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Biomedical subjects

D G Gibson

Publications and source records attributed to D G Gibson.

At least 19 recordsLinked to original sources
PubMed1997

Coronary artery problems during homograft aortic valve replacement: role of transesophageal echocardiography.

We describe 2 cases in which intraoperative transesophageal echocardiography detected complications related to the proximal coronary arteries during homograft aortic valve and root replacement. In both cases, cardiopulmonary bypass could not be discontinued despite the use of large doses of inotropic drugs. Transesophageal echocardiography demonstrated aliasing on color flow mapping in the left main coronary artery in 1 case and proximal right coronary artery in the other, along with severely depressed left ventricular anterior wall and right ventricular function, respectively. Coronary artery bypass grafting was performed in both cases, and the outcome was successful.

Aged↗
PubMed1997

Asynchronous left ventricular wall motion in unstable angina.

The objective of the study was to assess the nature of left ventricular wall motion disturbances in patients with unstable angina and the relative contributions of the severity of symptoms and the severity of coronary artery disease (CAD) to their genesis. A prospective examination was performed on 30 patients with unstable angina (UA) with triple CAD, 34 matched patients with chronic stable angina (CSA) (20 with triple CAD and 14 with isolated left anterior descending (LAD) artery disease), and compared to 21 normals. LV cavity size was normal in all three groups. Twenty-two of 30 patients with UA had marked (>3 mm) abnormal long axis shortening during isovolumic relaxation time (IVRT), 65% of LV sites being abnormal. In CSA, minor (<3 mm) shortening during IVRT occurred in 7 patients with triple CAD, and in 5 with LAD disease, with 12% of LV sites involved in both groups, P<0.001 vs. UA. The incidence of other long axis abnormalities, including reduced extent and peak rate of shortening and lengthening as well as the delay in the onset of shortening and lengthening was increased between patients with CSA and triple CAD compared with LAD but not between the two groups of patients with triple CAD, CSA and UA. Transmitral E/A ratio was also reduced in the two groups with triple vessel disease, CSA and UA. Thus, the incidence of minor long axis abnormalities is similar in CSA and UA and is related to the severity of CAD. However, abnormal shortening during IVRT is more severe and generalised in UA but not in CSA with triple vessel disease. We suggest that these abnormalities of wall motion bear a close relation to the development of instability within the setting of CAD.

Aged↗
PubMed1997

Left ventricular remodelling and improvement in Freestyle stentless valve haemodynamics.

OBJECTIVE: To assess how left ventricular (LV) hypertrophy, geometry and function change after stentless aortic valve replacement for aortic stenosis, and to elucidate the physiological mechanism of the improvement in stentless valve haemodynamics. METHODS: 81 patients with aortic stenosis (age 75 +/- 6 years, 47 male) underwent aortic valve replacement (plus CABG in 33 patients) with a Freestyle stentless porcine valve (mean size 23 +/- 2 mm). They were prospectively investigated by Doppler echocardiography at 2 weeks, 3-6, 12, and 24 months after operation. Two hundred and forty-six echocardiograms were obtained and analysed. Aortic valve performance was assessed from its effective orifice area (EOA), the transvalvular increase in mean flow velocity (delta mV), the deceleration time of aortic flow velocity, and mean pressure drop (mPG). LV hypertrophy was assessed from LV mass index; LV geometry, from the ratio of wall thickness to the radius (T/R ratio) and LV function, from stroke volume index (LVSVI) and myocardial stroke work (SW). RESULTS: By 2 years after operation, LV mass index had fallen from 162 +/- 64 to 109 +/- 36, g/m2, and T/R ratio from 0.61 +/- 0.25 to 0.43 +/- 0.10. LVSVI increased from 29.4 +/- 10 to 42 +/- 17, ml/m2, and myocardial SW from 3.1 +/- 1.6 to 5.2 +/- 2.2, mJ/cm3 (all P < 0.001 by ANOVA), while LV outflow tract diameter remained unchanged. At the same time, stentless valve EOA increased from 1.59 +/- 0.75 to 2.2 +/- 0.72, cm2, and delta mV (from 82 +/- 31 to 49 +/- 24, cm/s) and mPG (from 9.7 +/- 5.0 to 5.2 +/- 3.7 mmHg) both fell significantly (all P < 0.001 by ANOVA): as the deceleration time of aortic flow velocity increased from 153.6 +/- 64.1 to 202.7 +/- 37.6 ms (P < 0.001 by ANOVA). CONCLUSION: After stentless aortic valve replacement, LV mass index and wall thickness both fall towards normal, and myocardial stroke work increases. These ventricular remodelling processes are accompanied by a more physiological flow jet at valve cusp level, which permits a greater stroke volume to be ejected with a smaller transvavular velocity increase, so that effective orifice area increases.

