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T Menzel

Publications and source records attributed to T Menzel.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Determination of left ventricular mass by transthoracic three-dimensional echocardiography in patients with dilated cardiomyopathy].

Conventional echocardiographic methods of measuring left ventricular mass (LVM) are limited by assumptions of ventricular geometry and image plane positioning. Three-dimensional (3D) echocardiography offers a promising new approach for more accurate determination of LVM. This study was performed to compare LVM measurement by one- (1D), two- (2D), and 3D echocardiography with magnetic resonance imaging (MRI) in patients (pts) with dilated cardiomyopathy (DCM). 36 pts (age 18-74) with DCM underwent imaging by conventional 1D and 2D echocardiography as well as transthoracic 3D echocardiographic data acquisition. Also, pts were imaged with cardiac MRI. Due to echocardiographic and MRI quality and because of exclusion criteria's for MRI, it was not possible to accomplish each LVM determination method for each patient. LVM was determined by Devereux and area-length algorithm for the conventional echocardiography. 3D echocardiographic data was calculated after manual delineation of endo- and epicardial boundaries--slice by slice (5 mm)--in 3 perpendicular cut planes. LVM was determined by multiplying the myocardial volume by the specific density of the myocardium. To determine LVM in MRI, the even summation of slices method for myocardial volume measurement was used defined by the endo- and epicardium in short axis images. There was no significant correlation (r = 0.42) for measuring LVM between 1D echocardiography and MRI in pts with DCM. A significant correlation was obtained between 2D (r = 0.64, p < 0.01) echocardiography and MRI as well between 3D (r = 0.78, p < 0.01) and MRI in determination of LVM. Compared with 1D and 2D echocardiography, the 3D analysis achieved a significantly higher agreement with the results of the MRI (1D: 399.2 g, 2D: 285.9 g, 3D: 172.6 g versus MRI: 199.1 g). Interobserver variability was 5.1% for measuring LVM by 3D echocardiography (1D: 11.2%, 2D: 9.1%). In conclusion, in pts with DCM the determination of LVM was incompletely characterized by 1D and 2D echocardiography compared with results of MRI. The best correlation and high agreement for determination of LVM was obtained with 3D echocardiography compared with MRI.

Adolescent↗
PubMed1999

Long-term results after thromboendarterectomy for chronic pulmonary embolism.

OBJECTIVE: In patients with chronic thromboembolic pulmonary hypertension, pulmonary vascular resistance (PVR) can be reduced by pulmonary thromboendarterectomy (PTE). In this study, long-term symptomatic and hemodynamic effects were investigated. METHODS: Twenty-two patients (12 female, 10 male, mean age 40 years, preoperative NYHA functional class II/III/IV: n = 1/12/9) were re-evaluated 48-72 months (mean 60 months) after surgery. In addition to clinical assessment, radiologic, hemodynamic and echocardiographic investigations were performed. RESULTS: All patients reported a marked improvement of their clinical condition. At follow-up, 11 patients were identified as NYHA class I, 10 as NYHA class II and one patient was in class III. PVR and mean pulmonary artery pressure (mPAP) were significantly reduced (preoperative PVR 800+/-274 dynes/s per cm(-5), follow-up PVR 180+/-28.3 dynes/s per cm(-5); P < 0.001; preoperative mPAP 48.5+/-7.4 mmHg, follow-up mPAP 27.5+/-4.9 mmHg; P < 0.001). There was also a significant increase in arterial blood oxygen tension (preoperative PaO2 59+/-10 mmHg; follow-up PaO2 84+/-12 mmHg; P < 0.001). Chest roentgenograms and echocardiographic examinations revealed significantly decreased right heart dimensions and a recovery of right heart function. CONCLUSION: In patients with severe chronic thromboembolic pulmonary hypertension, persistent symptomatic and hemodynamic improvements can be achieved by PTE.

