Biomedical subjects

D G Gibson

Publications and source records attributed to D G Gibson.

At least 73 records · Page 4Linked to original sources

PubMed1995

Perioperative assessment of aortic homograft, Toronto stentless valve, and stented valve in the aortic position.

We investigated aortic valve hemodynamic performance and perioperative left ventricular function in 50 patients (mean [+/- SD] age, 64 +/- 9 years; 34 men, 16 women) undergoing elective aortic valve replacement, using an aortic homograft (n = 20), a Toronto stentless porcine valve (n = 20), or a stented bioprosthesis (n = 10), by transesophageal echocardiography combined with high-fidelity cavity pressure recordings and thermodilution cardiac output measurements. Thirty-nine patients had aortic stenosis; 11 had predominant regurgitation. Thirteen patients with concomitant coronary artery stenosis underwent grafting. Left ventricular mass index in all patients was 280 +/- 110 g/m2. The transvalvular pressure drop and energy consumption were significantly higher with stented than stentless valves (5 with aortic homograft and 11 with Toronto valve, with matched age and valve size; 20 +/- 12 versus 3 +/- 9 mm Hg; 21% +/- 13% versus 8% +/- 8%, both p < 0.01). However, there was no difference in these variables between the Toronto valve and the aortic homograft (3 +/- 12 versus 2 +/- 10 mm Hg; 5% +/- 14% versus 2% +/- 12%, both p > 0.05), although the Toronto valves (normalized to body surface area) were larger than the aortic homografts (14.4 +/- 1.9 versus 12.6 +/- 1.8 mm/m2, p < 0.01). There was no significant difference in left ventricular stroke volume index or stroke work index in the systemic circulation, either between stentless and stented valves or between aortic homografts and Toronto valves, although the cross-clamp time required to insert a stentless valve was 20 minutes longer than that for a stented valve.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

Doppler reconstruction of left ventricular pressure from functional mitral regurgitation: potential importance of varying orifice geometry.

OBJECTIVE: To assess the left ventricular pressure pulse, in particular its time course, reconstructed from the continuous wave Doppler signal of functional mitral regurgitation using the simplified Bernoulli equation. DESIGN: Prospective study with simultaneously recorded high fidelity left ventricular pressure and continuous wave Doppler traces of functional mitral regurgitation, along with indirect left atrial pressure, electrocardiograms, and phonocardiograms. SETTING: Tertiary referral cardiac centre. PATIENTS: 9 patients (age 60 (17) years) were studied immediately before or 1-20 h after routine cardiac surgery. RESULTS: 104 cardiac cycles were analysed. There were no consistent differences between directly measured and reconstructed pressures in the time intervals from Q to + dP/dt (mean (SD) 125 (35) v 130 (35) ms and from Q to -dP/dt (389 (30) v 387 (28) ms or from Q to maximum pressure (267 (40) v 270 (40) ms, all P = NS). The time from Q to the onset of pressure rise (67 (30) v 64 (30) ms, P < 0.01) and the duration of total left ventricular systole (404 (50) v 408 (50) ms, P < 0.01) measured by the two methods were effectively identical, though the small difference was consistent enough to be statistically significant. The calculated peak pressure drop between the left ventricle and the left atrium (45-100 mm Hg) significantly underestimated left ventricular pressure (72-150 mm Hg; 70 (11) v 105 (15) mm Hg, P < 0.01) even if mean left atrial pressure (14 (4.0) mm Hg) was taken into account. Compared with those directly derived from left ventricular pressure, values of pressure measured at + dP/dt (26 (6.5) v 53 (10) mm Hg, P < 0.01) and -dP/dt (30 (8.0) v 60 (10) mm Hg, P < 0.01), and those of the rates of increase (675 (155) v 815 (155) mm Hg/s, P < 0.01) and fall (610 (145) v 845 (175) mm Hg, P < 0.01) were all significantly underestimated by Doppler. The underestimation in peak rates of pressure change could not entirely be explained by a scaling effect of absolute pressure. To investigate interrelations between the two methods throughout the cardiac cycle, reconstructed left ventricular pressure was plotted against the direct record. The plots confirmed that the reconstructed pressure was always less than directly measured pressure, the relative degree of underestimation falling as the pressure rose. This was not the effect of acceleration but probably reflects changing geometry of the regurgitant orifice. CONCLUSION: The continuous wave Doppler trace of functional mitral regurgitation is suitable for studying the timing of overall mechanical events and normalised rates of change of pressure in the left ventricle. Estimates of atrioventricular pressure drop by this method and particularly its absolute rates of change seem to be less reliable.

