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Serial echocardiographic and angiographic measurements of left ventricular function were obtained in a patient with massive pulmonary embolism before and after pulmonary embolectomy. These data suggest that left ventricular dysfunction secondary to right ventricular failure is the results of markedly decreased left ventricular filling in this settings.
The acute dose-related effects of small to moderate doses of ethanol on right ventricular functioning were studied on 18 anesthetized, artificially ventilated dogs in 39 sessions. Diluted ethanol (from 25-37.5%) was infused during 40 minutes, yielding total doses of 1.0 g/kg (n = 15), and 1.5 g/kg (n = 12) with corresponding venous blood ethanol peak concentrations of 1.38 +/- 0.25 and 2.41 +/- 0.31 mg/ml, respectively. Heart rate increased up to 16% in groups receiving ethanol. In the control group receiving the equivalent volume of saline (n = 12) heart rate decreased 14%. Pulmonary arterial systolic pressure increased from 24 +/- 3 to 27 +/- 3 mmHg and diastolic pressure from 11 +/- 2 to 14 +/- 4 mmHg (p less than 0.05) when the ethanol dose was 1.0 g/kg. The pulmonary arterial resistance increased from 620 +/- 135 to 805 +/- 185 dyn.s.cm-5 (p less than 0.01). The peak dP/dt decreased maximally by 20% with increasing ethanol doses. Stroke volume decreased maximally by 14% but due to the increase in heart rate, cardiac output even increased. The changes in end-diastolic volume and pressure were not significant. Hence, the ethanol increased heart rate and afterload of the right ventricle but depressed the myocardium.
In this report we describe our first use of N-acetylcysteine in a patient with his first acute myocardial infarction in an effort to reduce the infarct size and to protect left ventricular function by pharmacological and mechanical therapy (thrombolysis and percutaneous transluminal coronary angioplasty). This comprehensive therapy caused normalization of previously depressed left ventricular systolic function.
A study of left ventricular diastolic function in early hypertension was performed by the new method of acoustic quantification and Doppler echocardiography. A total of 23 untreated patients, five males and 18 females (mean age 53.52 +/- 9.10 years) with mild or moderate hypertension (160 +/- 13/98 +/- 10 mmHg) and 12 normal, age- and heart-rate-matched, control subjects were studied. All subjects showed normal left ventricular systolic function and wall thickness on two-dimensional echocardiography. The following indices were obtained. (1) Acoustic quantification (AQ): the time rate of area change in early diastole (dA/dt)E, in late diastole (dA/dt)A and their ratio (dA/dt)E/(dA/dt)A. (2) Doppler echocardiography: the early peak E, the late peak A flow velocities, their ratio E/A and deceleration E-F slope in early diastole. Measurements of left ventricular diastolic function by acoustic quantification showed, in the patient group, that the time rate of area change in early diastole (dA/dt)E was significantly lower (64.7 +/- 11.0 cm2/second versus 74.3 +/- 5.9 cm2/second; P < 0.01), the rate of area change in late diastole (dA/dt)A was not significantly higher (43.3 +/- 9.2 cm2/second versus 38.4 +/- 6.0 cm2/second; P > 0.05), and the ratio between the above indices (dA/dt)E/(dA/dt)A was significantly lower (1.55 +/- 0.42 versus 1.95 +/- 0.20; P < 0.01), compared with normal values. Doppler diastolic indices were all significantly abnormal in patients, in comparison with the values of the control group. Reduced left ventricular diastolic function was found in nine of 23 patients (39.1%) by the AQ method and eleven of 23 patients (47.8%) by Doppler echocardiography. Acoustic quantification was in agreement with Doppler echocardiography in identifying left ventricular diastolic dsyfunction in nine of 11 hypertensive patients with reduced Doppler diastolic values (82% sensitivity, 100% specificity). The correlation between the two methods showed that the time rate of area change in early diastole (dA/dt)E correlated well with the early peak E flow velocity (r = 0.59), the ratio between the time rates in early and late diastole (dA/dt)E/(dA/dt)A also correlated well with the Doppler E/A ratio (r = 0.89), while a poor correlation was found between the time rate of area change in late diastole (dA/dt)A and peak A flow velocity (r = 0.26). Thus abnormal diastolic filling of the left ventricle can be seen in the early stages of hypertension, even in the presence of normal systolic function and wall thickness, while acoustic quantification could be considered as a useful noninvasive modality for the early identification of left ventricular diastolic abnormalities.
