Left Ventricular Internal Diameter In Diastole Research Articles

Effect of Atropine-dobutamine Stress Test on Left Ventricular Echocardiographic Parameters in Untrained Warmblood Horses

The aim of this study was to investigate the effect of combined atropine low-dose dobutamine stress test on left ventricular parameters in adult warmblood horses, to establish a potential protocol for pharmacological stress echocardiography. Seven healthy untrained warmblood horses aged 9 to 22 years were used. Heart rate (HR) and left ventricular B- and M-mode dimensions were recorded at baseline and during stress testing with 35 microg/kg atropine IV followed by incremental dobutamine infusion of 2 to 6 microg/kg/min. HR increased significantly (P < .05) during the pharmacological challenge, and a maximal HR of 156.6 +/- 12.5 bpm was reached at maximal dobutamine infusion rate. Systolic and diastolic interventricular septum thickness, systolic and diastolic left ventricular free wall thickness, and fractional shortening increased significantly and reached a maximum at the highest infusion rate (mean +/- SD: 4.51 +/- 0.27 versus 5.65 +/- 0.31 cm, 2.89 +/- 0.19 versus 3.78 +/- 0.10 cm, 3.72 +/- 0.34 versus 4.77 +/- 0.18 cm, 2.44 +/- 0.28 versus 3.11 +/- 0.34 cm, 34.98 +/- 3.82 versus 50.56 +/- 3.42%, respectively). Systolic and diastolic left ventricular internal diameter decreased significantly during dobutamine infusion. Left ventricular external and internal area were significantly lower at a dobutamine infusion rate of 2 microg/kg/min but no further decrease was observed during the subsequent steps. Systolic and diastolic myocardial area was significantly lower after the administration of dobutamine but not significantly different during dobutamine infusion, when compared to baseline values. This pharmacological stress test induced significant changes in left ventricular echocardiographic parameters in adult warmblood horses. Additional research should evaluate the value of this stress test in horses suffering from cardiac disease.

Low-intensity race training does not induce left ventricular hypertrophy in 2-year-old Standardbred trotters

The objective of the study was to evaluate the effect of low-intensity training on cardiac dimensions in young trotters compared with an untrained control group by use of echocardiography. Seventy-five 2-year-old Standardbred trotters undergoing low-intensity race training 3 to 4 days per week for 6 months were studied. Nine untrained age-matched Standardbred trotters served as controls. All horses were examined by echocardiography twice with an interval of 6 months. Left ventricular (LV) morphology and systolic function were studied with 2-dimensional guided M-mode echocardiography. An estimation of body weight was based on measurement of the chest girth circumference. A significant increase in LV internal diameter in diastole (LVIDd) (P = .005), LV muscle mass (LV mass) (P < .001), and mean wall thickness (MWT) (P < .001) during the 6-month study period for both the trained and untrained groups was observed. No significant differences in LVIDd, LV mass, MWT, and relative wall thickness (RWT) were observed between the 2 groups. Body weight was significantly correlated to the size of the cardiac measures LVIDd, LV mass, and MWT (P < .001). After the 6-month training period, the colts had larger LVIDd (P = .004) and LV mass (P = .002) than the fillies. The results indicate that the cardiac morphologic changes observed were mainly a result of normal physiologic growth. The amount of training over the 6-month period did not alter the different measures significantly from those of control group. When evaluating cardiac adaptive responses to training in young horses, serial echocardiographic measurements have to be performed. It is crucial to be aware of the considerable growth of the heart due to normal physiologic growth. In addition, it seems that an intense workload is required to achieve a training-induced increase in LV mass.

Severity of left ventricular remodeling defines outcomes and response to therapy in heart failure: Valsartan heart failure trial (Val-HeFT) echocardiographic data