Aged↗
PubMed1997

Effects of acute coronary occlusion and previous ischaemic injury on left ventricular wall motion in humans.

OBJECTIVE: To assess the acute effects of single and repeated coronary artery occlusions, during percutaneous transluminal coronary angioplasty (PTCA), on left ventricular long axis function in patients with stable and unstable angina. DESIGN: Prospective examination of ventricular systolic and diastolic long axis function using M mode echocardiography and transmitral Doppler in patients with significant coronary artery stenosis and either stable or unstable angina, during routine PTCA. SETTING: A tertiary referral centre for heart disease with cardiac catheterisation and echocardiographic facilities. SUBJECTS: 36 patients, age (SD) 60 (8) years, with significant coronary artery disease undergoing PTCA (mean duration 100-130 seconds) to the left anterior descending coronary artery (LAD) in 18 patients, native LAD or its vein graft in eight, and right coronary artery in 10. Controls were 21 normal subjects, age 58 (11) years. RESULTS-AT BASELINE: in systole, total long axis excursion was reduced at septal, posterior, and right sites in patients with LAD disease, at right site in those with vein grafts, and at septal and right sites in patients with right coronary artery disease. Peak shortening rate was often reduced in all patients and onset of shortening delayed with respect to the Q wave in patients with LAD disease. In diastole, onset of lengthening was always delayed, peak lengthening rate reduced, and relative A wave amplitude increased in all patients. There was a consistent abnormal shortening of the long axis during the isovolumic relaxation period in the 14 patients with unstable angina, not seen in the others. Transmitral A wave velocity was also increased and the onset of E wave delayed with respect to A2. At first balloon inflation: the extent of pre-existing systolic and particularly diastolic abnormalities consistently increased in patients with LAD or right coronary artery occlusion. This was associated with further delay in the onset of the transmitral Doppler E wave as its peak velocity fell and E/A ratio increased. In unstable angina, balloon inflation caused minor changes only in systolic function and no change in diastolic function. At second balloon inflation: systolic changes were the same as with the first inflation, while diastolic changes were attenuated by 10-15%. CONCLUSIONS: In stable angina intracoronary balloon inflation aggravated pre-existing systolic and diastolic abnormalities in the territory of the occluded vessel, indicating the dependence of both on coronary flow. In unstable angina balloon inflation caused only minor deterioration in systolic function, and diastolic changes-including the characteristic abnormal shortening during isovolumic relaxation-were unaffected. Thus resting abnormalities of left ventricular function in unstable angina are effectively dissociated from acute changes in coronary flow. Overall, the severity of systolic disturbances was unaltered by a second balloon inflation, but diastolic disturbances were attenuated by 10-15%, compatible with ischaemic preconditioning or recruitment of collaterals.

Aged↗
PubMed1996

Natural history of abnormal conduction and its relation to prognosis in patients with dilated cardiomyopathy.

To investigate the natural history of disturbances in ventricular activation, atrioventricular conduction, and ventricular cavity size, we retrospectively studied 58 patients from a total of 296 patients with dilated cardiomyopathy seen within 4 years. A total of 309 computerised electrocardiograms (ECGs) and 135 M-mode echocardiograms were analysed. In the majority of the patients, PR interval, QRS duration and QT interval prolonged progressively, though heart rate changed little. Their increase was much more striking in patients who died (n = 10) or had a pacemaker inserted (n = 9), compared to that in the clinically stable patients, though at entry all these values, as well as age and left ventricular cavity size, were similar. There were no significant differences between patients who died and those with a pacemaker inserted, except for QRS axis, which had shifted rightwards in 8 out of 10 who died, but only in 3 of 9 who subsequently had a pacemaker inserted and 14 of the 29 stable patients. A QRS duration over 160 ms was found in 8 out of the 10 patients who died, 6 of 9 who had a pacemaker and only in 5 out of the 39 stable patients (P < 0.001). The sum of PR interval and QRS duration over 375 ms was not found in any stable patient but was present in 6 of the 7 patients who were in sinus rhythm and died (P < 0.001). Left ventricular cavity size also increased with time, but did not correlate significantly with ECG progression, nor did it identify patients who subsequently died. Thus, a combination of increasing PR interval and QRS duration, particularly along with rightwards shift of QRS axis, appears to be a marker of high risk in patients with dilated cardiomyopathy.

