Change In Ventricular Diameter Research Articles

Field-of-view zoom during a single-shot short-axis image for cardiac contraction correction

Summary Evaluate a new method correcting for cardiac contraction during each single-shot image. Background Cardiac motion during a single-shot image causes blurring along the phase-encode axis and dark rim artefact (1). We attempt to correct for myocardial contraction during short-axis single-shot acquisition, to optimise subendocardial myocardium. Methods A myocardial perfusion sequence (balanced SSFP) was modified to vary field-of-view and in-plane offsets during each single-shot rawdata acquisition to “zoom” in [or out] following myocardial contraction [filling]. FOVzoom varied linearly during raw data acquisition, and for each phase-encode line ps caled the FOV and inplane offsets by factor Sc(p) = 1 + ((Db - De)/De) x (pN/2)/N where Db and De were LV short-axis diameter at the begin and end of the single-shot scan, and N was the total phase encode lines (96) for each single-shot. The diameters Db and De were measured using a shortaxis cine pre-scan in the same slice. The sequence acquired 300x225mm FOV (2.3x2.3x6mm). For in-vitro tests, a conical cup of fluid was imaged in circular cross-section. The slice was shifted along the cone during acquisition, so that the apparently changing diameter modelled contraction of a short-axis LV. In healthy volunteers without contrast agent, T2-preparation was used for endocardial image contrast (1). Each 200ms perfusion image was acquired during ventricular contraction, starting 80ms after the R-wave, repeated with and without FOV-zoom. Results Correct operation of the FOV-zoom was confirmed (Figure 1) including in-plane offsets. Gibbs artefact remained unfiltered in all images; the optimum setting of rawdata edge filters during FOV-tracking remains unsolved. Ironically, if FOV-zoom is setup correctly it clarified Gibbs artefact as well as the border. Blurring of the endocardial borders along the phase-encode direction (Figure 2) was reduced by FOV-zoom. The improvement was less than expected given the large change in ventricular diameter (top row) during the image. Although diastolic filling motion is most rapid, the myocardial sectors are more asynchronous even in healthy subjects, and FOV-zoom would be unsuccessful. Even for the more synchronous contraction, the origin of contraction was sometimes midway along the septal endocardial border, and this point must be positioned at the center of the FOV-zoom. Distortion of other tissues by FOV-zoom remained local causing no artefacts at the heart. FOV-zoom might be applied to other long singleshot sequences (e.g. 3D perfusion).

Hyperhomocysteinemia causes cardiac rhythm disturbances due to a shift in atrial and ventricular gap junction protein distribution

Homocysteine (Hcy) is an amino acid byproduct in the metabolism of methionine. Hyperhomocyseinemia (HHcy) is associated with thromboembolic events. Hcy has been identified to correlate with atrial fibrillation and stroke in humans. The role of Hcy and its influence on atrial and ventricular gap junction proteins has been investigated. We hypothesize that changes in the Connexin (Cx) distribution and localization are responsible for cardiac arrhythmia. ECG was monitored in freely moving mice (Hcy‐diet for 12 weeks) with a subcutaneously implanted telemetric ECG probe. 2D transthoracic echocardiography was performed to assess regional wall motion abnormalities and ventricular diameter changes in M‐Mode. Immunoblotting was used for quantification, immunohistochemistry was used to visualize the localization of the gap junction proteins Cx 40, 43 and 45. A shift of Cx 43 to Cx 45 was seen in the ventricular myocardium, a loss of Cx 40 was detected in the atrial myocardium in HHcy animals. Arrhythmia, sudden cardiac death and left ventricular dysfunction along with right ventricular diameter changes were detected in the HHcy animal group.

Effect of cardiac resynchronization therapy on ventricular remodeling

Cardiac resynchronization therapy (CRT) is a new non-pharmacological option for patients with advanced heart failure and ventricular conduction delay. Four randomized prospective studies have provided evidence that CRT increases exercise capacity, improves functional class and quality of life. There is also increasing evidence that CRT may trigger an inverse remodeling process leading to reduction of ventricular diameter and eventually of the atrial size. The pathophysiological mechanism throughout CRT may promote inverse remodeling is: (1) reduction of systolic and diastolic mitral regurgitation; (2) reduction of sympathetic/parasympathetic imbalance as well as reduction of neurohumoral activation due to increased systolic blood pressure and improved filling time; (3) reduction of regional wall stress. The structural changes taking place during CRT are directly related to continuous pacing, because lack of pacing immediately shows the new onset of remodeling. The duration of the reported changes of ventricular diameter is still unknown, and it is also unknown whether such reverse remodeling process of the ventricle and of the atria will lead to a reduction of cardiac death and incidence of ventricular arrhythmias.

