Pulsed-wave Doppler Echocardiography Research Articles

Myocardial, erythropoietic, and metabolic adaptations to anemia of prematurity in infants with bronchopulmonary dysplasia

Objectives: The effects of anemia of prematurity during bronchopulmonary dysplasia (BPD) as well as on the metabolic and erythropoietic functions were determined before and after a transfusion. Fourteen anemic (Hb range: 65-88 gm/L), oxygen dependent (fraction of inspired oxygen ≤35%), nonventilated, preterm infants with BPD were studied at a postnatal age of 6 ± 2 weeks. Study Design: Cardiac output, heart rate, mean velocity of circumferential fiber shortening, shortening fraction (SF), and stroke volume were assessed by pulsed and continuous wave Doppler echocardiography. Values for resting oxygen consumption, carbon dioxide production, and energy expenditure were obtained by indirect calorimetry. The affinity of oxygenated hemoglobin was determined by a blood oxygen dissociation analyzer. Results: An increased hemoglobin level resulted in auppression of erythropoietin secretion ( p < 0.001), whereas heart rate, cardiac output, stroke volume, and SF decreased ( p < 0.05). Weight gain before and after transfusion were similar. Plasma lactate levels decreased from 1.6 ± 0.3 to 1.2 ± 0.3. Oxygen consumption, carbon dioxide production, and energy expenditure were not affected. Conclusions: Anemia of prematurity and BPD increase heart rate, cardiac output, stroke volume, and SF. These hemodynamic compensatory responses are normalized by transfusion. (J Pediatr 1998;132:630-4.)

Restrictive Left Ventricular Filling Patterns Are Predictive of Diastolic Ventricular Interaction in Chronic Heart Failure

Objectives. The purpose of this study was to determine whether restrictive left ventricular (LV) filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure.Background. We recently demonstrated a diastolic ventricular interaction in ∼50% of a series of patients with chronic heart failure, as evidenced by paradoxic increases in LV end-diastolic volume despite reductions in right ventricular end-diastolic volume during volume unloading achieved by lower body negative pressure (LBNP). We reasoned that such an interaction would impede LV filling in mid and late diastole, but would be minimal in early diastole, resulting in a restrictive LV filling pattern.Methods. Transmitral flow was assessed using pulsed wave Doppler echocardiography in 30 patients with chronic heart failure and an LV ejection fraction ≤35%. Peak early (E) and atrial (A) filling velocities and E wave deceleration time were measured. Left ventricular end-diastolic volume was measured using radionuclide ventriculography before and during −30-mm Hg LBNP.Results. Nine of the 11 patients with and 2 of the 16 patients without restrictive LV filling patterns (E/A >2 or E/A 1 to 2 and E wave deceleration time ≤140 ms) increased LV end-diastolic volume during LBNP (p = 0.001). The change in LV end-diastolic volume during LBNP was correlated with the baseline A wave velocity (r = −0.52, p = 0.005) and E/A ratio (r = 0.50, p = 0.01).Conclusions. Restrictive LV filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. Volume unloading in the setting of diastolic ventricular interaction allows for increased LV filling. Identifying patients with chronic heart failure and restrictive filling patterns may therefore indicate a group likely to benefit from additional vasodilator therapy.

Surgical Delay for Acute Type A Dissection With Malperfusion

Background. An acute type A aortic dissection is considered a surgical emergency. Review of the risk factors for a type A dissection showed that preoperative malperfusion was associated with a 22% (2/9) intraoperative mortality and an 89% (8/9) hospital mortality. Intraoperative deaths were secondary to pulmonary failure resulting from capillary leak; the remaining patients died of multiorgan failure resulting from reperfusion injury. Methods. The surgical delay approach was adopted for malperfused patients, and treatment in these patients included percutaneous reperfusion, with aortic fenestration and branch stenting where appropriate. Twenty patients had a type A dissection and malperfusion shown by pulsed-wave Doppler echocardiography, transesophageal echocardiography, or spiral computed tomographic scanning. Malperfusion was documented by angiography. After reperfusion, all patients’ conditions were stabilized in the intensive care unit; intravenous beta-blockers were administered to decrease the maximum rate of increase of left ventricular pressure. Once patients completely recovered from the consequences of malperfusion, surgical repair was performed. Statistical comparison of the non-delay and delay groups was performed using Fisher’s exact test and Student’s t test. Multiple logistic regression analysis was used to establish independent predictors for mortality. Results. The mean delay to repair was 20 days (2 to 67 days). Four (31%) patients were discharged home and readmitted for operation. Three patients (15%) died preoperatively, 1 of retrograde dissection and rupture and 2 of reperfusion injury. Seventeen underwent surgical repair, with two deaths (12%); 15 (75%) were discharged, with an average follow-up of 16.8 months ( p < 0.003). Delay was the only independent predictor of outcome. Conclusions. Patients with an acute type A dissection and malperfusion should undergo percutaneous reperfusion, and surgical repair should be delayed until the reperfusion injury resolves.

