Images in cardiology. Acute recoil in sirolimus eluting stent: real time, in vivo assessment with optical coherence tomography.
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Catheterization↗
Biomedical subjects
J Schaar
Publications and source records attributed to J Schaar.
Myocardial lactate release after intracoronary verapamil application in humans: acute effects of intracoronary verapamil on systemic and coronary hemodynamics, myocardial metabolism, and norepinephrine levels.
Coronary and systemic hemodynamic effects of verapamil have been investigated previously in detail. The acute impact of intracoronary verapamil on coronary hemodynamics has, however, not been correlated to simultaneously changes in myocardial metabolism or norepinephrine levels in humans. After bolus application of 1 mg verapamil into the left coronary artery of 52 patients scheduled for routine coronary angiography, heart rate (HR) remained unchanged, whereas mean arterial blood pressure (MAP) decreased (93.8 +/- 14.9 mmHg to 85.1 +/- 13.7 mmHg, p = 0.001). Coronary blood flow (CBF), calculated from intracoronary Doppler measurements and quantitative coronary angiography, increased after verapamil administration (28.5 +/- 16.7 ml/min to 66.2 +/- 41.8 ml/min, p < 0.001), whereas coronary vascular resistance index (CVRI) decreased (1.43 +/- 0.92 to 0.46 +/- 0.23, p < 0.001). Blood samples, taken simultaneously from the aorta (Ao) and coronary sinus (CS) at baseline and at maximal flow velocity, showed an increase in norepinephrine concentrations in Ao (209 +/- 151 ng/l to 283 +/- 195 ng/l, p < 0.001) and CS (233 +/- 162 ng/l to 323 +/- 248 ng/l, p = 0.004). Myocardial metabolism of pyruvate and free fatty acids were not affected. Glucose release was augmented and initial lactate consumption changed to a net lactate release into the CS (Ao to CS differences: glucose: -1.92 +/- 9.9 mg/dl to -12.8 +/- 22.8 mg/dl, p < 0.001; lactate: 0.07 +/- 0.2 mmol/l to -0.08 +/- 0.3 mmol/l, p = 0.001). Similar results were obtained for the extraction ratios and flux of these metabolites. There was a weak correlation between the increase in CBF and lactate release into the CS. This is the first report of unexpected myocardial lactate release following intracoronary verapamil administration in humans. This lactate release was paralleled by an increased glucose release into the CS at an unchanged metabolism of free fatty acids and pyruvate. One explanation for this unexplained lactate release during increased coronary blood flow might be a wash out phenomenon of lactate from previous ischemic areas, other explanations might be the induction of paradox myocardial ischemia and/or a steal effect. Further studies are necessary to explain these unexpected findings of increased coronary flow and myocardial lactate release. Until reliable explanations are pending, studies using only lactate release as a marker of myocardial ischemia, without taken coronary and systemic hemodynamic parameters into account, should be interpreted with caution.
Adult↗
Tissue Doppler imaging: a new technique for assessment of pseudonormalization of the mitral inflow pattern.
