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Biomedical subjects

D G Gibson

Publications and source records attributed to D G Gibson.

At least 91 records · Page 5Linked to original sources

Effects of intravenous milrinone on left ventricular function in ischemic and idiopathic dilated cardiomyopathy.

M-mode echocardiography and Doppler were used to assess the effects of phosphodiesterase inhibition on subendocardial function in dilated cardiomyopathy, and in particular, to study interactions with both systolic and diastolic left ventricular function. Twelve adult patients with dilated cardiomyopathy were studied (6 ischemic in origin and 6 idiopathic), 7 of whom were being considered for cardiac transplantation. Cardiac index increased without significant change in heart rate or blood pressure. Longitudinal mitral ring motion, which had been uniformly reduced, increased markedly after intravenous milrinone. Left ventricular cavity size decreased, and shortening fraction, posterior wall thickness, and rates of posterior wall thickening and thinning increased markedly. Left atrial pressure decreased, and isovolumic relaxation time increased. However, the peak velocity and duration of the transmitral E wave increased, with no change in the A wave. Improved longitudinal (subendocardial) function was reflected by improved posterior wall dynamics, and early filling, possibly by augmentation of restoring forces. Thus, severely reduced subendocardial function in dilated cardiomyopathy is potentially reversible, with marked effects on systolic and diastolic function. These previously unrecognized actions of milrinone provide further evidence to justify its short-term use in supporting the severely depressed myocardium.

Cardiomyopathy, Dilated↗

Relationship between myocardial collagen and echo amplitude in non-fibrotic hearts.

The aim of the study was to investigate the relationship between myocardial collagen and regional echo amplitude in humans with non-fibrotic myocardium. The ratio of myocardial collagen to total myocardial protein was determined as the hydroxyproline/leucine ratio in endomyocardial biopsies obtained from the right ventricular side of the interventricular septum in orthotopically transplanted hearts. Regional echo amplitude was measured in the interventricular septum. Patients were studied prospectively. Twenty-five patients (five female, 20 male) who had undergone orthotopic cardiac transplantation were studied 355 to 2939 days (1009 +/- 718, mean +/- SD) post-transplantation at the time of annual cardiac catheterization and endomyocardial biopsy. Patient ages varied from 22 to 62 years (46 +/- 11). Donor ages were 14 to 47 years (25 +/- 8) and the ischaemic time, 90 to 245 min (151 +/- 42). Cardiac transplantation was performed for end-stage cardiac failure in all patients. The aetiology of cardiac failure was valvular heart disease in three, dilated cardiomyopathy in eight and ischaemic heart disease in the remainder. Echo amplitude studies were performed within 24 h of endomyocardial biopsy. All but one patient were on an immunosuppressive regime consisting of cyclosporine A and azathioprine with additional steroids in three. The remaining patient, who was the longest surviving patient in the study group, had never been treated with cyclosporine. This patient was maintained on steroids and azathioprine alone. No patient had clinical or histological evidence for acute cardiac rejection and all were clinically well. Five patients had angiographic evidence of coronary artery disease. All subject studies were performed at Harefield Hospital.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Differing effects of right ventricular pacing and left bundle branch block on left ventricular function.

OBJECTIVE: To compare the different effects of right ventricular pacing and classic left bundle branch block on left ventricular function. DESIGN: Retrospective and prospective study of 48 patients by electrocardiography, and M mode, cross sectional, and Doppler echocardiography. SETTING: A tertiary cardiac referral centre. PATIENTS: 48 patients (age range 21 to 89 years, 15 women), 24 with a VVI pacemaker implanted and 24 with classic left bundle branch block. Functional mitral regurgitation was present in all those with right ventricular pacing and 22 of those with left bundle branch block. RESULTS: Age, RR interval, and left ventricular size were similar in the two groups, as were conventional measurements of overall systolic function: shortening fraction and pre-ejection and aortic ejection times. In right ventricular pacing, however, QRS duration (p < 0.01) and electromechanical delay were much longer (p < 0.001), whereas the time intervals from onset of mitral regurgitation to aortic opening (contraction time) and from A 2 to the end of mitral regurgitation (relaxation time) were consistently shorter (p < 0.01) than corresponding values in patients with left bundle branch block. Reversed splitting of the second heart sound was much commoner in left bundle branch block (p < 0.02), and only these patients showed an early systolic ventricular septal contraction. Its onset followed the initial deflection of the QRS complex by 40(15) ms and preceded mitral regurgitation by a small but consistent interval of 10 ms (p < 0.01). The onset of posterior wall thickening was synchronous with the onset of mitral regurgitation in right ventricular pacing but much later (p < 0.01) in patients with left bundle branch block. The extent of incoordinate wall motion measure as relative dimension change during pre-ejection and isovolumic relaxation period was much greater (p < 0.01) in left bundle branch block. These major differences were not altered by left ventricular cavity size in either group, nor by the presence of previous left bundle branch block in patients who were subsequently paced. CONCLUSIONS: The left ventricle seems to be activated much more rapidly with right ventricular pacing than with left bundle branch block. This applies even when left bundle branch block is present before pacing. Electromechanical delay, contraction and relaxation times, and extent of incoordinate ventricular wall motion differ strikingly between the two conditions. The use of right ventricular pacing as an experimental model of left bundle branch block in humans must be re-examined.