ObjectivesThe objective of this study was to test the hypothesis that the severity of left ventricular remodeling predicts the response to treatment and outcomes in chronic heart failure. BackgroundReversal of remodeling should produce the most favorable outcome in patients with the most severe remodeling. MethodsIn 5,010 heart failure patients on background therapy and randomized to valsartan and placebo, serial recordings of left ventricular internal diastolic diameter (LVIDd) and ejection fraction (EF) were read at sites that had to meet qualifying standards before participating. Baseline LVIDd and EF were pooled across treatments and retrospectively grouped by quartiles Q1 to Q4, representing best to worst. Kaplan-Meier survival curves were obtained by the log-rank test. Q1 was compared with Q4 for mortality and combined mortality and morbidity (M + M) from Cox regression risk ratios (RRs). Valsartan versus placebo changes from baseline in LVIDd and EF were analyzed by quartiles from analysis of covariance. Valsartan and placebo were compared by RRs for M + M. ResultsSurvival rates were greater in the better quartiles for LVIDd and EF (p < 0.00001). The RR for Q1 versus Q4 in events approached 0.5 for both LVIDd and EF (p < 0.0001). An LVIDd decrease and EF increase were quartile-dependent and greater with valsartan than placebo at virtually all time points. The RR for M + M outcomes favored valsartan in the worse quartiles. ConclusionsStratification by baseline severity of remodeling showed that patients with worse LVIDd and EF are at highest risk for an event, yet appear to gain the most anti-remodeling effect and clinical benefit with valsartan treatment.

A pressure overload model to track the molecular biology of heart failure.

Pressure overload plays an important role in left ventricular remodelling and the development of heart failure. The underlying molecular mechanisms behind these processes are poorly understood at the myocyte level. To investigate this, we developed an ovine model of pressure overload-induced heart failure, in which serial left ventricular biopsies were obtained. Adult male sheep were chronically banded with a novel variable aortic constriction device. This was progressively inflated via a subcutaneous port to increase left ventricular afterload. The animals were monitored clinically and echocardiographically. Serial left ventricular endomyocardial biopsies were obtained via the right external carotid artery under fluoroscopic guidance. They were used to measure mRNA expression of the genetic regulators of apoptosis by reverse transcription polymerase chain reaction. In a subset of the animals, once left ventricular failure had been established, the constriction device was deflated to produce unloading of the left ventricle. Ten of the 17 sheep banded developed left ventricular failure. Over the first 3-4 weeks, left ventricular mass index increased acutely (88+/-18 vs. 44+/-10 g/m(2), P<0.01) followed by gradual left ventricular dilatation (diastolic left ventricular internal diameter 4.1+/-0.7 vs. 3.2+/-0.3 cm, P<0.01). Ventricular function remained stable until 7-8 weeks postoperatively, when there was significant deterioration (fractional shortening 17+/-8 vs. 40+/-8%, P<0.01) associated with clinical heart failure. Expression of the pro-apoptotic genes (bax and Fas) increased significantly following inflation of the constriction device and persisted through the transition to left ventricular failure. Following deflation of the constriction device, myocardial contractility gradually improved over a 3 week period (fractional shortening 32+/-1 vs. 17+/-8%). Progressively increasing the afterload on the left ventricle produces a clinical and echocardiographical picture of chronic heart failure. Obtaining myocardial tissue during this transition will allow the molecular correlates of pressure overload-induced heart failure and potential myocardial recovery to be investigated.

Spontaneous Feline Hypertension: Clinical and Echocardiographic Abnormalities, and Survival Rate

Systemic hypertension was diagnosed in 58 of 188 untreated cats referred for evaluation of suspected hypertension‐associated ocular, neurologic, cardiorespiratory, and urinary disease, or diseases frequently associated with hypertension (hyperthyroidism and chronic renal failure). Hypertensive cats were significantly older than normotensive subjects (13.0 ± 3.5 years versus 9.6 ± 5.0 years;P &lt;.01), and had a greater prevalence of retinal lesions (48 versus 3%;P &lt;.001), gallop rhythm (16 versus 0%;P &lt;.001), and polyuria‐polydipsia (53 versus 29%;P &lt;.01). Blood pressure was significantly higher(P &lt;.001) in cats with retinopathies (262 ± 34 mm Hg) than in other hypertensive animals (221 ± 34 mm Hg). Hypertensive cats had a thicker interventricular septum (5.8 ± 1.7 versus 3.7 ± 0.64 mm;P &lt;.001) and left ventricular free wall (6.2 ± 1.6 versus 4.1 ± 0.51 mm;P &lt;.001) and a reduced diastolic left ventricular internal diameter (13.5 ± 3.2 versus 15.8 ± 0.72 mm;P &lt;.001) than control cats. Left ventricular geometry was abnormal in 33 of 39 hypertensive subjects. No significant difference was found in age or blood pressure at the initial visit between cats that died or survived over a 9‐month period after initial diagnosis of hypertension. Mean survival times were not significantly different between hypertensive cats with normal and abnormal left ventricular patterns. Further prospective studies are needed to clearly identify the factors involved in survival time in hypertensive cats.

