Effect of nitroglycerin-induced reduction of left ventricular filling pressure on diastolic filling in acute dilated heart failure

Recent information has suggested that early diastolic filling may be influenced by the left ventricular filling pressure, especially in the failing left ventricle. Acute severe left ventricular dysfunction was induced in 14 dogs by severe left ventricular global ischemia produced by left main coronary artery microsphere embolization until the left ventricular end-diastolic pressure was greater than or equal to 20 mm Hg. To assess the importance of left ventricular filling pressure on left ventricular diastolic filling, nitroglycerin was infused and titrated to reduce left ventricular end-diastolic pressure to less than 15 mm Hg in seven dogs, whereas the remaining seven dogs were observed for 1 h after acute severe left ventricular dysfunction. In both groups of dogs, severe left ventricular dysfunction resulted in left ventricular dilation and elevation of end-diastolic pressure, reduction in area ejection fraction (echocardiographically determined) and an early redistribution of diastolic filling (increased filling fractions at one-third and one-half diastole) despite prolongation of the time constant of left ventricular pressure decline. Pressure-area plots shifted upward and rightward with severe left ventricular dysfunction and were unchanged at 1 h as were all other variables. Nitroglycerin infusion reduced left ventricular size and filling pressure, redistributed diastolic filling to later in diastole as characterized by reduced filling fraction at one-third diastole (left ventricular dysfunction 48.8 +/- 9.7%, nitroglycerin 17.9 +/- 7.9%, p less than 0.001) and shifted downward left ventricular pressure-area plots. Nitroglycerin also improved the time constant of relaxation (left ventricular dysfunction 83 +/- 15 ms, nitroglycerin 52 +/- 15 ms, p less than 0.001) and lengthened the diastolic filling period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mitral valve motion during diastole in patients with complete heart block: relation of pressure gradients between left atrium and left ventricle

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.     

Left atrial and left ventricular diastolic function during acute myocardial ischaemia.

OBJECTIVE--To study indices of diastolic left ventricular function during the first few seconds of myocardial ischaemia. DESIGN--Isovolumic and total relaxation times and left atrial and left ventricular dP/dt were identified from high fidelity (micromanometer) pressure recordings in the left ventricle and left atrium during percutaneous transluminal angioplasty of the left anterior descending coronary artery. PATIENTS--20 patients with isolated disease of the left anterior descending artery and normal left ventricular function. RESULTS--The isovolumic relaxation time lengthened during the first seven to nine seconds of ischaemia; then it shortened by an average of 15% up to the twentieth second, initially as a result of increased left atrial contractility and subsequently because of impaired ventricular relaxation. Ventricular ischaemia resulted in impaired left ventricular diastolic compliance, as shown by an increase in the total relaxation time, before there was evidence of systolic impairment. Minimum dP/dt decreased progressively (by -37% at the twentieth second of ischaemia), whereas maximum dP/dt fell only after 20 seconds of ischaemia (by -11%). CONCLUSIONS--Relaxation and filling of the left ventricle (indices of diastolic function) are more sensitive to myocardial ischaemia than myocardial contractility and systolic function. Left atrial contractility increases during left ventricular ischaemia.     

Clinical, hemodynamic and cineangiocardiolographic findings in congestive cardiomyopathy]

Sixteen patients affected by congestive cardiomyopathy were studied by means of right and left cardiac catheterization and cineangiocardiography. Cardiac output and mean pulmonary circulation time were determined by the radiocardiographic method. Left ventriculograms were obtained in all the patients in the 45 degrees RAO projection; the left ventricular end diastolic and end systolic volumes were calculated both by the area-length and by the slice method. Among the several hemodynamic data (stroke index, mean pulmonary circulation time, left ventricular end diastolic pressure, left ventricular volumes and ejection fraction) the most early impaired and therefore usefull for an early diagnosis, were: the left ventricular end-systolic volume, the left ventricular end-diastolic volume and the left ventricular ejection fraction.     