Adult↗

PubMed1995

Suppression of left ventricular early diastolic filling by long axis asynchrony.

OBJECTIVE: To assess how early diastolic transmitral flow is suppressed in a group of patients in whom effective ventricular filling occurred exclusively with atrial systole. DESIGN: Prospective examination of the left ventricular transverse and longitudinal axes and transmitral Doppler flow. SETTING: A tertiary referral centre for cardiac diseases. SUBJECTS: 20 patients (mean (SD) age 65 (10) years) with isolated transmitral late diastolic flow were studied. None had sinus tachycardia, prolonged PR interval or a summation flow pattern. 21 normal individuals of similar age served as controls. RESULTS: The left ventricle was usually dilated, end diastolic diameter (6.6 (1.0) v 4.9 (0.5) cm, P < 0.001) and end systolic diameter (5.4 (1.1) v 3.3 (0.5) cm, P < 0.001) were both increased, and fractional shortening of the minor axis reduced (16 (7)% v 30 (10)%, P < 0.001) in patients in whom left ventricular early diastolic filling was absent compared with those of normal controls. Mitral valve opening was late after aortic valve closure (A2) (115 (30) v 60 (10) ms, P < 0.001). The minor axis increased during this period (30 (20)% v 8.6 (2.5)%, P < 0.001). Onset of detectable transmitral flow was further delayed after cusp separation (85 (25) v 25 (10) ms, P < 0.001). Left ventricular long axis function was very abnormal. Onset of shortening was delayed with respect to the q wave at the left and septal sites (150 (40) v 90 (20) ms and 145 (30) v 80 (10) ms respectively, P < 0.001) and major shortening occurred after, rather than before, A2 (25 (12) v -10 (2.5)% and 50 (30) v -6.6 (0.3)% total excursion, P < 0.001). Although the long axis lengthened a little at the start of early diastole, its dominant component occurred in late diastole to coincide with atrial systole. The relative A wave was thus greatly increased at both sites (67 (17) v 29 (6)% and 77 (13) v 33 (8)%, P < 0.001). CONCLUSION: Prolonged left ventricular long axis shortening and delayed onset of lengthening effectively suppress early diastolic transmitral flow even though the minor axis increases and mitral cusps separate apparently normally. This grossly asynchronous left ventricular relaxation may interfere with filling by dissipating normal ventricular restoring forces.

Aged↗

PubMed1995

Architecture of atrial musculature in humans.

OBJECTIVE: To investigate the gross arrangement of the principal muscular bundles of the two atria, and to suggest how it may contribute to contraction and spread of atrial excitation. DESIGN: A prospective analysis based on anatomical examination of adult human hearts. SETTING: A national heart and lung institute and a tertiary referral centre for cardiac disease. MATERIAL: 9 normal postmortem human hearts. METHODS: Dissection of atrial muscles with macrophotography. RESUltS--The atrial walls consist of circumferential and longitudinal muscular bundles, the former being arranged at the base of the atria with the latter predominating in the parietal walls. The muscular bundles in the right atrium are larger than those in the left. The main muscles forming the right atrial wall are the terminal crest and terminal pectinate muscles. The terminal crest, the most obvious muscle, is arranged longitudinally with its pectinate muscles connecting to the musculature of the atrioventricular vestibule. No structure resembling the terminal crest is seen in the left atrium. Instead the left atrial wall is composed of intermingled series of muscles, chief of these being the interatrial band and the septoatrial bundle. The former is arranged circumferentially at the atrial base, while the latter is mainly longitudinal. The wall of the right atrium is not of uniform thickness because of the presence of the terminal crest and its pectinate muscles on its internal surface. By contrast, the left atrial wall is much more uniform and its average thickness is greater than that of the right atrium. The rim of the oval fossa is the most important muscular structure on the septal surface and is formed by the infolded atrial walls. The other principal muscles of the atria attach to it, so that the rim provides mechanical support for overall movement of the atrial walls. Comparison of the gross arrangement of the atrial musculature with earlier echocardiographic measurements showed that this arrangement of the muscle explains movement of the atrioventricular ring and overall atrial contraction, and provides a suitable substrate for preferential conduction. CONCLUSION: The anatomical features of the atrial musculature explain the known facts concerning atrial contraction and preferential conduction.

