Myocardial infarction during coronary artery bypass surgery.

Ventricular aneurysms are circumscribed, thin-walled fibrous, noncontractile outpouchings of the ventricle. The majority are apically located, true aneurysms of the left ventricle (LV) that occur as a consequence of transmural myocardial infarction (MI). The precursor of aneurysm formation appears to be infarct expansion early after acute MI and occurrence generally relates to infarct size. The presence of underlying hypertension and the use of steroids and nonsteroidal antiinflammatory agents may promote aneurysm formation. The clinical sequelae include congestive heart failure (CHF), thromboembolism, angina pectoris, and ventricular tachyarrhythmias. Late rupture is a particular complication of false aneurysms in which the pericardium is the aneurysm wall. The diagnosis may be suspected by the clinical finding of a diffuse, pansystolic apical thrust, persistent ST-segment elevation on the electrocardiogram, and distortion of the cardiac silhouette on chest x-ray. This can be confirmed using echocardiography, radionuclide ventriculography, and cardiac catheterization. The latter has the additional advantage of being able to delineate the coronary anatomy. Management involves prevention, specific therapy for the various clinical manifestations, and surgery. Therapeutic interventions with thrombolytic agents, aspirin, heparin, and beta blockers that are applied early in the evolution of an MI may limit infarction size, thereby reducing the tendency toward infarct expansion and aneurysm formation. Patients with mild CHF can usually be controlled with the standard combination of angiotensin-converting enzyme inhibitors, diuretics, and digoxin. Thromboembolism is best prevented by anticoagulation with warfarin for at least 3 months after the acute MI. The choice of pharmacotherapy for ventricular tachyarrhythmias should be guided by electrophysiologic studies. The treatment of patients with angina pectoris utilizes conventional therapeutic modalities.(ABSTRACT TRUNCATED AT 250 WORDS)

https://onlinelibrary.wiley.com/doi/pdf/10.1002/clc.4960180905

Postinfarction ventricular aneurysms.

Typical three dimensional (3D) reconstruction techniques of coronary arteries from intravascular ultrasound (IVUS) have assumed that the artery was straight and disregarded the angular orientation of IVUS slices. The authors achieved accurate 3D reconstruction of coronary arteries by following the transducer in time with the aid of biplane angiograms. Simultaneously acquired IVUS images were then placed perpendicular to the transducer path. Angular orientation of the IVUS slices was determined by using the lumen outlines and the biplane contrast angiograms. Tracking the transducer eliminates the need for assisted pullback, making the procedure more accurate and suitable for clinical use. The reconstruction algorithm was evaluated for consistency using a self-validation scheme that created simulated angiograms, which were then compared with acquired angiograms. A good correlation (rep to 68% area overlap) was found between the two.

Fusion of intravascular ultrasound and biplane angiography for three-dimensional reconstruction of coronary arteries

The enhanced echocontrast associated with the gas microbubbles produced when a liquid is rapidly injected into a large blood vessel was first reported by Gramiak and Shah in 1968 [1]. Twenty-eight years later, microbubbles remain the standard echocontrast enhancers. They have been used clinically to verify the presence of intracardiac shunts [2] and valvular regurgitation [3, 4] and for the measurement of cardiac output [5]. Contrast echocardiography (CE) has also been used as a means of defining myocardial perfusion non-invasively [6]. In recent times this rapidly developing diagnostic technique has been more accurately named myocardial contrast two-dimensional echocardiography (MC-2DE). Contrast enhancers have extended the applications of cardiac color Doppler imaging, and gas bubbles have also found applications outside the cardiovascular system, in establishing tubal patency during investigations of infertility and in the diagnostic evaluation of potential malignancies [7, 8]. In the early days of CE, clinical investigators speculated that the gaseous microbubbles present in the echocontrast agents (ECA) were probably the source of the observed contrast [6, 9]. This discovery was confirmed [10–13] and it is now accepted that the ultrasonic targets in contrast-enhanced ultrasonography are the microbubbles themselves.

Echo-enhancing agents: safety

Myocardial contrast echocardiography (MCE) with high-mechanical-index (MI), triggered harmonic imaging is the best-established technique to date for the assessment of myocardial perfusion. A high signal-to-noise ratio, which is significantly influenced by precontrast tissue signals, is an important prerequisite. Our goal was to evaluate the efficacy of ultraharmonic MCE, a technique that rejects tissue signals by receiving signals beyond the second but below the third harmonic. Imaging was performed in 6 closed-chest dogs and in 15 healthy volunteers (11 of whom also had dipyridamole stress). Analyses of videointensity (VI) confirmed uniformly low precontrast tissue VI, a significant increase of postcontrast VI (before and after dipyridamole), and a significant decrease in VI after microbubble destruction. We conclude that ultraharmonic MCE produces low precontrast tissue signals, thus optimizing postcontrast myocardial opacification, and exhibits efficient microbubble destruction with use of multiple-frame triggering. Thus this new technique opens up a new possibility of further optimizing coronary microcirculation imaging with microbubbles.

Ultraharmonic myocardial contrast imaging : In vivo experimental and clinical data from a novel technique

This study was performed to examine the transmural (endocardial vs. epicardial) heterogeneity of myocardial blood flow during the cardiac cycle (systole vs. diastole). Twenty-four contrast echocardiographic injections were performed in seven open-chest anesthetized dogs either into left anterior descending or circumflex coronary artery or into the aortic root. Two-dimensional echocardiography in short-axis view was performed and was digitized off-line into a 256 x 256 pixel matrix with 256 gray levels/pixel. All end-diastolic and end-systolic frames before and to peak contrast were analyzed. A region of interest corresponding to the most intensely opacified myocardial segment was traced, the mean videodensity measured, and the frame of initial contrast appearance detected. The region of interest was divided into three equal parallel layers corresponding to the endocardial, midcardial, and epicardial myocardium. When the echocardiographic contrast effect initially appeared in diastole, the increment in videodensity was greater for the endocardium (131 +/- 48%) than for the epicardium (71 +/- 37% of the increment in videodensity of the entire wall) (p less than 0.05). This inhomogeneity subsequently disappeared in the following end-systolic frame. When the initial echocardiographic contrast effect appeared in systole, intensity was higher in epicardium (136 +/- 83%) than in endocardium (60 +/- 60%) (p less than 0.05). However, in the following diastole, intensity was not significantly different for the two layers. Thus, myocardial contrast echocardiography demonstrates that coronary blood flow is primarily subendocardial in distribution during diastole and subepicardial during systole.

Se Nissen

Papers

Nonuniformity of the transmural distribution of coronary blood flow during the cardiac cycle. In vivo documentation by contrast echocardiography.

Automated identification of luminal and medial adventitial borders in intravascular ultrasound images of human coronary arteries