Identification of floral genes for sex determination in Calamus palustris Griff. by using suppression subtractive hybridization.

Calamus palustris Griff. is an economically important dioecious rattan species in Southeast Asia. However, dioecy and onset of flowering at 3-4 years old render uncertainties in desired female:male seedling ratios to establish a productive seed orchard for this rattan species. We constructed a subtractive library for male floral tissue to understand the genetic mechanism for gender determination in C. palustris. The subtractive library produced 1536 clones with 1419 clones of high quality. Reverse Northern screening showed 313 clones with differential expression, and sequence analyses clustered them into 205 unigenes, including 32 contigs and 173 singletons. The subtractive library was further validated with reverse transcription-quantitative polymerase chain reaction analysis. Homology identification classified the unigenes into 12 putative functional proteins with 83% unigenes showing significant match to proteins in databases. Functional annotations of these unigenes revealed genes involved in male flower development, including MADS-box genes, pollen-related genes, phytohormones for flower development, and male flower organ development. Our results showed that the male floral genes may play a vital role in sex determination in C. palustris. The identified genes can be exploited to understand the molecular basis of sex determination in C. palustris.

Isolation and characterization of CCoAOMT in interspecific hybrid of Acacia auriculiformis x Acacia mangium--a key gene in lignin biosynthesis.

This study was directed at the understanding of the function of CCoAOMT isolated from Acacia auriculiformis x Acacia mangium. Full length cDNA of the Acacia hybrid CCoAOMT (AhCCoAOMT) was 1024-bp long, containing 750-bp coding regions, with one major open reading frame of 249 amino acids. On the other hand, full length genomic sequence of the CCoAOMT (AhgflCCoAOMT) was 2548 bp long, containing three introns and four exons with a 5' untranslated region (5'UTR) of 391 bp in length. The 5'UTR of the characterized CCoAOMT gene contains various regulatory elements. Southern analysis revealed that the Acacia hybrid has more than three copies of the CCoAOMT gene. Real-time PCR showed that this gene was expressed in root, inner bark, leaf, flower and seed pod of the Acacia hybrid. Downregulation of the homologous CCoAOMT gene in tobacco by antisense (AS) and intron-containing hairpin (IHP) constructs containing partial AhCCoAOMT led to reduction in lignin content. Expression of the CCoAOMT in AS line (pART-HAS78-03) and IHP line (pART-HIHP78-06) was reduced respectively by 37 and 75% compared to the control, resulting in a decrease in the estimated lignin content by 24 and 56%, respectively. AhCCoAOMT was found to have altered not only S and G units but also total lignin content, which is of economic value to the pulp industry. Subsequent polymorphism analysis of this gene across eight different genetic backgrounds each of A. mangium and A. auriculiformis revealed 47 single nucleotide polymorphisms (SNPs) in A. auriculiformis CCoAOMT and 30 SNPs in A. mangium CCoAOMT.

The utility of transoesophageal echocardiography to determine management in suspected embolic stroke.

BACKGROUND: Assessment for source of stroke is a common indication for transoesophageal echocardiography (TOE). Although an abnormality is frequently found, it remains uncertain how frequently the findings alter patient management. Also, the role of transthoracic echocardiography (TTE) prior to or instead of TOE is not well defined. We sought to determine the use of TTE prior to TOE, the outcome of the TOE and its impact on management. METHODS: We retrospectively reviewed the records and echocardiography results of 100 consecutive patients who underwent TOE for any reason at a tertiary hospital. In 35 subjects (35%), the indication was evaluation for source of stroke. Among these, we determined clinical risk factors for stroke, if a TTE was performed prior to their TOE, the results of the TOE and its effect on management. RESULTS: The mean age of the stroke patients was 64.6 years (17-90) and 49% were women. Eighty per cent had at least one risk factor for stroke and 17% had atrial fibrillation. A TTE, performed in 40% prior to the TOE, found an abnormality in 14% (2/14). The TOE showed an abnormality in 71% of patients; 54% had aortic atheroma; 17% PFO; 14% spontaneous echo contrast; 6% left atrial appendage thrombus, 3% left ventricular thrombus and 3% vegetation. In only one patient (3%) the management was altered based on the abnormal TOE findings. CONCLUSION: An abnormality on TOE, although common (71%) and more sensitive than TTE, altered management in only 3% of subjects referred for stroke assessment. Its role requires further consideration.