Adult↗
PubMed1996

Absent septal q wave on electrocardiogram: a forgotten marker of myocardial disease.

Though absence of the septal q wave on a standard ECG was recognised by Willem Einthoven, this abnormality has received little attention. Nevertheless it is common in patients with coronary artery disease, and strongly associated with fibrosis of the septum with or without infarction. Furthermore, the associated disturbance of ventricular activation has clear mechanical consequences, impairing both systolic and diastolic left ventricular performance. Its structural, functional, and possible prognostic significance combined with ease of its detection all suggest that the cardiographic sign of absence of the septal q wave should be more widely recognised as a noninvasive marker of ventricular disease.

Biomarkers↗
PubMed1996

Effects of valve substitute on changes in left ventricular function and hypertrophy after aortic valve replacement.

BACKGROUND: Residual left ventricular hypertrophy adversely affects long-term outcome after aortic valve replacement. A stentless biological valve in the aortic position has been shown to offer a better hemodynamic profile than a stented one. However, it remains to be defined whether this difference is translated into inter-mediate-term effects on left ventricular structure and function. METHODS: One hundred thirty-seven patients receiving single aortic valve replacement (52 with concomitant coronary artery bypass graft) were enrolled in this study. Ninety-eight were men, and the mean age was 68 years (range, 55 to 90 years). Of the 137 patients, 39 had an aortic homograft, 72 a Toronto stentless porcine valve, and 26 had a stented porcine or bileaflet mechanical valve, with mean valve size of 25 +/- 2.5 mm (mean +/- standard deviation). Left ventricular muscle mass and function were assessed by M-mode echocardiography performed before and 0.5, 6, 12, 24, and 36 months after operation, and recorded on paper for off-line digitizing. Peak valve prosthesis pressure gradients were quantified by continuous wave Doppler. RESULTS: A total of 330 echocardiograms obtained during this study were adequate for computer digitizing. Clinical data, preoperative left ventricular function, and hypertrophy were similar between the three groups. Significant improvement in left ventricular function and major regression of left ventricular hypertrophy had occurred in the entire population by 6 months after operation. Multivariate analysis of variance showed that patients with previous aortic regurgitation had a larger left ventricular cavity size (p < 0.001) and greater mass index (p = 0.001) postoperatively than those with previous aortic stenosis. In addition, peak valvular gradient was lower (p < 0.001), mass index less (p < 0.001), and left ventricular function more normal both systolic, by a greater peak velocity of dimension shortening (p = 0.05) and wall thickening (p = 0.002), and diastolic, by a greater peak velocity of dimension lengthening (p = 0.046), with an aortic homograft or stentless porcine valve compared with a mechanical or stented biological valve. There was no significant difference in peak valve gradient, left ventricular mass index, or function between the aortic homograft and the stentless porcine valve. Age, sex, and concomitant coronary artery bypass graft, as well as aortic cross-clamp time, cardioplegia method, and valve size all proved to be insignificant determinants of postoperative left ventricular hypertrophy or function. CONCLUSIONS: In the first 2 years after implantation, the superior hemodynamic performance of aortic homograft and stentless porcine valve appears to result in more extensive regression of ventricular hypertrophy and greater improvement of left ventricular function than occurs with a mechanical or stented biological valve. These findings encourage the use of a stentless biological valve in older patients requiring aortic valve replacement, and a larger scale long-term randomized study of stentless versus stented biological valve or mechanical valve seems warranted.

Aged↗
PubMed1996

Effect of acute alterations in afterload on left ventricular function in patients with combined coronary artery and peripheral vascular disease.