Left ventricular diastolic dysfunction (LVDD) is a frequent cause of heart failure. Doppler echocardiography has become the method of choice for the noninvasive evaluation of LVDD. However, pseudonormalization (PN) of the mitral inflow often presents a diagnostic challenge in clinical practice. In this setting, we sought to define the role of tissue Doppler imaging (TDI) of the septal mitral annulus. Echocardiography was performed in 36 consecutive subjects (age 59 +/- 10 years). Eighteen of these had diagnosed coronary artery disease (CAD) with recent onset of symptoms (within 3 months), 18 had clinical suspicion of CAD, and 15 had symptoms of heart failure (New York Heart Association [NYHA] Class 2.4 +/- 0.5). The mitral inflow profile (E, A, E/A) was measured by pulsed Doppler, and the deceleration time (DT) and the isovolumic relaxation time (IVRT) were calculated. Peak diastolic velocities of the septal mitral annulus (E(T), A(T), E(T)/A(T)) and the time interval from Q in the ECG to the onset of E(T) were derived from pulsed TDI. Left heart catheterization was performed for direct measurement of left ventricular end-diastolic pressure (LVEDP). PN defined by an E/A ratio > 1 and an LVEDP > or = 16 mmHg was found in nine patients. All patients with PN had symptoms of heart failure (NYHA Class 2.8 +/- 0.5). Patients with and without PN did not differ with respect to the E/A ratio (1.29 +/- 0.44 vs 1.16 +/- 0.23, P = ns), DT (182 +/- 38 msec vs 205 +/- 42 msec, P = ns), and IVRT (88 +/- 24 msec vs 92 +/- 18 msec, P = ns). In the group with PN, a significant reduction of E(T) (5.6 +/- 1.8 cm/sec vs 8.8 +/- 2. 9 cm/sec, P < 0.05) and E(T)/A(T) (0.5 +/- 0.16 vs 0.82 +/- 0.37, P < 0.05) was detected. In the PN group, the Q-E(T) interval was prolonged (404 +/- 48 msec vs 346 +/- 50 msec, P < 0.05). Receiver operating characteristic curve analysis for E(T) yielded an area under the curve of 0.78 +/- 0.06 (P = 0.034) for separating patients with versus without PN. When the combination of E(T) < 7 cm/sec and E(T)/A(T) < 1 was used as cutpoint, PN could be identified with a sensitivity of 83% and a specificity of 79%. There was no significant relation between LVEDP and either E(T) (r = 0.32, P > 0. 2) or the Q-E(T) interval (r = 0.14, P > 0.5). In conclusion, E(T) and the Q-E(T) interval appear to be useful parameters for assessing LV diastolic dysfunction in symptomatic patients with a pseudonormal mitral inflow pattern and elevated filling pressures.
Aged↗
Tei-index in patients with mild-to-moderate congestive heart failure.
BACKGROUND: Congestive heart failure is related to contraction and relaxation abnormalities of the ventricle. Isolated analysis of either mechanism may not be reflective of overall cardiac dysfunction. A combined myocardial performance index (isovolumic contraction time plus isovolumic relaxation time divided by ejection time, 'Tei-Index') has been described which may be more effective for analysis of global cardiac dysfunction than systolic and diastolic measures alone. It was the aim of the present investigation to evaluate the Tei-Index against invasive examination. METHODS AND RESULTS: Eighty-one subjects were included in a consecutive manner, among 125 patients undergoing left heart catheterization for invasive measurement of left ventricular end-diastolic pressure; 43 patients had congestive heart failure (35 male, 8 female, 68+/-6 years) defined by NYHA functional class >/=2 (mean 2.5+/-0.5) and left ventricular end-diastolic pressure >/=16 mmHg (mean 20+/-4) and 38 subjects (32 male, 6 female, 66+/-5 years) without symptoms of heart failure (NYHA functional class I) and with normal left ventricular end-diastolic pressure (mean 12+/-3 mmHg) served as a control group. Using conventional echo-Doppler methods, parameters assessed were: ejection fraction, peak velocities of early (E) and late (A) diastolic filling, the E/A ratio, deceleration time, isovolumic contraction time, isovolumic relaxation time and ejection time. The Tei-Index was obtained by subtracting ejection time from the interval between cessation and onset of the mitral flow. The control group and patients with congestive heart failure did not differ with respect to the E/A ratio (0.86+/-0.27 vs 0.90+/-0.44, P=ns), deceleration time (203+/-42 ms vs 206+/-36 ms, P=ns) and isovolumic relaxation time (97+/-16 ms vs 94+/-26 ms, P=ns). The ejection fraction was slightly reduced in patients with congestive heart failure (46+/-11% vs 55+/-8%, P<0.05). The Tei-Index was easily and reproducibly measured in all subjects. The mean value of the Tei-Index was significantly different between the control group and patients with congestive heart failure (0.39+/-0.10 vs 0.60+/-0.18, P<0.001). Receiver operating characteristic curve analysis for the Tei-Index yielded an area under the curve of 0.88+/-0.038. Using a Tei-Index >/=0.47 as the cutpoint, congestive heart failure was identified with a sensitivity of 86% and a specificity of 82%. No correlation was observed between the Tei-Index and heart rate (r=0.22, P=ns), systolic blood pressure (r=0.16, P=ns) or diastolic blood pressure (r=0.08, P=ns). The Tei-Index was significantly related to left ventricular end-diastolic pressure (r=0.46, P<0.01). CONCLUSION: The Tei-Index is a sensitive indicator of overall cardiac dysfunction in patients with mild-to-moderate congestive heart failure. The Tei-Index is easily obtained and may be used in the work-up of patients with suspected cardiac dysfunction.