In order to determine the influence of right ventricular artificial pacing on left ventricular function, particularly on diastolic specificity and regional myocardial perfusion, 99mTc multigated blood pool study and 201Tl myocardial SPECT at rest were performed on 12 patients with a DDD pacemaker implanted due to atrio-ventricular block at various degrees and on 7 normal adults without pacemaker as controls. Studies were performed on the pacing group during both ventricular pacing (VP) and atrio-ventricular sequential pacing (AVSP) at a rate of 80 beats/min. Although global left ventricular ejection fraction (LVEF) showed no significant differences between the control group (63.7 +/- 9.1%) and the pacing group, or between during AVSP (57.8 +/- 9.6%) and during VP (55.8 +/- 10.0%), global early diastolic peak filling rate (EDPFR) in the pacing group were significantly lower during AVSP (0.90 +/- 0.52 counts/second/end-diastolic counts) than during VP (1.55 +/- 0.52) (p less than 0.01), which were both found to be lower than those seen in control group (2.37 +/- 0.48 (p less than 0.01). Functional images disclosed regional prolongation of left ventricular ejection time (ET) in septal and apical areas of the left ventricle adjacent to the pacing site in 7 of the 12 patients (58.3%) during AVSP and in 3 of them (25%) during VP, and also revealed regional decrease in EDPFR in the similar areas in all of the patients during both modes, being more remarkable during AVSP than during VP. On 201Tl myocardial SPECT at rest, regional perfusion impairment was observed in septum, apex and the infero-posterior wall on the septal side adjacent to the pacing site in 8 of 10 patients (80%) during AVSP and in 6 of 9 patients (66.7%) during VP. These results suggest that a change in electrical conduction by right ventricular pacing may disturb regional myocardial relaxation, probably resulting in a regional impairment of myocardial perfusion.
Diltiazem is a calcium channel blocker whose effects on left ventricular function (LVF) are controversial. We studied 12 patients with ischemic heart disease (IHD) before starting and 15 and 30 days after having initiated Diltiazem 60 mg t.i.d. LVF was accessed by means of the normalized indexes of the calibrated apexcardiogram: nS for systolic LVF evaluation and nA for diastolic LVF evaluation. Recent works have shown that these indexes have a good correlation with invasive parameters of LVF. We verified that nS did not change and nA decreased significantly (p < 0.05) after Diltiazem. We preliminary concluded that Diltiazem has no deleterious effect on LV systolic function and improves LV diastolic function, by decreasing nA, a parameter which correlates well with LV end diastolic pressure.
BACKGROUND: Measurement of tricuspid annulus motion (TAM) is an easy way to estimate right ventricular ejection fraction (RVEF). However the accuracy of two-dimensional (2-D) methods for analyzing the three-dimensional (3-D) structure of the tricuspid annulus has not been evaluated. OBJECTIVE: This study evaluated the accuracy with which 2-D measurements of TAM reflect RVEF using 3-D reconstructions of the heart at end diastole (ED) and end systole (ES). METHODS: 2-D echocardiographic studies were performed on 12 subjects and used to reconstruct the RV and tricuspid annulus in 3-D at ED and ES. Measurements of TAM from medial and lateral positions on the annulus were selected from the standard echocardiographic apical four-chamber view. The minimum and maximum possible TAM values, RV volumes, and movement of the apex of the heart along the trajectory of TAM were calculated from the 3-D reconstructions. RESULTS: TAM correlated highly with RVEF (r > or = 0.90). Values found by 2-D and 3-D techniques were not significantly different. Correcting TAM for apex motion did not improve correlation. Summation of medial and lateral TAM data increased correlation values slightly relative to lateral TAM alone. Regional aberrant contractility degraded the predictive value of TAM. CONCLUSION: Estimation of RVEF from 2-D echo measurement of TAM is accurate, especially when medial and lateral TAM are summed, except in patients with severe apical RV dysfunction.