Autopsy↗

PubMed1995

Right ventricular filling in dilated cardiomyopathy.

PURPOSE: To assess right ventricular filling in dilated cardiomyopathy. PATIENTS: 32 patients with dilated cardiomyopathy and 24 healthy controls. METHODS: Stroke distances were measured by pulsed Doppler echocardiography at left ventricular outflow and left and right ventricular inflow. The inflow tract dimensions of both ventricles and the outflow tract dimension of the left ventricle were measured from two dimensional images. Right and left sided atrioventricular (AV) ring excursions were measured by M mode echocardiography at the tricuspid and mitral rings. Stroke volume was derived as stroke distance multiplied by left ventricular outflow tract area. Total stroke distances were calculated as the sum of AV valve Doppler stroke distances and ring excursion. The effective orifice areas of the two AV valves were thus defined as stroke volumes divided by total stroke distance. RESULTS: Total tricuspid stroke distance was normally less than mitral (6.0 (1.7) v 7.6 (1.7) cm, P < 0.05), implying that effective orifice area of the tricuspid valve was consistently greater (6.6 (1.6) v 4.5 (0.8) cm2, P < 0.01). Total tricuspid ring excursion was normally more than mitral (2.30 (0.30) v 1.62 (0.22) cm, P < 0.01). Total tricuspid stroke distance in dilated cardiomyopathy was also less than mitral (7.8 (2.4) v 9.7 (2.8) cm, P < 0.05). Tricuspid stroke distance was significantly increased in patients with dilated cardiomyopathy compared with that in healthy controls (P < 0.05 v controls), though stroke volume was much smaller (26 (10) v 63 (11) ml, P < 0.01) so that tricuspid effective orifice area was reduced to less than half normal (2.7 (1.2) cm2, P < 0.01). Total tricuspid ring long axis excursion was more than mitral (1.37 (0.6) v 0.74 (0.21) cm, P < 0.01). Right ventricular end diastolic inflow dimension was increased compared with that in healthy controls (3.9 (0.7) v 2.8 (0.5) cm, P < 0.01), correlating inversely with tricuspid effective orifice area (r = -0.71, P < 0.01). Total tricuspid ring excursion was bimodally distributed as a low amplitude group (less than 1.6 cm, n = 23) and a high amplitude group (more than 1.6 cm, n = 9), in which the interval P2 to onset of tricuspid flow was much longer (100 (35) v 50 (14) ms, P < 0.01). CONCLUSIONS: Enlargement of the right ventricular inflow tract in dilated cardiomyopathy, especially to more than 5 cm, is accompanied by a progressive decrease in effective tricuspid orifice area, sometimes to less than 1 cm2 and increased inflow velocities. Right ventricular relaxation was incoordinate in 28% of the patients studied. These disturbances of right ventricular filling are likely to compromise overall cardiac function independently of left ventricular disease.

Blood Volume↗

PubMed1995

Atrial electromechanical sequence in normal subjects and patients with DDD pacemakers.

OBJECTIVE: To assess the effect of right atrial appendage pacing on atrial electromechanical interrelations in patients with DDD pacemakers. DESIGN: Prospective study by M mode echocardiogram, Doppler echocardiogram, and apexcardiogram, along with electrocardiogram and phonocardiogram. SETTING: Tertiary cardiac referral centre. PATIENTS: 20 patients with DDD pacemakers and 20 age matched normal controls. RESULTS: Age, RR interval, atrial size, left ventricular size, and fractional shortening were similar in the two groups. Atrial electromechanical delay (the time from the onset of P wave or atrial pacing spike on ECG to the onset of atrial contraction on M mode echogram) was 68 (SD 7) ms at the lateral site of right atrium, 82 (9) ms at the central fibrous body, 93 (11) ms at the lateral site of left atrium in normals. In patients with DDD pacing, however, this delay increased to 85 (22) ms, 117 (23) ms, and 138 (25) ms respectively (all P < 0.01). Interatrial mechanical delay (the time from the onset of right atrial motion to the onset of the left) increased from 25 (6) ms in normal controls to 53 (18) ms in patients (P < 0.01). Intra-atrial mechanical dispersion (the time from the earliest to the latest onset of regional atrial motion around the atrioventricular ring) in the right atrium increased from 6 (2) ms in normals to 19 (2) ms in patients (P < 0.01), but it remained unchanged in the left atrium (6 (2) ms in normal controls v 7 (2) ms in patients, P > 0.05). Peak atrial shortening rate was not different between the two groups. Differences of atrial electromechanical activity between the two groups were also reflected on Doppler echocardiogram and apexcardiogram. CONCLUSIONS: Right atrial appendage pacing disturbs the normal coordinate sequence of right atrial mechanical activity and leads to a striking and variable increase in intra-atrial conduction time as well as in interatrial conduction time. Left atrial contraction remains synchronous although the timing of the start of its contraction was delayed. These values can be determined in individual patients to allow optimal setting of DDD pacemakers.