Adult↗
PubMed1998

Overexpression of basic fibroblast growth factor in MCF-7 human breast cancer cells: lack of correlation between inhibition of cell growth and MAP kinase activation.

Basic fibroblast growth factor (bFGF, FGF-2) is progressively lost from mammary epithelial cells as they become malignant. To investigate the effects of restoring the expression of bFGF in breast cancer cells, we constructed MCF-7 cells that permanently overexpress 18-kD cytoplasm-localizing bFGF (MCF-7/deltaA(FGF)(18) cells) and cells that express both the 18-kD along with the 22- and 24-kD nucleus-localizing bFGF peptides (MCF-7/NCF(FGF)(18,22,24) cells), using retroviral transduction. These stable cell constructs grew more slowly and had a larger fraction of their populations in the G0/G1 phase of the cell cycle than control cells. All forms of bFGF were eluted from MCF-7/NCF(FGF)(18,22,24) cell monolayers with 2 M NaCl, in contrast to fibroblasts that were demonstrated to secrete only the 18-kD bFGF isoform. High-affinity binding of 18-kD 125I-bFGF to these cells was significantly decreased, probably because of competitive binding by the autocrine-secreted bFGF. Recombinant 18-kD bFGF that was previously demonstrated in our laboratory to inhibit proliferation, activate MAP kinase, and induce the cyclin-dependent kinase inhibitor p21WAF1/CIP1 in MCF-7 cells, further inhibited MCF-7/deltaA(FGF)(18) cells but had no effect on MCF-7/NCF(FGF)(18,22,24) cells. The total cellular content of the high-affinity FGF receptors 1-3 was unchanged, but FGF receptor 4 was decreased in MCF-7/NCF(FGF)(18,22,24) cells. Both cell types overexpressing bFGF isoforms had elevated levels of the cyclin-dependent kinase inhibitor p27Kip1 but not that of p21WAF1/CIP1. In MCF-7/deltaA(FGF)(18) cells, FGFR1 and MAP kinase were constitutively phosphorylated. Exogenous recombinant 18-kD bFGF did not accentuate these effects but did induce an increase in the levels of p21WAF1/CIP1 corresponding to the further inhibition induced by exogenous bFGF in these cells. In MCF-7/NCF(FGF)(18,22,24) cells, FGFR1 and MAP kinase were not phosphorylated at baseline nor upon stimulation with recombinant bFGF, and exogenous bFGF only had a minimal effect on low steady-state p21WAF1/CIP1 levels. However, stimulation of these cells with phorbol ester or insulin did result in MAP kinase phosphorylation. While growth-inhibited in the G1 phase of the cell cycle, MCF-7/NCF(FGF)(18,22,24) cells retained active isoforms of cdk2 and the hyperphosphorylated form of Rb. These data suggest that high molecular weight forms of bFGF overexpressed in MCF-7 cells do not activate the receptor-mediated MAP kinase pathway, and do not induce p21WAF1/CIP1 in an autocrine manner, but inhibit proliferation through other, possibly direct nuclear signalling mechanisms.

Breast Neoplasms↗
PubMed1998

Calculation of left ventricular outflow tract area using three-dimensional echocardiography. Influence on quantification of aortic valve stenosis.

In 23 patients with aortic valve stenosis (14 male, 9 female, mean age 66 +/- 21.5 years) left ventricular outflow tract cross-sectional area was determined in planimetric fashion using three-dimensional echocardiography. The 3-D data-set for each patient had been acquired in the course of a multiplane transesophageal examination. Aortic valve area was determined using the continuity equation. Results obtained were compared to those calculated by continuity equation using to the conventionally determined LVOT area (a = pi [d/2]2). As reference method the results were compared to invasive measurements. 3-D planimetric determination of LVOT cross-sectional area was possible in 20 of 23 patients. In three patients, this method failed due to artefacts. The mean difference to the conventionally calculated LVOT area amounted to 0.18 cm2 (SD = 0.46). The comparison of AVA determined by continuity equation and by invasive measurement showed a mean difference of -0.074 cm2 (SD = 0.21) for the conventionally calculated LVOT area; for the planimetrically determined LVOT area the mean difference of AVA amounted to -0.03 cm2 (SD = 0.14) (p < 0.05). Planimetric determination of LVOT area using 3-D echocardiography improves the agreement of the continuity equation with invasive measurement.