Preload dependence of Doppler-derived indexes of left ventricular diastolic function in humans.

To determine the effect of filling pressure on the pattern of left ventricular filling in humans, the mitral flow velocity profile was measured by pulsed wave Doppler echocardiography during right and left heart catheterization in 11 patients before and during nitroglycerin infusion. Nitroglycerin reduced mean arterial pressure from 90 +/- 9 to 80 +/- 11 mm Hg (p less than 0.001) and mean pulmonary capillary wedge pressure from 9 +/- 4 to 4 +/- 2 mm Hg (p less than 0.001). Cardiac output fell from 6.6 +/- 1.5 to 5.5 +/- 1.4 liters/min (p less than 0.001) and heart rate increased from 60 +/- 13 to 65 +/- 14 beats/min (p less than 0.002). The time constant of isovolumic relaxation (TI.) decreased from 51 +/- 9 to 46 +/- 8 ms (p less than 0.01), indicating faster left ventricular relaxation. Nitroglycerin altered the Doppler characteristics of the early filling (E) wave but not those of the atrial contraction (A) wave. Peak velocity of the E wave decreased from 56 +/- 14 to 44 +/- 9 cm/s (p less than 0.001), peak velocity of the A wave did not change and the ratio of peak velocities of the E and A waves decreased from 0.97 +/- 0.33 to 0.77 +/- 0.20 (p less than 0.02). The deceleration of the E wave decreased from 289 +/- 138 to 186 +/- 71 cm/s2 (p less than 0.02). The ratio of velocity-time integral of the A wave to total velocity-time integral (that is, contribution of atrial contraction to total filling) increased from 0.31 +/- 0.09 to 0.36 +/- 0.08 (p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of the early transmitral Doppler velocity curve: effect of primary physiologic changes and compensatory preload adjustment.

Left ventricular filling (as assessed by Doppler echocardiography) has previously been shown to depend in a complex fashion on ventricular diastolic function (compliance and relaxation) as well as other variables, such as atrial pressure and compliance, ventricular systolic function and mitral valve impedance. To study the effect of isolated physiologic alterations on individual Doppler indexes, a mathematic model of mitral flow was analyzed. By varying one physiologic variable at a time, it was shown that mitral velocity acceleration is affected directly by atrial pressure and inversely by the ventricular relaxation time constant, with relatively little impact of chamber compliance. Deceleration rate was directly influenced by mitral valve area, atrial pressure and ventricular systolic dysfunction and inversely affected by atrial and ventricular compliance relations, with little impact of relaxation unless it was so delayed as to be incomplete during deceleration. Peak velocity was directly affected most strongly by initial left atrial pressure, and lowered somewhat by prolonged relaxation, low atrial and ventricular compliance and systolic dysfunction. Strikingly different filling patterns emerged when the primary physiologic alterations were accompanied by simultaneous compensatory changes in atrial pressure designed to maintain stroke volume constant. Low ventricular compliance with preload compensation produced characteristic E waves with very short acceleration and deceleration times and high peak velocity. Thus, mathematic analysis of ventricular filling helps to explain the physical and physiologic basis for the transmitral velocity curve.

Echocardiographic evaluation of mitral valve structure and function in patients followed for at least 6 months after percutaneous balloon mitral valvuloplasty.

Although beneficial results have been reported immediately after percutaneous mitral balloon valvuloplasty, little information is available concerning the longer-term outcome of this procedure. The anatomic and functional results of percutaneous mitral valvuloplasty were assessed in 20 patients, in whom two-dimensional and Doppler echocardiographic examination could be obtained both immediately and 6 to 11 months (mean 7.5 +/- 2.0) after balloon dilation. Mean valve area measured by planimetry decreased slightly but significantly from 1.90 +/- 0.59 cm2 immediately after valvuloplasty to 1.62 +/- 0.55 cm2 (p less than 0.001) at follow-up. Individual changes in valve area were variable, and in four patients valve area decreased by greater than 25%. Echocardiographic scores of valvular morphology were obtained by assigning scores of 0 to 4 (with increasing abnormality) to each of four morphologic characteristics of the valve, namely, leaflet mobility, thickening, calcification and subvalvular thickening. This score was higher in the four patients with a decrease in valve area greater than 25% at follow-up than in the other patients (11 +/- 2 versus 7 +/- 2, p less than 0.002). Multiple regression analysis of several hemodynamic and echocardiographic factors identify first the echocardiographic score and second the valve area postvalvuloplasty as the only significant predictors of the percent decrease in valve area (r = 0.70, p less than 0.006). Mitral regurgitation graded by pulsed Doppler ultrasound decreased from 1.9 +/- 1.2 immediately after valvuloplasty to 1.0 +/- 0.9 (p less than 0.003) at follow-up, whereas there was no change in mean transmitral pressure gradient by Doppler echocardiography (5 +/- 2 versus 6 +/- 3 mm Hg, p = NS) and left atrial volume (74 +/- 34 versus 72 +/- 27 cm3, p = NS). Thus, 6 to 11 months after balloon mitral valvuloplasty, mean mitral valve area decreases slightly. Individual changes in valve area, however, are variable. Valvular morphology assessed by two-dimensional echocardiography may be useful for identifying those patients who have an increased likelihood of developing valvular restenosis.