Aged↗

PubMed1995

Early diastolic left ventricular inflow pressures in normal subjects and patients with dilated cardiomyopathy. Reconstruction from pulsed Doppler echocardiography.

OBJECTIVE: To estimate early diastolic left ventricular inflow pressures in normal subjects and patients with dilated cardiomyopathy, and thus to assess the potential effect of restoring forces. METHODS: Early diastolic left ventricular inflow pressures were reconstructed using the ventricular blood as an accelerometer, by measuring velocity at 1 cm intervals within the left ventricle from mitral ring to apex by pulsed Doppler echocardiography, and differentiating the records to obtain the acceleration. Aortic component of second heart sound (A2) was used to fix relative timings. The local pressure gradient was determined from the acceleration at each level, and the total pressure drop during the acceleration (+ peak PD) and deceleration (- peak PD) phases of the filling interval were determined by summing the local increments. The total stroke volume (SV) at the left ventricular outflow tract and the mitral stroke distances (MSD) were also determined, using the time-velocity integral at mitral ring level. Effective flow orifice area was thus SV/MSD. Inflow jet width across the mitral valve was estimated by cross sectional colour Doppler flow mapping. PATIENTS: 32 patients with dilated cardiomyopathy with a dominant mitral E or summation wave, and 24 normal subjects of similar ages. RESULTS: Normal + peak PD was 3.9 (SD 0.7) v 7.4 (2.2) mm Hg in dilated cardiomyopathy (P < 0.01). Normal - peak PD was 2.5 (0.9) v 5.6 (2.8) mm Hg in cardiomyopathy (P < 0.01). Normal effective flow orifice area was 5.9 (1.3) v 1.9 (0.8) [range 0.9 approximately 3.7] cm2 in cardiomyopathy (P < 0.01). This corresponded to 71 (18)% of the end systolic cavity cross section in normals v 11 (6)% in dilated cardiomyopathy (P < 0.01). Normal cross sectional colour inflow jet width was 2.7 (0.3) v 1.5 (0.4) cm in cardiomyopathy (P < 0.01). The jet width correlated with flow width calculated from effective flow orifice area (r = 0.82, P < 0.01). CONCLUSIONS: (1) Total early diastolic positive and negative peak pressure drop are normally low, so that significant negative left ventricular pressures are not needed to explain normal resting early diastolic mitral flow velocities. (2) These low pressure drops are only possible with a large effective orifice area approaching end systolic left ventricular cavity area. (3) Atrioventricular pressure drops are much greater in dilated cardiomyopathy, where increased inflow accelerations are due to reduced effective flow orifice area. These disturbances will impair filling independently of any abnormality of relaxation or compliance.

Adult↗

PubMed1995

Non-invasive detection of left atrial mechanical failure in patients with left ventricular disease.

