Clinical applications of transesophageal echocardiography.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Toma.
Explore the source record for details and available documents.
The relation between the left atrial systolic pressure waveform and left ventricular end-diastolic pressure was observed in 17 patients who underwent diagnostic cardiac catheterization. Left atrial pressure and left ventricular pressure were simultaneously recorded from a multisensor catheter before and during angiotensin infusion. Left ventricular systolic pressure and left ventricular end-diastolic pressure were 133 +/- 17 and 12.3 +/- 3.2 mm Hg, respectively, before angiotensin infusion and increased to 168 +/- 18 (p less than 0.01) and 19.4 +/- 4.5 mm Hg (p less than 0.01), respectively, during infusion. The left atrial systolic pressure curve consisted of two positive waves--a first wave (A) and a second wave (A'). The A and A' wave pressures were 11.6 +/- 2.3 and 10.2 +/- 3.9 mm Hg, respectively, before angiotensin infusion and 16.5 +/- 2.9 (p less than 0.01) and 18.1 +/- 4.7 mm Hg (p less than 0.01), respectively, during infusion. The ratio of A'/A of left atrial systolic pressure was 0.81 +/- 0.27 before angiotensin infusion and 1.08 +/- 0.14 (p less than 0.01) during infusion. The ratio of A' to A of left atrial systolic pressure was linearly related to left ventricular end-diastolic pressure before and during (p less than 0.01) angiotensin infusion. The amplitude of the A wave exceeded that of the A' wave at normal left ventricular end-diastolic pressures. However, as the left ventricular end-diastolic pressure increased either at rest or during angiotensin infusion, the amplitude of the A' wave increased and often exceeded that of the A wave. These results suggest that the second (A') wave might be attributed to the increased reflection associated with increased left ventricular end-diastolic pressure.
This study observed the left function in determining filling dynamics of the left ventricle in patients with myocardial infarction. The study consisted of eight control subjects and ten patients with myocardial infarction. The left ventricular filling volume is considered to be composed of the left atrial passive emptying, active emptying, and conduit volumes. The change of left ventricular filling volume was correlated with that of conduit volume (r = .87, P less than .01). However, the change of left ventricular filling volume did not have any correlation to those of left atrial passive emptying and active emptying volumes. These results suggested that the left atrial conduit function was important in determining filling dynamics of the left ventricle.
To determine whether bunazosin (alpha 1-adrenoceptor blocking agent) can alter the hemodynamic profile of chronic heart failure secondary to myocardial infarction, the drug was administered to Wistar rats 4 weeks after coronary ligation, and continued for 4 weeks. In rats without bunazosin treatment, the left ventricular end-diastolic pressure (LVEDP) and the total vascular resistance index (TVRI) increased as a function of infarct size, while the cardiac index (CI) decreased. But in infarcted rats with bunazosin treatment, the mean aortic pressure and TVRI were reduced, the LVEDP was modestly lessened, and the CI was maintained. The greatest increase in CI after the treatment occurred in rats with infarcts of small and moderate size. Thus, long-term therapy with bunazosin improved LV dysfunction, relative to the size of infarction. This study suggests the beneficial effects of bunazosin therapy in patients with chronic heart failure.
