Late Systolic Bulging of Left Ventricle in Patients with Angina Pectoris

Hamby, Robert I.; Aintablian, Agop; Tabrah, Farouk; Reddy, K N; Wisoff, George

doi:10.1378/chest.65.2.169

Cited by 29 publications

(14 citation statements)

References 22 publications

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“…The former explanation seems more likely, since there was close correlation between these changes and the extent of outward wall movement before mitral valve opening, which is a direct measure of the severity of the isovolumic disturbance. Such changes have previously been documented angiographically (Altieri et al, 1973;Ruttley et al, 1974;Hamby et al, 1974;Wilson et al, 1975;, and by echocardiography (Upton et al, 1976).…”

Section: Discussionmentioning

confidence: 77%

Relation between apex cardiogram and changes in left ventricular pressure and dimension.

Venco¹,

Gibson²,

Brown³

1977

Heart

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The relation between the apex cardiogram and changes in left ventricular pressure measured by micromanometer, and dimension measured by echocardiography, was studied in 12 normal subjects and 64 patients with heart disease. In 12 patients, the apex cardiogram was delayed with respect to simultaneous left ventricular pressure by 17±18 ms during the upstroke and 28±16 ms during the downstroke. In the normal subjects, changes in left ventricular dimension during the upstroke and downstroke of the apex cardiogram were small, amounting to 6±5 and 21 ± 7 per cent total excursion, respectively. In 10 patients with mitral regurgitation, there was significant inward wall movement during the upstroke and in 10 patients with aortic regurgitation, significant outward movement during the downstroke, both reflecting valvular regurgitation. In 20 patients with ischaemic heart disease and segmental abnormalities on left ventricular angiography, apex cardiogramecho dimension relations were abnormal in all, because of inward or outward wall movement during the upstroke, increased outward movement before the 'O' point, or abnormal inward movement during the downstroke. These disturbances were displayed by constructing apex cardiogram-echo dimension loops, which appear to be a sensitive means of detecting incoordinate left ventricular contraction, analogous to those between pressure and dimension.A limitation in the use of M-mode echocardiography in studying left ventricular function is that wall movement is recorded from only a localized region of cavity, so that it is not possible to tell whether a change in dimension results from filling or ejection on the one hand, or from an isovolumic shape change on the other. The value of the technique would, therefore, be increased if information were simultaneously available allowing this distinction to be made, and incoordinate contraction and relaxation detected and quantified. We have previously shown that these abnormalities may lead to characteristic alterations in the time relations between left ventricular dimensions measured by echocardiography and left ventricular pressure , particularly when a pressure-dimension loop is constructed. In the present study, we have explored the possibility of substituting the apex cardiogram for the pressure pulse in order to obtain the same information noninvasively. We have, therefore, investigated the time relations between the various phases of the

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Section: Discussionmentioning

confidence: 77%

Relation between apex cardiogram and changes in left ventricular pressure and dimension.

Venco¹,

Gibson²,

Brown³

1977

Heart

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“…It therefore assumes a shape of smaller radius that will support intracavitary pressure, which results in the initial formation of an aneurysmal bulge.25 While the mechanism by which the aneurysmal bulge forms is understood, the factors that affect the amplitude and timing of radially directed motion 108 CIRCULATION by guest on May 11, 2018 http://circ.ahajournals.org/ Downloaded from within the ischemic region are less well defined. The net motion of any point along the endocardial interface at any interval in time should be determined by the residual tension that can be developed by the ischemic muscle, the stress on the wall in the affected area (which is proportional to the intracavitary pressure and the local radius of curvature of the involved segment), and the passive mechanical motion imparted to the region by the contraction of normal adjacent myocardium.…”

Section: Discussionmentioning

confidence: 99%

Importance of temporal heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia.