Functional abnormality due to a deformation of the left ventricle: dynamic anatomy revealed using echocardiography

A deformation of the left ventricular cavity is commonly observed in myocardial infarction, which directly influences the ventricular function. Even in cases without ischemia, a deformation of the left ventricle during systole or diastole is presumed to affect its function. Inward bending of the left ventricular posterobasal wall in giant left atrium is an example of the unfavourable effects of such a deformation. Systolic flattening of the left ventricle is atrial septal defect complicated by pulmonary hypertension is an example of the favourable influences by such a deformation. A regional wall motion abnormality observed in these cases is explained by the deformation attributed to the relationship between the left ventricle and left atrium or between the left and right ventricles. The relationship between the deformation and the function of the left ventricle in ventricular aneurysm can be explained well by the mode of blood turnover within the left ventricle. Contrast studies via the left atrium revealed that blood flow into the left ventricle did not reach the cardiac apex with an aneurysm, but immediately turned upwards towards the outflow tract. These results indicate that, although the left ventricle is anatomically a single cavity, it consists of functioning and non-functioning portions for blood turnover. A morphological abnormality of the left ventricle influences its function even without myocardial ischemia. It is necessary to relate all morphological changes of the left ventricle to cardiac function, regardless of the causes of a deformation.     

Role of the left atrium in adaptation of the heart to chronic mitral regurgitation in conscious dogs

The manner in which the left atrium adapts to chronic mitral regurgitation and the role of the adapted left atrium as a modulator of excessive central blood volume were analyzed in seven conscious dogs, instrumented with high-fidelity pressure transducers and ultrasonic dimension gauges for measurement of left atrial and left ventricular pressure and cavity size. After obtaining data in a control situation, mitral regurgitation was produced by transventricular chordal sectioning. Heart rate was matched by right atrial pacing. In the "early" stage (7-14 days), left ventricular end-diastolic and mean left atrial pressures increased from 6 to 16 mm Hg and from 4 to 12 mm Hg, respectively. Both left ventricular end-diastolic segment length and left atrial diameter prior to atrial contraction increased by 7%. In the "late" stage (20-35 days), despite significant decreases in left ventricular filling pressure (11 mm Hg) and left atrial pressure (8 mm Hg), there was a continuous increase in left ventricular end-diastolic dimension (10%) and atrial end-diastolic diameter (10%). After the onset of mitral regurgitation, the left atrium performed greater work with a more enlarged cavity. Left atrial chamber stiffness was progressively decreased. These changes were associated with progressive increase in the left atrial diameter at zero stress, and there was a significant increase in the diameter of the left atrial myocyte. These results indicate that during chronic mitral regurgitation, the left atrium enlarges in size and mass, with a more potent booster action. The left atrial chamber becomes more compliant. Thus, the enlarged left atrium appears to exert an important compensatory mechanism in the case of excessive central blood volume by buffering pressure rise in the atrium and by providing an adequate ventricular filling volume.     

三维经食管超声心动图对室壁瘤患者左心室容积与功能的评价

目的:探讨应用三维经食管超声心动图(3D-TEE)定量评价左心室室壁瘤形成后左心室的形态、结构与功能。方法:35例心肌梗死后合并左心室室壁瘤形成的患者,于术前3 d之内进行经胸三维超声心动图和三维经食管超声心动图检查。对所获得的左心室舒张末期容积、收缩末期容积、左心室射血分数、收缩期二尖瓣口反流面积和室壁瘤容积等数据进行处理,对照分析2种方法所测得的结果。结果:32例患者可以获得优质图像,三维经食管超声心动图所测得左心室舒张末期容积、收缩末期容积、室壁瘤容积较三维经胸超声心动图所测得的数据偏高,而三维经食管超声心动图所测得的左心室射血分数偏低,二者差异有统计学意义(P<0.05)。结论:应用3D-TEE对心室重构、心腔扩大或室壁瘤形成的左心室评价更为精确。3D-TEE可以作为定量评价心肌梗死后室壁瘤形成患者的左心室容积、功能和室壁瘤大小的有效手段。     

Effects of renal transplantation on left ventricular size and function.