Aged↗
PubMed1997

[Excision and open wound treatment of pilonidal sinus. Rate of recurrence and duration of work incapacity].

BACKGROUND AND OBJECTIVE: There is controversy whether open or closed operative treatment of pilonidal sinuses is better, especially with regard to postoperative recurrence rate and duration of work incapacity in these mostly young patients. Having performed radical excision with subsequent open wound healing, we have analysed recurrence rate, duration of sickness certification, amount of pain and general impairment in our group of patients. PATIENTS AND METHODS: All 103 patients operated on for pilonidal sinus between January 1992 and December 1994 (84 men, 19 women, mean age 28.1 [16-68] years) were sent a questionnaire to record any recurrence, duration of certified incapacity to work, amount of pain and general satisfaction of the operation, using visual analogue scales. Complete answers were obtained from 86 patients (83.5%). RESULTS: The follow-up period ranged from 12 to 47 months postoperatively. The recurrence rate was 12.8%, median duration of work incapacity was 4 weeks, longer for the employed and manual workers than for self-employed. Postoperative pain (scale of 0-6) averaged 3.3 and 2.3, respectively, for the in-hospital and post-hospital periods. CONCLUSION: Taking into account duration of incapacity, general patient satisfaction and recurrence rate, the radical excision method with subsequent open wound granulation provides a reasonable alternative to closed methods. But a definitive assessment of the advantages of the open method with respect to these criteria must await the results of prospective randomized series.

Adolescent↗
PubMed1997

[Intraventricular obstructions in dobutamine stress echocardiography: determinants of their development and clinical sequelae].

UNLABELLED: Dobutamine stress echocardiography (DSE) leads to strong hypercontraction, tachycardia, and peripheral vasodilatation. In previous studies systolic obstruction of the left ventricular outflow tract (LVOT) was observed as a result of these factors. To evaluate left ventricular function and morphology in patients (pts) with induced systolic LVOT obstruction, we used continuous wave (CW) doppler registrations in combination with quantitative 2-D-echocardiography in 100 pts during routinely performed DSE (5-40 micrograms/kg/min). In addition left ventricular wall thickness was measured. Symptoms were registered using a standardised questionnaire and cardiac arrhythmias were counted over a two minute interval at rest and during the maximal heart rate of each patient. During DSE dynamic flow acceleration with late systolic peak velocity above 2 m/second (s) was considered to represent LVOT obstruction in pts with normal flow profiles in the LVOT before infusion of dobutamine. For invasive studies pts were investigated with femoral catheterisation by the method of Judkins. A greater than 50% stenosis was judged to be significant. RESULTS: Examinations in 73 pts provided data of sufficient quality for echocardiographic and Doppler sonographic evaluations. 39 pts, 26 men, 13 women, mean age 64 +/- 8 years, developed late systolic flow velocities above 2 m/s and therefore formed the obstructive group (grp A). Grp B consisted of 34 pts, 26 men and 8 women, mean age 66 +/- 10 years, who showed normal time velocity integrals during DSE. In 41 pts invasive data provided information concerning the existence and severity of coronary artery disease. There were no significant differences in the increase of heart rate, the product of maximal systolic blood pressure and maximal heart rate or the percentage of pts, who reached their age corrected submaximal heart rate during DSE. Obstructive pts (group A) showed late systolic dynamic acceleration of systolic flow with a mean maximal speed of 315.4 +/- 139.8 cm/s, which peaked 0.12 +/- 0.04 s after the R-wave. From the velocities we calculated a mean pressure gradient of 47.5 +/- 39.7 mm Hg using the modified Bernoulli equation. Group B patients showed lower and earlier maximal speeds with a mean value of 158.2 +/- 37.6 cm/s, 0.09 +/- 0.04 s after the R-wave, corresponding to a pressure gradient of 10.6 +/- 4.9 mm Hg (p < 0.001). Ejection fractions were higher (p < 0.001) before the test in grp A: 68.2 +/- 8% compared to 55.7 +/- 10.4% in B. This difference increased during peak stress: 74.1 +/- 7.7% compared to 59.5 +/- 12.8%. End diastolic (EDVI) and end systolic volume indexes (ESVI) were lower in grp A (p < 0.001). During DSE, the decrease in ESVI was somewhat stronger for pts in grp A. Left ventricular hypertrophy was more often seen with obstruction. Septal thickness was increased in A: 1.45 +/- 0.34 cm compared to 1.13 +/- 0.27 cm in B (p < 0.001). Left ventricular posterior wall measured 1.03 +/- 0.28 cm in A and 0.83 +/- 0.23 cm in B (p < 0.01). 27 pts in grp B and only 9 in grp A had a history of previous myocardial infarction. Showing no difference at rest, wall motion score indexes raised under DSE in both groups and developed significantly higher scores in grp B at peak stress: 1.30 (1.0-1.90) compared to 1.18 (1.0-1.75) in A. We observed typical chest pain more often in grp B. Unspecific symptoms and arrhythmogenic complications were not statistically different, with the exception of ventricular bigeminy which was more often observed in grp B. A decline in the diastolic blood pressure was observed in pts with very severe obstruction (> 3.5 m/s, p < 0.05). Sensitivity of DSE was 84%, specificity 79%. No significant differences between pts with and without obstruction were observed. SUMMARY: Intraventricular obstructions during DSE are often observed in pts with normal systolic function at rest and during peak stress, especially in the case of left ventricular hypertrophy. (ABSTRACT TRU