Spontaneous feline hypertension: clinical and echocardiographic abnormalities, and survival rate.

Systemic hypertension was diagnosed in 58 of 188 untreated cats referred for evaluation of suspected hypertension-associated ocular, neurologic. cardiorespiratory, and urinary disease, or diseases frequently associated with hypertension (hyperthyroidism and chronic renal failure). Hypertensive cats were significantly older than normotensive subjects (13.0 +/- 3.5 years versus 9.6 +/- 5.0 years; P < .01), and had a greater prevalence of retinal lesions (48 versus 3%; P < .001), gallop rhythm (16 versus 0%; P < .001), and polyuria-polydipsia (53 versus 29%: P < .01). Blood pressure was significantly higher (P < .001) in cats with retinopathies (262 +/- 34 mm Hg) than in other hypertensive animals (221 +/- 34 mm Hg). Hypertensive cats had a thicker interventricular septum (5.8 +/- 1.7 versus 3.7 +/- 0.64 mm; P < .001) and left ventricular free wall (6.2 +/- 1.6 versus 4.1 +/- 0.51 mm; P < .001) and a reduced diastolic left ventricular internal diameter (13.5 +/- 3.2 versus 15.8 +/- 0.72 mm; P < .001) than control cats. Left ventricular geometry was abnormal in 33 of 39 hypertensive subjects. No significant difference was found in age or blood pressure at the initial visit between cats that died or survived over a 9-month period after initial diagnosis of hypertension. Mean survival times were not significantly different between hypertensive cats with normal and abnormal left ventricular patterns. Further prospective studies are needed to clearly identify the factors involved in survival time in hypertensive cats.

Echocardiographic characteristics of professional football players

ObjectivesWe examined the echocardiographic characteristics of highly trained American football players. BackgroundIntense physical training is associated with morphologic and physiologic cardiac changes often referred to as the “athlete’s heart.” Echocardiographic features peculiar to elite football players have not been described. MethodsWe studied cardiac morphology and function as assessed by rest and stress echocardiography in 156 asymptomatic National Football League players. Resting and stress ejection fraction (EF), wall thickness, and diastolic left ventricular internal diameter (LVID) were measured. Left ventricular (LV) mass was calculated, as was relative wall thickness (RWT) defined as septal and posterior wall thickness divided by LVID. Control data were obtained from published studies. ResultsThe mean LVID (53 ± 0.5 mm) and maximal wall thickness (11.2 ± 0.2 mm) were increased over normal reported control subjects. There was a correlation between LVID and body weight (p = 0.01) and body surface area (BSA) (p = 0.01). The average LVID indexed to BSA was 23 ± 2 mm/M2. There was also a correlation between maximal wall thickness and body weight (p = 0.01) and BSA (p = 0.01). The average wall thickness indexed to BSA was 5.05 ± 0.88 mm/M2. Of the players, 23% had evidence of LV hypertrophy. Two players had an increased septal-to-posterior-wall-thickness ratio (≥1.3), although no player had an outflow gradient. The RWT for the players was 0.424 (± 0.1). The mean resting EF was 58% (± 4.4%), and every player undergoing exercise testing had an appropriate hyperdynamic response in cardiac function. ConclusionsBoth wall thickness and LVID of elite American football players are increased and correlate with body size. There is a high RWT, reflecting an emphasis on strength training. The LV EF was normal and not supranormal, as is sometimes believed. Regardless of the resting EF, all players had hyperdynamic cardiac responses with exercise.

Valsartan benefits left ventricular structure and function in heart failure: Val-HeFT echocardiographic study