Three cases are reported in which cerebral infarction developed due to blunt cervical trauma. All of these patients had external signs of cervical trauma and presented focal cerebral ischemic symptoms. Cerebral angiography demonstrated characteristic findings in each case. The first case: A 27 year-old man developed left hemiparesis four days after hitting his neck against a bed rail. Cerebral angiography showed complete occlusion of the right extracranial internal carotid artery 1.5 cm distal to its origin and emboli in distal branches of the right middle cerebral artery. He was treated conservatively. The second case: A 32 year-old man developed disturbance of consciousness with motor aphasia and right hemiparesis a few hours after hitting his chest and neck against baggage hanging from a crane. Cerebral angiography showed complete occlusion of the left middle cerebral artery and no abnormalities of the left internal carotid artery. He was treated with STA-MCA anastomosis two weeks after the accident. The third case: An 84 year-old man, who failed in a suicidal hanging, was semicomatose on admission and had right hemiparesis. Computed tomography demonstrated massive cerebral infarction of the territory of both anterior and left middle cerebral arteries. Cerebral angiography showed linear shadow defect of the left extracranial internal carotid artery corresponding with the site of the ligature. He was treated conservatively. From these angiographic findings, it was thought that intimal tear, intramural hematoma, vasospasm of the internal carotid artery and emboli given might bring about cerebral infarction. In such cases of blunt cervical trauma, cerebral angiography should be undertaken as soon as possible if focal cerebral ischemic symptoms can be seen.(ABSTRACT TRUNCATED AT 250 WORDS)
We analyzed the high-fidelity left atrial and left ventricular pressures and the echocardiograms of the mitral valve, left atrium, and left ventricle in patients with complete heart block. During left ventricular diastole, the mitral valve opened, and no pressure gradient was observed between the left atrium and the left ventricle before the left atrial contraction. After the left atrial contraction, the mitral valve closed with persistent higher left ventricular than left atrial pressure. These findings indicated that during the left ventricular diastole in patients with complete heart block, the mitral valve closed after the left atrial contraction, which appeared to be maintained by the pressure gradient between the left ventricle and the left atrium.
To correlate blood flow velocities with thrombogenesis in the left atrium (LA) and left atrial appendage (LAA), we performed transesophageal two-dimensional echocardiography (Eso 2-D Echo) combined with pulsed Doppler flowmetry, which was developed in our laboratory. Thirty-eight patients were studied; 1) 15 who had sinus rhythm including four with mitral stenosis (MS) and 11 normal subjects, and 2) 23 with atrial fibrillation (Af). The patients with Af were classified as lone Af (nine cases); Af-CI: Af with cerebral infarction having no MS (four cases); and Af-MS: Af with MS (10 cases). In four of 10 patients with Af-MS, mural thrombi were detected in the LA or LAA by Eso 2-D Echo, but they were not visualized by conventional echocardiography. In lone Af and Af-CI, however, abnormal echoes in the LAA were not observed by Eso 2-D Echo. Thus, Eso 2-D Echo proved superior to conventional 2-D echocardiography in detecting mural thrombi in the LA or LAA. In sinus rhythm, a biphasic flow pattern followed the P wave on the ECG. It was observed in the vicinity of the junction between the LA and LAA. In Af a flow with a saw-tooth appearance was observed throughout the cardiac cycle. The peak flow velocity in the LAA was significantly less in Af than in sinus rhythm (p less than 0.05). Especially in Af-MS, the peak flow velocity was markedly decreased (1 +/- 4 cm/sec: mean +/- SD) compared with those of the other Af groups (p less than 0.01), and it was significantly less in Af-CI (11 +/- 5 cm/sec) than in patients with lone Af (21 +/- 9 cm/sec) (p less than 0.05). These results indicate that analysis of blood flow velocities in the LAA by Eso 2-D Echo is of great value in assessing thrombogenesis in the LAA, and the patients with Af, even without MS, who have markedly reduced peak flow velocities in the LAA, should be prophylactically anticoagulated, because stagnation of blood is strongly suspected.
Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.