Doppler Evaluation of Left Ventricular Diastolic Inflow and Outflow Waveforms in Normal Subjects.

The measurements of the left ventricular inflow parameters do not necessarily reflect the measurements of the respective outflow ones. The A wave transit time from the mitral valve to the left ventricular outflow tract has been demonstrated to have a fair correlation with measures of the left ventricular late diastolic stiffness. We performed this study to obtain the normal patterns of the diastolic left ventricular outflow as well as inflow waveforms and to evaluate the roles of aging and other physiological parameters in their evolution. The study population consisted of 60 healthy subjects (aged 22-66 years). They were divided into three groups: group 1 (aged 20-34 years), group 2 (aged 35-49 years), and group 3 (aged 50-70 years). Pulse-wave Doppler echocardiography was performed to get the patterns of diastolic left ventricular inflow and outflow waveforms. With aging, the peak velocity and velocity-time integral of the transmitted transmitral E wave decreased, and those of the transmitted transmitral A wave increased with a progressive decrease in their ratio of transmitted transmitral E to A wave. The diastolic left ventricular inflows followed a similar aging course. There was no obvious aging trend in the A wave transit time from the mitral valve to the left ventricular outflow tract. Multiple linear regression analyses selected age as the most important determinant in the differences in most left ventricular inflow and outflow indices among normal subjects. Besides, heart rate had modest influences on some Doppler indices. This study confirms the age related changes in the left ventricular inflow waveforms and further establishes the concept that the diastolic left ventricular outflow waveforms are also significantly influenced by age and heart rate. Hence, both factors should be taken into account in interpreting the diastolic left ventricular outflow as well as inflow indices.

Use of Pulsed-Wave Doppler Echocardiography to Measure Changes in MPAP: Is Further Validation Required?

Use of Pulsed-Wave Doppler Echocardiography to Measure Changes in MPAP: Is Further Validation Required?

Determinants of Functional Capacity in Chronic Mitral Regurgitation Unassociated With Coronary Artery Disease or Left Ventricular Dysfunction

Impaired functional capacity is common in patients with mitral regurgitation (MR), but the determinants of functional capacity in patients with normal left ventricular (LV) function are unclear. Forty patients with chronic, isolated, nonrheumatic MR with no coronary artery disease underwent exercise echocardiography with continuous expired gas analysis. Cardiac output and regurgitant stroke volume were measured at rest and immediately after exercise by pulsed-wave Doppler echocardiography. For controls, 17 healthy volunteers without MR were also studied. Patients achieved a significantly lower VO2max compared with controls (25.6 ± 7.7 vs 31.7 ± 7.7 ml/kg/min, p = 0.008). VO2max showed better correlations with exercise cardiac output than with cardiac output at rest in both patients and controls. Multiple linear regression identified exercise cardiac output (partial r = 0.65), patient age (partial r = −0.56), and gender as independent determinants of VO2max (multiple R = 0.85, p <0.001). Cardiac output at rest, LV ejection fraction, regurgitant stroke volume, and fraction were not significant determinants. With exercise, the regurgitant stroke volume increased in 13 patients and decreased in 27 patients. The former 13 patients had a significantly lower exercise cardiac output (7.4 ± 2.5 vs 9.4 ± 2.6 L/min, p = 0.026). Patients who stopped exercise due to dyspnea (n = 7) had a significantly lower exercise cardiac output and VO2max compared with those who stopped due to fatigue (n = 33), with no differences in resting or exercise regurgitant volume. Patients with an increase in LV end-systolic volume with exercise (n = 8) also had a significantly lower exercise cardiac output (6.9 ± 1.9 vs 9.2 ± 2.7 L/min, p = 0.037) and showed a trend toward a lower VO2max (21 ± 7.5 vs 26 ± 6.4 ml/kg/min, p = 0.07). In patients with chronic MR, exercise cardiac output is the major determinant of VO2max. Regurgitant volume and fraction are not related to functional capacity. Limitations in functional capacity in these patients may be more related to a diminished cardiac reserve than to a large regurgitant volume.Maximum oxygen consumption (VO2max) showed better correlations with exercise cardiac output than with cardiac output at rest in both patients with chronic mitral regurgitation and controls. Multiple linear regression identified only exercise cardiac output (partial r = 0.65), patient age (partial r = −0.56), and gender as independent determinants of VO2max (multiple R = 0.85, p <0.001). Severity of regurgitation was not related to VO2max.