ObjectivesThe objective of the study was to evaluate the effect of an angiotensin receptor blocker on left ventricular (LV) structure and function when added to prescribed heart failure therapy. BackgroundThe clinical benefit derived from heart failure therapy is attributed to the regression of LV remodeling. MethodsAt 302 multinational sites, 5,010 patients in New York Heart Association (NYHA) classification II to IV heart failure taking angiotensin-converting enzyme inhibitor (ACEI) and/or beta-blocker (BB) were randomized into valsartan and placebo groups and followed for a mean of 22.4 months. Serial echocardiographic measurements of left ventricular internal diastolic diameter (LVIDd) and ejection fraction (EF) were recorded. Total study reproducibility calculated to 90% power at 5% significance defined detectable differences of 0.09 cm for LVIDd and 0.86% for EF. ResultsBaseline LVIDd and EF for valsartan and placebo groups were similar: 3.6 ± 0.5 versus 3.7 ± 0.5 (cm/m2) and 26.6 ± 7.3 versus 26.9 ± 7.0 (%). Mean group changes from baseline over time were compared. Significant decrease in LVIDd and increase in EF began by four months, reached plateau by one year, and persisted to two years in valsartan compared with placebo patients, irrespective of age, gender, race, etiology, NYHA classification, and co-treatment therapy. Changes at 18 months were −0.12 ± 0.4 versus −0.05 ± 0.4 (cm/m2), p < 0.00001 for LVIDd, and +4.5 ± 8.9 versus +3.2 ± 8.6 (%), p < 0.00001 for EF. The exception occurred in patients taking both ACEI and BB as co-treatment, in whom the decrease in LVIDd and increase in EF were no different between valsartan and placebo groups. ConclusionsThe Val-HeFT echocardiographic substudy of 5,010 patients with moderate heart failure demonstrated that valsartan therapy taken with either ACEI or BB reversed LV remodeling.

Echocardiographic features of peripartum cardiac failure: the Zaria syndrome.

Zaria has the highest incidence of peripartum cardiac failure, a syndrome of unsettled aetiology. Over the years it has been noted that there has been a decrease in the period of treatment by traditional methods from an average of 90 days to 30 days and with a complete avoidance of hot bed treatment. Twenty-one subjects with the syndrome were studied: they exhibited the same clinical findings as evinced in previous reports from our centre. Echocardiography findings of dilated heart with depressed left ventricular function were noted. There was a statistically significant relationship between the duration of practice and ejection fraction (EF), r=0.36 and P<0.05, duration of practice and left ventricular internal diameter in diastole (LVIDd), r=0.28, P<0.05. Were these subjects suffering from a quiescent heart muscle disease from a previous viral myocarditis and did they require an expanded volume as a trigger? Or are they intolerant of salt requiring only a small increase from the traditional method of treatment to precipitate cardiac failure? Further investigation in the field of molecular biology is required.

Cardiac responses to training in 2-year-old thoroughbreds: an echocardiographic study.

Guided M-mode echocardiography was performed in seven 2-year-old Thoroughbreds before commencement of commercial flat-race training, and 18 weeks later, when all horses were either racing regularly (5 horses), or at racing fitness (2 horses). M-mode echocardiography was performed using a 2.5 MHz annular phased array ultrasound transducer and a Vingmed 800 Supervision echocardiograph. Images were obtained from the right hemithorax; a short axis view of the left ventricle (LV) at the level of the chordae tendinae was used to position the M-mode cursor. The following variables were measured: left ventricular (LV) internal diameter in diastole (LVIDd) and systole (LVIDs) and interventricular septal (IVS) and left ventricular free wall thickness (LVFW) in systole and diastole. The following variables were also calculated: LV fractional shortening (%FS), LV ejection fraction (EF), LV relative and mean wall thickness and muscle mass. Values before and after training were compared using a paired Student's t test. Training resulted in significant reductions in %FS and EF. Left ventricular internal diameter increased from 11.38 s.d = 0.58) cm before training to 12.16 (s.d. = 0.7) cm after training (P < 0.001). Calculated left ventricular mass also increased significantly (mean increase of 33% P < 0.001). Bodyweight was unchanged in the present study. Relative wall thickness was significantly increased in all horses, suggesting that eccentric cardiac hypertrophy occurs in response to commercial flat-race training. The mean post training value for relative wall thickness of 0.45 (s.d. = 0.05) for the horses in the present study is similar to that of human athletes in power/endurance disciplines.

Weaning from mechanical cardiac support in patients with idiopathic dilated cardiomyopathy.