Mitral regurgitation after percutaneous balloon mitral valvuloplasty in adults: evaluation by pulsed Doppler echocardiography.

Percutaneous balloon mitral valvuloplasty is a new technique used in the treatment of adult patients with mitral stenosis. To evaluate the occurrence and severity of mitral regurgitation after balloon valvuloplasty, 24 patients (20 women and 4 men, mean age 57 years) were studied using two-dimensional and Doppler echocardiography before and less than 24 h after this procedure. Mitral valve area increased after valvuloplasty in all patients, from 0.89 +/- 0.07 to 1.61 +/- 0.09 cm2 (p less than 0.001). Before valvuloplasty, 10 patients had no mitral regurgitation, 4 had 1+, 4 had 2+ and 6 had 3+ mitral regurgitation. After valvuloplasty, new mitral regurgitation occurred in six patients. Regurgitation grade did not change in 13 patients (54%), increased by one grade in 8 patients (33%) and by two grades in 3 patients (13%). Left atrial volume decreased in all except one patient from 100 +/- 12 to 83 +/- 12 cm3 (p less than 0.001). Neither age, sex, cardiac rhythm, initial mitral valve area, increase in mitral valve area, morphologic characteristics of the valvular and subvalvular apparatus, previous mitral commissurotomy nor effective balloon dilating area discriminated between those patients with and without an increase in mitral regurgitation after valvuloplasty. Thus, mitral balloon valvuloplasty is frequently associated with an increase in mitral regurgitation. However, in this series, no patient developed severe mitral regurgitation, and left atrial volume decreased in nearly all patients. An increase in mitral regurgitation could not be predicted from any features of the valve or subvalvular apparatus, clinical characteristics of the patients or technical aspects of the procedure.

Effects of nifedipine on arterial oxygenation at rest and during exercise in patients with stable angina.

The effects of nifedipine on arterial oxygenation and hemodynamics were studied at rest and during bicycle exercise in 12 men (mean age 55 years, range 41 to 67) with stable exertional angina. The study was conducted double-blind on 2 days, 1 week apart, using a placebo-controlled crossover design. On each day, measurements at rest were made before and 20 minutes after 20 mg sublingual nifedipine or placebo and were followed by measurements made during exercise. Compared with placebo, nifedipine reduced mean arterial pressure, systemic vascular resistance and pulmonary vascular resistance, and increased heart rate and cardiac output at rest and during exercise. It did not alter mean pulmonary artery or pulmonary artery wedge pressures at rest, but decreased them during exercise. Nifedipine decreased arterial oxygen tension (PaO2) from 96 +/- 10 to 90 +/- 13 mm Hg (p less than 0.05) at rest and from 99 +/- 11 to 92 +/- 12 mm Hg (p less than 0.005) at submaximal exercise (33 +/- 21 W), but did not alter it (100 +/- 12 versus 100 +/- 16 mm Hg, p = NS) at maximal exercise (68 +/- 30 W). The reduction in PaO2 was not due to alveolar hypoventilation, because nifedipine did not alter arterial carbon dioxide tension, or to changes in mixed venous oxygen tension, which nifedipine increased at rest (39 +/- 2 versus 43 +/- 3 mm Hg, p less than 0.001) and during submaximal exercise (31 +/- 4 versus 33 +/- 4 mm Hg, p less than 0.03) and maximal exercise (27 +/- 3 versus 31 +/- 3 mm Hg, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside.