Blood Flow Velocity↗
PubMed1997

[Early results of pulmonary thromboendarterectomy in chronic thromboembolic pulmonary hypertension].

Pulmonary thromboendarterectomy (PTE) is a potentially curative procedure in chronic thromboembolic pulmonary hypertension. From June, 1989, to December, 1994, we performed PTE in 109 consecutive patients. Multiple changes in surgical approach and postoperative management have been implemented since January, 1995. We report the early results of 32 thromboendarterectomies performed from January, 1995, to January, 1997. Thirty-two patients (16 females, 16 males; mean age 55 years) were operated using cardiopulmonary bypass, deep hypothermia and circulatory arrest. Preoperative NYHA functional class was III in 21 and IV in 11 patients. Pulmonary vascular resistance (PVR) and mean pulmonary artery pressure (mPAP) were elevated to 967 +/- 238 dynes.s.cm-5 and 51 +/- 11 mm Hg respectively. The perioperative mortality rate was 9.3% (3 of 32). Twenty-nine survivors were weaned from mechanical ventilation and extubated after a mean of 35 hours (12 to 190 hours). PVR was reduced to 301 +/- 151 dynes.s.cm-5 (p < 0.001) and mPAP was reduced to 28 +/- 10 mm Hg (p < 0.001). Pulmonary thromboendarterectomy is an effective surgical procedure for chronic thromboembolic pulmonary hypertension. By means of modifications in surgical approach and postoperative management, early results can be improved and perioperative mortality can be decreased to less than 10%.

Chronic Disease↗
PubMed1997

[Reversibility of changes in left and right ventricular geometry and hemodynamics in pulmonary hypertension. Echocardiographic characteristics before and after pulmonary thromboendarterectomy].