OBJECTIVE: To assess the effect of acute alterations in afterload by aortoiliac clamping, during peripheral vascular surgery, on left ventricular function. DESIGN: Prospective examination of the left ventricular long axis and transmitral Doppler flow preoperatively and intraoperatively; before aortic clamping, during clamping and 5 min, 15 min, and 5 days after unclamping. SETTING: A tertiary referral centre for cardiac and vascular disease equipped with invasive and non-invasive facilities. PATIENTS: 20 patients (11 men; mean (SD) age 61 (8) years) with significant aortoiliac disease and documented coronary artery disease and 21 normal controls of similar age. RESULTS: Preoperatively: long axis function was abnormal compared with that in normal controls. In systole total long axis excursion and peak shortening rate were reduced, onset of shortening delayed, and there was pre-ejection lengthening (P < 0.001). In diastole there was abnormal shortening during isovolumic relaxation, delaying the onset of long axis lengthening (P < 0.001). Peak lengthening rate was also reduced and A wave excursion increased (P < 0.001). Transmitral Doppler showed increased A wave velocity and reduced peak E/A diastolic flow velocities ratio (P < 0.001). Intraoperatively: preclamping results did not differ from those before operation. With clamping the extent of systolic and diastolic abnormalities promptly increased as to a lesser extent did those of transmitral flow velocity, although heart rate and blood pressure did not change significantly. Total long axis excursion and A wave amplitude were more reduced by aortic than iliac clamping, whereas the onset of lengthening was more delayed and the lengthening velocity more reduced with iliac clamping. Some 5 min after unclamping systolic long axis function had already returned towards normal; total excursion increased, as did the peak shortening rate, and the onset of shortening became less delayed (P < 0.001). In diastole the delayed onset of lengthening regressed, its lengthening velocity increased, and A wave excursion fell (P < 0.001). Early diastolic transmitral flow velocity also increased. This improvement in systolic and diastolic long axis function had progressed 15 min after unclamping but showed no further change at 5 days. At 5 days after operation, however, systolic and diastolic measurements had improved compared with those preoperatively. CONCLUSION: Resting left ventricular long axis function is abnormal in patients with combined coronary artery disease and peripheral vascular disease. It is unaffected by anaesthesia but deteriorates with aortic or iliac clamping, although blood pressure remains unchanged. It promptly improves with unclamping after successful peripheral arterial reconstruction. Thus, even in apparently stable coronary artery disease, resting subendocardial function is labile, showing pronounced alterations with changing after-load, even when arterial pressure itself does not change.

Blood Pressure↗
PubMed1996

ACE inhibitors unmask incoordinate diastolic wall motion in restrictive left ventricular disease.

OBJECTIVE: To assess the effect of ACE-inhibition on left ventricular filling and wall motion in patients with a clinical diagnosis of heart failure. DESIGN: Prospective examination of left ventricular systolic and diastolic function using M mode echocardiography and pulsed and continuous wave Doppler before and three weeks after starting an ACE inhibitor. SETTING: A tertiary referral centre for cardiac disease equipped with non-invasive facilities. SUBJECTS: 30 outpatients with a clinical diagnosis of heart failure in whom treatment with an ACE inhibitor was started; age 61 (SD 11) years; 27 male; 3 female; 21 healthy controls of similar age. RESULTS: Left ventricular cavity was dilated both at end systole and end diastole, and fractional shortening reduced. Although mean isovolumetric relaxation time (IVRT) and transmitral E (early) to A (late) filling velocity (E/A) ratio were not different from normal, a value of 1.0 on the normal frequency plot of the E/A ratio divided the patients bimodally into two groups: 20 patients (group A) with E/A ratio > 1.0 and 10 patients (group B) < 1.0. In group A patients, IVRT was short as was transmitral E wave deceleration time compared to normal (P < 0.001), fulfilling the criteria of restrictive left ventricular physiology. Left ventricular wall motion during IVRT was coordinate and left ventricular end diastolic pressure was raised on the apex-cardiogram (P < 0.001). In group B, E wave deceleration time was longer, relaxation incoordinate, and apexcardiogram normal. With an ACE inhibitor: in group A, left ventricular dimensions fell at end diastole (P < 0.05) and end systole (P < 0.01) but fractional shortening did not change; long axis total excursion (P < 0.01) and peak rate of shortening (P < 0.05) both increased; IVRT increased (P < 0.001) with the appearance of markedly incoordinate wall motion, minor axis lengthening, and long axis shortening (P < 0.001 for both); A wave amplitude also consistently increased (P < 0.001); finally, transmitral E wave velocity fell and A wave velocity increased. ACE inhibition did not alter any of the left ventricular minor and long axis or transmitral Doppler variables in patients in group B. CONCLUSIONS: Patients with a clinical diagnosis of heart failure differ in their presentation and response to ACE inhibition according to baseline haemodynamics. In restrictive left ventricular physiology, ACE inhibition reduces cavity size and prolongs IVRT, compatible with a fall in left atrial pressure. At the same time, ventricular relaxation becomes very delayed and incoordinate, greatly reducing early diastolic left ventricular filling velocity. Thus ACE inhibition unmasks major diastolic abnormalities in patients with restrictive left ventricular disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Effects of incoordination on left ventricular force-velocity relation in aortic stenosis.