We studied the interrelation of changes in ventricular external work, myocardial blood flow, and O2 consumption at birth. Eleven fetal sheep were instrumented under general anesthesia at 133-134 days gestation with arterial, peripheral venous, and left atrial catheters, and in five fetuses, a catheter was also inserted into the coronary sinus. Fetal left ventricular (LV) and right ventricular (RV) outputs and myocardial blood flows (radioactive microspheres), hemodynamics, and LV O2 consumption were measured 1 wk later. Fetuses were delivered by cesarean section, and measurements were repeated 1 and 4 h after birth. RV minute work (mmHg.l.kg-1) was greater in fetuses (10.8 +/- 0.5 vs. 15.6 +/- 1.0 P < 0.001), but because of increased LV minute work (to 20.9 +/- 1.4, P < 0.005) and unchanged RV minute work, this pattern was reversed by 1 h after birth. RV myocardial blood flow (ml.min-1.100 g-1) was predominant in fetuses (234 +/- 25 vs. 306 +/- 27, P < 0.001), but this also reversed in lambs; this reversal was related to unchanged 1-h (248 +/- 16) and lower 4-h LV myocardial blood flow (199 +/- 9, P < 0.05) and a progressive fall in RV myocardial blood flow (1 h: 245 +/- 20, P < 0.05; 4 h: 174 +/- 12, P < 0.005). LV O2 consumption (ml.min-1.100 g-1) increased between fetal (8.1 +/- 0.6) and 1-h lambs (18.9 +/- 1.3, P < 0.005) because of a rise in the LV arteriovenous O2 content difference (3.6 +/- 0.4 vs. 7.5 +/- 0.6 ml/dl, P < 0.005). External work performed per unit myocardial blood flow (mmHg.l.ml-1) in the LV increased between fetal and 1-h lambs (1.92 +/- 0.14 to 3.33 +/- 0.15, P < 0.001) and, in the RV, between fetal and 4-h lambs (2.09 +/- 0.18 to 2.92 +/- 0.24, P < 0.01). The proportion of consumed O2 converted to external work was, however, similar in fetal (34.6 +/- 3.1%) and 1-h (31.3 +/- 2.9%) and 4-h lambs (34.5 +/- 3.6%). These findings indicate that 1) a switch from a fetal RV to a newborn LV dominance is due to increased LV pumping performance, 2) an associated switch in LV and RV myocardial blood flow patterns is mainly related to a fall in RV myocardial blood flow, 3) a postnatal rise in LV O2 consumption results from enhanced LV arteriovenous O2 extraction, not increased LV myocardial blood flow, 4) ventricular external work per unit myocardial blood flow increases postnatally, particularly in the LV, and 5) LV mechanical efficiency is not altered after birth.
We measured the right ventricular ejection fraction (RVEF) before and during unilateral pulmonary artery occlusion test (UPAO) by thermodilution method. We also measured the right ventricular end-diastolic volume index (RVEDVI), right ventricular end-systolic volume index (RVESVI), and right ventricular stroke volume index (RVSVI). RVEF and RVSVI were significantly decreased by UPAO (p less than 0.05), but there were no obvious changes in RVEDVI and RVESVI. Some cases showed only a small decrease in RVEF by UPAO, even though their total pulmonary vascular resistance indices were over 700 dyne.sec.cm-5/m2 during UPAO. On the other hand, some cases had a decreased in RVEF of more than 10% by UPAO, even though their total pulmonary vascular resistance indices were under 400 dyne.sec.cm-5/m2 during UPAO. We consider that it is important to measure right ventricular functions such as RVEF together with pulmonary vascular hemodynamics in the pre-operative evaluation of cases of lung resection.