To assess the accuracy of digital subtraction angiography in evaluating coronary flow reserve in cases with critical coronary artery stenosis, time-density curves were obtained from digital subtraction coronary angiograms in the myocardial region of interest. Time to peak contrast (TPC) and time constant of the washout exponential curve (T) were measured in 14 patients with stable effort angina pectoris and critical one vessel lesion before and after percutaneous transluminal coronary angioplasty (PTCA). All patients had normal left ventricular ejection fraction (59 +/- 7%) and 201T1 myocardial images at rest. The values of TPC and T were significantly shortened from 5.4 +/- 1.3 to 4.5 +/- 1.0 sec (p less than 0.02) and from 10.9 +/- 3.8 to 5.3 +/- 1.3 sec (p less than 0.001) after PTCA, respectively. However, in 9 patients TPC values were approximately the same before and after PTCA. In five experimental dogs with critical circumflex coronary artery stenosis, coronary flow (CF; Doppler flowmeter) and systolic thickening of the posterior wall (by sonomicrometry) at rest did not differ from those of the controls. However, contrast media-induced reactive hyperemia was markedly attenuated, accompanied by a significant increase in T (7.7 +/- 4.5 vs 15.8 +/- 10.9 sec, p less than 0.01) and totally unchanged TPC (both 6.8 sec). With simultaneous tracings of CF and time-density curves, TPC and washout phases corresponded with contrast-induced transient CF reduction and hyperemic phases, respectively. We concluded that T may be more sensitive for estimating CF maintained nearly normal, e.g., in patients with stable effort angina pectoris having normal left ventricular wall motion at rest.
Relations between left atrial contraction and left atrial early filling were studied in eight subjects with atypical chest pain from simultaneous left atrial pressure recordings and left atrial cineangiograms. The left atrial ejection phase was defined as the interval from the onset of the sharp systolic rise in left atrial pressure (a point) to the point of minimum left atrial volume (Vmin). The left atrial filling phase was divided into (a) the early filling phase, the period from Vmin to the nadir of left atrial pressure (x), and (b) the late filling phase, the period from x to the point of maximum left atrial volume (Vmax). During the early filling phase, when the left atrium filled as left atrial pressure diminished, approximately 37% of total atrial filling took place. There was a direct relation between left atrial volume measured at a and x points (r = 0.91, p less than 0.01). The extension fraction, measured as the ratio of filling volume during the early filling phase to minimum left atrial volume, was significantly correlated with ejection fraction, measured as the ratio of ejected volume (delta V) during ejection phase to left atrial volume at the a point (r = 0.97, r = 0.01). Both mean and peak filling rates of left atrial volume change during the early filling phase were directly proportional to the ejected volume, the ejection fraction, and the mean ejection rate of left atrial volume change during the ejection phase. Thus these results suggest that there is close interaction between left atrial contraction and left atrial early filling.
To evaluate interatrial septal motion throughout the cardiac cycle, echocardiograms of the septum were obtained by esophageal echocardiography simultaneously with left and right atrial pressures using Millar's micromanometers in nine subjects with sinus rhythm. There were four patients with atypical chest pain but with normal coronary arteries, two with old myocardial infarction, one with angina pectoris, one with aortic regurgitation and one with sick sinus syndrome. The relationship between interatrial pressure gradient (IAPG: left atrial pressure minus right atrial pressure) and the motion of the septum was examined. In all nine patients, the curves of IAPG showed two peaks near the second heart sound and during the atrial contraction period, and the motion of the septum throughout the cardiac cycle showed a similar pattern except during the late diastolic period. During atrial contraction the septum moved posteriorly (decrease in left atrial dimension) against the IAPG. Therefore, except during the atrial contraction period, the motion of the atrial septum is considered to be dependent on this pressure gradient. During the atrial contraction period, the direction of the septal movement might be dependent on the force of active contraction of the left atrial muscles.
Dual echocardiogram was recorded simultaneously with phonocardiogram (PCG) to analyze the isovolumic relaxation time (IRT) of the left ventricle (LV) in 85 patients with various heart diseases and in 23 normal subjects. The measurements used were time intervals from the onset of the aortic component of the second heart sound (IIA) to the onset of the posterior deflection of the posterior aortic wall in the aortic root echocardiogram (X) (IIA-X interval), and to the onset of the most rapid opening motion of the anterior mitral leaflet (D') (IIA-D' interval) during early diastole. 1. The IIA-X interval was directly proportional to the IIA-D' interval in the entire study population. 2. The IIA-X interval was prolonged with advancing age in normal subjects. 3. The IIA-X interval was significantly increased in patients with hypertensive heart disease, old myocardial infarction, hypertrophic cardiomyopathy, and dilated cardiomyopathy, but significantly decreased in patients with mitral stenosis. Thus, the IIA-X interval, which was measured easily and noninvasively from the aortic root echocardiogram is a reliable indicator of the isovolumic relaxation time of the left ventricle, as well as of the IIA-D' interval.