Aged↗
M-mode analysis of mitral annulus motion for detection of pseudonormalization of the mitral inflow pattern.
Left ventricular (LV) diastolic dysfunction is a frequent cause of heart failure. Doppler echocardiography has become the method of choice for the noninvasive evaluation of LV diastolic dysfunction. However, pseudonormalization of mitral inflow often presents a diagnostic problem in clinical practice. We sought to define the role of mitral annulus motion in this setting. We performed echocardiography in 36 consecutive subjects (age 59 +/- 10 years). Eighteen had recently (within 3 months) been diagnosed with coronary artery disease, 18 had clinical suspicion of coronary artery disease, and 15 had symptoms of heart failure (New York Heart Association class 2.4 +/- 0.5). The amplitude (E(M)) and the slope (slope E) of early diastolic motion of the septal mitral annulus were derived from M-mode analysis. Left heart catheterization was performed for direct measurement of LV end-diastolic pressure. Pseudonormalization defined by an E/A ratio > 1 and a LV end-diastolic pressure > or = 16 mm Hg was found in 9 patients. All patients with pseudonormalization were symptomatic (New York Heart Association class 2.8 +/- 0.5). Patients with and without pseudonormalization did not differ with respect to the E/A ratio (1.29 +/- 0.44 vs 1.16 +/- 0.23, p = NS), deceleration time (182 +/- 38 vs 205 +/- 42 ms, p = NS), and isovolumic relaxation time (88 +/- 24 vs 92 +/- 18 ms, p = NS). In the group with pseudonormalization, a significant reduction of E(M) (3.9 +/- 1.6 vs 5.7 +/- 1.5 mm, p = 0.008) and slope E (24.5 +/- 11.8 vs 43.9 +/- 7.7 mm/s, p <0.001) was detected. Using E(M) <4.3 mm and slope E <35 mm/s as cut points, sensitivity and specificity for the detection of pseudonormalization were 66% and 82% for E(M) and 77% and 87% for slope E, respectively. There was no significant relation between LV end-diastolic pressure as a measure of preload and either E(M) (r = 0.44, p >0.5) or slope E (r = 0.30, p >0.2). Thus, E(M) and slope E may be preload-independent tools for assessing LV diastolic dysfunction in symptomatic patients with a pseudonormal mitral inflow pattern and elevated filling pressures.
Adult↗
[Anti-ischemic effect of verapamil within the scope of interventional recanalization].
We report on a 46-year-old male with unstable angina pectoris due to a total proximal occlusion of the left circumflex artery. At the side of a plaque rupture there was a thrombotic occlusion. With PTCA recanalization was possible, but a dissection occurred, therefore coronary stents were implanted. Besides an optimal morphological result and recurrent applications of nitroglycerin, the baseline blood flow velocity declined from initial 16 cm/s to 11 cm/s after PTCA down to 8.4 cm/s after stent implantation. Because peak flow velocity remained almost unchanged, the low baseline velocity ("slow flow phenomenon") did not lead to an impaired coronary flow velocity reserve (CFVR). Only after application of 1 mg verapamil, a sustained flow velocity on a higher baseline level was reached (17 cm/s), at the same time typical signs of ischemia in the ECG (ST-segment depressions) improved. Additionally, in the non-treated LAD there was an increase in coronary blood flow velocity from 10 cm/s up to 25 cm/s. The reduction in coronary blood flow velocity with increasing manipulations might be due to an impairment of the coronary microcirculations with increasing alpha-adrenergic vasoconstriction, a distribution of vasoactive agents and peripheral microembolizations. Only after administration of verapamil, a calcium channel blocker with non-specific anti-adrenergic effects, the slow flow was removed and ECG signs of ischemia improved. The blood flow velocity in the non-treated LAD was low at baseline and improved after verapamil. This phenomenon leads to the conclusion that mechanisms with vasoconstrictive effect are present in the whole coronary system, but these mechanisms are less pronounced in non-treated vessels.
Angina, Unstable↗
[Analysis of mitral annulus excursion with tissue Doppler echocardiography (tissue Doppler echocardiography = TDE). Noninvasive assessment of left ventricular, diastolic dysfunction].