OBJECTIVE: To define patients with left atrial mechanical failure and identify its echocardiographic, physiological, and clinical associations. DESIGN: Prospective study with cross sectionally guided M mode and Doppler echocardiograms, and with apexcardiograms, electrocardiograms, and phonocardiograms. SETTING: Tertiary cardiac referral centre. PATIENTS: 10 patients with left atrial mechanical failure and 20 healthy controls of similar age. RESULTS: 10 patients with left atrial mechanical paralysis were identified among 4036 adults over a 1 year interval. Nine were in sinus rhythm and one had a DDD pacemaker. Left atrial mechanical activity was absent on M mode echocardiograms of the left sided atrioventricular ring and the aortic root. A Doppler A wave on transmitral flow and a clearly defined A wave on the left ventricular apexcardiogram were also absent, though evidence of right atrial mechanical movement was present in nine patients. Mean (SD) age was 63 (19) years and six were men. Nine had left ventricular disease and one had undergone extensive resection of the left atrium. Abnormal measurements of left ventricular end diastolic dimension (62 (13) mm), fractional shortening (15 (6)%), isovolumic relaxation time (19 (12) ms), left atrial size (45 (10) mm), and transmitral Doppler E wave deceleration time (110 (35) ms) were recorded. CONCLUSION: Left atrial mechanical failure may be present in patients with left ventricular disease despite normal sinus rhythm. Normal atrial activation on 12 lead electrocardiogram suggests it is primarily mechanical in origin. The possibility of left atrial mechanical failure must be considered when Doppler patterns of transmitral flow are used to assess left ventricular diastolic function.

Adult↗

PubMed1995

Abnormal ventricular long-axis function in systemic sclerosis.

STUDY OBJECTIVE: To assess possible effects of systemic sclerosis on ventricular function. DESIGN: Retrospective analysis of patients referred for echocardiographic examination to assess ventricular function. SETTING: Tertiary referral center for cardiac and chest diseases equipped with invasive and noninvasive facilities. PATIENTS: Thirty-four patients with clinical diagnosis of systemic sclerosis, aged 49 +/- 12 years; 24 had pulmonary fibrosis and 10 did not. There were 21 normal controls of similar age. MEASUREMENTS: Two-dimensional guided M-mode echocardiographic recordings of the left ventricular minor and long axis at the left and septal sites and right ventricle were obtained. Transmitral and transtricuspid Doppler flow velocities were also obtained with ECG and phonocardiogram. RESULTS: In 24 patients with pulmonary fibrosis, long-axis excursion was reduced 2.1 +/- 0.5 vs 2.7 +/- 0.4 cm/s as was peak rate of shortening and lengthening, 8.5 +/- 3.3 vs 10.8 +/- 2.4 cm/s and 7.5 +/- 2.5 vs 12 +/- 3.6 cm/s, respectively (p < 0.001), at the right side compared with 10 patients without. The onset of right long-axis shortening and lengthening was delayed with respect to the Q wave of the ECG and P2 of the phonocardiogram (p < 0.001 in both vs controls). The onset of tricuspid forward flow from the second heart sound was also delayed in the two groups, 110 +/- 15 ms and 100 +/- 20 ms vs 80 +/- 15 ms, respectively (p < 0.001). Right ventricular late diastolic filling velocities were increased 35 +/- 15 and 35 +/- 12 cm/s vs 20 +/- 10 cm/s in both groups (p < 0.01), and hence E:A ratio reduced 1.25 +/- 0.5 and 1.4 +/- 0.3 vs 1.9 +/- 0.4, respectively (p < 0.001). Pulmonary flow acceleration time was reduced only in patients with pulmonary fibrosis, 105 +/- 30 ms vs 125 +/- 30 ms (p < 0.001). At the left side, total long-axis excursion was reduced only in patients with pulmonary fibrosis (p < 0.01), while peak shortening and lengthening rates were reduced in both groups (p < 0.05). The onset of shortening from the Q wave and lengthening from the second heart sound were both delayed in the two groups with the latter greatly delayed in patients with pulmonary fibrosis (p < 0.05). CONCLUSIONS: Right and left ventricular long-axis function is frequently abnormal in patients with systemic sclerosis. Abnormalities are more profound in patients with CT evidence of pulmonary fibrosis than in those without. We suggest that these disturbances are due to myocardial fibrosis which, from the anatomic distribution of longitudinally directed fibers, is likely to have been subendocardial.

Blood Flow Velocity↗

PubMed1994

Early changes in left ventricular function after aortic valve replacement for isolated aortic stenosis.