Comparison of ultrasound and invasive measurements has shown that accuracy and reproducibility of echocardiographic assessment of left ventricular performance are suitable for clinical use. We determined the influence of changes in heart rate, afterload, inotropic state and diastolic cycle length after premature beats and in atrial fibrillation on various ejection phase indices of myocardial contractility in man. Mean and maximal velocity of circumferential fiber shortening (VCF mean' VCF max) showed a slight increase during rapid atrial pacing. In contrast fractional shortening (FS%) and delta-VCF were not influenced by acute changes in heart rate. During intravenous infusion with Dobutamine VCF max and delta-VCF proved to be particular sensitive indices of left ventricular function. After permature beats and in atrial fibrillation the results indicate a linear correlation between all indices of the ejection phase and diastolic cycle length.
BACKGROUND: Left ventricular assist devices (LVADs) are frequently used to maintain patients with severe heart failure until heart transplantation becomes possible. Some patients may experience recovery of LV function during such support. Therefore, it is essential to be able to monitor changes in LV function in this setting. METHODS: We studied LV function in 10 patients (median age 34 years, 9 male) who had LVADs implanted because of severe heart failure due to dilated cardiomyopathy a median of 4 months previously. Median pre-implant ejection fraction was 27% and all patients had been on maximal medical therapy, including intravenous inotropic support, prior to insertion of the LVAD. RESULTS: During LVAD support there were cyclical variations in LV dimensions, fractional shortening (FS) and transmitral flow, related to changes in the phase relationship of the LV and the LVAD. The "best" FS occurred when LV systole coincided with device filling and the "worst" FS when LV systole coincided with device ejection. Median FS with the pump switched off was 18% (10% to 32%). Pump-off FS was significantly greater than the "worst" FS with the pump on (5%, p = 0.002), and similar to the "best" pump-on FS (19%, p = NS). CONCLUSIONS: LV function could be studied echocardiographically during LV support and brief periods of interruption in support. Function varied according to the phase relationship of the LV and LVAD. The "best" FS measured during LVAD support was more closely related to the FS with the device switched off than the "worst" pump on FS. The "best" pump-on LV function is therefore most representative of intrinsic LV performance and can be used as a guide to recovery and the potential need for pump-off studies.
The study population consisted of 248 patients with at least five-year (mean 8.7+/-4.2 yrs.) history of drinking, mean age (48+/-4.2 years), including 132 subjects with arterial hypertension (mild or moderate according to WHO/ISH guidelines) and 116 normotensives. A group of 48 patients with essential arterial hypertension not consuming alcohol served as controls. Groups of alcoholics with hypertension, alcoholics with normal blood pressure and the controls were compared with respect to differences in standard BP measurements and 24hr blood pressure monitoring, left ventricular mass index, systolic and diastolic left ventricular function by echocardiography. In alcohol-dependent subjects the left ventricular mass index progressed with the increasing declared consumption of ethanol and duration of abuse. The incidence of LVH in drinking hypertensives (28%) did not differ from that in non drinking hypertensives (26%), p>0.05. In hypertensives irrespective of ethanol consumption delayed relaxation was a marker of left ventricular diastolic dysfunction. The present study did not confirm the hypothesis that left ventricular hypertrophy was responsible for diastolic impairment in alcohol abusers. Chronic ethanol consumption significantly deteriorated left ventricular diastolic function irrespective of its effect on blood pressure and left ventricular mass. In patients with the highest level of ethanol consumption and the longest duration of abuse ejection fraction was significantly lower than in patients with the lowest level of alcohol consumption and the shortest duration of abuse (EF 61.8% vs. EF 67.4%, p<0.05). Thus, the deterioration of systolic function is significantly related with the level of alcohol consumption and duration of abuse.