Ductus arteriosus-dependent pulmonary circulation secondary to cardiac malformations in fetal life.

The objective of this study was to describe the characteristic prenatal findings of a ductus arteriosus-dependent pulmonary circulation secondary to cardiac malformations. B-mode, color and pulsed wave Doppler echocardiography were performed in seven fetuses with severe pulmonary stenosis or atresia. All findings were confirmed postnatally by echocardiography and cardiac catheterization or autopsy. Severe fetal pulmonary stenosis or atresia was characterized by decreased pulmonary valve diameters, frequently with reduced pulmonary artery diameters, increased flow velocities or absent flow across the stenotic pulmonary valve, increased ascending aorta diameters, slightly increased aortic velocities and normal umbilical and middle cerebral artery Doppler wave forms. In all cases, prenatal assessment of neonatal ductus dependence was possible by demonstrating reverse flow across the fetal ductus with peak systolic velocities ranging from 0.9-2.0 m/s and absent diastolic flow. Ductal diameters were slightly decreased, ranging from 2-4 mm. Prenatal detection of a ductus-dependent pulmonary circulation is a strong indication of the presence of severe pulmonary stenosis or atresia. Its diagnosis allows avoidance of maternal administration of drugs with constrictive effects upon the ductus, interdisciplinary planning of perinatal management, early postnatal confirmation of the diagnosis, and early postnatal intervention, in particular administration of prostaglandins to prevent life-threatening ductal closure.

A Study for Diastolic Functions in Patients with Early Acute Myocardial Infarction

Background:Doppler echocardiography is a non-invasive technique that has been used to evaluate LV diastolic dysfunction. Impaired left ventricular diastolic filling is known to occur in patients with coronary artery disease. Compared with those in normal subjects, Doppler-derived transmitral blood flow velocities have been reported to be reduced during early diastolic filling and to be compensatory elevated subsequent to atrial systole in patients with coronary artery disease. But stiffness of myocardium normalize the E/A ratio, and normal E/A ratio may reveal increased ventricular filling pressure. We tried to investigate left ventricular filling parameters by Doppler echocardiography in patients with early myocardial infarction, and to compare left ventricular diastolic function regarding infarct location on EKG, one or multi vessel disease on coronary angiography, and treatment modality. Methods:From September 1993 to August 1995, Pulsed wave Doppler echocardiography was performed in patients with early acute myocardial infarction(N=95 and control group(N=20 within 5 days after admission, and parameters of diastolic function was evaluated. Results:Echocardiographic data showed significant differences in mean ejection fraction, mean left ventricular mass, and mean left ventricular mass index between two groups. There was no significant difference in E/A ratio, deceleration time, and isovolumetric relaxation time between two groups. Neither, there was significant difference in each diastolic parameter for infarct related wall on EKG. And there was no significant difference in deceleration time for one or multi vessel disease on coronary angiography, treatment modality(conservative treatment, thrombolytic therapy, or primary PTCA. Conclusion:In patients with early acute myocardial infarction, left ventricular diastolic dysfunc- * 본 논문의 요지는 1995년도 대한 순환기확회 추계 학술대회 석상에서 발표되었음.

Retrograde atrial kick in acute aortic regurgitation. Study of mitral and pulmonary venous flow velocities by transthoracic and transesophageal echocardiography.