Adult↗

Shortened left ventricular filling time in dilated cardiomyopathy: additional effects on heart rate variability?

OBJECTIVE: To assess possible mechanical influences underlying the reduced heart rate variability in patients with dilated cardiomyopathy. DESIGN: Comparison of standard non-spectral indices of heart rate variability with echocardiographic Doppler measures of left ventricular function in patients and normal controls. PATIENTS: 20 patients with dilated cardiomyopathy and 15 normal subjects of similar ages were studied. METHODS: Standard non-spectral indices of heart rate variability were measured over 24 hours. These were correlated with left ventricular cavity size, shortening fraction, and isovolumic relaxation time measured by M mode echocardiography, and the duration of functional mitral regurgitation and left ventricular filling time assessed by continuous wave Doppler. RESULTS: Mean RR interval and estimates of short term variability (root mean square difference of successive RR intervals, proportion of adjacent RR intervals > 50 ms different, and SD indices) were not different from normal. The overall mean (SD) of the RR interval (65 (35)), and SD of five minute mean RR intervals (55 (30)), however, were reduced compared with normal values (115 (40) and 105 (45); p < 0.01 for both). Neither correlated with left ventricular cavity size or shortening fraction, but both were strongly related to left ventricular filling time (coefficient of variation, r = 0.82 and r = 0.81 respectively). Correlation persisted when the SD was corrected for RR interval (r = 0.69) although this correlation was not found in the controls. In individual patients, the difference between RR interval at the time of echo and minimum value during the 24 hours, a measure of ability to increase heart rate, also correlated closely with filling time (r = 0.92). CONCLUSION: As the duration of functional mitral regurgitation is effectively fixed, its presence can limit the time available for left ventricular filling in dilated cardiomyopathy when heart rate is high. This may become the mechanism by which maximum heart rate is set, becoming fixed to optimise cardiac output. This manifestation of dilated cardiomyopathy may be an important factor in reduction of heart rate variability in these patients.

Adult↗

Berheim "a" wave: obstructed right ventricular inflow or atrial cross talk?

OBJECTIVE: To study the possible mechanisms underlying the dominant "a" wave in the jugular venous pulse seen in patients with left ventricular hypertrophy (Bernheim "a" wave). DESIGN: Prospective examination of the left ventricular transverse and longitudinal axes, transmitral and transtricuspid flows, and jugular venous pulse recordings. SETTING: Tertiary referral centre for cardiac disease. SUBJECTS: 23 patients with left ventricular hypertrophy of various aetiologies and a dominant "a" wave in the jugular venous pulse. Controls were 21 normal volunteers. RESULTS: Early diastolic filling of the right ventricle was normal. During right atrial systole the (mean(SD)) tricuspid ring motion was exaggerated (1.2(0.4) v 0.8(0.2) cm, p < 0.001) and Doppler A wave velocity slightly increased (0.3(0.1) v 0.2(0.08) m/s, p < 0.01), although the E wave remained dominant. By contrast left ventricular isovolumic relaxation time was longer than normal (70(20) v 55(10) ms, p < 0.001) with wall motion incoordinate in the septal long axis, 15%(9.5%) v 6.6%(3%) total excursion occurring before mitral valve opening. During early filling the extent of long axis motion was decreased to 0.6(0.5) cm from 1.1(0.2) cm, (p < 0.001) and 0.5(0.2) cm from 0.9(0.2) cm, (p < 0.0001) at the left and septal sites, and similarly its peak lengthening rate reduced to 5.4(2.5) cm/s from 10(3) cm, (p < 0.001) and 4.3(2.2) cm/s from 8(2) cm, (p < 0.001). The atrial component of long axis lengthening was increased to 43%(18%) from 29%(6%) (p < 0.01) and 55%(15%) from 33%(8%) of the total excursion (p < 0.0001). Left ventricular E/A ratio was less than normal (0.9(0.8) v 1.4(0.4), p < 0.05). CONCLUSIONS: There is no evidence of obstruction or any other disturbance of early diastolic right ventricular inflow in Bernheim's syndrome. It is possible that the haemodynamically appropriate increase in left atrial activity is mirrored on the right side due to shared interatrial myocardial fibres. This could represent a form of atrial interaction.