The influence of acute volume loading on right ventricular function immediately after extracorporeal circulation (ECC) was investigated in 25 patients undergoing elective aortocoronary bypass grafting. In addition to commonly monitored hemodynamic variables, right ventricular (RV) ejection fraction (EF) was measured by thermodilution technique using a new fast-response thermodilution catheter. In eight patients with concomitant severe stenosis (greater than 89%) of the right coronary artery (RCA), volume loading was followed by a decreased RVEF and cardiac output. In contrast, RVEF in the 17 patients without diseased RCA increased significantly, with an increase in cardiac output. Duration of aortic cross-clamping (i.e., ischemia) was more pronounced in the group with decreased RVEF due to RCA grafting. Increased end-diastolic volume and decreased RV contractility index indicated that patients with myocardial ischemia during cardiac surgery procedures sometimes were unable to make the adaptations required. We conclude that cardiocirculatory dysfunction associated with ECC may be caused by depressed RV function. Acute volume loading in this situation may lead to further deterioration of myocardial function due to RV failure, a condition which cannot be diagnosed readily at the bedside with the usual monitoring techniques.
Human immunodeficiency virus-infected (HIV) patients frequently present left ventricular dysfunction. Its etiology is not elucidated but zidovudine has been postulated as a possible cause factor. This study is an attempt to clarify this issue by evaluating the effect of zidovudine therapy on left ventricular function in these patients. We prospectively studied by echocardiographic examination 11 consecutive HIV-infected patients who were assigned for zidovudine therapy. We excluded patients that had a history or a physical examination suggestive of ischemic, rheumatic, congenital, or hypertensive heart disease. Patients with diabetes mellitus, excessive ethanol intake and patients on potentially cardiodepressant drugs were also excluded. Echocardiographic examination was performed immediately before the initiation of zidovudine therapy and 1 and 3 months later. Left ventricular diameters, mass and fractional shortening showed no significant difference from baseline, at 1 or 3 months after the initiation of zidovudine therapy. Our results suggest that zidovudine therapy has no effect on left ventricular diameters, mass or fractional shortening during a short term.
The recent expansion of interventional cardiovascular technologies has stimulated a concomitant expansion of noninvasive cardiac studies, both to assist in diagnosis and to evaluate treatment outcomes. Radionuclide ventricular function studies provide a reliable, reproducible means to quantify global left ventricular systolic performance, a critical determinant of prognosis in patients with cardiovascular disease. In addition, the ability to evaluate regional left ventricular wall motion and to assess ventricular performance during exercise have secured a fundamental role for such studies in the screening and treatment of patients with coronary artery disease. Radionuclide techniques have been extended to the evaluation of left ventricular relaxation/filling events, left ventricular systolic/diastolic function in the ambulatory setting, and with appropriate technical modifications, to the assessment of right ventricular performance at rest and with exercise. As a complement to radionuclide perfusion studies, cardiac blood-pool imaging allows for thorough noninvasive description of cardiac physiology and function in both normal subjects and in patients with a broad range of cardiovascular diseases.