The purpose of this study was the comprehensive evaluation of the changes in pulmonary venous and mitral flow velocities of patients with acute and chronic severe aortic regurgitation. Transmitral flow velocities obtained with pulsed-wave Doppler echocardiography have been used to provide information on left ventricular (LV) filling and diastolic function. Pulmonary venous flow tracings are an important adjunct to LV inflow pattern in assessing LV diastolic function. Fourteen patients with severe aortic regurgitation (8 chronic and 6 acute) and in sinus rhythm were examined by transthoracic and transesophageal pulsed Doppler echocardiography. Mitral and pulmonary flow velocities were recorded and compared. All patients had ejection fractions > 40%. Early mitral flow peak velocity was higher in patients with acute regurgitation (p < 0.001). The mitral A wave was absent in five patients with acute regurgitation. In contrast, a prominent reverse atrial pulmonary systolic wave AR was demonstrated in these patients. Peak diastolic velocity of the pulmonary venous flow was greater in patients with acute aortic regurgitation (0.76 +/- 0.13) than in patients with chronic aortic regurgitation (0.40 +/- 0.09) (p < 0.001). Peak systolic velocity did not differ significantly between the two groups. The systolic fraction of pulmonary venous flow in patients with acute aortic regurgitation was lower (0.43 +/- 0.05) than that of patients with chronic regurgitation (0.63 +/- 0.1) (p < 0.01). All patients with acute aortic regurgitation had an S/D ratio < 1, while those with chronic regurgitation had an S/D > 1 (p < 0.001) and an E/A < 1. Patients with severe acute aortic regurgitation showed a retrograde atrial kick (absence of transmitral A wave with prominent pulmonary AR wave). These patients had an S/D ratio < 1 (restrictive Doppler pattern). Patients with chronic aortic regurgitation exhibited a Doppler pattern of abnormal LV relaxation (E/A < 1, S/D > 1).

Heart Function in Patients with Chronic Glomerulonephritis and Mildly to Moderately Impaired Renal Function: An Echocardiographic Study

Schroeder AP, Kristensen Bø, Nielsen CB, Pedersen EB. Heart function in patients with chronic glomerulonephritis and mildly to moderately impaired renal function.Left ventricular hypertrophy and diastolic heart dysfunction have been reported in essential hypertension and in patients with chronic renal failure, treated with haemodialysis, but a close association with blood pressure (BP) level has not been uniformly documented. Thus, other factors could be involved in the pathogenesis of cardiac dysfunction. The aims of the present echocardiographic study were to investigate cardiac morphology and function in patients with chronic glomerulonephritis with mildly to moderately impaired renal function, and to study the relation between echocardiographic findings and glomerular filtration rate (GFR), BP and age. Twenty patients with chronic glomerulonephritis and 14 healthy controls, of the same age- and sex-distribution, were examined by 2D-, M-mode and pulsed-wave Doppler echocardiography. In patients, GFR was determined as plasma clearance of Cr-EDTA. The patients had significantly thicker left ventricular (LV) posterior walls in end diastole (8.7 vs 8.1 mm, p<0.05), and a higher LV mass index (106.5 vs 93.8 g/m2, p<0.05). Systolic functional indices, i.e. LV fractional shortening and LV ejection fraction, were statistically significantly lower in patients than in controls (p<0.05). LV diastolic function in patients was characterized by a statistically significantly lower early peak flow velocity (E-Vmax) (0.66 compared with 0.8 ds) and early to late peak flow velocity ratio (E/A ratio) (1.07 vs 1.41), as well as E/A ratio of time velocity indices (VTI-E/A) (1.45 vs 1.99) (p<0.05). The right ventricular filling indices showed a tendency towards a lower E-Vmax in patients (0.55 compared with 0.62 ds, p=0.1). In patients, statistically significant negative correlations were found between age and mitral E/A ratio (F-0.76, p<0.0001), as well as LV VTI-E/A (F-0.81, p<0.0001). The same trend was seen for the tricuspid E/A ratio. No statistically significant correlations were found in patients between mitral or tricuspid E/A ratio and GFR, BP, LV mass or heart rate. In conclusion: in a group of patients with chronic glomerulonephritis and mildly to moderately impaired renal function, it was found by means of echocardiography that there was a higher LV mass index and decreased systolic function, when compared with healthy controls. In addition, the patients had diastolic dysfunction of primarily the left ventricle. The echocardiographic findings were not correlated to BP level or renal function. 'This suggests that factors other than GFR or BP per se might be involved in the pathogenesis of cardiac dysfunction, at an early stage.