Adult↗

Early changes in left ventricular subendocardial function after successful coronary angioplasty.

OBJECTIVE: To study the early effects of coronary angioplasty on resting left ventricular long axis function, reflecting that of the subendocardium. DESIGN: Prospective echocardiographic and Doppler examination of patients with coronary artery disease, before and after single vessel coronary angioplasty. SETTING: A tertiary referral centre for cardiac diseases with facilities for invasive and non-invasive investigation. PATIENTS: 23 patients with significant left coronary disease being considered for coronary angioplasty. RESULTS: Before angioplasty the mean (SD) isovolumic relaxation time was longer than normal (75(19) ms v 55 (10), p < 0.001) with a significant increase in transverse dimension change before mitral valve opening, and peak rate of early diastolic thinning (8(3) v 10.4 (2.6) cm/s (p < 0.001)) was reduced. Long axis motion was frequently abnormal. The interval from the onset of the Q wave to the onset of shortening was prolonged (118 (30) ms v 90 (19) at the left site and 115 (26) ms v 81 (9) at the septal site, p < 0.001) and the onset of early diastolic rapid lengthening delayed with respect to the aortic valve closure sound (A2) by 85 (34) ms v 58 (11) at the left site and 88 (33) ms v 60 (9) at the septal site (p < 0.001). Although overall amplitude was reduced at the septal site only (1.23 (0.3) cm v 1.5 (0.4), p < 0.05), the extent (0.8 (0.2) cm v 1.04 (0.3) at the left site and 0.66 (0.2) cm v 0.9 (0.3) at the septal site, p < 0.001) and peak rate (6.2 (2) cm/s v 10 (2.5) at the left site and 5.4 (2.3) cm/s v 8.5 (2) at the septal site, p < 001) of early diastolic lengthening were both much lower than normal. The E/A ratio on transmitral Doppler was modestly reduced (1.0 (0.7) v 1.4 (0.4), p < 0.05). After angioplasty: isovolumic relaxation time shortened to 64 (18) ms (p < 0.001) and left ventricular incoordination regressed. Long axis shortening with respect to Q (98 (32) ms v 118 (30) at the left site and 94 (23) ms v 115 (26) at the septal site, p < 0.01) and that of lengthening with respect to A2 both normalised. Early diastolic peak lengthening rate increased (7.5 (2.1) cm/s v 6.2 (2) at the left site, and 6.3 (2.4) cm/s v 5.4 (2.3) at the septal site, p < 0.001). The early diastolic peak thinning rate of the posterior wall significantly increased (10 (3.5) cm/s v 8 (3), p < 0.005) as did mitral E/A ratio 1.2 (0.7) v 1.0 (0.7), p < 0.05). CONCLUSION: Long axis motion, representing the function of longitudinally arranged subendocardial fibres, is consistently abnormal in the resting state in coronary artery disease. These systolic and diastolic abnormalities return towards normal after successful angioplasty, suggesting that they are the direct effect of coronary artery stenosis.

Angioplasty↗

Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy.