BACKGROUND: Mitral inflow velocity, deceleration time, and isovolumic relaxation time recorded by Doppler echocardiography have been widely used to evaluate left ventricular diastolic function but are affected by age, heart rate, loading conditions, and other factors. The diastolic mitral anulus velocity assessed by tissue Doppler echocardiography (TDE) was suggested to provide additional information about LV relaxation less affected by filling pressures. AIM OF THE STUDY: This study was designed to assess the clinical utility of mitral anulus velocity in the evaluation of left ventricular diastolic function. PATIENTS AND METHODS: Three groups of patients with a systolic ejection fraction > 45% were separated: 10 normal volunteers (60 +/- 10 y, CON group), 15 asymptomatic patients with known coronary artery disease (60 +/- 11 y, CAD group) and 15 patients with long-term arterial hypertension and heart failure symptoms (58 +/- 9 y, HYP group). The mitral inflow profile (E, A, E/A) was measured by pulsed Doppler, and the deceleration time (DT) and the isovolumic relaxation period (IVRT) were calculated. Systolic, early, and late diastolic velocities of the septal mitral anulus (ST, ET, AT, ET/AT) were assessed by pulsed TDE. All study subjects had invasive measurements of left ventricular end diastolic filling pressures during left heart catheterization. RESULTS: In the AH group, ET (6.9 +/- 4.8 cm/s) and ET/AT (0.71 +/- 0.28) were reduced compared to the CON group (11.7 +/- 4.7 cm/s and 1.11 +/- 0.36, p < 0.05, respectively) and the CAD group (8.9 +/- 5.4 cm/s and 0.85 +/- 0.26, respectively, p = ns). The groups did not differ with respect to the mitral E/A ratio, the deceleration time and the isovolumic relaxation time. LVED in the HYP group (16 +/- 8 mm Hg) was elevated compared to the CON group (8 +/- 3, p < 0.05) and the CAD group (12 +/- 6 mm Hg, p = ns). No correlation was found between ET and LVED (r = 0.26). When the combination of mitral E/A ratio > 1 with LVED > or = 15 mm Hg was classified as pseudonormalization, the pseudonormalization could be identified by a peak early diastolic mitral anulus velocity (ET) < 7 cm/s and an ET/AT ratio < 1 with a sensitivity of 77% and a specificity of 88%. CONCLUSIONS: The early diastolic mitral anulus velocity assessed by TDE (ET) is a preload-independent index of LV relaxation. TDE permits the detection of diastolic dysfunction in patients with a pseudonormal mitral inflow and elevated filling pressures.
Adult↗
Tissue Doppler imaging (TDI) for on-line detection of regional early diastolic ventricular asynchrony in patients with coronary artery disease.
Diastolic filling of the left ventricle is often impaired in patients with coronary artery disease (CAD) in the absence of systolic wall motion abnormalities or previous myocardial infarction. The current study was designed to assess the ability of tissue Doppler imaging (TDI) for on-line detection of regional diastolic wall motion abnormalities to identify CAD in patients with preserved systolic function. 20 normal subjects (age 51 +/- 13 years) and 17 CAD patients with normal systolic function and > or = 70% luminal narrowing of the LAD (age 56 +/- 11 years) were included. Coronary anatomy was unknown to the echocardiographer. In the parasternal short axis and the apical 4-chamber-view, peak tissue velocities of the anterior/inferior and the midseptal/midlateral LV segments during rapid ejection (RE), isovolumic relaxation (IR), rapid filling (RF) and atrial contraction (AC) were analyzed by color-M-Mode-TDI. In the apical view, in 13 of 35 (37%) patients with adequate recordings, myocardial asynchrony was detected during IR: while the septum was moving inwards (red color-coding), the lateral wall was moving outwards (blue/green coding). In the remaining 22 patients (63%) a slow, synchronous outward motion of septum and lateral wall with homogeneous color-coding (blue/green) was seen. Unblinding of the coronary status revealed a critical LAD stenosis in all 13 patients (100%) with myocardial asynchrony. Analysis of midseptal peak velocities during IR revealed positive velocities (1.22 +/- 1.64 cm/s) in CAD patients and negative velocities (-1.39 +/- 0.81 cm/s) in normal subjects. Thus, TDI allowed for the on-line detection of early diastolic asynchrony in 13 of 16 (82%) patients with critical LAD-narrowing. Due to the rapid assessment of regional wall motion abnormalities, TDI might help to identify CAD in patients with normal systolic function.