Doppler echocardiographic index for assessment of global right ventricular function

Echocardiographic assessment of right ventricular function remains difficult and challenging. However, there is considerable clinical need for a simple, reproducible, and reliable parameter of right ventricular function in patients with right-sided heart disease. The purpose of this study was to assess the clinical value of a Doppler-derived index, combining systolic and diastolic intervals of the right cycle, in assessing global right ventricular function in patients with primary pulmonary hypertension. The study population comprised 26 consecutive patients with primary pulmonary hypertension and 37 age-matched normal subjects. The sum of right ventricular isovolumetric contraction time and isovolumetric relaxation time was obtained by subtracting right ventricular ejection time from the interval between cessation and onset of the tricuspid inflow velocities with pulsed-wave Doppler echocardiography. An index of combined right ventricular systolic and diastolic function was obtained by dividing the sum of both isovolumetric intervals by ejection time. The index was compared with available parameters of systolic or diastolic function, clinical symptoms, and survival. Right ventricular isovolumetric contraction time and isovolumetric relaxation time were prolonged significantly in patients with primary pulmonary hypertension (85 ± 41 msec and 135 ± 43 msec) compared with normal subjects (38 ± 7 msec and 49 ± 9 msec, respectively; p < 0.001). Ejection time was shortened significantly in patients with pulmonary hypertension (241 ± 43 msec versus normal [322 ± 21 msec]; p < 0.001). However, the index was the single most powerful variable to discriminate patients with primary pulmonary hypertension from normal subjects (0.93 ± 0.34 versus 0.28 ± 0.04; p < 0.001) and was the strongest predictor of clinical status and survival. The index was not significantly affected by heart rate, right ventricular pressure, right ventricular dilation, or tricuspid regurgitation. It is well known that right ventricular systolic and diastolic dysfunction coexist in patients with primary pulmonary hypertension. This article reports the use of an easily obtainable Doppler-derived index that combines elements of systolic and diastolic function. This index appears to be a useful noninvasive means that correlates with symptoms and survival in patients with primary pulmonary hypertension.

Echocardiographic Study of Residual Shunt after Hemoclip Closure of Patent Ductus Arteriosus in Neonates

Residual shunt was determined by postoperative echocardiogram after hemoclip closure of patent ductus arteriosus in 22 neonates, and compared with the findings in 15 neonates who had conventional ligation of the ductus between January 1992 and December 1994. There were no significant postoperative complications related to the surgery. The study showed no residual shunt across the ductus by color and pulsed wave Doppler echocardiography in either group, with the exception of one patient who required a second hemoclip operation. We conclude that the method of closure with a hemoclip is safe and effective.

Regional left atrial stasis during fibrillation and flutter determinants and relation to stroke

Objectives. This study sought to 1) determine the location of left atrial stasis during atrial arrhythmia; 2) define the degree of stasis associated with significant risk of stroke; and 3) identify clinical or transthoracic echocardiographic data useful for predicting left atrial stasis.Background. Prior studies suggest that stroke during atrial arrhythmia is related to stasis in either the body of the left atrium or the appendage. Recent data indicate that appendage stasis is associated with appendage thrombus formation, but stroke during atrial arrhythmia occurs frequently in the absence of appendage stasis.Methods. Blood flow velocity was measured in multiple sites in the body of the left atrium and in the appendage by transesophageal pulsed wave Doppler echocardiography in 89 patients with atrial fibrillation or flutter. Regional velocities were related to the frequency of probable embolic stroke and to clinical and transthoracic echocardiographic variables.Results. The lowest velocity region was either the posterior left strium or the appendage. Stroke frequency increases progressively and steeply with velocity <15 cm/s is either region; this cutoff value had an 87% sensitivity and 40% specificity for stroke. Factors related to stasis were low left atrial ejection fraction, mitral regurgitation <3+, fibrillation (vs. type 1 flutter), left ventricular dilation and mitral valve area <2.0 cm2.Conclusions. Posterior left atrial stasis appears to the as important as appendage statis for the risk of stroke, which increases sleeply with lower blood flow velocity in either region. Patients likely to have severe stasis during atrial arrhythmia are those with left ventricular dilation and low atrial ejection fraction accompanying left atrial dilation. Direct measurement of atrial velocity by transesophageal echocardiography appears to be useful for the identification of patients at risk for stroke during atrial arrhythmia.