Implantation of mechanical cardiac support systems (MCSS) in patients with idiopathic dilated cardiomyopathy (IDC) may improve cardiac function and allow explantation of the device. We report of long-term effects of ventricular unloading on cardiac function, humoral anti-beta1-adrenoceptor autoantibodies (A-beta1-AABs), and myocardial fibrosis. Seventeen patients in New York Heart Association functional class IV with nonischemic IDC received MCSS. All had a cardiac index of < 1.6 L x min(-1) x m(-2) of body surface area, a left ventricular ejection fraction (LVEF) of <16%, and a left ventricular internal diameter in diastole (LVIDd) of >68 mm and tested positive for A-beta1-AABs. Echocardiographic evaluation, serum tests for A-beta1-AABs, and histological assessment of myocardial fibrosis were performed before and after MCSS implantation. The mean support duration was 230+/-201 days. Six patients died, four were transplanted, and two are still on MCSS. Five patients with significant cardiac recovery (mean LVIDd, 54+/-2.3 mm; LVEF, 47+/-3.7%) were weaned after 160 to 794 days and are now device free for 51 to 592 days. A-beta1-AABs disappeared gradually during MCSS without increase after weaning; cardiac function and volume density of fibrosis remained normal. Nine patients' cardiac function hardly improved during ventricular unloading. Cardiac function can be normalized in selected patients with end-stage IDC by MCSS. The degree of preoperative myocardial fibrosis may be an indicator for outcome; A-beta1-AABs can be used to monitor myocyte recovery. Weaning from MCSS offers an alternative to cardiac transplantation in certain patients.

Anthropometric, Demographic, and Cardiovascular Predictors of Left Ventricular Mass in Young Children ,

Left ventricular (LV) mass is a strong independent predictor of cardiovascular morbidity and mortality. Few longitudinal studies have examined predictors of LV mass in children. This study assessed the contributions of anthropometric, demographic, and cardiovascular parameters (at rest and after exposure to laboratory stressors) as predictors of LV mass 3.6 years after the initial examination in a sample of 68 Caucasian and African-American children 7.9 ± 0.7 years old. At the initial examination, all subjects had standard anthropometrics measured and hemodynamics assessed at rest and during 3 stressors: postural change, forehead cold stimulation, and treadmill exercise. On the follow-up examination 3 to 4 years later, echocardiographic evaluations were conducted to estimate LV mass and related LV geometry. LV mass and LV internal diameter in diastole were adjusted for linear growth (LV mass/height 2.7 and LV internal dimension during diastole/height 0.80, respectively). Hierarchical stepwise multiple regression analyses were conducted using parameters significant in univariate comparisons (p <0.05). Initial weight (R 2 = 0.38), height (R 2 = 0.42), and cardiac output reactivity to standing and treadmill exercise (final model R 2 = 0.55) were significant predictors of LV mass, whereas LV mass/height 2.7 was predicted by initial adiposity (R 2 = 0.07) and cardiac output and systolic pressure reactivity to postural change (final model R 2 = 0.25). Follow-up relative wall thickness was significantly predicted by ethnicity (African-Americans greater than Caucasians, R 2 = 0.15), adiposity (R 2 = 0.20), and systolic pressure reactivity to postural change (final model R 2 = 0.28). These findings suggest the potential benefit of weight control in childhood as a primary prevention for later onset of cardiovascular disease. (Am J Cardiol 1996;78:323–326)

Validation of an echocardiographic assessment of cardiac function following moderate size myocardial infarction in the rat.

1. The present study determined whether two dimensional guided M-mode echocardiography could assess left ventricular (LV) geometry and function following a moderate size myocardial infarction in the rat. 2. Myocardial infarction (MI) was induced by left coronary artery ligation and rats were studied 4 weeks later. Infarct rats showed increased LV internal diastolic diameter (7.33 +/- 0.8 vs 5.91 +/- 0.6 mm; P < 0.001), LV systolic diameter (3.73 +/- 1.2 vs 1.87 +/- 0.6 mm; P < 0.001) and thickening of the noninfarcted posterior wall compared with sham operated rats (1.81 +/- 0.2 vs 1.47 +/- 0.3; P < 0.001; n = 10/group; mean +/- s.d.). Systolic function was impaired in infarct rats who showed reduced fractional shortening (50 +/- 12 vs 68 +/- 9%; P < 0.001) and fractional area change (41 +/- 14 vs 78 +/- 5%; P < 0.001). Infarct size measured echocardiographically was comparable to that measured by quantitative histological examination (29 +/- 10 vs 28 +/- 5%; NS). 3. The present study indicates that postinfarction remodelling leading to LV cavity dilation, hypertrophy of surviving myocardium and impaired systolic function is apparent 4 weeks following moderate size MI in the rat. 4. Transthoracic echocardiography is a noninvasive technique that may be used to assess serially the efficacy of therapeutic interventions designed to prevent remodelling in moderate size MI in the rat.