Aged↗
[Aortic rupture after blunt chest trauma. Rapid diagnosis using transesophageal echocardiography when radiographic and computed tomographic findings are unclear].
HISTORY AND CLINICAL FINDINGS: A 37-year-old woman who was not wearing a seat-belt while driving a car had a head-on collision at 70 km/h. On arrival of the emergency physician she was awake and responsive but complained of pain with bruising over the sternum and the epigastrium. Pressure on the sternum was painful. Arterial pressure was 95/60 mm Hg, heart rate 112/min. On admission the heart sounds were unremarkable and peripheral pulses normal. Vesicular sounds were heard over both lungs. In addition to multiple facial abrasions voluntary movements were impaired and the right knee-joint was swollen. INVESTIGATIONS: The ECG showed sinus tachycardia (103 beats/min) with left axis deviation, but was otherwise unremarkable. Initially the haemoglobin was 12.6 g/dl with normal white cell and platelet counts. Clotting tests, serum transaminases, creatine kinase, lactate dehydrogenase and other routine laboratory tests were within normal limits. TREATMENT AND COURSE: Because the haemoglobin level had fallen to 7.7 g/dl within the first 4 hours erythrocytes concentrate was infused. The chest radiogram and subsequent computed tomography showed a mediastinal and paraaortic haematoma of unclear origin. Transoesophageal echocardiography (TEE) demonstrated rupture of the descending aorta with free floating intraluminal parts of the intima in the isthmal region, just distal to the origin of the left subclavian artery, which was not occluded. Colour Doppler echocardiography revealed abnormal flow into mediastinal and paraaortic tissues. At operation the echocardiographic findings were confirmed and part of the descending aorta was replaced by a 3 cm dacron tube during an aortic crossclamping time of 37 min. The patient was discharged after a postoperative stay of average length, during which her other injuries were treated. CONCLUSION: After blunt thoracic or deceleration trauma earliest possible TEE is indicated, because it can at once provide details of extent and degree of injury to heart and/or aorta.
Accidents, Traffic↗
[Improved structure identification with tissue Doppler echocardiography].
Tissue Doppler echocardiography (TDE) has been shown to be of particular value in patients with impaired myocardial function. Recently, the technique was successfully employed to localize the ventricular insertion of accessory atrioventricular pathways. The identification of abnormal cardiac structures is coming up now as a new field of clinical interest. The purpose of this study was to differentiate anomalous cardiac and aortic from native structures by physical properties of tissue motion using transesophageal TDE. Characteristic motion patterns of anomalous structures have not been described in detail and tissue Doppler findings have not been associated with clinical features up to now. Forty consecutive patients were included after anomalous cardiac or vascular structures had been detected by conventional transesophageal echocardiography (TEE). A control group consisted of 20 subjects. Rapidity of diagnosis in anomalous structures was divided into 3 categories, and TDE signals were related to particular pathology by a blinded, 2nd observer. Three different motion patterns could be defined: incoherent motion due to free oscillation of an anomalous structure which is independent of the surrounding tissue (Figure 1b); coherent motion with a phase difference meaning that motion depends on the motion of the surrounding tissue but is out of phase (Figure 2); concordant motion showing no difference in direction, velocity, or phase of motion compared with the surrounding tissue. Incoherent motion was present in endocarditic vegetations, 4th degree aortic plaques, Chiari network, valvular prolapse, intracavitary tumors, and freely oscillating thrombi as well as in normal valve leaflets and papillary muscles. Especially if endocarditic vegetations are present its incoherent motion facilitates to recognize these small structures. The colorcode of this motion pattern demarcates the vegetation reliably from the surrounding tissue (Figure 1b). Within 15 seconds vegetations could be detected in 9 (82%) vs 2 (18%) patients employing only conventional imaging. Using conventional echocardiographic approaches detection of vegetations is frequently hindered by their small size and minor echo intensity (Figure 1a). In contrast, size and echo intensity do not affect the tissue Doppler signal. Normal papillary muscles and distal portions of the mitral and tricuspid valves were demonstrated to regularly meet the criterion of incoherent tissue motion in the control group. In part, this was also observed with respect to the aortic and pulmonary valves. In valvular tissue incoherent motion was caused by passive floating, whereas papillary muscles show an active inverse motion for short time intervals. Nevertheless, physiologic incoherent motion did