Left atrial function in patients with hypertensive heart disease was compared with that in control subjects. In patients with hypertensive heart disease, the time constant of left ventricular relaxation was significantly greater than that in controls (54 +/- 18 vs 31 +/- 16 msec; p less than 0.01). The ratio of left ventricular filling volume before atrial contraction (left atrial reservoir volume/left atrial emptying volume before atrial contraction, and conduit volume/flow volume from the pulmonary vein into the left ventricle) to left ventricular stroke volume was significantly smaller than that in controls (65 +/- 13 vs 76 +/- 7%; p less than 0.05). In patients with hypertensive heart disease, the ratio of reservoir volume to stroke volume was not significantly different from that in controls, while the ratio of conduit volume to stroke volume was significantly smaller than that in controls (43 +/- 13 vs 57 +/- 9%; p less than 0.05). The latter ratio was inversely correlated with the time constant of left ventricular relaxation (r = -0.05, p less than 0.05). In patients with hypertensive heart disease, the ratio of left ventricular filling volume during atrial contraction to stroke volume was significantly larger than that in controls (35 +/- 13 vs 24 +/- 7%; p less than 0.05). The ratio of left ventricular filling volume during atrial contraction to stroke volume had a significant inverse correlation with the ratio of conduit volume to stroke volume (r = -0.84, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Atrial filling fraction obtained by left ventricular echocardiogram (AFF by LV echo) is considered to be a reliable measure of AFF of LV. However, in patients with LV asynergy, AFF by LV echo cannot be evaluated correctly by this method. To obtain AFF, we devised a new echocardiographic index of AFF, obtained from the aortic-left atrial echogram (AFF by Ao echo), and examined the significance of this index in 9 normal subjects (Normals) and 49 patients with various heart diseases. The correlation between AFF by Ao echo and left ventricular end-diastolic pressure (LVEDP) also was examined. In an additional 20 patients with acute myocardial infarction (acute MI), the relationship between AFF by Ao echo and pulmonary arterial end-diastolic pressure (PAEDP) was studied for several days following the onset of MI. Results were as follows: In Normal patients and patients without asynergy, a significant correlation was seen between AFF by LV echo and AFF by Ao echo (r = 0.710, p less than 0.001). The value of AFF by Ao echo was always greater than that by LV echo. AFF by Ao echo in patients with hypertensive heart disease (HHD), angina pectoris (AP) and old myocardial infarction (old MI) was significantly higher than that in Normal patients. A significant curvilinear correlation was seen between AFF by Ao echo and LVEDP (r = 0.673, p less than 0.005). In patients with acute MI, AFF by Ao echo correlated well with PAEDP.(ABSTRACT TRUNCATED AT 250 WORDS)
To evaluate the effects of left ventricular (LV) distortion on its pump function, the LV cavity shape was analyzed by two-dimensional echocardiography in normal subjects and in patients with right ventricular (RV) volume or pressure overload. The functional significance of LV distortion in the short-axis sections was evaluated by an index of the efficiency of ejection (E) of endocardial circumferential fiber length (ECL) shortening in reducing LV cavity area during systole; E = measured systolic area reduction/ideal systolic area reduction X 100 (%), where an ideal area at end-diastole or end-systole was computed for the measured ECL, assuming its shape to be perfectly circular (ideal area = ECL2/4 pi), and then an ideal systolic area reduction was determined. E at the chordal level was termed Ech. In patients with atrial septal defect (ASD), the LV cavity was distorted at end-diastole and became more circular at end-systole. Since this characteristic change during systole diminished the E, and the values of E at the chordal level (Ech) were significantly lower in ASD than those in normal subjects (89.4 +/- 4.4% vs 98.3 +/- 0.8%, p less than 0.001), strongly suggesting impairment of the efficiency of LV pump function in ASD. In patients with pulmonary hypertension, the LV cavity was more distorted at systole, and a decrease in cavity area at end-systole with the distorted LV contributed to increased systolic area reduction. Thus, the values of Ech in this group exceeded 100% in five of nine patients (103.8 +/- 12.3%). In other words, when marked RV systolic overload exists, an increase in LV systolic area reduction due to progressive LV compression will occur against LV systolic pressure. This phenomenon suggests the existence of "cardiac massage on the LV by the RV with elevated pressure". In conclusion, it was strongly suggested that the efficiency of LV pump function is modulated by RV overload through dynamic changes in the LV shape.