To assess the immediate effects of aortic valve replacement (AVR) for valvular aortic stenosis (AS) on left ventricular (LV) systolic and diastolic function and global hemodynamics, 17 patients with AS underwent transesophageal echocardiography combined with high-fidelity LV pressure recording and thermodilution cardiac output measurements before cardiopulmonary bypass and 0.5, 6, 12, and 20 hours after AVR. Compared with results before bypass, LV systolic function had already changed 30 minutes after AVR, and remained constant thereafter: peak LV systolic wall stress decreased (from 210 +/- 60 to 130 +/- 40 g.cm-2), peak rate of dimension shortening increased (from 7.3 +/- 2.2 to 9.7 +/- 2.1 cm.s-1), both p < 0.01. Peak segmental external power thus remained constant (16.6 +/- 6.7 vs 17.7 +/- 7.6 mW.cm-3); p = NS. Changes in LV diastolic function and global hemodynamics were delayed. The peak rate of ventricular pressure decrease, normalized to developed end-systolic pressure, increased (from 15 +/- 3.2 to 19 +/- 5.2 s-1) by 6 hours. The minimal ventricular pressure of early diastole decreased (from 8.9 +/- 4.9 to 4.3 +/- 3.7 mm Hg), the peak rate of dimension lengthening of early diastole increased (from 6.0 +/- 3.0 to 8.8 +/- 2.0 cm.s-1), and LV stroke volume index increased (from 24 +/- 7 to 31 +/- 6 ml.m-2) by 12 hours, all p < 0.01. LV incoordination, defined as the dimension changes during isovolumic periods, had also improved significantly at 20 hours. Heart rate and LV enddiastolic dimension did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Effects of intermittent left bundle branch block on left ventricular diastolic function: a case report.

We investigated systolic and diastolic left ventricular function in a patient with an echocardiographically normal left ventricle and rate dependent left bundle branch block. Abnormal activation was associated with asynchronous left ventricular wall motion and secondary changes in filling pattern. The latter were similar to those seen in severe left ventricular disease. When the activation pattern reverted to normal, all of these abnormalities regressed. This case provides further evidence that abnormal activation can, on its own, cause left ventricular diastolic as well as systolic dysfunction.

Bundle-Branch Block↗

PubMed1994

Re-evaluation of normal splitting of the second heart sound in patients with classical left bundle branch block.

To study the mechanism of normal splitting of the second heart sound in patients with classical left bundle branch block, we investigated 43 such patients and 15 normal controls, using electro-, phono- and echo-cardiography and comparing the relative timing of mechanical activity in the two ventricles. The splitting of the second heart sound is reversed in only two-thirds of the patients and normal in remaining one-third. Comparing patients with and without reversed splitting, there are no significant differences in left ventricular cavity size, heart rate, pre-ejection period and the distribution of age, gender, or aetiology. QRS duration is longer (P < 0.01) in patients with reversed splitting. Diastolic events of the left ventricle do not differ between groups. The onset of the left ventricular free wall motion is delayed compared with normal by a similar extent in the two groups. In patients with normal splitting, the onset of the right ventricular wall motion is also delayed, both with respect to normal and to those with reversed splitting to an extent similar to that seen in classical right bundle branch block. Normal splitting of the second heart sound associated with an electrocardiographic pattern of left bundle branch block therefore suggests bilateral block. This combination can be documented from the precise timing of the movement of the two ventricles by M-mode echocardiography and identified by simple auscultation.

Aged↗

PubMed1994

Relations between resting ventricular long axis function, the electrocardiogram, and myocardial perfusion imaging in syndrome X.

OBJECTIVE: To investigate interrelations between ventricular long axis function, resting electrocardiogram, and myocardial perfusion imaging in a group of patients with syndrome X in order to define possible underlying mechanisms. DESIGN: Prospective echocardiographic, electrocardiographic, and myocardial perfusion imaging. SETTING: A tertiary referral centre for cardiac diseases with invasive and non-invasive facilities. PATIENTS: 50 consecutive patients with syndrome X selected on the basis of a history of angina, ST segment depression on exercise, and normal coronary arteriograms and 21 controls of similar age. RESULTS: Long axis motion of one or both ventricles assessed by echocardiography was abnormal in 37 patients. The onset of systolic shortening was delayed by > 130 ms (upper limit of normal 95% confidence interval) in eight patients, and was associated with prolonged shortening during the isovolumic relaxation period in seven (p < 0.01) (systolic abnormalities). The onset of diastolic lengthening was delayed by > 80 ms in 20. Early diastolic peak lengthening rate was < 4.5 cm.s-1 in 13 patients, and the relative amplitude of lengthening during atrial systole was > 45% in 18. On the resting electrocardiogram septal q waves were absent in 12 patients. This was associated with long axis systolic disturbances in seven patients (p < 0.05). T waves were abnormal in 10 and associated with delayed onset of early diastolic lengthening in all (p < 0.001). Late diastolic long axis disturbances were not associated with any consistent electrocardiographic abnormality. Myocardial perfusion imaging was abnormal in six of 33 patients, four of whom had systolic abnormalities (p < 0.03). Imaging was normal in the rest, but in 13 of them long axis function was abnormal in the left side and in four it was abnormal on the right ventricle. Both electrocardiography and imaging were normal in 10 patients. No patient with an abnormal electrocardiogram or myocardial perfusion had normal long axis motion on echocardiography. CONCLUSION: The function of the left and right ventricular long axes was abnormal in about 70% of a sample of patients with syndrome X. Systolic disturbances were consistently associated with absent septal q wave and abnormal myocardial perfusion imaging, while early diastolic disturbances correlated with T wave abnormalities. These associations suggest that the three different investigations detect related objective abnormalities in one or more subgroups of patients with syndrome X.