Weyman¹,

Franklin²,

Hogan³

et al. 1984

Circulation

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A number of recent two-dimensional echocardiographic studies have attempted to relate quantitative changes in short-axis left ventricular radial wall motion to underlying myocardial ischemia/infarction. The significance of temporal variation in the contraction sequence within these ischemic regions in the overall evaluation of segmental left ventricular dysfunction, however, remains undefined. To assess this, we examined the motion of 192 individual radii that intersected known ischemic segments at 16.7 msec intervals from end-diastole to end-systole. The studies were performed in 13 dogs 1 hr after acute coronary ligation (six of the left anterior descending and seven of the circumflex coronary artery). Zones of infarction were confirmed by triphenyltetrazolium chloride staining at the termination of the experiment and by a corresponding decrease of more than 75% in myocardial perfusion at the 1 hr sampling period. Dyskinesis (defined for each radius as negative or outward excursion relative to the end-diastolic reference on two consecutive fields) was noted along 168 of 192 radii (88%) at some point in the contraction sequence. The maximal outward or dyskinetic motion occurred most commonly in the fourth decile of the normalized contraction sequence. In 147 of the 168 dyskinetic radii (88%) the maximal outward motion occurred during the first half of systole while in only two radii in one animal was the maximal outward motion noted at end-systole. The total number of radii showing dyskinetic motion at any given point in the contraction sequence likewise varied with time. Although again the greatest number of radii showed abnormal motion during the fourth decile of the normalized contraction sequence, only 66 of 168 or 39% remained dyskinetic to end-systole. No relationship was observed between the point of maximal dyskinesis (time-weighted average of all dyskinetic radii for a given animal) and (1) the total number of radii showing dyskinesis, (2) the total number of radii within the infarct zone, or (3) the infarct area expressed as a percent of the slice area. The major factor determining persistence of dyskinesis to end-systole for any radius was the maximal outward motion of the endocardial segment at the point of maximal dyskinesis. Therefore, simple measurement of endocardial excursion from end-diastole to end-systole may fail to detect important wall motion abnormalities and, in some cases, may miss dyskinetic segments completely. Circulation 70, No. 1, 102-112, 1984. A NUMBER of recent two-dimensional echocardiographic studies have attempted to quantitate the changes in regional wall motion and wall thickening that occur after acute coronary ligation and to relate these changes to infarct location and density.' -2 In most instances, wall motion and thickening have been

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“…involved region and the damaged vessel. 3,7 Apart from the study of Gibson and co-workers,8'9 quantitative data have not been available, and the LV cineangiograms have been analyzed only qualitatively. Although this phenomenon may not be specific to any particular pathology, the characteristic pattern of wall motion is well recognized by cardiologists.…”

Section: Introductionmentioning

confidence: 99%

“…Early end of contraction in anterior segments (% of systolic time interval : 88±14% vs 96±6% in group I, p < 0.001) 2. Asynchronism at end systole (maximal velocity of shortening — 0.4±2.3 circ/sec in anterior segments vs 0.05±1.9 in inferior segments, p < 0.02) 3. An early but poor outward anterior wall motion (anterior lengthening at 0.04 sec after the end of ejection 2.9±10% in group II versus 5.4±7.2% in group I, p < 0.05) These abnormalities are strongly correlated with a significant impairment of peak negative diastolic pressure/diastolic time (dP/dt) (1500 ±400 mmHg.…”

mentioning

confidence: 96%

Long-Term Beneficial Effects of PTCA on Segmental Early Relaxation in Disease of the Left Anterior Descending Coronary Artery

et al. 1988

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The relationship between regional left ventricular (LV) motion and global pressure relaxation of the left ventricle remains unclear. To clarify the recent concept of segmental early relaxation in coronary artery disease, the authors investigated two groups of patients. In group I, all 12 patients (mean age 47 +/- 7 years) exhibited evidence of a normal heart after an extensive investigation. In group II, 25 patients (55 +/- 7 years) presented an isolated stenosis of the left anterior descending coronary artery, and they underwent a hemodynamic investigation before and after (six to nine months) a durable successful percutaneous transluminal coronary angioplasty (PTCA). After all conventional hemodynamic measurements had been done, a quantitative frame-by-frame analysis of left ventricular wall motion was conducted. The authors' method is derived from that of Ingels, applying to LV cineangiograms filmed in 30 degrees right anterior oblique view at a 50 frames/second rate. Thus segmental wall motion is analyzed in terms of amplitudes (%), velocities of shortening and lengthening in circumferences/second (circ/sec), and times of events (%). Statistical results took into account the reproducibility of the method. Main results regarding the control state of group II consisted of an asynergic motion of the anterior region taking place from end systole to early diastole: 1. Early end of contraction in anterior segments (% of systolic time interval: 88 +/- 14% vs 96 +/- 6% in group I, p less than 0.001) 2. Asynchronism at end systole (maximal velocity of shortening - 0.4 +/- 2.3 circ/sec in anterior segments vs 0.05 +/- 1.9 in inferior segments, p less than 0.02) 3. An early but poor outward anterior wall motion (anterior lengthening at 0.04 sec after the end of ejection 2.9 +/- 10% in group II versus 5.4 +/- 7.2% in group I, p less than 0.05) These abnormalities are strongly correlated with a significant impairment of peak negative diastolic pressure/diastolic time (dP/dt) (1500 +/- 400 mmHg. sec-1 vs 1850 +/- 410 in group I, p less than 0.02). Long-term beneficial effects of PTCA in group II were characterized by an almost complete normalization, both asynergy and relaxation taking place back within the normal range. The authors conclude that in this kind of patient, peak negative dP/dt could be an index of an asynergic segmental motion, this one being correctly analyzed and quantified on LV cineangiograms with our method.

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Late Systolic Bulging of Left Ventricle in Patients with Angina Pectoris

Cited by 29 publications

References 22 publications

Relation between apex cardiogram and changes in left ventricular pressure and dimension.

Relation between apex cardiogram and changes in left ventricular pressure and dimension.

Importance of temporal heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia.

Long-Term Beneficial Effects of PTCA on Segmental Early Relaxation in Disease of the Left Anterior Descending Coronary Artery

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