Balloon aortic valvuloplasty in adults: Failure of procedure to improve long-term survival

This study sought to determine the long-term outcome of adult patients undergoing percutaneous balloon aortic valvuloplasty. Percutaneous balloon aortic valvuloplasty has been offered as an alternative to aortic valve replacement for selected patients with valvular aortic stenosis. Although balloon aortic valvuloplasty produces an immediate reduction in the transvalvular aortic gradient, a high incidence of restenosis frequently leads to recurrent symptoms. Therefore, it is unclear whether balloon aortic valvuloplasty impacts on the long-term outcome of these patients. Clinical, hemodynamic and echocardiographic data were collected at baseline in 165 patients undergoing balloon aortic valvuloplasty and examined for their ability to predict long-term outcome. The median duration follow-up was 3.9 years (range 1 to 6). Ninety-nine percent follow-up was achieved. During this 6-year period, 152 patients (93%) died or underwent aortic valve replacement, and 99 (60%) died of cardiac-related causes. The probability of event-free survival (freedom from death, aortic valve replacement or repeat balloon aortic valvuloplasty) 1, 2 and 3 years after valvuloplasty was 40%, 19% and 6%, respectively. In contrast, the probability of survival 3 years after balloon aortic valvuloplasty in a subset of 42 patients who underwent subsequent aortic valve replacement was 84%. Survival after aortic valvuloplasty was poor regardless of the presenting symptom, but patients with New York Heart Association functional class IV congestive heart failure had events earliest. Univariable predictors of decreased event-free survival were younger age, advanced congestive heart failure symptoms, lower ejection fraction, elevated left ventricular end-diastolic pressure, presence of coronary artery disease and increased left ventricular internal diastolic diameter. Stepwise multivariable logistic regression analysis found that only younger age and a lower left ventricular ejection fraction contributed independent adverse prognostic information (chi-square 14.89, p = 0.0006). Long-term event-free and actuarial survival after balloon aortic valvuloplasty is dismal and resembles the natural history of untreated aortic stenosis. Aortic valve replacement may be performed in selected subjects with good results. However, the prognosis for the remainder of patients who are not candidates for aortic valve replacement is particularly poor.

Interactions between the effects of exercise and weight loss on risk factors, cardiovascular haemodynamics and left ventricular structure in overweight subjects

To assess the individual and combined effects of exercise and weight loss on the cardiovascular risk factors and cardiac left ventricular structure and function in overweight individuals. A randomized, parallel-group, crossover study design was adopted. The following treatments were employed: exercise three times a week at 70% maximum work capacity for 30 min; dietary modification to achieve weight loss involving 4200 kj/day dietary restriction; and a combination of both exercise and dietary modification weight-loss programmes. Each subject was randomly assigned to one group only and was studied after a 12-week treatment and 12-week control period, performed in a random order. Thirty subjects entered the trial, 23 completing both treatment and control phases. Body weight remained unchanged with exercise alone and fell significantly both with weight loss and with the combination. The corresponding effects on blood pressure were also significant. Exercising groups also showed a significant increase in maximal oxygen consumption and a reduction in heart rate. Serum cholesterol and triglycerides fell significantly only after the combination, whereas high-density lipoprotein-cholesterol increased with exercise, decreased with weight loss and did not change with the combination. Interventricular septum and posterior wall thickness measurements remained unchanged after 12 weeks' treatment in all groups. No significant changes occurred in left ventricular internal diastolic diameter, wall thickness:radius ratio or the heart rate corrected ratio of peak early diastolic filling velocity:peak late diastolic filling velocity. Left ventricular mass and mass indexed to body surface area were not changed in any group. The results indicate that the effects of exercise and weight reduction on blood pressure are additive, although a positive interaction may exist with respect to lipids. Despite lowering blood pressure, exercise and weight loss had no effect on cardiac left ventricular structure or function in these overweight individuals.

Dynamic effects of pericardial effusion without tamponade. Respiratory responses in the absence of pulsus paradoxus.

Fourteen patients with pericardial effusions without clinical signs of tamponade (pulsus paradoxus or other cardiac and circulatory abnormalities) showed inspiratory reductions in echocardiographic left ventricular internal diastolic diameter which correlated directly with the exaggerated respiratory changes in systolic time intervals (both pre-ejection period and left ventricular ejection time). Excessive pericardial fluid affects left ventricular function even in the absence of clinical manifestations.