Mitral or tricuspid regurgitation of long duration may so shorten the ventricular filling time in dilated cardiomyopathy that stroke volume is limited. We assessed the effects of changing the atrioventricular interval during temporary or permanent dual-chamber DDD pacing in twelve dilated cardiomyopathy patients with short ventricular filling times due to regurgitation. We measured ventricular filling time and cardiac output with doppler echocardiography and exercise capacity on a treadmill, at baseline and with the best atrioventricular delay during pacing. The durations of both mitral and tricuspid regurgitation were significantly shorter at the shorter atrioventricular interval (mean reductions 85 [95% CI 60-110] ms and 110 [75-150] ms, respectively; p < 0.001 for both). There were consequent increases in left-ventricular and right-ventricular filling times (65 [35-95] ms and 90 [60-120] ms, p < 0.001). For each 50 ms reduction in atrioventricular delay, left-ventricular filling time increased by 35 ms in six subjects with presystolic mitral regurgitation and right-ventricular filling time by 30 ms in nine subjects with presystolic tricuspid regurgitation. At the short atrioventricular interval, cardiac output was greater than baseline (by 1.1 [0.8-1.4] l/min, p < 0.01) and there were rises in exercise duration (104 [45-165] s, p < 0.05) and maximum oxygen consumption (2.1 [1.5-2.7] ml kg-1 min-1, p < 0.05). There was a decrease in the Likert visual analogue score of breathlessness at peak exercise (8.6 [SD 2.1] vs 4.9 [3.1], p < 0.01). Although from a small sample, these findings suggest that DDD pacing with a short atrioventricular delay may have therapeutic potential in patients with dilated cardiomyopathy, even in the absence of conventional indications for pacemaker implantation.

Aged↗

Culture of amebocytes in a nutrient mist bioreactor.

We report the first use of nutrient mist bioreactor (NMB) technology to culture animal cells. The nutrient mist approximated the amebocyte stem tissue's natural environment, which is a thin layer of fluid in the gill leaflets of the horseshoe crab Limulus polyphemus. NMB culture was tried in an attempt to increase production of amebocytes, which are the source of the Limulus Amebocyte Lysate (LAL), the basis for a sensitive and commercially valuable endotoxin assay. Amebocyte growth in the nutrient mist bioreactor is comparable to growth in liquid medium. However, the current design of the bioreactor presents problems for primary cultures such as ours where a pyrogen-free environment is necessary and fungal decontamination is difficult.

Animals↗

Factors influencing left-ventricular stiffness.

The aim of the study was to investigate the relative contributions of geometrical and material factors to overall left-ventricular cavity stiffness. Left-ventricular cavity shapes were reconstructed using a computer and the variation of myocardial elastic modulus was calculated, by the finite element method, through the passive phase of diastole when rising volume coincided with rising pressure. Geometric data were obtained from biplane cineangiography, with micromanometer pressure measurements, for ten patients with left ventricular disease. Dimensional analysis was applied to the initial and derived data from which the influences of myocardial compliance, wall thickness-to-long dimension ratio, and aspect ratio (long-to-short axes) were determined. The ratio between the volume elasticity and the myocardial modulus of elasticity, the normalized stiffness ratio (NSR), is proposed as a useful index of left ventricular mechanical behaviour in diastole. The volume elasticity of the chamber is dependent not only upon the myocardium elastic modulus and the wall thickness ratio, but also on the shape of the chamber. Changes in the thickness/radius ratio of the ventricle have less effect upon its distention than those in the long dimension/radius ratio. The left ventricle becomes more spherical in shape through diastole and hence becomes stiffer by this geometric mechanism.

Cineangiography↗

Assessment of the peak tricuspid regurgitant velocity from the dynamics of retrograde flow.

We describe a simple, non-invasive and practical method to determine the peak velocity of tricuspid regurgitant flow (and hence derive systolic pulmonary artery pressure) from examination of the dynamics of retrograde tricuspid flow on Doppler. Based on a previously described relationship between right ventricular systolic pressure and the time interval between pulmonary valve closure and tricuspid valve opening, our technique does not require the peak tricuspid regurgitant velocity to be recorded; nor, as in previous studies does it rely upon recording the jugular venous pulse, right ventricular apexcardiogram or invasive pressure measurements. We have studied 65 patients with right ventricular disease (53 with pulmonary hypertension), and 24 with dilated cardiomyopathy, with M-mode, two-dimensional echocardiography, Doppler, and phonocardiography. The peak tricuspid regurgitant velocity could be predicted from the interval between pulmonary closure and the end of the tricuspid regurgitant signal on Doppler in patients with pulmonary hypertension and those with right ventricular disease with normal pulmonary artery pressure, but not in patients with dilated cardiomyopathy. In patients with pulmonary hypertension or right ventricular dilatation, this may be a useful alternative method in estimating pulmonary artery pressure from Doppler, in cases where it is not possible to record the peak tricuspid regurgitant velocity.