To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic and metabolic basis of impaired exercise tolerance in patients with severe left ventricular dysfunction.

Hemodynamic and metabolic changes were measured at rest and during exercise in 23 patients with chronic heart failure and in 6 control subjects. Exercise was limited by leg fatigue in both groups and capacity was 40% lower in the patients with failure. At rest, comparing patients with control subjects, heart rate and right atrial and pulmonary wedge pressure were higher; cardiac output, stroke volume and work indexes and ejection fraction were lower; mean arterial and right atrial pressure and systemic resistance were similar. During all phases of exercise in patients with heart failure, pulmonary wedge pressure and systemic vascular resistance were higher and pulmonary vascular resistance remained markedly elevated compared with values in control subjects. Cardiac output was lower in the patients with failure, but appeared to have the same physiologic distribution in both groups during exercise. Although arterial-femoral venous oxygen content difference was higher in patients with heart failure, this increase did not compensate for the reduced blood flow. Even though the maximal oxygen consumption was significantly reduced, femoral venous lactate and pH values were higher than values in control subjects, but femoral venous pH was similar in both groups at their respective levels of maximal exercise. Ejection fraction was lower in those with heart failure at rest and did not increase with exercise. Ventilation in relation to oxygen consumption was higher in patients with failure than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Antianginal effects of nitroglycerin during exercise-induced angina: hemodynamic and left ventricular function changes related to indexes of myocardial oxygen consumption.

In 14 patients during exercise, intravenous nitroglycerin improved anginal threshold and increased workload compared with control subjects. At similar workloads, the decreased left ventricular volumes suggested decreased myocardial oxygen consumption due to peripheral unloading. At maximal exercise with nitroglycerin (50 +/- 17 to 79 +/- 15 watts), rate-pressure product and end-diastolic volumes were higher with less ischemia, suggesting myocardial supply was improved by nitroglycerin.

Effects of upright and supine position on cardiac rest and exercise response in aortic regurgitation.

The effects of upright and supine position on cardiac response to exercise were assessed by radionuclide ventriculography in 15 patients with moderate to severe aortic regurgitation (AR) and in 10 control subjects. In patients with AR, heart rate was higher during upright exercise, but systolic and diastolic blood pressure and left ventricular (LV) output were similar during both forms of exercise. LV stroke volume and end-diastolic volume were not altered during supine exercise. LV end-systolic volume increased and ejection fraction decreased during supine exercise, but both were unchanged during upright exercise. Of 15 patients, 5 in the upright and 12 in the supine position had an abnormal LV ejection fraction response to exercise (p less than 0.01). Right ventricular ejection fraction increased and regurgitant index decreased with both forms of exercise and was not significantly different between the 2 positions. Thus, posture is important in determining LV response to exercise in patients with moderate to severe AR.

Left ventricular volume and ejection fraction response to exercise in chronic congestive heart failure: difference between dilated cardiomyopathy and previous myocardial infarction.

To determine if cause influences the left ventricular (LV) volume and ejection fraction (EF) response to exercise, 24 patients with chronic congestive heart failure (CHF) (13 dilated cardiomyopathy [DC], CHF-DC group; 11 previous myocardial infarction [MI], CHF-MI group) and 6 age-matched control subjects underwent simultaneous hemodynamic monitoring and radionuclide ventriculography during semiupright bicycle exercise. Both CHF groups had similar hemodynamic values, LV volumes and EF at rest. Exercise hemodynamics were also similar, but LV volume and EF responses to exercise were different. In the CHF-DC group LV end-diastolic volume increased by 15% during exercise, significantly less (p less than 0.01) than the 44% increase in CHF-MI group. During exercise, EF increased in CHF-DC group, but did not change in CHF-MI group because of a larger increase in end-systolic volume. The slope of mean pulmonary wedge pressure-LV end-diastolic volume relation was steeper in CHF-DC group than in CHF-MI group (p less than 0.01). The study suggests that LV volume and EF response to exercise in patients with CHF depends on the origin of the CHF.

Improvement in exercise capacity and associated changes in hemodynamics and left ventricular function after the addition of metoprolol to nifedipine in patients with stable exertional angina.