Thirteen patients with chronic renal failure and uraemia were investigated by echocardiography preoperatively before and after haemodialysis and again after a successful renal transplantation to evaluate the cardiac changes caused by renal transplantation. After renal transplantation, the left ventricular end-diastolic and end-systolic diameters, as well as the cardiac index, decreased, probably because of the decreased left ventricular filling pressure. The left ventricular wall thickness and mass decreased, apparently as a result of the decrease of the left ventricular preload and also of the decrease of the afterload, because the systolic blood pressure decreased. The left atrial diameter decreased in response to the decreased left ventricular preload and wall hypertrophy. The changes in the indices of left ventricular function as a result of haemodialysis appeared to predict the changes seen after renal transplantation. Renal transplantation appears to have a tendency to result in normal left ventricular and left atrial volumes, as well as to lessen left ventricular hypertrophy, without significantly improving left ventricular function.     

Location, size and morphological characteristics of left atrial thrombi as assessed by echocardiography in patients with rheumatic mitral valve disease.

AIMS: This study aimed to assess the use of transthoracic and transoesophageal echocardiography in diagnosing the thrombi located in the left atrium and/or left atrial appendage in patients with rheumatic mitral valve disease, and to investigate the characteristics of thrombi in comparison to intraoperative findings. METHODS AND RESULTS: The study group was comprised of 474 patients who underwent transthoracic and transoesophageal echocardiography prior to mitral valve surgery. Location, thickness and morphological characteristics of thrombi were determined by transoesophageal echocardiography. Intraoperative assessment disclosed left atrial thrombi in 105 patients. Thickness of thrombi < or = 1cm, and thrombi confined to left atrial appendage were associated with false-negative results by transthoracic echocardiography. However, diameter and morphological characteristics of thrombi, left atrial and left atrial appendage size, and the presence of the spontaneous echo contrast were not associated with the diagnosis of thrombi by transthoracic echocardiography. For overall left atrial thrombi, sensitivity and specificity of transthoracic echocardiography were 32%, and 94%, respectively. Sensitivity and specificity of transoesophageal echocardiography for thrombi in the left atrial appendage were 98%, and 98%, for thrombi in the main left atrial cavity were 81%, and 99%, and for thrombi located in both left atrium and appendage cavities were 100%, and 100%, respectively. CONCLUSION: In patients with rheumatic mitral valve disease, detection of left atrial thrombi by transthoracic echocardiography seems to be determined by thickness and location of thrombi. The multilobed structure of the left atrial appendage and artifacts over posterior wall of the left atrium may still prevent precise diagnosis even with transoesophageal echocardiography.     

Significance of echocardiographic left atrial enlargement in aortic stenosis

This study investigated the significance of echocardiographic left atrial enlargement as measured by the left atrial dimension corrected for body surface area in 24 patients with pure aortic stenosis established by cardiac catheterization. Echocardiographic evidence of left atrial enlargement occurred in 11 of 15 patients (73%) with an aortic valve area below 0.8 cm2 and in none of nine patients (0%) with an aortic valve area above 0.8 cm2, p less than 0.0025. All 11 patients (100%) with an enlarged left atrial dimension had an increased diastolic left ventricular dimension, whereas 1 of 13 patients (8%) with a normal left atrial dimension had an increased diastolic left ventricular dimension, p less than 0.00001. The 11 patients (100%) with an enlarged left atrial dimension had increased posterior left ventricular wall thickness, whereas 2 of 13 patients (13%) with a normal left atrial dimension had increased posterior left ventricular wall thickness (p less than 0.0005). These data lead one to conclude that in patients with pure aortic stenosis, echocardiographic evidence of left atrial enlargement as measured by an increased left atrial dimension corrected for body surface area should lead one to suspect severe aortic stenosis.     

Vectorcardiographic findings in concentric and eccentric left ventricular hypertrophy as determined by angiocardiograms. 1. Preliminary report.

