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Biomedical subjects

S J Brecker

Publications and source records attributed to S J Brecker.

At least 37 records · Page 2Linked to original sources
PubMed1994

Relative effects of left ventricular mass and conduction disturbance on activation in patients with pathological left ventricular hypertrophy.

OBJECTIVE: To investigate the relative effects of left ventricular mass and conduction disturbance on the duration and axis of the QRS complex in patients with left ventricular hypertrophy and a normal cavity size. STUDY DESIGN: Retrospective and prospective study of 42 patients with pathological left ventricular hypertrophy and 17 normal controls by electrocardiography, echocardiography, and pulsed Doppler recordings. SETTING: Tertiary cardiac referral centre. PATIENTS: 42 patients (mean (SD) age 58(16)) with left ventricular hypertrophy and normal cavity size. 17 had stenotic or replaced aortic valves, 14 had hypertension, 9 had hypertrophic cardiomyopathy and 2 had left ventricular hypertrophy without obvious cause. 17 normal people (mean (SD) age 47(20)) were used as controls. RESULTS: The values of QRS duration segregated into two normally distributed populations, with a cut off point at 135 ms. When patients with QRS duration of < 135 ms (n = 30) were compared with those with QRS duration of > or = 135 ms (n = 12), there were no significant differences in age, heart rate, left ventricular size, shortening fraction, left ventricular mass and total QRS amplitude. Both the PR and QT intervals were, however, longer in patients with a QRS duration of > or = 135 ms, and the extent of incoordinate left ventricular wall motion during the preejection period was greater. When it was < 135 ms the QRS duration was strikingly correlated with left ventricular mass (r = 0.81, p < 0.01). The onsets of transverse septal motion and of posterior wall thickening were normal, as were the onsets of the longitudinal motion of left, septal, and right atrioventricular junctions. When the QRS duration was > or = 135 ms the onset of transverse septal motion and of the longitudinal right atrioventricular junction were both normal, but that of the posterior wall thickening (p < 0.01) and the longitudinal motion of the septum (p < 0.05) and lateral left ventricular wall (p < 0.01) were significantly delayed. Peak rates of left ventricular dimension decrease (p < 0.01) and increase (p < 0.01) were both reduced, as were the peak rates of the long axis shortening of the septum (p < 0.01) and left atrioventricular junction (p < 0.05), whereas the peak rates of posterior wall thickening and thinning did not differ between the two groups. Mean isovolumic relaxation time was longer (p < 0.05) in patients with QRS duration of > or = 135 ms and the peak velocity of the A wave and thus the A to E ratio was greater than in patients with a QRS duration of < 135 ms and that of the E wave was similar in the two groups. CONCLUSION: In patients with left ventricular hypertrophy the values of QRS duration are bimodally distributed, with a cut off point at 135 ms. When QRS duration is < 135 ms, left ventricular mass seems to be closely related to QRS duration, making it the dominant factor determining the activation time. Once QRS duration reaches > or = 135 ms the correlation with mass no longer exists. The statistical distribution, electrocardiographic characteristics, and incoordination pattern of left ventricular wall motion all suggest the development of a proximal left bundle branch block.

Adolescent↗
PubMed1994

Comparison of Doppler derived haemodynamic variables and simultaneous high fidelity pressure measurements in severe pulmonary hypertension.

OBJECTIVE: To assess relations between right ventricular pressure measured with a high fidelity transducer tipped catheter and the characteristics of tricuspid regurgitation recorded with Doppler echocardiography. DESIGN: A prospective non-randomised study of patients with severe pulmonary hypertension referred for consideration of lung transplantation. SETTING: A tertiary referral centre for cardiac and pulmonary disease, with facilities for invasive and non-invasive investigation, and assessment for heart and heart-lung transplantation. PATIENTS: 10 patients with severe pulmonary hypertension being considered for lung transplantation. ENDPOINTS: Peak right ventricular, pulmonary artery, and right atrial pressures; peak positive and negative right ventricular dP/dt; peak Doppler right ventricular-right atrial pressure drop; Doppler derived peak positive and negative right ventricular dP/dt; and time intervals of Q to peak right ventricular pressure and to peak positive and negative right ventricular dP/dt. RESULTS: The mean (SD) pulmonary artery systolic pressure was 109 (29) mm Hg. The peak Doppler right ventricular-right atrial pressure drop underestimated peak right ventricular pressure by 38 (21) mm Hg, and by 21 (18) mm Hg when the Doppler value was added to the measured right atrial pressure (P values < 0.05). This discrepancy was greater for higher pulmonary artery pressures. The timing of peak right ventricular pressure differed, with the Doppler value consistently shorter (mean difference 16 ms, P < 0.05). Values of peak positive and negative right ventricular dP/dt and the time intervals Q-peak positive right ventricular dP/dt and pulmonary closure to the end of the pressure pulse differed between the two techniques in individual patients, but not in a consistent or predictable way. CONCLUSIONS: Doppler echocardiography significantly underestimates the peak right ventricular pressure and the time interval to peak right ventricular pressure in pulmonary hypertension, particularly when severe. These differences may be related to orifice geometry. Digitisation of Doppler records of tricuspid regurgitation provides useful semiquantitative estimates of absolute values and timing of peak positive and negative right ventricular dP/dt. Clinically significant differences may exist, however, and must be considered in individual patients.