OBJECTIVE: Tension development is often incoordinate in the hypertrophic left ventricle (LV). The present study aimed to elucidate the possible effects of incoordination on standard LV force-velocity relations in patients with aortic stenosis (AS). DESIGN: Prospective study during aortic valve replacement with transoesophageal cross sectionally guided M mode echocardiogram, combined with high-fidelity LV pressure recorded by pressure transducer tip catheter, and thermodilution cardiac output. SETTING: Tertiary cardiac referral centre. PATIENTS: 37 patients (mean (SD) age 63 (12)) years were studied before and 20 hours after aortic valve replacement. MAIN OUTCOME MEASURES: LV function was assessed regionally by peak velocity of circumferential fibre shortening (peak Vcf), mean systolic wall stress, and peak myocardial power; and globally by LV stroke work index. LV coordination was quantified as cycle efficiency, derived from LV pressure-dimension loop (lower normal limit > or = 76%). RESULTS: 22 patients with a coordinate LV had significantly higher peak Vcf (1.85 (0.47) v 1.46 (0.64) s-1) peak myocardial power (20.8 (8.5) v 12.0 (6.1) mW.cm-3) and global stroke work index (440 (155) v 325 (150) mJ.m-2) than those of 15 patients with an incoordinate ventricle, all P < 0.05; though there was no significant difference in LV end diastolic dimension, mean systolic wall stress, LV mass index, or the incidence of coronary artery disease (P > 0.05, respectively). Furthermore, when contraction was coordinate, mean systolic circumferential wall stress correlated inversely with peak Vcf (r = - 0.71) and positively with peak myocardial power (r = 0.83), both P < 0.01. When contraction was incoordinate, these correlations did not apply; instead peak Vcf (r = 0.65) and peak myocardial power (r = 0.73) both correlated positively with cycle efficiency (P < 0.02 and 0.01, respectively). By 20 hours after surgery, values of cycle efficiency, peak Vcf, and myocardial power were indistinguishable in the previously coordinate and incoordinate groups. CONCLUSIONS: In aortic stenosis, incoordination causes a fall in LV peak Vcf proportional to the increase in systolic wall stress, and thus modifies the standard LV force-velocity relation to mimic depressed contractility. However, incoordination and subsequent ventricular dysfunction were largely reversible once the aortic stenosis had been relieved.

Aortic Valve↗
PubMed1995

Early changes in regional and global left ventricular function after aortic valve replacement. Comparison of crystalloid, cold blood, and warm blood cardioplegias.

BACKGROUND: The clinical effects of different cardioplegic methods on left ventricular (LV) function have not been fully elucidated, particularly in the setting of myocardial hypertrophy. METHODS AND RESULTS: Sixty-four patients (mean age, 62 +/- 12 years; 41 men, 23 women) who were undergoing elective aortic valve replacement (stenosis, 49; regurgitation, 15; concomitant coronary artery bypass grafting, 22), with LV mass index 230 +/- 70 g/m2, were randomized to the following groups: antegrade crystalloid cardioplegia (CCP, 21 patients), antegrade/retrograde cold blood cardioplegia (CBP, 23 patients), or continuous retrograde warm (37 degrees C) blood cardioplegia (WBP, 20 patients). Mean aortic cross-clamp and cardiopulmonary bypass times were 100 +/- 20 and 126 +/- 24 minutes. Positive inotropic drug therapy was required postoperatively in 9 patients after CBP, 14 after CCP, and 18 after WBP. Perioperative LV function was assessed using transesophageal M-mode echocardiography, combined with high-fidelity LV pressure recording and thermodilution cardiac output, before bypass and 0.5, 1, 3, 6, 12, and 20 hours after cross-clamp removal. There was a similar fall in LV peak circumferential wall stress at constant LV end-diastolic dimension in each group after aortic valve replacement. The increase in contraction velocity was significant from 0.5 hour with CBP; however, no significant increase occurred until 12 hours with CCP and until 20 hours with WBP. The rate and extent of LV pressure fall and early diastolic filling rate both increased with CBP, and only in this group did ventricular coordination improve. LV stroke work index was maintained with CBP throughout the postoperative period with less inotropic support than with the other two methods. CONCLUSIONS: In the hypertrophied LV, CBP offers the best preservation of myocardial physiological response and ventricular function with less inotropic support.