In forty-one patients with various heart diseases including 29 with LVH, the vectorcardiograms of Frank system and angiocardiographic findings correlated minutely. Based on the left ventricular wall thickness in end-diastole, left ventricular end-diastolic volume, and the length of the long axis of the left ventricle obtained in angiocardiograms, typical left ventricular hypertrophy was classified into types 1a, 1b, 2a, 2b anatomically. The vectorcardiograms in these 4 types represented different patterns with regard to the QRS and T loops respectively. The QRS voltage in the left ventricular hypertrophy closely correlated to the left ventricular wall thickness in end-diastole, the left ventricular end-diastolic volume, and the left ventricular mass. Marked ST and T changes in the left ventricular concentric hypertrophy characterized by increase in wall thickness without definite chamber enlargement may be closely related to the abnormal muscle state with the increased left ventricular wall thickness, the probably due to relative hypoxia in origin. The Q loop of patients with severe left ventricular concentric hypertrophy was definitely differentiated from that of most patients with the pure left ventricular eccentric hypertrophy which was characterized by chamber enlargement with usually slight thickening of the wall. A possible mechanism regarding inconspicuous or prominent Q loops in both concentric and eccentric LVH was presented. An important factor of the delay of the time of occurrence of the spatial R vector in the left ventricular eccentric hypertrophy is the greater distance of the intraventricular conducting pathways caused by the left ventricular dilatation. By means of assessing the vectorcardiogram of the left ventricular hypertrophy, relatively exact anatomy of the left ventricular hypertrophy can be determined.     

Model studies of the contribution of ventricular interdependence to the transient changes in ventricular function with respiratory efforts

The effects of variations in intrathoracic pressure on left ventricular function were studied using a mathematical model of the circulation. The variations in intrathoracic pressure directly affect the left ventricular afterload, and indirectly alter left ventricular filling by changing the right ventricular volume. The decrease in intrathoracic pressure with sustained inspiratory efforts increased the left ventricular afterload and thus reduced the left ventricular stroke volume. Secondary to the reduction in stroke volume, the left ventricular end systolic and end diastolic volumes increased. Decreasing intrathoracic pressure also increased the systemic venous return, thereby increasing right ventricular volume. The model predicted that an enlarged right ventricular volume would, through diastolic ventricular interdependence, immediately reduce the left ventricular end diastolic volume (which in turn reduced the left ventricular stroke volume), while through systolic ventricular interdependence it would increase left ventricular stroke volume and reduce left ventricular end systolic volume. An increased right ventricular volume would also increase right ventricular stroke volume and after a delay of a few heart beats raise left ventricular end diastolic and stroke volumes. The net effect of respiratory variations in intrathoracic pressure on left ventricular function would be a combination of these effects. Thus on sustained inspiration the left ventricular stroke volume initially decreased (left ventricular afterload and diastolic interdependence secondary to the increase in right ventricular volume partly counteracted by the effects of systolic interdependence), followed by an increase as the increased venous return reached the left ventricle. The model indicated that the response to a forced expiratory effort was not simply the opposite of the inspiratory response, since the increase in intrathoracic pressure during a forced expiration is accompanied by increases in abdominal pressure. On sustained expiration the left ventricular stroke volume initially increased, with no significant initial change in end diastolic volume. The cardiovascular response to respiration is complex, and model studies can help to isolate and identify the various components involved.     

Echocardiographic study of abnormal position and motion of the posterobasal wall of the left ventricle in cases of giant left atrium

In 35 of 70 patients with rheumatic mitral valve disease, two dimensional echocardiography revealed the posterobasal wall of the left ventricle to be entrapped between the left ventricular and atrial cavities and bent inward. The motion of the bending segment was paradoxical. This abnormality was assumed to be induced by the left atrial dilatation extending inferiorly behind the left ventricle, because the length of the bending segment correlation with the left atrial dimension. There was no correlation between the degree of abnormal bending and left atrial pressure, mitral valve pressure gradient or left ventricular dimension. The systolic excursion of the posterobasal wall of the left ventricle was reduced according to the length of the bending segment. This abnormal feature was also observed in five postmortem heart specimens with an extremely dilated left atrium. The macroscopic and microscopic findings in the myocardium of the bending segment were not different from those of the remaining segment of the left ventricle. Therefore, the asynergic motion of the bending segment is assumed to be caused by the abnormal spatial orientation of the left ventricle and the left atrium. It should be considered that the giant left atrium not only oppresses the surrounding organs but also affects the left ventricle.     