Adolescent↗

Changes in myocardial echo amplitude during reversible ischaemia in humans.

OBJECTIVE: This study investigated the changes in regional myocardial ultrasonic backscatter, measured as myocardial echo amplitude, that occur during reversible myocardial ischaemia in humans. DESIGN: Left anterior descending coronary angioplasty was used to produce reversible myocardial ischaemia in human subjects. Regional myocardial echo amplitude was studied in the interventricular septum and left ventricular posterior free wall before, during, and after coronary occlusion with the angioplasty balloon. Wall motion analysis of the left ventricle was performed from simultaneous cross sectional echocardiographic imaging. Patients were studied prospectively. PATIENTS: Six patients (mean age 56 (SD 11), range 46 to 69 years) with single vessel, left anterior descending coronary artery stenoses, were investigated during elective coronary angioplasty. A total of 11 balloon inflations were studied. SETTING: All patient studies were performed at Harefield Hospital. Echo amplitude analysis was performed at the Royal Brompton Hospital. INTERVENTIONS: Angioplasty was performed by the usual procedure at Harefield Hospital for elective coronary angioplasty. All routine medication including beta blockers and calcium antagonists were continued. Inflation pressures were up to 12 atm (1212 kPa) and mean inflation time ranged from 30 to 120 (86 (31)) s. In four studies the first inflation was examined, in three the second, in two the third, and in one each the fourth and fifth inflations. Echo amplitude and cross sectional echo-cardiographic studies were recorded with a 3.5 MHz Advanced Technology Laboratories (ATL) (720A/8736 series) mechanical sector scanner and an ATL Mark III (860-1 series) echocardiograph system with 45 dB logarithmic grey scale compression. MAIN OUTCOME MEASURES: Regional echo amplitude was examined in four regions of the left ventricle--namely, the basal and mid-septum, and basal and mid-posterior wall. Consecutive end diastolic and end systolic frames were analysed and cyclic variation was determined as the difference between the level of echo amplitude at end diastole and at end systole. Measurements were made before balloon inflation, at peak inflation, and after balloon deflation. Regional wall motion and systolic wall thickening were analysed qualitatively. RESULTS: Before balloon inflation, cyclic variation in echo amplitude was noted in all regions (basal septum, 2.4 (SD 1.1) dB; mid-septum, 2.5 (1.1) dB; basal posterior wall, 3.3 (2.1) dB; mid-posterior wall, 3.9 (1.6) dB). During balloon inflation there was a significant fall in cyclic variation to 0.4 (0.9) dB (p < 0.0002) in the mid-septum. This was predominantly owing to an increase in end systolic echo amplitude from 5.4 (2.0) dB to 9.3 (1.9) dB (p < or = 0.01). This was associated with the development of severe hypokinesis or akinesis in the mid-septum. No significant changes in echo amplitude occurred in the three other regions examined. Changes were completely reversed after balloon deflation. CONCLUSIONS: These results suggest a causal relation between occlusion of the supplying coronary artery and blunting of myocardial echo amplitude cyclic variation. It is suggested that balloon occlusion produced myocardial ischaemia. The resultant impairment of myocardial contraction then caused a blunting of cyclic variation in echo amplitude. The results of this study provide further data about the ability of quantitative studies of ultrasonic backscatter to identify alterations in the myocardium during injury.

Aged↗

Effects of abnormal activation on the time course of the left ventricular pressure pulse in dilated cardiomyopathy.