ANEMIA OF PREMATURITY (AOP) DURING BRONCHOPULMONARY DYSPLASIA (BPD): MYOCARDIAL, METABOLIC AND ERYTHROPOIETIC ADAPTATIONS. † 1145

The benefits of transfusion in AOP during BPD remain to be defined. Myocardial dysfunction has. been shown to be a sensitive and early indicator of the adverse effects of anemia. To determine the effects of AOP during BPD on myocardial as well as on the metabolic and erythropoietic functions, a study was planned to evaluate these parameters (mean±SEM) before (PR) and after (PO) a transfusion (20cc/kg of Packed RBC'S). Twelve anemic (Hb range: 71-88g/L) preterm infants (gest.age: 27.8±0.6 wks, birthweight: 1022±71.7g) were studied at a postnatal age of 6.6±0.5 wks with clinically stable BPD with O2 supplement (FiO2 30-35%). All measurements were done before and 48 hrs after the transfusion. Cardiac output(CO, L/kg/min), heart rate (HR,bpm) and myocardial function (mean velocity of circumferential fiber shortening, shortening fraction (SF%) and peak aortic velocity) were assessed by pulsed and continuous wave Doppler echocardiography. Resting O2 consumption (VO2, mL/kg/min), CO2 production (VCO2) and energy expenditure (REE, Kcal/kg/d) were obtained by indirect calorimetry. Hb-O2 affinity was assessed by determining P50 (mm Hg) by gas mixing tonometry. Erythropoietin (EPO)(mU/ml), 2,3DPG (μmol/g Hb) and lactate (mmol/L) were measured by RIA & enzymatically respectively. RESULTS: Table Lactate levels decreased from 1.6±0.2 to 1.0±0.1 (p<.01). This study showed that increased Hb level resulted in a suppression of EPO secretion (**p<.01). HR & CO decreased (*p<.05); there was a decrease in SF (p<.01) an indice of myocardial function. Weight gain / day× 7 days prior and after transfusion were similar (14.5±2 vs 15.3±1 g/kg/d). Metabolic demands as shown by VO2, VCO2 and REE were not affected. Transfusion of preterm infants with AOP and BPD decreases SF therefore diminishing the risk of high output cardiac failure. These findings could be of importance when establishing indications for transfusion for anemia of prematurity during BPD.

Cardiac-specific overexpression of phospholamban alters calcium kinetics and resultant cardiomyocyte mechanics in transgenic mice.

Phospholamban is the regulator of the cardiac sarcoplasmic reticulum (SR) Ca(2+)-ATPase activity and an important modulator of basal contractility in the heart. To determine whether all the SR Ca(2+)-ATPase enzymes are subject to regulation by phospholamban in vivo, transgenic mice were generated which overexpressed phospholamban in the heart, driven by the cardiac-specific alpha-myosin heavy chain promoter. Quantitative immunoblotting revealed a twofold increase in the phospholamban protein levels in transgenic hearts compared to wild type littermate hearts. The transgenic mice showed no phenotypic alterations and no changes in heart/body weight, heart/lung weight, and cardiomyocyte size. Isolated unloaded cardiac myocytes from transgenic mice exhibited diminished shortening fraction (63%) and decreased rates of shortening (64%) and relengthening (55%) compared to wild type (100%) cardiomyocytes. The decreases in contractile parameters of transgenic cardiomyocytes reflected decreases in the amplitude (83%) of the Ca2+ signal and prolongation (131%) in the time for decay of the Ca2+ signal, which was associated with a decrease in the apparent affinity of the SR Ca(2+)-ATPase for Ca2+ (56%), compared to wild type (100%) cardiomyocytes. In vivo analysis of left ventricular systolic function using M mode and pulsed-wave Doppler echocardiography revealed decreases in fractional shortening (79%) and the normalized mean velocity of circumferential shortening (67%) in transgenic mice compared to wild type (100%) mice. The differences in contractile parameters and Ca2+ kinetics in transgenic cardiomyocytes and the depressed left ventricular systolic function in transgenic mice were abolished upon isoproterenol stimulation. These findings indicate that a fraction of the Ca(2+)-ATPases in native SR is not under regulation by phospholamban. Expression of additional phospholamban molecules results in: (a) inhibition of SR Ca2+ transport; (b) decreases in systolic Ca2+ levels and contractile parameters in ventricular myocytes; and (c) depression of basal left ventricular systolic function in vivo.