Adult↗
PubMed1995

Association of reduced PR-AC interval with ventricular early potentials in dilated cardiomyopathy.

We studied 31 patients with dilated cardiomyopathy, correlating mitral valve cusp motion with the continuous wave Doppler signal of mitral regurgitation and the signal averaged electrocardiogram (ECG). Sixteen patients had a B point (early partial closure) on the mitral echogram and 15 did not. Fifteen normal cases were used as controls. The duration of ventricular early potentials (< 40 microV) was measured on the signal averaged ECG of the QRS complex. The PR interval was increased in patients with a B point (190 (33) ms vs. 145 (16) ms in normal, P < 0.01) and PR-AC interval was reduced (25 (71) ms vs. 65 (11) ms in normal, P < 0.05). The B point itself was effectively synchronous with the onset of low velocity early systolic mitral regurgitation, and followed the Q wave of the succeeding beat by 20 ms or less. Early low velocity on mitral regurgitation was not present in patients without a B point. The duration of early potentials was greatly increased in patients with a B point (43 (26) ms) compared both to those without (17 (20) ms, P < 0.01) and to normals (12 (7) ms, P < 0.01) and their duration correlated with B-C interval (r = 0.6, P < 0.02). We conclude that a B point on the mitral echogram in patients with left ventricular disease is due to early systolic low velocity mitral regurgitation which itself results from an abnormal pattern of left ventricular activation, probably bilateral bundle branch block. Once established, this low velocity jet delays complete mitral valve closure.

Adult↗
PubMed1995

Magnetic resonance velocity mapping of normal human transmitral velocity profiles.

We used magnetic resonance imaging (MRI) velocity mapping to assess the velocity profile of early diastolic mitral inflow in 11 normal subjects. Velocity maps of left ventricular inflow were obtained in the horizontal long axis of the left ventricle at the time of peak early diastolic filling. Velocity profile curves across the mitral inflow were obtained at 1-cm intervals from the mitral ring to 4 cm into the cavity. The jet width was 3.06 +/- 0.64 cm at the mitral ring level, increasing to 3.6 +/- 0.61 cm at 4 cm. The peak/mean velocity was 1.2 +/- 0.07 at the mitral ring and increased to around 1.4 at 3-4 cm from the mitral ring. The point at which the peak velocity was recorded at each level was skewed towards the septal side by 10%-13% of jet width from the center at the mitral ring and 2-4 cm from the ring. However, at a depth of 1 cm, corresponding to the mitral tip level, the peak velocity was at the center of the jet. The ratio of vertical and horizontal dimensions of the jet cross section was 1.11 +/- 0.05. Thus, the mitral inflow velocity profile is relatively flat at the mitral ring and tip level; the inflow jet cross section is effectively circular.

Adolescent↗
PubMed1995

Detection and localization of early diastolic forces within the left ventricle from inflow jet dynamics. A comparison between normal subjects and patients with dilated cardiomyopathy.

We studied the properties of the jet of blood entering the left ventricle from the left atrium during early diastole in 32 patients with dilated cardiomyopathy, and 24 normal subjects of similar age. The diameter of the jet was measured from the cross-sectional color Doppler image and its cross-sectional area (JA) was derived. Pulsed Doppler records of flow velocity were made at 1-cm intervals into the ventricle from the mitral ring. Peak (Vp) and mean (Vm) E wave velocity and time velocity integral (TVI) were determined. At any level in the ventricle, therefore, the early diastolic volume of blood remaining in the jet, i.e., the flow time integral, is given by JA.TVI; the local flow rate, Q, by JA.Vm; and jet momentum along the long axis of the ventricle by Q.Vp. In normals, the jet cross-sectional area fell from 5.9 (1.3) cm2 at the mitral ring to 4.9 (0.7) cm2 at 4 cm (P < 0.05), but the flow time integral fell proportionately more, from 46.0 (15.2) ml at the ring level to 15.9 (3.4) ml at 4 cm (P < 0.01). Axial momentum flux was 44 (13) x 10(2) cm4s-2 at the ring level, falling to 28 (10) x 10(2) cm4s-2 at 4 cm (P < 0.01). In dilated cardiomyopathy, the jet cross-sectional area was much smaller than normal, 1.9 (0.8) cm2 at the ring level, and it remained effectively constant, being 2.0 (0.9) cm2 at 6 cm (P < 0.01 vs normals).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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↗