Pulmonary thromboendarterectomy (PTE) leads to an acute decrease of right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension. We investigated the changes in right and left ventricular (LV) geometry and hemodynamics by means of transthoracic echocardiography. The prospective study was performed in 14 patients (8 female, 6 male; age 55 +/- 20 years) before and 18 +/- 12 days after PTE. Total pulmonary vascular resistance and systolic pulmonary artery pressure were significantly decreased (PVR: preoperative 986 +/- 318, postoperative 323 +/- 280 dyn x s/cm5, p < 0.05; PAP preoperative 71 +/- 40, postoperative 41 +/- 40 mm Hg + right atrial pressure, p < 0.05). End diastolic and end systolic RV area decreased from 33 +/- 12 to 23 +/- 8 cm2, respectively, from 26 +/- 10 to 16 +/- 6 cm2, p < 0.05. There was an increase in systolic RV fractional area change from 20 +/- 12 to 30 +/- 16%, p < 0.05. RV systolic pressure rise remained unchanged (516 +/- 166 vs. 556 +/- 128 mm Hg/sec). LV ejection fraction remained within normal ranges (64 +/- 16 vs. 62 +/- 12%). Echocardiographically determined cardiac index increased from 2.8 +/- 0.74 to 4.1 +/- 1.74 l/min/m2. A decrease in LV excentricity indices (end diastolic: 1.9 +/- 1 vs. 1.1 +/- 0.3, end systolic: 1.7 +/- 0.6 vs. 1.1 +/- 0.4, p < 0.05) proved a normalization of preoperatively altered septum motion. LV diastolic filling returned to normal limits: (E/A ratio: 0.62 +/- 0.34 vs. 1.3 +/- 0.8; p < 0.05); Peak E velocity: 0.51 +/- 0.34 vs. 0.88 +/- 0.28 m/sec, p < 0.05; Peak A velocity: 0.81 +/- 0.36 vs. 0.72 +/- 0.42 m/sec, ns; E deceleration velocity: 299 +/- 328 vs. 582 +/- 294 cm/sec2, p < 0.05; Isovolumic relaxation time: 134 +/- 40 vs. 83 +/- 38 m/sec, p < 0.05). We could show a marked decrease in RV afterload shortly after PTE with a profound recovery of right ventricular systolic function--even in case of severe pulmonary hypertension. A decrease in paradoxic motion of the interventricular septum and normalization of LV diastolic filling pattern resulted in a significant increase of cardiac index.

Aged↗
PubMed1997

Quantitative assessment of aortic stenosis by three-dimensional echocardiography.

The purpose of this study was to assess the feasibility of three-dimensional echocardiography in aortic stenosis. Planimetric determination of valve area and dynamic volume-rendered display were performed. Three-dimensional echocardiography permits display of any desired plane of the cardiac structure. Thus in the case of aortic stenosis, the plane used for planimetric evaluation can be positioned exactly through the valve orifice. Dynamic volume-rendered display may provide a spatial demonstration of the stenotic valve. In 48 patients aortic valve area was measured by planimetry. The three-dimensional data set was acquired by a workstation in the course of a multiplane transesophageal examination. Results were compared with those obtained by multiplane transesophageal two-dimensional planimetric technique and invasive measurement. A dynamic three-dimensional reconstruction was displayed. Planimetric determination of valve area was possible in 42 (88%) of 48 cases. Statistical analysis of the data acquired showed a good agreement between three-dimensional echocardiography and transesophageal echocardiography (mean difference +0.018 cm2; SD = 0.086) and between three-dimensional echocardiography and the invasive technique (mean difference +0.012 cm2; SD = 0.12). Dynamic volume-rendered display was possible in 42 of 48 cases. Three-dimensional echocardiography permits accurate and reliable determination of aortic valve area. Preoperative spatial recognition of the stenotic valve is possible by dynamic volume-rendered display.

Adult↗
PubMed1997

Basic fibroblast growth factor (bFGF) upregulates the expression of bcl-2 in B cell chronic lymphocytic leukemia cell lines resulting in delaying apoptosis.