In 10 men with stable exertional angina, the changes in exercise capacity, hemodynamics, and left ventricular (LV) function were measured after 20 mg sublingual nifedipine (N) and again after adding 100 mg oral metoprolol (M). Nifedipine alone did not significantly improve exercise workloads (+18%) and duration (+21%), but the addition of metoprolol increased both parameters by a further 37 and 32%, respectively (both p less than 0.005 vs. N). After nifedipine the onset of angina was slightly delayed (5.14 +/- 2.41 min placebo (P), 6.00 +/- 2.31 min N, p less than 0.1) and occurred at higher workloads (36 +/- 17 W P, 43 +/- 8 W N, p less than 0.1). After the addition of metoprolol, the onset of angina was delayed substantially more (9.57 +/- 2.22 min, p less than 0.001 vs. P and N) and occurred at much higher workloads (62 +/- 20 W, p less than 0.001 vs. P and N). At rest (R) and during exercise (E), nifedipine decreased systemic vascular resistance (-36% R, -27% E, both p less than 0.001) and mean arterial pressure (-18% R, -21% E, both p less than 0.001), and increased heart rate (+15% R, +11% E, both p less than 0.001), Pulmonary artery wedge pressure on exercise increased less (22 +/- 7 mmHg P, 13 +/- 5 mmHg N, p less than 0.001). After adding metoprolol, the major change was a reduced heart rate (-25% vs. N at R and E, both p less than 0.001), and arterial pressure was unaltered. Pulmonary artery wedge pressure on exercise increased to 18 +/- 5 mmHg (p less than 0.05 vs. N). Exercise LV ejection fraction and volume did not change significantly after adding metoprolol despite marked improvement in angina. In this acute exercise study in patients with stable exertional angina, metoprolol added to nifedipine markedly improved exercise capacity by preventing the increase in heart rate seen with nifedipine. In our patients with relatively normal LV function at rest, the combination was safe and produced no deleterious effects on LV function.

Physical and physiological determinants of transmitral velocity: numerical analysis.

The Doppler transmitral velocity curve is commonly used to assess left ventricular diastolic function. Recent investigations, however, relating Doppler mitral indexes to ventricular compliance, relaxation, and preload have been inconclusive and at times contradictory. We used a mathematical formulation to study the physical and physiological determinants of the transmitral velocity pattern for exponential chamber pressure-volume relationships with active ventricular relaxation (2,187 combinations investigated). We showed that transmitral velocity is fundamentally affected by two principal physical determinants, the transmitral pressure difference and the net atrioventricular compliance, as well as the impedance characteristics of the mitral valve. These physical determinants in turn are specified by the compliance and relaxation parameters of physiological interest. We found that the peak mitral velocity is most strongly related to initial left atrial pressure but lowered by prolonged relaxation, low atrial and ventricular compliance, and systolic dysfunction. Peak acceleration varies directly with atrial pressure and inversely with the time constant of isovolumic relaxation, with little influence of compliance, whereas the mitral deceleration rate is approximately valve area divided by atrioventricular compliance. We then used these data to suggest possible strategies for improved analysis of noninvasive data (Doppler indexes, planimetered valve area, and isovolumic relaxation time) to estimate ventricular compliance and relaxation and atrial pressure.

Identification of high-risk and low-risk subgroups of patients with mitral-valve prolapse.

Mitral-valve prolapse is a common cardiac valvular disorder with a wide range of severity and diverse clinical outcomes. The lack of a standard definition of mitral-valve prolapse may explain the variation in reported complication rates. To identify high-risk and low-risk subgroups, we retrospectively analyzed clinical and two-dimensional echocardiographic data from 456 patients with mitral-valve prolapse. Mitral-valve prolapse was defined on the basis of echocardiographic findings as systolic displacement into the left atrium of one or both leaflets beyond the plane of the mitral annulus in the parasternal long-axis view. Two groups of patients were compared: those with thickening of the mitral-valve leaflets and redundancy (designated the classic form; n = 319) and those without leaflet thickening (designated the nonclassic form; n = 137). The two groups were similar in age and sex ratio. Complications or a history of complications was more prevalent in the classic than the nonclassic form: infective endocarditis, 3.5 percent and 0 percent, respectively (P less than 0.02); moderate-to-severe mitral regurgitation, 12 percent and 0 percent (P less than 0.001); and the need for mitral-valve replacement, 6.6 percent and 0.7 percent (P less than 0.02). However, the frequency of stroke was similar in the two groups: 7.5 percent and 5.8 percent (P not significant). We conclude that in a selected population of patients with mitral-valve prolapse, those with the classic form (leaflet thickening and redundancy) are at higher risk than those without these features for the infectious and hemodynamic complications of mitral-valve prolapse, but not for stroke.