Short- and long-term effects of nisoldipine on cardiac function and exercise tolerance in patients with hypertrophic cardiomyopathy

Nisoldipine is a second generation dihydropyridine calcium antagonist having characteristics of strong coronary artery dilating effect and less negative inotropic action. The purpose of this study was to evaluate the effect of nisoldipine on the cardiac function (systolic and diastolic) and the exercise tolerance, in patients with hypertrophic cardiomyopathy (HCM). Twenty-three patients with HCM were studied. We measured the following indices using M-mode and pulsed wave Doppler echocardiography before and after nisoldipine therapy; left ventricular fractional shortening (LVFS), isometric relaxation time (IRT), deceleration half-time (DHT) of early diastolic mitral (E) flow, late diastolic mitral (A) flow and A/E ratio. Symptom-limited treadmill exercise test was performed. Exercise tolerance (EX) time was measured. Nisoldipine of 10 mg/day was orally administered. Same tests were repeated on day 14 and after 6 months. 1) Short-term effects; LVFS did not change (55.9 +/- 5.9%-->57.0 +/- 7.4%, NS) after 2 weeks. However, LV diastolic function significantly improved (IRT; 92.1 +/- 7.7 ms-->85.2 +/- 11.6 ms, p < 0.05, DHT; 70.7 +/- 16.2 ms-->63.3 +/- 3.7 ms, p < 0.05). EX time increased (8.9 +/- 2.6 min-->10.0 +/- 3.3 min, p < 0.05), 2) Long-term effects; LV diastolic function had a tendency toward improvement, but is statistically not significant (IRT; 91.1 +/- 7.6-->83.8 +/- 11.6 ms, DHT; 73.1 +/- 23.4-->61.0 +/- 11.4 ms, A/E; 1.26 +/- 0.29-->1.11 +/- 0.36) after 6 months. EX time was significantly increased (9.4 +/- 1.7--> 10.1 +/- 1.7 min, p < 0.05). Nisoldipine improved LV diastolic dysfunction and exercise tolerance in patients with HCM. These effects were similar to the first generation calcium antagonists. LV diastolic dysfunction may be improved due to the reduction of intracellular calcium concentration and the relief of myocardial ischemia by strong coronary artery dilating effect. However, nisoldipine did not affect the LV systolic function because of its less negative inotropic effect.

Acute hypoxic pulmonary vasoconstriction in man is attenuated by type I angiotensin II receptor blockade

We examined the hypothesis that angiotensin II (ANG II) is a modulator of acute hypoxic pulmonary vasoconstriction (HPV) by looking at the effect of losartan, a selective type 1 ANG II receptor antagonist, on acute HPV in man. Ten normal volunteers were studied on two separate days. They either received pre-treatment with losartan 25, 50, 100, 100 mg respectively on four consecutive days or matched placebo. They were then rendered hypoxaemic, by breathing an N2/O2 mixture for 20 min to achieve an SaO2 of 85-90% adjusted for a further 20 min to achieve an SaO2 of 75-80%. Pulsed wave Doppler echocardiography was used to measure mean pulmonary artery pressure (MPAP), cardiac output and hence pulmonary vascular resistance (PVR). Baseline MPAP and PVR (during normoxaemia) were unaffected by losartan pre-treatment compared with placebo. However, losartan significantly reduced MPAP at both levels of hypoxaemia compared with placebo: 14.7 +/- 0.7 vs 19.0 +/- 0.7 mmHg at an SaO2 85-90% (P < 0.01) and 20.0 +/- 0.7 vs 25.7 +/- 0.8 mmHg at an SaO2 75-80% (P < 0.05) respectively. Similarly losartan significantly reduced PVR compared to placebo: 191 +/- 9 vs 246 +/- 10 dyne.s.cm-5 at an SaO2 85-90% (P < 0.005) and 233 +/- 12 vs 293 +/- 18 dyne.s.cm-5 at an SaO2 75-80% (P < 0.05), respectively. Pre-treatment with losartan, however, had no significant effect on systemic vascular resistance although losartan compared to placebo resulted in a significant (P < 0.05) reduction in mean arterial pressure at an SaO2 75-80%: 78 +/- 2 vs 87 +/- 2 mmHg. Losartan had no effect on baseline pulmonary haemodynamics but significantly attenuated acute hypoxic pulmonary vasoconstriction, suggesting that angiotensin II plays a role in modulating this response in man via its effects on the type 1 angiotensin II receptor.