Basic fibroblast growth factor (bFGF) is a pleiotropic cytokine which has recently been shown to delay fludarabine-induced apoptosis in B cell chronic lymphocytic leukemia (B-CLL) cells. To investigate the potential mechanism of bFGF-mediated delay of apoptosis, two EBV-transformed B prolymphocytic cell lines (JVM-2, JVM-13), one EBV-transformed B-CLL cell line (I83CLL), and one non-EBV-transformed B-CLL cell line (WSU-CLL) were used as a model for chronic lymphoid malignancies. Viability data of cells treated with fludarabine alone or in combination with bFGF demonstrated that the addition of bFGF to the cells resulted in prolonged survival. Quantitative assessment of apoptosis-associated DNA strand breaks by in situ TdT labeling showed a protective effect of bFGF on fludarabine-treated cells. The potential effect of bFGF on bcl-2 mRNA expression was analyzed by Northern blotting. Stimulation with bFGF led to a time-dependent accumulation of bcl-2 specific mRNA in all three cell lines. Maximal levels of bcl-2 mRNA expression were detected after 8 h in JVM-2, and after 18 h in JVM-13 and I83CLL. Intracellular bcl-2 protein was also found to be increased upon bFGF stimulation in both EBV- and non-EBV-transformed cells. In addition, exposure of cells from three patients with B-CLL to bFGF showed an upregulation of bcl-2 protein after 4-8 h. Our data demonstrate that bFGF upregulates the expression of bcl-2 in these cells, suggesting that this increase in bcl-2 expression may play a role in the delay of fludarabine-induced apoptosis.

Apoptosis↗
PubMed1997

Low level expression of basic FGF upregulates Bcl-2 and delays apoptosis, but high intracellular levels are required to induce transformation in NIH 3T3 cells.

We investigated the roles of basic fibroblast growth factor (bFGF) in the transformation and survival of NIH 3T3 cells. We constructed NIH 3T3-derived cell lines expressing human bFGF using retroviral gene transfer with an N2-based vector. Clonally derived cell lines containing a single copy of the vector overexpress bFGF mRNA and produce more immunoreactive protein (0.407 +/- 0.010-3.028 +/- 0.087 ng bFGF/10(6) cells) which is biologically active than nontransduced (0.151 +/- 0.013 ng bFGF/10(6) cells) or N2-transduced (0.211 +/- 0.029 ng bFGF/10(6) cells) NIH 3T3 cells. All cells producing excess amounts of bFGF achieve greater density at confluence, show delayed apoptosis and increased survival and have elevated intracellular levels of Bcl-2. However, only cells expressing from 8-15 times background levels of bFGF are phenotypically transformed. The transformed cells form dense foci at confluence, have decreased adherence to tissue culture plates and grow colonies in soft agar. Exogenous bFGF induces higher Bcl-2 levels in a dose dependent manner and recapitulates the antiapoptotic effects of the overexpressed species but fails to induce changes associated with the transformed phenotype. In this study, we demonstrate a dissociation between phenotypic transformation secondary to bFGF overexpression and upregulation of cellular Bcl-2 that correlates with a delay in programmed cell death. Although low level expression of bFGF or exogenous bFGF is sufficient to upregulate Bcl-2 and delay apoptosis, high intracellular levels are required for cellular transformation. These data suggest that overexpression of bFGF modulates cellular transformation and Bcl-2-mediated inhibition of apoptosis through alternate molecular mechanisms.

3T3 Cells↗
PubMed1996

Elevated intracellular level of basic fibroblast growth factor correlates with stage of chronic lymphocytic leukemia and is associated with resistance to fludarabine.