not lead to any false differential diagnosis. The phase difference of coherent motion results from damped oscillation. This phenomenon was visualized by tissue Doppler M-mode in 5 thrombi of the left atrial appendage (LAA) (100%) and in 1 ventricular thrombus (50% of all clots). Concordant motion was shown in 3rd degree aortic plaques and postrheumatic and calcified vegetations. These structures were found to be completely embedded or closely attached, so that their passive motion corresponded to the motion of the surrounding regular tissue. Detection and assessment of anomalous structures are based on their motion patterns which can be synchronous or asynchronous in comparison with the surrounding tissue. Another goal of this investigation was to test if the sensitivity of TEE to spontaneous echo contrast can be improved using TDE. In 21 patients presenting with left atrial dilation (left atrial diameter > 44 mm) due to mitral stenosis (n = 8), mitral regurge (n = 5), arterial hypertension (n = 5) and multiple valvular disease (n = 3) fundamental multiplane TEE and transesophageal TDE were performed with standardized gain setting. The control group consisted of 20 randomized individuals with normal left
Aorta, Thoracic↗
[Asynchrony of ventricular contraction and relaxation--pathophysiologically recognized phenomenon, now can be clinically assessed].
When regional myocardial dysfunction is present, the physiological pattern of ventricular filling and contraction is impaired. During acute coronary occlusion, characteristic changes are observed in the ischemic myocardial segment: the amplitude of the systolic wall thickening is reduced (hypokinesia), then virtually absent (akinesia) and finally replaced by a paradoxical outward motion (dyskinesia). The maximum amplitude is reached in early diastole ("post-ejection thickening"). Since hyperkinesis develops in the normal region, the ischemic and the normal region contract asynchronously. Experimentally left ventricular asynchrony can be detected by means of subendo- and subepicardially implanted ultrasonic crystals ("sonomicrometry") or by the analysis of the phase difference of the first Fourier harmonic of dysfunctional versus control myocardial wall motion. In the clinical setting, digitized cineventriculography, radionuclide angiography and digitized M-mode echocardiography were used to assess left ventricular asynchrony in patients with coronary artery disease and hypertrophic cardiomyopathy. However, these imaging modalities are time-consuming and require complicated off-line analysis. Tissue Doppler echocardiography (TDE) is a new ultrasound modality that is based on color Doppler principles and allows for quantification of myocardial wall motion velocity by detection of consecutive phase shifts of the ultrasound signal reflected from the myocardium. The Doppler signals are displayed as a color or pulsed Doppler image by rejecting low-amplitude echoes from the blood pool due to changes in thresholding and filtering algorithms. In addition, the ability to measure low velocity is improved in the TDE system so that the lowest measurable velocity is 0.2 cm/s, a velocity level associated with cardiac tissue motion (Table 1). Due to its high temporal and spatial resolution, TDE provides valuable information on regional myocardial wall motion during different intervals of the cardiac cycle. In healthy subjects, patients with coronary artery disease and patients with hypertrophic cardiomyopathy, tissue Doppler echocardiography was used to assess myocardial synchrony/asynchrony on a 2-fold temporal and spatial analysis. Peak myocardial velocities in different myocardial regions were detected during rapid ejection, isovolumic relaxation, rapid filling and atrial contraction (Figure 1). In the apical view, during the isovolumic relaxation time (IVRT) healthy subjects showed slow, synchronous outward motion of the septum and the lateral wall with homogeneous color-encoding (blue/green, Figure 2). Analysis of peak velocities revealed low, negative velocities in both the septum and the lateral wall (Figure 3). In patients with a significant luminal narrowing of the LAD myocardial asynchrony was detected during the isovolumic relaxation period: while the septum was moving inwards (red color-encoding with low, positive velocities), the lateral wall was moving outwards (blue/green encoding, low, negative velocities). A representative example of a patient with CAD is given in Figure 4. The M-mode analysis of the abnormally contracting interventricular septum reveals positive peak tissue velocities during the isovolumic relaxation period (Figure 5). In hypertrophic cardiomyopathy, TDE was able to detect an abnormal inward motion of the interventricular septum during IVRT and a delay in the onset of rapid filling (Figure 6). Thus, tissue Doppler echocardiography is a feasible method for the on-line detection of myocardial asynchrony. Sensitivity and specificity of the findings have to be explored in further, prospectively randomized trials.