高血压病患者左房容积改变及其影响因素

应用二维超声心动图,采用双平面面积长度法,测定65例高血压病患者及40例正常人的左房最大容积(MAXV)、左房容积指数(MAXVI)。结果显示,高血压病患者MAXV和MAXVI较正常人显著增大(P<0.001)。对导致高血压病患者左房容积改变的可能因素进行研究分析,发现高血压病患者左房容积增大与左室重量指数(LVMI)、年龄、体循环舒张压有关。     

Percutaneous transluminal coronary angioplasty of left main stenosis--results of the German PTCA registry

In cases with protected left main stenosis by previous bypass surgery or as an emergency intervention in patients presenting with acute myocardial infarction and cardiogenic shock, percutaneous transluminal coronary angioplasty is performed as an alternative treatment strategy to bypass surgery. A review of 262 left main angioplasties revealed a procedure-related mortality in cases without protection of the left main coronary artery of 9.1% (4/44), in cases with partially protected left main stenosis by collaterals to either left coronary artery of 4.8% (1/21) and 0.5% (1/187) in cases with nonobstructed bypass grafts to either left coronary artery. Coronary angioplasty of an unprotected left main coronary artery, had an unacceptably high procedure-related mortality rate and should therefore not be performed even in cases of emergency intervention. The risk stratification of the procedure can be evaluated by the proposed grading of left main artery protection.     

Effect of inotropic and vasodilator therapy on left ventricular diastolic filling in dogs with severe left ventricular dysfunction

Inotropic and vasodilator therapy for congestive heart failure improve left ventricular systolic performance by different mechanisms. However, the nature and extent to which diastolic filling is altered have not been well described. Acute severe left ventricular dysfunction was induced in 21 dogs by severe left ventricular global ischemia produced by left main coronary artery microsphere embolization until left ventricular end-diastolic pressure was greater than or equal to 18 mm Hg. Dobutamine was infused in seven dogs until the peak positive first derivative of left ventricular pressure (dP/dt) increased by greater than or equal to 33%. Nitroprusside was infused in seven dogs until left ventricular end-diastolic pressure was less than 15 mm Hg. Seven dogs were observed for 1 h after the induction of acute severe left ventricular dysfunction and served as the control group. In all groups of dogs, severe left ventricular dysfunction resulted in left ventricular dilation, reduction in area ejection fraction, elevation of left ventricular end-diastolic pressure and an early redistribution of diastolic filling (increased 1/3 and 1/2 filling fractions) despite a markedly abnormal time constant of relaxation. No changes were noted in any variable after 1 h of observation in the seven control dogs. Nitroprusside reduced left ventricular size and filling pressure, increased cardiac output, improved relaxation and redistributed diastolic filling to later in diastole as characterized by a reduced 1/3 filling fraction (19.4 +/- 7.4% versus 51.4 +/- 10%, p less than 0.001). The pressure-area curve was shifted downward and leftward.(ABSTRACT TRUNCATED AT 250 WORDS)     

Change in filling pattern with preload reduction reflects left ventricular relaxation