Adult↗
PubMed1994

Evaluation of unstented aortic homografts for the treatment of prosthetic aortic valve endocarditis.

BACKGROUND: Prosthetic aortic valve endocarditis is a serious complication that carries a high morbidity and mortality. Aortic homografts have been used in this setting, but long-term results are not available. METHODS AND RESULTS: Over a 23-year period, 48 patients presented with infected aortic valve substitutes: 28 homografts, 15 mechanical, and 5 xenografts. Nineteen patients had emergency surgery, and the mean interval between the first and second operation was 5.9 years (range, 1 month to 22 years). In 28 patients, the preoperative New York Heart Association (NYHA) class was III or IV. Active endocarditis was present in 39 patients, and the microorganisms grown were Staphylococcus epidermidis (n = 13), Staphylococcus aureus (n = 6), Streptococcus viridans (n = 6), Streptococcus faecalis (n = 4), Candida albicans (n = 5), and Gram-negative spp (n = 2). Aortic root abscesses were found in 28 (58%) patients, and transesophageal echocardiography was 95% accurate in their localization. All patients received homograft aortic valves, 19 as root replacement and 29 using the freehand technique. There were four (8.3%) early deaths; poor left ventricular function and concomitant procedure were identified as risk factors. At a mean follow-up of 4 years (range, 2 months to 19 years) 95% of the patients were in NYHA class I or II without significant aortic regurgitation. The actuarial survival at 5 years was 97% (confidence limit, 84% to 100%), and freedom from endocarditis at 10 years was 97% (confidence limit, 84% to 100%). Multivariate analysis did not identify risk factors for these late events. CONCLUSIONS: Homograft aortic valves offer good early and long-term results in patients with infected aortic valve substitutes.

Actuarial Analysis↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

Comparison of coronary angiographic findings in acute and chronic first presentation of ischemic heart disease.

BACKGROUND: It is generally assumed that the clinical manifestations of ischemic heart disease occur randomly on the same underlying pathological process. Therefore, coronary angiographic findings should be similar whether the first presentation of ischemic heart disease is acute myocardial infarction or uncomplicated chronic stable angina. METHODS AND RESULTS: We studied 102 patients (men < or = 60 years old, women < or = 65 years old) presenting with either acute myocardial infarction as first manifestation of coronary artery disease with a concomitant coronary angiogram (55 patients; mean age, 50.2 years) or stable angina for at least 2 years with no history, ECG, or left ventriculographic evidence of any acute event and with an angiogram performed at least 2 years after initial symptoms (47 patients; mean age at symptom onset, 51.7 years). These angiograms were evaluated blindly for severity (number of vessels diseased, stenoses > or = 50%, occlusions), extent of disease (with an index derived by assigning a score of 0-3 per segment, depending on the proportion of lumen length irregularity and dividing the sum by the number of visualized segments), and pattern (discrete: three or fewer loci of disease never involving more than 50% of the length of any segment or diffuse: anything exceeding this). Patients with unheralded myocardial infarction had fewer vessels diseased, fewer stenoses and occlusion, and a lower extent index than those with uncomplicated stable angina (mean +/- SD of 1.3 +/- 0.8 versus 2.1 +/- 0.8, p < 0.001; 2.1 +/- 1.8 versus 3.9 +/- 1.8, p < 0.001; 0.6 +/- 0.6 versus 1.0 +/- 0.9, p < 0.02; and 0.6 +/- 0.5 versus 1.2 +/- 0.5, p < 0.001, respectively). A discrete pattern was present in 54.5% of patients with unheralded infarction and in only 8.5% of those with uncomplicated angina (p < 0.001). CONCLUSIONS: These very different angiographic findings suggest that unheralded acute myocardial infarction and uncomplicated chronic stable angina do not occur randomly on a common atherosclerotic background but rather that additional factors, such as a varying propensity to thrombosis, may predispose to one or the other of these two clinical syndromes.

Angina Pectoris↗
PubMed1993

Delay in presentation after myocardial infarction.

Thrombolytic therapy reduces mortality in acute myocardial infarction (AMI), giving maximal benefit with early treatment. In the UK delayed presentation after AMI may reduce the advantages of thrombolysis. To assess this, 103 patients presenting with AMI to two London Hospitals were interviewed to determine the length and cause of delay from onset of chest pain to arrival at hospital. Forty-nine per cent of patients took longer than 2 h to arrive at hospital, and 21% took longer than 4 h. Patients who contacted their general practitioner (GP) had a significantly prolonged time delay (160 mins; 65-730: median; range) compared to those who went directly to hospital by ambulance (82 mins; 15-395; P < 0.0005), or on their own (90 min; 15-855; P < 0.005). Patients calling their GP took a similar duration to decide to seek help [decision time (30 min versus 25 mins) P = NS], but significantly longer to reach hospital once the decision was made (110 min versus 56 min; P < 0.0001), than those proceeding directly to hospital. Believing the pain was cardiac in origin significantly shortened decision time (15 min versus 45 min; P < 0.05), as did knowledge of the existence of thrombolysis (15 min versus 50 min; P < 0.05) and lack of prior cardiac symptoms (18 min versus 42 min; P < 0.05). Only 14% were aware of thrombolysis. Rank correlation confirmed that decision and total delay time were age independent. Delays of this magnitude may compromise the efficiency of thrombolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1992

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↗