OBJECTIVE: To investigate the effects of QRS duration on characteristics of the left ventricular pressure pulse derived from the time course of functional mitral regurgitation by continuous wave Doppler. DESIGN: Retrospective and prospective study of 50 patients with dilated cardiomyopathy, by electrocardiography, echocardiography, and Doppler cardiography. SETTING: Tertiary cardiac referral centre. PATIENTS: 50 patients (mean age (SD) 58 (16)) with dilated cardiomyopathy, all with functional mitral regurgitation. RESULTS: The values of QRS duration ranged widely, from 70 to 190 ms with a mean value of 110 ms, and were unimodally distributed. The overall duration of mitral regurgitation correlated positively with QRS time (r = 0.65) over the entire range of values. When the duration of mitral regurgitation was divided into contraction, aortic ejection, and relaxation times, increased QRS duration prolonged contraction (r = 0.51) and relaxation (r = 0.52) times. Aortic ejection time was affected by RR interval (r = 0.74). Duration of QRS correlated negatively with peak rate of rise in left ventricular pressure (+dP/dt) (r = -0.48), and positively with the time intervals from Q to peak pressure (r = 0.49) and to peak +dP/dt (r = 0.72), and also with those from the start of mitral regurgitation to peak pressure (r = 0.49) and to peak +dP/dt (r = 0.76). Duration of QRS did not directly affect the peak rate of left ventricular pressure fall (-dP/dt), or the isovolumic relaxation period. CONCLUSIONS: Values of QRS duration are unimodally distributed in patients with dilated cardiomyopathy, without evidence of a discrete group of patients with left bundle branch block. Prolonged QRS duration reduces peak +dP/dt, prolongs overall duration of the pressure pulse, the time to peak +dP/dt, and relaxation time. Duration of QRS must therefore be taken into account in assessing standard measurements of myocardial function in patients with dilated cardiomyopathy.

Adolescent↗

Relation of left ventricular isovolumic relaxation time and incoordination to transmitral Doppler filling patterns.

OBJECTIVE: To investigate factors during isovolumic relaxation that determine Doppler filling patterns in patients with left ventricular disease, and thus to identify the underlying mechanisms. DESIGN: 85 patients (50 ischaemic heart disease, 35 left ventricular hypertrophy due to aortic stenosis) and 26 controls were studied with Doppler and M mode echocardiography and phonocardiography. 16 patients underwent two studies on separate occasions, to find whether changes in isovolumic relaxation time were reflected by a change in the Doppler A/E ratio. SETTING: A tertiary cardiac referral centre. SUBJECTS: Patients referred for assessment of coronary artery disease or aortic stenosis with left ventricular hypertrophy. MAIN OUTCOMES MEASURES: Doppler filling velocities during early (E wave) and late (A wave) diastole and the A/E ratio, acceleration of the E wave, digitised M mode indices of incoordinate relaxation (change in cavity dimension before mitral valve opening and time from minimum dimension to mitral valve opening), isovolumic relaxation time, M mode measures of diastolic function after mitral valve opening (peak rate of posterior wall thinning and peak rate of dimension increase), and left ventricular end diastolic pressure. RESULTS: A/E correlated with age in normal subjects (r = 0.74), to a lesser extent in left ventricular hypertrophy (r = 0.41), but not significantly in ischaemic heart disease. In all patients, isovolumic relaxation time was significantly and negatively correlated with the acceleration of the E wave, showing its fundamental relation to the force responsible for early diastolic filling (r = -0.71 for left ventricular hypertrophy, and -0.74 for ischaemic heart disease, p value < 0.01). In left ventricular hypertrophy and those ischaemic patients without left ventricular dilatation A/E was correlated both with isovolumic relaxation time (r = 0.68 and 0.60 respectively), and with incoordinate relaxation (r = 0.65 and 0.61). In those ischaemic patients with left ventricular dilatation, the influence of incoordination was lost and isovolumic relaxation time became the dominant influence upon A/E (r = 0.82). Weak correlations of end diastolic pressure and RR interval with A/E, became insignificant once isovolumic relaxation time had been taken into account. Isovolumic relaxation time and incoordination together accounted for over 50% of the variance in the A/E ratio in our patients. Isovolumic relaxation time and the A/E ratio were linearly related. Patients with a short isovolumic relaxation time had evidence of considerable diastolic abnormalities, despite a normal Doppler A/E ratio. In the 16 patients who had two echocardiographic studies, changes in the duration of isovolumic relaxation were accompanied by a change in the Doppler A/E ratio. The relation between these two variables, derived from the group as a whole was similar. CONCLUSIONS: The main factors influencing the A/E ratio in patients with left ventricular disease are two distinct properties of isovolumic relaxation--namely the duration and the extent of incoordinate wall motion. Filling pressure and RR interval are not significant independent determinants, but act only through an effect upon isovolumic relaxation time. Age is an important influence in normal people, but this effect is attenuated in left ventricular hypertrophy and lost in ischaemic ventricular disease.