Chronic lymphocytic leukemia (CLL) is characterized by delayed senescence and slow accumulation of monoclonal, small lymphocytes. Basic fibroblast growth factor (bFGF) is a pleiotropic cytokine that plays a role in hematopoiesis and apoptosis. Elevated bFGF levels have been detected in urine from patients with a variety of neoplastic diseases including various leukemias; however, the cellular source of the bFGF has not been determined. In this study, the intracellular bFGF level in lymphocytes of 36 patients with B-CLL and 15 normal donors was determined using an enzyme-linked immunoassay. In cells derived from patients with high-risk disease, the median level of intracellular bFGF was 381.5 pg/2 x 10(5) cells, compared with a median of 90.5 pg/2 x 10(5) cells in patients with intermediate disease. In patients with low-risk disease, the median bFGF level was 4.9 pg/2 x 10(5) cells, and in normal controls, it was 6.0 pg/2 x 10(5) cells. The difference in the bFGF levels was significant for the comparison between low- and intermediate-risk (P = .00119), low- and high-risk (P < .0001), and intermediate- and high-risk disease (P = .0001). Immunofluorescent stains of peripheral blood mononuclear cells confirmed CLL lymphocytes as a cellular source of bFGF. To evaluate the potential contribution of elevated intracellular bFGF levels to the phenotype of CLL cells, leukemic cells were cultured in vitro with an apoptotic stimulus (fludarabine). CLL cells with high intracellular levels of bFGF appeared to be more resistant to fludarabine treatment. The addition of bFGF to fludarabine-treated CLL cells resulted in a delay of apoptosis and prolonged survival. These data suggest that bFGF may contribute to the resistance of CLL cells to an apoptotic stimulus.

Adult↗
PubMed1996

Quantification of mitral valve stenosis by three-dimensional transesophageal echocardiography.

The aim of this study was the evaluation of the diagnostic potentials of transesophageal 3D- echocardiography in the determination of mitral valve stenosis. 54 patients were investigated by transthoracic and multiplane transesophageal echocardiography. In 41 patients cardiac catheterization was performed. 3D- echocardiographic data acquisition was performed by automatic transducer rotation at 2 degree increments over a span of 180 degrees. The transesophageal probe was linked to an ultrasound unit and to a 3D- workstation capable of ECG- and respiration gated data acquisition, postprocessing and 2D/3D image reconstruction. The mitral valve was visualized in sequential cross-sectional planes out of the 3D data set. The spatial position of the planes was indicated in a reference image. In the cross-sectional plane with the narrowest part of the leaflets the orifice area was measured by planimetry. For topographic information a 3D view down from the top of the left atrium was reconstructed. Measurements were compared to conventional transthoracic planimetry, to Doppler-echocardiographic pressure half time and to invasive data. The mean difference to transthoracic planimetry, pressure half time and to invasive measurements were 0.3 +/- 0.1 cm2, 0.2 +/- 0.1 cm2 and 0.1 +/- 0.1 cm2, respectively. Remarkable differences between the 3D- echocardiographic and the 2D- or Doppler- echocardiographic methods were observed in patients with severe calcification or aortic regurgitation. In 22% of the patients the 3D data set was not of diagnostic quality. New diagnostic information from a 3D view of the mitral valve could be obtained in 69% of the patients. Thus, although image quality is limited, 3D- echocardiography provides new topographic information in mitral valve stenosis. It allows the use of a new quantitative method, by which image plane positioning errors and flow-dependent calculation is avoided.

Adult↗
PubMed1996

[Determination of systolic left ventricular time interval using the doppler technique. Analysis of aortic flow spectrum with transthoracic echocardiography].