BACKGROUND: The early diastolic mitral valve pressure gradient and the rate of left ventricular filling are determined by the rate of left ventricular relaxation and left atrial pressure at the time of mitral valve opening. Accordingly, we hypothesized that the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved systolic function. METHODS: We evaluated the relationship between the logistic time constant of left ventricular relaxation and left ventricular filling pattern calculated from the time derivative of left ventricular volume using a microtipmanometer and a conductance catheter in 26 consecutive patients with preserved left ventricular ejection fraction (>45%). Left ventricular filling patterns were determined from the maximal rates of early diastolic left ventricular filling (E velocity) and atrial filling (A velocity) before and after preload reduction by inferior venal caval occlusion. RESULTS AND CONCLUSIONS: There was no significant relationship between the logistic time constant of left ventricular relaxation and the E/A velocity ratio at baseline. However, the time constant was correlated with the E/A velocity ratio after venal caval occlusion (r=-0.47, p=0.02). Furthermore, the time constant was correlated with %E/A velocity change, which was defined as the rate of change of E/A before and after caval occlusion divided by E/A after caval occlusion, more significantly (r=-0.67, p<0.01) than with the E/A velocity ratio after caval occlusion. Thus, the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved left ventricular ejection fraction.     

Radionuclide left ventricular absolute volume determination by ejection fraction measurement data and a left posterior oblique blood pool image

A new method for the calculation of left ventricular volumes called the "semi-geometric" method, was reported by Nichols et al in 1984. This method, however, still had certain limitations for practical use. This paper describes a modified semi-geometric method in which the left ventricular volume was obtained from conventional left ventricular ejection fraction measurement data collected from the modified left anterior oblique position with a caudal tilt of 10 degrees or more and a left posterior oblique blood pool image. The left ventricular end-diastolic volumes obtained by this method were compared with those calculated by combining the thermodilution cardiac output and the left ventricular ejection fraction. The correlation coefficient was r = 0.93 (n = 20). In the phantom experiment, the true volumes and those obtained by this method showed an excellent correlation (r = 0.99). This method is considered accurate and practical.     

咪哒普利对冠心病心衰患者左房功能的影响

目的评价咪哒普利对冠心病心衰患者的左房功能。方法：应用M型超声和心内膜自动边缘检测技术（ABD）与用药前后检测左房最大内径，左房面积及容量曲线。结果：应用咪哒普利1个月后左房最大内径（LAdiam),左房最小面积（LAAmin)，左房最大面积（LAAmax)，左房最小容量（LAVmin)，左房最大容量（LAVmax)显著减少（P＜0．05，P＜0．01，P＜0．05，P＜0．01，P＜0．05），左房面积变化率（FAC）及左房射血分数（LAEF）显著升高（P＜0．01，P＜0．01）。结论：咪哒普利可以显著改善冠心病心衰患者左房功能。     

Effect of oral propranolol on rest and exercise left ventricular ejection fraction, volumes, and segmental wall motion in patients with angina pectoris. Assessment with equilibrium gated blood pool imaging.

The effect of oral propranolol on left ventricular ejection fraction, left ventricular volumes, cardiac output, and segmental wall motion was assessed with multigated blood pool imaging both at rest and during supine exercise in 15 patients with angina pectoris. Propranolol had no effect on resting left ventricular ejection fractions. Before propranolol, they did not change during exercise, whereas after propranolol the ejection fractions increased slightly. Exercise left ventricular ejection fractions increased with propranolol in three patients with resting left ventricular ejection fractions of less than 40 per cent. More specifically, left ventricular end-diastolic volume index, end-systolic volume index, stroke volume index, and cardiac index were not altered significantly at rest or during exercise by propranolol. Exercise left ventricular ejection fractions were increased in five and unchanged in eight patients by propranolol. Those patients with increases in left ventricular ejection fractions had a greater change in left ventricular end-diastolic volume indices and a greater change in left ventricular end-systolic volume indices during exercise while on propranolol. Left ventricular segmental wall motion was not altered significantly during exercise by propranolol. We conclude that: (1) Left ventricular functional responses to propranolol during exercise are heterogeneous and not easily predicted; (2) propranolol causes no consistent deterioration in exercise left ventricular ejection fraction even in patients with resting ventricular ejection fractions less than 40 per cent; (3) increased exercise left ventricular ejection fraction with propranolol is contributed to by significant increases in end-diastolic volume during exercise; and (4) gated blood pool imaging is a useful method for characterising rest and exercise left ventricular ejection fractions and left ventricular volumes during propranolol therapy.