simply by the "laminar flow" theory, by a change in transducer angulation, nor by a change in ultrasound imaging frame rate. This phenomenon was limited to Albunex microbubbles and was not observed with a contrast medium (corn starch) devoid of the acoustic properties of Albunex.

Ability of the no-reflow phenomenon during an acute myocardial infarction to predict left ventricular dysfunction at one-month follow-up.

Despite angiographically successful opening of an infarct-related vessel within a 6-hour time frame, some patients do not recover left ventricular regional wall function in the infarct zone after an acute myocardial infarction (AMI). Recent evidence suggests that this finding is due to the no-reflow phenomenon, or failure to recover tissue perfusion despite patient epicardial arteries. We performed myocardial contrast echocardiography to assess tissue perfusion before and after opening of an infarct-related artery. Coronary angiograms, regional wall motion scoring, and myocardial contrast enhancement were graded by 3 observers. Of 24 patients with AMI, 7 (29%) failed to recover tissue perfusion in > or = 1 region of myocardium. Of 106 regions subtended by the infarct-related artery, 16 (15%), 43 (41%), and 47 (44%) regions had no-reflow, partial, or normal flow, respectively, after arterial patency was established. There was a spectrum of reperfusion patterns ranging from no-reflow to normal perfusion. One-month follow-up angiographic and myocardial contrast echocardiographic studies were performed in 12 of the 24 patients. At 1 month, all segments of myocardium that had immediate normal perfusion had regained normal wall motion. In contrast, 17 segments that had partial or no-reflow were identified. Of these 17, 3 regained normal function, 10 segments were hypokinetic, and 4 segments were akinetic. We conclude that myocardial contrast echocardiography can be used to identify the no-reflow phenomenon in up to 29% of patients with AMI. Additionally, we found that the immediate-reflow pattern can predict degree of left ventricular dysfunction at 1-month follow-up.

Retrograde cardioplegia does not adequately perfuse the right ventricle.

UNLABELLED: Surgeons often rely primarily on retrograde cardioplegia for myocardial protection, because it provides adequate left ventricular perfusion even in the presence of coronary artery disease. Clinically, however, adequate right ventricular perfusion by retrograde delivery has not been demonstrated. Using intraoperative transesophageal echocardiography, we examined retrograde delivery of cardioplegic solutions by contrast echocardiography, which directly assesses myocardial perfusion. In 15 patients (seven having coronary bypass and eight having valve operations), 4 ml of sonicated Isovue medium was injected retrograde via a coronary sinus catheter. Myocardial perfusion was assessed quantitatively by visual inspection and back-ground-subtracted videodensitometric analysis. In five patients undergoing aortic valve replacement, right and left coronary ostial drainage was estimated during retrograde infusion. Before the aortic crossclamp was removed, myocardial oxygen extraction was calculated in all 15 patients by first delivering warm blood cardioplegic solution for 2 minutes in a retrograde fashion and then taking samples from the cardioplegia line and aortic root. This determined the oxygen extraction ratio across the myocardium at the end of retrograde delivery. Warm blood cardioplegic solution was next given antegrade, and 15 seconds later samples were taken from the cardioplegia line and a right ventricular (acute marginal) vein to determine the oxygen extraction ratio across the right ventricle. As assessed by contrast echocardiography, retrograde infusion resulted in almost four times more perfusion to the left ventricular free wall and septum than to the right ventricular free wall (74 +/- 2 versus 69 +/- 2 versus 20 +/- 2, p < 0.05). In those five patients with an aortotomy the right ostial drainage was less than 5 ml/min whereas left ostial drainage was estimated at 80 ml/min during retrograde administration. Oxygen extraction across the myocardium supplied by retrograde infusion was low after 2 minutes. Conversely, when antegrade cardioplegia was started, right ventricular oxygen extraction rose fourfold (42% +/- 5% versus 11% +/- 1%, p < 0.05), demonstrating that retrograde cardioplegia had not adequately perfused the right ventricular myocardium. CONCLUSIONS: 1. Retrograde cardioplegia provides poor right ventricular myocardial perfusion as assessed by contrast echocardiography and coronary ostial drainage. (2) This poor perfusion is inadequate to meet myocardial demands as demonstrated by the high right ventricular oxygen extraction after a prolonged retrograde infusion. (3) Therefore surgeons must not rely solely on retrograde cardioplegia for right ventricular myocardial protection. This concept is especially important if continuous warm blood cardioplegia is used, because myocardial requirements are then higher.

Warm blood cardioplegic induction: an underused modality.

Warm blood cardioplegic induction (WBCI) improves recovery of cardiogenic shock hearts by repaying their energy debt before cold ischemic arrest. This study tests the hypothesis that despite the absence of shock, many hearts are energy depleted and would benefit from WBCI. Twenty-five consecutive (nonshock) patients undergoing open heart operations received antegrade WBCI. Simultaneous samples were drawn from the aortic root and coronary sinus 15 seconds and 2 minutes after cardiac arrest. Samples were analyzed and compared to determine the oxygen consumption, oxygen extraction ratio, and glucose uptake across the left ventricular myocardium. There was a positive linear correlation between oxygen and glucose uptake (p < 0.001). By univariate analysis, severe multivessel disease and high Parsonnet (severity) score were predictors (p < 0.05) of increased metabolic uptake during warm induction. In addition, patients requiring urgent operations (unstable angina, left main disease, or congestive heart failure) and those with a history of hypertension (coronary artery bypass grafting) or left ventricular overload (valve patients) had higher consumption of oxygen and glucose (p < 0.05) compared with patients undergoing elective operations or those without a history of hypertension. In conclusion, warm cardioplegic induction in nonshocked hearts results in increased metabolic uptake indicating energy repayment and correlates with severity of underlying myocardial disease. The need for WBCI is especially great in patients with a history of hypertension or left ventricular overload and those requiring an urgent operation, where increased metabolic extraction was still present after 2 minutes. In addition, even for completely elective patients, WBCI may be useful if the patient has severe multivessel disease or a high Parsonnet score.

Contrast echocardiography.

Myocardial contrast echocardiography (MCE) is an ultrasound imaging technique which promises to provide a safe, noninvasive means of assessing myocardial perfusion. A contrast agent, consisting of a suspension of air-filled microspheres, serves as an ultrasound tracer. When these microspheres are injected intravascularly, the acoustic interface created between the blood and the microspheres enhances the reflected ultrasound signals. Thus, the flow pattern of the microspheres represent the actual blood flow patterns. This paper will review the field of contrast echocardiography, its background and history, the development of ultrasound contrast agents, and a variety of experimental as well as clinical uses. Contrast echocardiography has been utilized in the cardiac catheterization laboratory for the assessment of "risk area," assessment of collateral blood flow and assessment of coronary blood reserve. In the operating room, contrast echo is utilized for the determination of cardioplegic perfusion, assessment of graft patency and evaluation of valvular regurgitation. In the future, with the technical advancement in ultrasound imaging and the active interest and growth in the field of myocardial perfusion imaging using contrast echocardiography, the ability to provide routine real-time perfusion imaging may become a reality.