Review Article: Echocardiography

SummaryEchocardiography encompasses a number of specific imaging techniques. The two‐dimensional (2‐D) echocardiogram is used to identify lesions of the heart and great vessels, assess myocardial function and provide a template for guiding contrast echocardiography, colour‐coded Doppler echocardiography and spectral Doppler studies. M‐mode echocardiography is used to measure cardiac size and ventricular function and can be combined with contrast or colour‐coded Doppler studies for accurate timing of flow events. Pulsed wave and continuous wave Doppler echocardiography display the direction and velocity of red blood cells within the heart and circulation. Continuous wave Doppler studies are used to calculate pressure gradients in the circulation. Any of the Doppler techniques can be used to identify abnormal or high velocity flow responsible for pathologic heart murmurs. Each Doppler format is complementary to the others: colour‐coded Doppler is used to screen large areas for flow disturbances; pulsed wave Doppler can pinpoint regions of abnormal flow; and continuous wave Doppler quantifies the maximal velocities of blood flow across cardiac lesions. Echocardiographic studies are very useful for the diagnosis and assessment of horses with cardiac murmurs, arrhythmias, and poor exercise performance. A number of cardiac disorders can be evaluated by echocardiography, including: cardiac malformation, valvular heart disease, cardiomyopathy, bacterial endocarditis, pericardial effusion, and congestive heart failure. When combined with a careful clinical examination, exercise evaluation and results of electrocardiography, the echocardiogram provides the best overall clinical assessment of the equine heart.

Diastolic Left‐to‐Right Shunting in Uncomplicated Ventricular Septal Defect

The systolic left‐to‐right shunt in patients with uncomplicated ventricular septal defect is associated with a classic loud murmur, and is well described. The additional diastolic left‐to‐right shunt, always silent, is less well recognized. Left‐to‐right diastolic shunt flow is directly related to the defect size, to the diastolic pressure gradient between the left and right ventricle, and to the duration of diastole. The purpose of this study was to evaluate by Doppler echocardiography the duration, magnitude, and flow velocity characteristics of the diastolic left‐to‐right shunt. There were 30 adult patients with uncomplicated ventricular septal defects studied by color, pulsed, and continuous wave Doppler echocardiography. In each patient, the uncomplicated ventricular septal defect was visualized by two‐dimensional echocardiography and/or Doppler echocardiography, and the systolic and diastolic left‐to‐right shunt flow was identified by Doppler echocardiography. Accurate Doppler flow velocity peaks twice, in beginning and again at end diastole. The mean diastolic flow velocity was 0.5–1.5 msec (average 0.83 ± .22 msec). This flow velocity was markedly lower than the mean systolic shunt flow velocity (2.4–5.3 msec, average 3.8 ± .7 msec). The Doppler flow velocity integral was 0.17–0.64 m (average 0.36 ± 0.14), markedly smaller than the systolic flow velocity integral (0.8–1.8 m, average 1.3 ± 0.3). The diastolic left‐to‐right shunt flow was 12–41% (average 21 ± 8) of total (systolic and diastolic) shunt flow. In conclusion: Diastolic left‐to‐right shunts can be identified in all patients with uncomplicated ventricular septal defects, and analyzed in the majority of patients. A significant degree of the left to right shunting in uncomplicated ventricular septal defects occur during diastole.

Pulmonary vein doppler echocardiography after left atrial operation

Intraoperative transesophageal echocardiography provides the surgical team with important guidance during operations for congenital heart disease. Doppler echocardiography adds hemodynamic information to that provided by two-dimensional imaging. Here we describe intraoperative pulmonary vein Doppler echocardiography after operation involving the left atrium. Intraoperative two-dimensional and pulsed-wave Doppler echocardiography of pulmonary veins were performed after surgical repair of anomalous pulmonary venous return in 4 patients. In 3 patients, intraoperative pulmonary vein Doppler findings were suggestive of obstruction. The surgical repair was thought to be excellent, and there was no obstruction apparent anatomically or clinically. No further intervention was performed, and all patients recovered uneventfully. No pulmonary venous obstruction was noted on follow-up two-dimensional echocardiography, and follow-up pulmonary vein Doppler echocardiography showed the expected pattern. An obstructive pattern in the pulmonary vein Doppler was seen in 3 of 4 patients studied immediately after repair of anomalous pulmonary venous return. No obstruction, however, was manifest then or subsequently. The abnormal Doppler pattern, thus, is not indicative of pulmonary venous obstruction. We propose that acute postoperative changes in left atrial volume and compliance and acute postoperative tissue changes in the left atrium explain the abnormal pulmonary vein Doppler patterns observed.