UNLABELLED: In 10 healthy volunteers (age 21-28 years; mean age 24.8 years +/- 1.9 years) systolic left ventricular time intervals (STI) were determined by analysis of aortic Doppler flow pattern. This method was compared with conventional calculation of STI, using electrocardiogram, carotid pulse curve and phonocardiography, which were registered in synchronicity to the Doppler examination. Both, CW- and PW Doppler echocardiography constantly showed slightly lower values than the conventional method. This referred to basic measurements as well as to measurements after the application of isoprenaline and quinidine. The PW Doppler method underestimated the conventional method concerning the electromechanic systole (QS2) by on average 3.98%, the left ventricular ejection period (LVET) by on average 2.24% and the pre-ejection period (PEP) by on average 7.3%. Using CW-Doppler-method, QS2 was on average 5.31% and LVET was on average 6.67% smaller than the values determined by conventional method, whereas PEP was overestimated by on average 1.69%. The study documented that positive and negative inotropic pharmacological effects were measured reliably by the Doppler-echocardiographic method. Isoprenaline caused a significant shortening of frequency corrected QS2 (QS2c) from -55 +/- 17 to -85 +/- 20 ms (p < 0.05) using the PW-Doppler method; frequency corrected PEP (PEPc) was shortened from -40 +/- 14 to -67 +/- 14 ms (p < 0.05). The CW Doppler method also showed a statistically significant reduction of QS2c (from -64 +/- 18 to -89 +/- 25 ms; p < 0.05) and PEPc (from -37 +/- 16 to -64 +/- 12; p < 0.05). Likewise, the conventional method demonstrated statistically significant shortening of QS2c and PEPc after application of isoprenaline. LVETc did not change in a state of positive inotropy, no matter which method was used for determination. The negative inotropic effect of quinidine, measured by PW-Doppler, resulted in a prolongation of QS2c from -55 +/- 16 to -32 +/- 24 ms (p < 0.05) and of LVETc from -20 +/- 11 to +6 +/- 17 ms (p < 0.05). Using CW Doppler method, quinidine led to a lengthening of QS2c from -63 +/- 16 to -42 +/- 22 (p < 0.05) and of LVETc from -33 +/- 11 to -12 +/- 8 ms (p < 0.05). The conventional method also demonstrated a statistically significant increase of QS2c and LVETc. None of the 3 methods in question showed a statistically significant alteration of PEPc in the negative inotropic state. CONCLUSIONS: Doppler-echocardiographic analysis of aortic flow pattern constitutes a new method for the measuring of systolic time intervals. Basic values as well as changes due to positive or negative inotropic effects are reliably determined, in comparison with conventional methods the measurements are slightly lower.

Adult↗
PubMed1996

[Prospective study of subjective stress caused by dobutamine stress echocardiography--effect on diagnostic accuracy].

UNLABELLED: We used a standardized questionnaire to assess physical and mental distress caused by dobutamine stress echocardiography (DSE). The examination was performed according to a standardized protocol (5-40 micrograms/kg/min including atropine). 91 patients (pts), 68 men (62 +/- 9 years), 23 women (65 +/- 7 years) were asked to quantify the severity of the following symptoms: palpitations, anxiety, headache, nausea, discomfort of left lateral position, angina pectoris and dyspnea. Numbers on a rating scale from 1-10 defined the degree of distress. Absence of a symptom equalled mark, 1, slight expression marks 2-4. Moderate expression was defined by marks 5-7 and very strong expression by marks 8-10. RESULTS: 86% of pts felt affected by one or more symptoms to a slight to moderate extent (mark 4 +/- 2.17). Palpitations were felt by 85% of the pts (mark 6 +/- 2.83), anxiety by 42% (mark 3 +/- 2.5), headache by 50% (3 +/- 2.54), nausea by 20% (2 +/- 1.72), angina pectoris by 42% (3 +/- 2.5), dyspnea by 30% (2 +/- 2.42) and discomfort of left lateral recumbent position by 43% (mark 3 +/- 2.59). 43 pts underwent coronary angiography. The negative predictive value of DSE to identify pts without a coronary artery stenosis extending a 50% diameter reduction was 85% for the 16 pts who reached their individual submaximal heart rate compared to 60% for those 27 pts who did not reach it. Unspecific symptoms led to test termination in these pts. The positive predictive values were comparable (89 and 94%). CONCLUSION: DSE causes physical and mental distress. If symptoms lead to test termination before age corrected submaximal heart rate is reached, normal wall motion does not exclude significant coronary artery disease.

Angina Pectoris↗