Echocardiography↗

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

Absent septal q wave: a marker of the effects of abnormal activation pattern on left ventricular diastolic function.

OBJECTIVE: To investigate the possible mechanical associations of the presence or absence of the septal q wave. STUDY DESIGN: Retrospective and prospective study of 63 patients with various left ventricular diseases and 10 controls by electrocardiography, echocardiography, and pulsed Doppler recordings. SETTING: Tertiary cardiac referral centre. PATIENTS: 73 subjects were studied. 26 had absent septal q waves and a QRS duration < 120 ms, 25 had classic left bundle branch block, and the rest had a normal electrocardiogram. Pathologically, 34 had left ventricular disease and 29 had a structurally normal heart. 10 subjects with structurally normal hearts and normal septal q waves were taken as controls. RESULTS: The timing of left ventricular minor axis motion was consistently normal in patients with abnormal activation, but long axis motion was considerably altered, with delayed "post-ejection shortening" of a mean amplitude of 4 mm. The post-ejection shortening began 10 (15) ms and reached its peak 90(20) ms after aortic closure (A2). Peak lengthening rate did not differ from normal (6.2 (3.5) v 8.5 (3.5) cm/s, NS) though it occurred significantly later. Post-ejection shortening was unrelated to age, amplitude of left ventricular wall motion, or QRS axis on the surface electrocardiogram. Post-ejection shortening was commoner when QRS duration was > 115 ms, but an absent septal q wave predicted its presence with a specificity of 90% and sensitivity of 86%. In patients with a post-ejection shortening, the onset of left ventricular systolic long axis shortening was delayed and the extent of its lengthening during the pre-ejection period increased, indicating delayed and incoordinate onset of tension development. During diastole, post-ejection shortening was associated with a prolonged isovolumic relaxation period and the time from A2 to the onset of transmitral flow. Peak mitral E wave flow velocity was reduced due to a fall in acceleration time although acceleration rate itself was unchanged. CONCLUSION: Loss of the normal septal q wave is associated with considerable mechanical consequences throughout the cardiac cycle, from the pre-ejection period to atrial systole, and apparently causes asynchronous subendocardial function.

Cardiovascular Diseases↗

PubMed1994

Nature of ventricular activation in patients with dilated cardiomyopathy: evidence for bilateral bundle branch block.