Improved accuracy of echocardiographic endocardial borders by spatiotemporal filtered Fourier reconstruction: description of the method and optimization of filter cutoffs.

The usefulness of digitized echocardiographic borders in quantitative regional left ventricular function analysis has been limited by the wide reported range for normal wall motion with this technique. We postulated that random error in endocardial border positioning is a major cause of this limitation. To test this hypothesis, we traced the endocardial borders field by field from 17 complete echocardiographic cycles in six dogs. These cycles showed a great deal of random movement, with each endocardial point reversing its motion an average of 18.5 times per cardiac cycle. Spatiotemporal Fourier analysis of these sequences demonstrated that most of the valid information on endocardial motion was contained in the first four temporal harmonics and the first seven spatial harmonics and that beyond these points the Fourier transform has the spectral characteristics of noise. Reconstruction of these 17 cycles eliminating all Fourier components above the sixth temporal and eighth spatial harmonics reduced the mean number of endocardial reversals per cycle to 2.3 (p less than .00001). To derive the optimal temporal and spatial cutoffs, we compared reconstructions of each of the 17 cycles with three M mode echocardiograms obtained simultaneously with the cross-sectional images. Fourier cutoffs were varied between two and 20 harmonics and demonstrated that the optimal temporal cutoff was 5.5 harmonics and optimal spatial cutoff 6.9. With optimal filtering, the correlation between ventricular diameter derived from the M mode and from the cross-sectional images was r = .965, compared with .877 for the M mode vs unfiltered cross-sectional data (p less than .0001). We conclude that two-dimensional filtered Fourier reconstruction significantly improves the accuracy of traced echocardiographic borders. This technique should be useful in the postprocessing of endocardial borders extracted by automated edge detection schemes and should also be applicable to cardiac images derived from modalities other than echocardiography.

Combined influence of ventricular loading and relaxation on the transmitral flow velocity profile in dogs measured by Doppler echocardiography.

The relation of the Doppler transmitral flow velocity profile to left ventricular loading conditions and diastolic properties remains poorly described. We studied seven adult mongrel dogs with an open-chest right heart bypass model in which left atrial pressure, representing preload, was varied by controlling blood flow into the pulmonary artery and left ventricular systolic pressure, representing afterload, was controlled independently by pumping blood into or from the femoral arteries. Heart rate was kept constant by crushing the sinus node and pacing the right atrium. Mitral inflow velocity profiles were measured by pulsed-wave Doppler echocardiography at multiple left atrial and left ventricular systolic pressures. In individual dogs, the peak E-wave velocity increased linearly with increasing left atrial V-wave pressure at constant left ventricular systolic pressure and decreased with increasing left ventricular systolic pressure at constant left atrial pressure. Stepwise multiple linear regression analysis of data pooled from all experimental stages in all dogs identified left atrial V-wave pressure, the time constant of relaxation (TL), and left ventricular systolic pressure, in order of decreasing significance, as predictors of the peak E-wave velocity (n = 82, multiple r = 0.87, p less than 0.0001). Multivariate analysis with the same three factors in individual dogs yielded higher r values (mean r = 0.89; range, 0.85-0.97), suggesting the presence of important interdog differences that were not accounted for by these three factors alone. When the values of codeterminant hemodynamic factors were kept within narrower limits, correlations between peak E-wave velocity and left atrial V-wave pressure (n = 35, multiple r = 0.83, p less than 0.0001), TL (n = 76, multiple r = -0.54, p less than 0.0001) and left ventricular systolic pressure (n = 20, multiple r = -0.59, p less than 0.005) improved substantially. In the pooled data, the relation of the peak E-wave velocity to left atrial V-wave pressure was shifted downward by an increase in TL (reduced relaxation rate), and the relation of the peak E-wave velocity to TL was shifted upward by an increase in left atrial V-wave pressure. Multivariate analysis also selected left atrial V-wave pressure and TL as the two most significant correlates of the velocity-time integral and deceleration rate of the E wave.(ABSTRACT TRUNCATED AT 400 WORDS)