A case of acute tuberculous pericarditis with massive pericardial effusion progressed to constrictive pericarditis under echocardiographic observation during one year. This 59-year-old man was hospitalized because of dyspnea. On admission, his physical examination revealed a paradoxical pulse, engorged jugular veins, hepatomegaly, and pitting edema in the pretibial regions. Chest radiography revealed an enlarged cardiac silhouette and a marked left pleural effusion. His echocardiogram showed a massive pericardial effusion. A biatrial echogram recorded by esophageal echocardiography showed a massive pericardial effusion anterior to the right atrial free wall. Echocardiography performed four months after commencing therapy revealed a reduction in the pericardial effusion, and normal motion of the interventricular septum and posterior wall. However, the motion of the interatrial septum was already abnormal and the excursion of the right atrial free wall was markedly reduced. These finding were similar to those in constrictive pericarditis, as previously reported. Eleven months after admission, both conventional and esophageal echograms showed findings typical of constrictive pericarditis. Thus, in this case, the abnormal biatrial dynamics were recognized earlier than the abnormal left ventricular wall motion.
To compare two expressions of the time constant for ventricular relaxation, 39 patients with various heart diseases (six normal, six angina pectoris [AP], 13 myocardial infarction [MI], eight hypertrophic cardiomyopathy [HCM], and six congestive cardiomyopathy [CCM]) were studied. One time constant was obtained by the method of Weiss et al. (T1) and the other was the ratio of left ventricular pressure at peak (-) dP/dt (Pm) to peak (-) dP/dt (T2). The deviation of T2 from T1 was expressed as 100 X (T2 - T1)/T1 (delta %). In normal subjects, T1 was nearly equal to T2 (32 +/- 3 and 32 +/- 6 msec, respectively), resulting in a low value of delta (-1 +/- 9). However, delta values in AP (20 +/- 23, p less than 0.05), MI (24 +/- 26, p less than 0.05), HCM (37 +/- 21, p less than 0.001), and CCM (46 +/- 24, p less than 0.001) were significantly higher than in normal subjects. Thus T1, T2, or delta separated the patient groups from the control subjects, and there were significant differences between T1 and T2 among the types of heart disease.
Coronary angiography was performed at rest and during bicycle exercise immediately after the onset of angina and significant ST segment elevation or depression in the ECG. Of 11 patients, six showed significant reduction of coronary lumen diameter at the site of organic stenosis; mean values of stenosis (range) before and during exercise were 55% (25% to 88%) and 98% (89% to 100%), respectively. Five patients did not have any diameter change of the organic lesion; mean values of stenosis (range) before and during exercise were 84% (74% to 89%) and 84% (73% to 92%), respectively. Excluding the areas of these stenoses, diameters of left main coronary artery, proximal, middle, and distal left anterior descending, circumflex, and right coronary artery segments were measured before and during exercise. Diameter in each coronary artery segment during exercise was not significantly changed from that before exercise, both in the groups with and without diameter reduction. Exercise provoked a localized worsening of coronary artery stenosis without changing the diameter in the remaining artery. These findings suggest that the worsening of stenosis might be caused by a regional abnormality of the coronary artery that is not necessarily related to the degree of organic stenosis.