Measuring left ventricular function after heart transplantation via digitization of M-mode echocardiograms.

The aim of the study was to assess the usefulness of M-mode echocardiography for noninvasive diagnosis of cardiac rejection. For this purpose, 292 M-mode images of 26 heart transplant recipients were analyzed. The echocardiographic images were digitized into an image analysis system. The curves of left ventricular diameter changes were obtained and its first differential calculated. A total of 23 parameters were measured. The most important parameters were: peak velocity of systolic diameter change, peak velocity of diastolic diameter change, time to peak velocity of systolic diameter change, time to peak velocity of diastolic diameter change (TPEAK-D), isovolumetric relaxation time (IVRT), rapid filling time (RFT), shortening fraction (SF), and mean velocity of circumferential fiber shortening (MVCF). The echocardiographic parameters were compared to biopsy results. In 18 patients, 23 biopsy-proven moderate rejections occurred. When rejection occurred, IVRT decreased 23% +/- 6% (P < 0.05), SF decreased 13% +/- 14% (P<0.05), MVCF decreased 18% +/- 18% (P<0.05), and TPEAK-D increased 27% +/- 27% (P<0.05). We concluded that the analysis of digitized M-mode images can identify heart transplant rejection.

Can cardiac tamponade be diagnosed by echocardiography? Experimental studies.

The purpose of this study was to determine if respiratory variation and/or absolute size of echocardiographically measured right or left ventricular internal dimension at end-diastole (RVIDd or LIVIDd) are accurate indicators of the presence or severity of cardiac tamponade. We measured RVIDd or LVIDd by echocardiography in nine closed-chest, spontaneously breathing dogs in control and during hypotensive tamponade. With tamponade, the end-expiratory RVIDd and LVIDd were significantly smaller than control. Inspiratory increases in RVIDd and decreases in LVIDd were exaggerated during tamponade. Because of the wide range and overlap of RVIDd and LVIDd, no single expiratory value or amount of respiratory change indicated the presence or severity of tamponade. We conclude that if serial echocardiograms show a pericardial effusion, a decreasing end-expiratory RVIDd and LVIDd and an increasing percentage change in ventricular diameter with inspiration, a progressive degree of tamponade should be suspected However, a single echocardiogram cannot accurately predict the presence or severity of tamponade.

An ultrasonic gauge for measurement of ventricular dimensions.

Abstract The paper describes a relatively simple and inexpensive ultrasonic instrument which is used for the continuous measurement of organ dimensions. A d.c. voltage is produced at the output by measuring the transit time of a burst of ultrasound to pass from one transducer to the other. The instrument is easily calibrated and a linear range of 100 mm length has been achieved. Digital technique is used throughout and it is small in size and self-contained, so that it can be easily converted to a portable instrument. This instrument has been used in studies concerned with left ventricular diameter changes on dogs under drug treatment.

Specificity of autonomic influences on cardiac responses during myocardial ischemia.

A possible role of the autonomic nervous system in the left ventricular response to acute regional myocardial ischemia was sought in conscious dogs instrumented for measurement of left ventricular pressure, internal diameter, and aortic flow. Ischemia produced by occluding the left circumflex coronary artery caused tachycardia and reduced contractility. Changes during control occlusions were compared with those during occlusion.s after beta-adrenergic blockade, parasympathetic blockade, and combined sympathetic and parasymphatetic blockade. Beta-blockade did reduce the tachycardia and slightly reduced left ventricular diameter changes in response to coronary occlusion. Results obtained in animals following surgical cardiac sympathectomy indicated reduced tachycardia and no effects on other parameters. The principal effect of parasympathetic blockade was to augment the increase in end diastolic diameter during occlusion Right atrial pacing indicated this change was due to higher initial heart rates. Combined parasympathetic and sympathetic blockade did not alter inotropic responses to coronary occlusion. Results indicated that inotropic support due to changes in activity in autonomic nerves is not increased during acute occlusion of the left circumflex coronary artery.