Adult↗

Left ventricular filling characteristics in pulmonary hypertension: a new mode of ventricular interaction.

OBJECTIVE: To examine the effects of pulmonary hypertension on left ventricular diastolic function and to relate the findings to possible mechanisms of interdependence between the right and left sides of the heart in ventricular disease. DESIGN: A retrospective and prospective analysis of echocardiographic and Doppler studies. SETTING: A tertiary referral centre for both cardiac and pulmonary disease. PATIENTS: 29 patients with pulmonary hypertension (12 primary pulmonary hypertension, 10 pulmonary fibrosis, five atrial septal defect (ASD), and two scleroderma) were compared with a control group of 10 patients with an enlarged right ventricle but normal pulmonary artery pressure (six ASD, one after ASD closure, one ASD and pulmonary valvotomy, one tricuspid valve endocarditis and repair, and one pulmonary fibrosis). None had clinical or echocardiographic evidence of intrinsic left ventricular disease. MAIN OUTCOME MEASURES: M mode echocardiographic measurements were made of septal thickness, and left and right ventricular internal cavity dimensions. Doppler derived right ventricular to right atrial pressure drop, and time intervals were measured, as were isovolumic relaxation time, and Doppler left ventricular filling characteristics. RESULTS: The peak right ventricular to right atrial pressure gradient was (mean (SD)) 60 (16) mm Hg in pulmonary hypertensive patients, and 18 (5) mm Hg in controls. The time intervals P2 to the end of the tricuspid regurgitation, and P2 to the start of tricuspid flow were both prolonged in patients with pulmonary hypertension compared with controls (115 (60) and 120 (40) v 40 (15) and 45 (10) ms, p values less than 0.001). Pulmonary hypertensive patients commonly had a dominant A wave on the transmitral Doppler (23/29); however, all the controls had a dominant E wave. Isovolumic relaxation time of the left ventricle was prolonged in pulmonary hypertensive patients compared with controls, measured as both A2 to mitral valve opening (80 (25) v 50 (15) ms) and as A2 to the start of mitral flow (105 (30) v 60 (15) ms, p values less than 0.001). The delay from mitral valve opening to the start of transmitral flow was longer in patients with pulmonary hypertension (30 (15) ms) compared with controls (10 (10) ms, p less than 0.001). At the time of mitral opening there was a right ventricular to right atrial gradient of 12 (10) mm Hg in pulmonary hypertensive patients, but this was negligible in controls (0.4 (0.3) mm Hg, p less than 0.001). CONCLUSIONS: Prolonged decline of right ventricular tension, the direct result of severe pulmonary hypertension, may appear as prolonged tricuspid regurgitation. It persists until after mitral valve opening on the left side of the heart, where events during isovolumic relaxation are disorganised, and subsequent filling is impaired. These effects are likely to be mediated through the interventricular septum, and this right-left ventricular asynchrony may represent a hitherto unrecognised mode of ventricular interaction.

Adolescent↗

Characteristics of presystolic flow in the superior vena cava: new thoughts on a forgotten sound.

Cross sectional, M mode, and Doppler echocardiography, apexcardiography, and phonocardiography were used to characterise presystolic cardiovascular sounds in three patients with ventricular disease. Although the aetiology was different (dilated cardiomyopathy, primary pulmonary hypertension, and chronic pulmonary thromboembolic disease), in each case the presystolic sound was associated with a rapid change in acceleration of blood and with flow reversal in the superior vena cava, and could only be recorded at the right sternal edge or over the jugular veins. Such flow characteristics may be explained by a raised ventricular end diastolic pressure with reduced compliance. Use of these techniques helps to understand the cause of a previously described but little recognised heart sound, and adds weight to the interpretation of its presence in disease.

Adult↗

Jugular venous 'a' wave in pulmonary hypertension: new insights from a Doppler echocardiographic study.