OBJECTIVE: To investigate the nature of ventricular activation and its relation with mechanical events in patients with dilated cardiomyopathy. STUDY DESIGN: Retrospective and prospective study with 12 lead electrocardiograms, signal averaged electrocardiograms, and M mode and Doppler echocardiograms. SETTING: Tertiary cardiac referral centre. PATIENTS: 77 patients (mean (SD) age 59(13)) with dilated cardiomyopathy, four after aortic valve replacement and three after coronary bypass surgery, and six patients with a normal sized left ventricle and complete right bundle branch block were studied. 15 normal subjects (age 45(20)) were used as controls. RESULTS: In patients with dilated cardiomyopathy, QRS duration was longer (127(25) ms v 90(10), P < 0.05) than normal and was normally distributed (r = 0.991, P < 0.01) on a normal probability plot. 20 had classic left bundle branch block, 29 intraventricular conduction delay, four right bundle branch block, and one bifascicular block. The PR interval was prolonged (185(30) ms v 150(15), P < 0.05). Electromechanical delay, Q to the onset of thickening of the interventricular septum as seen on the transverse M mode echocardiogram, was 75(15) ms in controls, but reduced to 43(15) ms in the patients (P < 0.01). Q to the onset of mitral regurgitation was also short (50(15)) ms, and correlated inversely with PR interval (r = -0.67, n = 73, P < 0.01). Early potentials (< 40 microV) were recorded on the signal averaged electrocardiogram in 33 representative patients and in all controls. Their overall duration was 30(12) ms in the patients, much longer than normal (12(7), P < 0.01)). Early potential time correlated positively with PR interval (r = 0.75, P < 0.01) and QRS duration (r = 0.60, P < 0.01) on a 12 lead electrocardiogram, and negatively with apparent electromechanical delay (r = -0.71, P < 0.01, n = 33), but not with true electromechanical delay (73(15)ms) or true PR interval (163(30)ms), calculated by correcting apparent values for early potential. The onset of left ventricular free wall motion was delayed with respect to the septum beyond 95% of the upper normal limit in all the patients with classic left bundle branch block and intraventricular conduction defect. Motion in the right ventricular free wall was delayed in 13 of 20 patients with left bundle branch block and 24 of 29 with intraventricular conduction defect by 65(20) ms, similar to that (75(10) ms) in patients with right bundle branch block. CONCLUSION: In most patients with dilated cardiomyopathy and an electrocardiographic pattern of left bundle branch block or intraventricular block, the onset of mechanical systole is strikingly and symmetrically delayed in both ventricles, compatible with bilateral bundle branch block. Complete atrioventricular block does not occur. The ventricle is activated through the upper septum and this activation is detectable only by signal averaged electrocardiography. The anatomical substrates for this abnormal activation could be the high connections described by Mahaim and Winston.

Bundle-Branch Block↗

PubMed1994

Abnormal subendocardial function in restrictive left ventricular disease.

OBJECTIVE: To study possible disturbances in left ventricular long axis function in patients with a restrictive filling pattern. DESIGN: Prospective examination of the left ventricular transverse and longitudinal axes, transmitral flow, and the apexcardiogram. SETTING: A tertiary referral centre for cardiac diseases. SUBJECTS: 21 normal subjects, age (SD) 51(11); 30 patients of similar age with a restrictive left ventricular filling pattern, defined as short early diastolic deceleration time less than the lower 95% confidence limit of the normal value (120 ms). 20 patients had a normal and 10 had an increased left ventricular end diastolic cavity size. RESULTS: Mitral Doppler echocardiography: E wave velocity was high only in patients with a normal cavity size. A wave velocity was greatly reduced in the two groups (P < 0.001) so that the E/A ratio was abnormally high. The relative A wave amplitude on the apexcardiogram was greatly increased in the two groups: 46(15)% (mean (SD)) and 54(4)% v 15(5)%. Minor axis: Fractional shortening was reduced from 30(10)% to 17(7)% in patients with normal cavity size and to 13(4.2)% in those with a dilated cavity (P < 0.001), as was the posterior wall thickening fraction from 100(30)% to 42(20)% and 50(25)% respectively (P < 0.001). Total systolic epicardial motion was normal and isovolumic relaxation time was short in the two groups. Long axis: Left ventricular abnormalities included reduced total amplitude of motion and its component during atrial systole (P < 0.001 for the two groups at both sites). Peak long axis shortening and lengthening were decreased at both left ventricular sites (P < 0.001). The time intervals from q wave of the electrocardiogram and A2 (aortic valve closure) to the onset of shortening and lengthening respectively were increased (both P < 0.001). Right ventricular long axis function was similarly affected but to a lesser extent. CONCLUSION: Left ventricular long axis function is consistently abnormal in patients with restrictive disease whether or not cavity size is increased. Not only are the extent and peak velocity of shortening reduced, but during diastole the peak early diastolic lengthening rate and amplitude during atrial systole are impaired. Early diastolic long axis motion is asynchronous with respect to transmitral flow and left ventricular minor axis. These effects will impair the overall left ventricular systolic and diastolic function independently of any decrease in passive cavity compliance. Unlike fibrosis, these long axis abnormalities are potentially amenable to treatment.

Cardiomyopathy, Restrictive↗

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↗