Global left ventricular function (LVF) and segmental wall motion of the left ventricle are registered in 113 patients presenting a pure mitral stenosis (MS) and in a control group of 50 individuals. The segmental wall motion is measured on the end-diastolic-end-systolic frames of the left ventricle, obtained from right anterior oblique (RAO) monoplane cineangiography. Measurement of the segmental wall shortening is performed using the Stanford method. Group 1 includes 68 patients (60% of the total number of patients studied). These patients show no pathological contraction abnormality. In this group, the global LVF is not different from the control group. Group 2 includes 45 patients (40% of the total) for whom contraction abnormalities are present: anterior hypokinesis in 20% of the cases (anterior area mean shortening (AAS) = 18 +/- 8%; p less than 0.001 vs. group 1 and control group), and posterior hypokinesis in 20% of the cases (posterior area mean shortening (PAS) = 9.8 +/- 5.8%, p less than 0.001 vs. group 1 and control group). In this group, global LVF is impaired; ejection fraction (EF) = 0.57 +/- 0.1% (p less than 0.001 vs. group 1); velocity of circumferential fiber shortening (VCF) = 1 +/- 0.3 circ/s (p less than 0.001 vs. group 1); enddiastolic pressure (EDP) = 11 +/- 5 mmHg (p less than 0.01 vs. group 1). Segmental contraction abnormalities appear to be the main factor involved in the global LVF impairment. Segmental wall motion abnormalities could be related to subvalvular fibrosis, or LV filling difficulties, or principally, to a possible interplay between the right and the left ventricles.
Left ventricular function is an important prognostic indicator in patients with coronary artery disease. We have assessed a method of providing this information as an adjunct to myocardial perfusion imaging using Tc-99m MIBI (2-methoxy-2-methyl-isopropyl-1-isonitrile). Two separate studies, at rest and during exercise, were performed following an injection of 400-600 M Bq of Tc-99m MIBI in 62 patients. Cardiac gating permitted excellent myocardial edge definition during the cardiac cycle. Radionuclide fractional shortening (RFS) was calculated from the anteroposterior (AP) and the septum to lateral wall (SL) axes in diastole and systole. Results were compared with echocardiographic fractional shortening (EFS) and the ejection fraction (EF) obtained from the gated equilibrium blood pool using Tc-99m-labelled red blood cells. The RFS in the AP axis correlated closely with echocardiographic FS (r = 0.89, P less than 0.001). The RFS in both axes was averaged to provide a global RFS. Global RFS correlated closely with LV radionuclide EF (r = 0.83, P less than 0.001). Inter- and intra-observer reproducibility studies have shown a variability for the procedure of less than 10%. In conclusion, gated perfusion imaging with Tc-99m MIBI, provides useful functional information as an adjunct to perfusion imaging.
Right ventricular ejection fractions have been difficult to estimate clinically. It has been recently suggested that right ventricular ejection fractions can be calculated by thermodilution techniques with a fast-response thermistor and computer. These studies were performed to compare right ventricular ejection fractions obtained from thermodilution and biplane ventriculography. Ten pigs were instrumented with a right ventricular angiographic, thermodilution, and systemic arterial catheter. Right ventricular ejection fractions were determined by thermodilution and ventriculography at four times: (1) baseline, (2) infusion of isoporterenol (5 micrograms/min), (3) 50% of baseline mean arterial pressure produced by hemorrhage, and (4) reinfusion of isoproterenol during hypovolemia. A significant correlation existed between thermodilution and ventriculographic ejection fractions (r = 0.74, p = 0.004). However, during hypovolemia, thermodilution measurements of right ventricular ejection fraction were significantly lower than ventriculographic measurements (p less than 0.05). To determine if the position of the thermistor had a significant effect on thermodilution computations, right ventricular ejection fractions were computed by thermodilution in 10 additional pigs by means of a jugular and femoral insertion, as well as by ventriculography in each pig. Femoral insertion resulted in a greater distance from pulmonic valve to thermistor as compared with jugular placement (p = 0.005). Right ventricular ejection fractions obtained from femoral placement were significantly less than those obtained by jugular insertion (p = 0.008) and ventriculography (p = 0.006). There was no significant difference between jugular and ventriculographic ejection fractions (p = 0.35). Results from these studies demonstrates that thermodilution right ventricular ejection fraction measurements are strongly correlated to ventriculographic methods over a wide hemodynamic range and that improved accuracy is obtained when the pulmonic valve to thermistor distance is minimized. Thus thermodilution may provide a simple and repeatable means to monitor right ventricular function in the critical care setting.