OBJECTIVE: To study the mechanisms underlying the dominant 'a' wave seen in patients with primary pulmonary hypertension. DESIGN: Retrospective and prospective examination of the jugular venous pulse recording, flow in the superior vena cava, and Doppler echocardiographic studies. SETTING: A tertiary referral centre for both cardiac and pulmonary disease, with facilities for invasive and non-invasive investigation, and assessment for heart and heart-lung transplantation. PATIENTS: 12 patients with primary pulmonary hypertension, most being considered for heart-lung transplantation. RESULTS: Two distinct patterns of venous pulse and superior vena caval flow were identified: a dominant 'a' wave with no 'v' wave, an absent or poorly developed 'y' descent, and exclusively systolic downward flow in the superior vena cava (group 1, n = 8), and a dominant 'v' wave, deep 'y' descent and exclusively diastolic downward flow in the superior vena cava (group 2, n = 4). A comparison between the two groups showed age (mean (SD)) 42 (18) v 36 (7) years, RR interval 700 (65) v 740 (240) ms, left ventricular end diastolic dimension 3.6 (0.8) v 3.2 (1.0) cm and end systolic dimension 2.1 (0.5) v 2.3 (0.3) cm, right ventricular end diastolic dimension 2.6 (0.5) v 2.8 (0.6) cm, and pressure drop between right ventricle and right atrium 60 (8) v 70 (34) mm Hg to be similar. Duration of tricuspid regurgitation 520 (30) v 420 (130) ms and the time interval of pulmonary closure to the end of the tricuspid regurgitant signal 140 (30) v 110 (40) ms were longer in group 1 compared with group 2, whereas right ventricular filling time was much shorter 180 (70) v 350 (130) ms. In seven patients from group 1, a single peak of forward tricuspid flow was present, but this pattern was seen in only one patient from group 2. CONCLUSION: In patients with primary pulmonary hypertension, the apparent 'a' wave seen in the venous pulse is, in fact, a summation wave. It is probably the result of large pressure changes that must underlie rapid acceleration and deceleration of blood across the tricuspid valve when the right ventricular filling time is short.

Adult↗

Echocardiographic diastolic abnormalities of the left ventricle in inflammatory joint disease.

Echocardiographic early diastolic abnormalities have been shown recently in 50% of men with ankylosing spondylitis. Similar techniques were used to investigate subjects with rheumatoid arthritis and psoriatic arthritis with or without spondylitis. These subjects had no clinical, radiographic, or electrocardiographic evidence of cardiac or respiratory disease. Echocardiographic abnormalities seen resembled those of ankylosing spondylitis in that the interval between minimum left ventricular dimension and mitral valve opening was prolonged in 12 of 22 subjects with rheumatoid arthritis and in seven of 11 subjects with psoriatic arthritis. Isovolumic relaxation time was significantly prolonged in four subjects with rheumatoid arthritis and one with psoriatic arthritis. Unlike ankylosing spondylitis, however, there was consistent reduction in peak rate of left ventricular dimension increase in subjects with rheumatoid arthritis and psoriatic arthritis. In addition, the dimension increase during atrial systole was greater than normal in nine subjects with rheumatoid arthritis and two with psoriatic arthritis. The most likely cause of these abnormalities is increased connective tissue deposition in the myocardium.

Adult↗

An echocardiographic assessment of atrial mechanical behaviour.

Relations between movement of the atrioventricular ring and changes in left atrial and ventricular dimensions were studied by echocardiography and compared with apexcardiography and Doppler mitral flow velocity traces in 20 healthy controls and in patients with left ventricular hypertrophy (n = 28) or dilatation (n = 16). During left ventricular systole the atrioventricular ring, a structure common to ventricle and atrium, moved towards the ventricular apex, thus increasing left atrial volume. This action matched pulmonary venous return because it was in phase with the transverse left atrial dimension measured from aortic root to posterior left atrial wall. During early diastole, the mitral ring moved rapidly towards the atrium as transmitral flow accelerated. This requires a force directed from ventricle to atrium, likely to be the result of elastic recoil arising from compression of the ventricular myocardium or stretching of the atrial myocardium during ventricular systole. Two additional mechanisms of ventricular filling with atrial systole were recognised: (a) an increase in ventricular volume as the atrioventricular ring moved upwards and (b) transverse left ventricular expansion by pressure driven transmitral flow. The former is undetectable by Doppler from the apex; it accounted for 10% of ventricular filling in the healthy controls, but for significantly less in those with ventricular dilatation. In left ventricular hypertrophy, left ventricular filling was maintained by both mechanisms compensating for the reduced increase in volume early in diastole. Interactions between the atrium and ventricle are functionally important during ventricular systole, early diastole, and in atrial systole. They are not included in the traditional separation of atrial function into reservoir, conduit, and pump functions.

Atrial Function, Left↗