Cardiomyopathy, Hypertrophic↗
Influence of nitric oxide on renal function in toxic acute renal failure in the rat.
Besides other mechanisms, nitric oxide (NO) plays a major role in maintaining the high renal blood flow (RBF) and is also involved in the regulation of glomerular hemodynamics and contractility of mesangial cells. We examined the hypothesis that L-arginine-derived NO exerts beneficial effects in toxic acute renal failure (ARF) in the rat. To induce ARF uranyl nitrate (UN) was given intravenously as a bolus injection (25 mg/kg over 5 min) following a basal period. After the initiation phase of ARF (3 h) saline in the control group (C) and drugs in the experimental groups (I-III, each n = 8) were administered for 60 min. Group I: Arg (= L-arginine, 300 mg/kg), group II: MeArg (= N-methyl-L-arginine, 30 mg/kg), group III: Arg + MeArg (300 mg/kg, 30 mg/kg respectively). The experiments were continued for additional 60 min following the infusion period. Glomerular filtration rate (GFR, inulin clearance) was reduced 3 h after UN to about 50% of normal values in group I-III and control group. After infusion of Arg GFR had significantly improved, but remained unchanged after MeArg in relation to control. One hour after the infusion period these effects were even more pronounced. We conclude that NO exerts beneficial effects on renal function in this animal model of ARF. These results underline the regulatory role of the L-arginine/NO pathway for renal function not only under basal conditions but also in ARF.
Acute Kidney Injury↗
Toxic acute renal failure in the rat: effects of diltiazem and urodilatin on renal function.
Beneficial effects of natriuretic peptides have been reported in different models of acute renal failure (ARF). Calcium antagonists can also improve renal function, especially in ischemic models of ARF. The aim of our study was to investigate the effects of urodilatin and diltiazem alone and in combination in uranyl nitrate-induced toxic ARF in the rat. Three hours after induction of ARF glomerular filtration rate (GFR) was clearly diminished to about 50% compared to basal values. Intravenous infusion of diltiazem and urodilatin revealed a significant increase of GFR that even continued after cessation of drug delivery. Combined administration of urodilatin and diltiazem had no additional effect, probably due to a more pronounced fall in blood pressure in this group. Besides their vasorelaxing and blood pressure lowering effects both drugs also revealed diuretic activity. In conclusion both urodilatin and diltiazem are able to elevate GFR in the early phase of toxic ARF in the rat.
Acute Kidney Injury↗
Toxic acute renal failure in the rat: effects of L-arginine and N-methyl-L-arginine on renal function.
Nitric oxide (NO) is generated from L-arginine (Arg) by different isoforms of nitric oxide synthase (NOS) and plays a major role in maintaining the high basal renal blood flow. NO also is involved in the regulation of glomerular haemodynamics and contractility of mesangial cells. We examined the hypothesis that L-arginine-derived NO modifies toxic ARF in the rat. After a basal period uranyl nitrate (UN) was given intravenously as a bolus injection (25 mg/kg over 5 min) to induce ARF. After the initiation phase of ARF (3 h) saline in the control group (C) and drugs in the experimental groups (I-III, each n = 8) were administered for 60 min. Group I, Arg (300 mg/kg); group II, MeArg (30 mg/kg); group III, Arg + MeArg (300 mg/kg, 30 mg/kg resp.). The experiments were continued for further 60 min following the infusion period. Glomerular filtration rate (GFR, inulin clearance) was reduced 3 h after UN to about 50% of normal values in groups I-III and control group (I, 0.52 +/- 0.06; II, 0.51 +/- 0.05; III, 0.49 +/- 0.05; C, 0.50 +/- 0.07 ml/min). After infusion of Arg GFR had significantly improved (0.64 +/- 0.07), but further declined after MeArg (0.46 +/- 0.06) in relation to control (0.47 +/- 0.07). This negative effect could be overcome by combined administration of Arg + MeArg (0.59 +/- 0.07). One hour after the infusion period these effects were even more pronounced (Arg, 0.71 +/- 0.06; MeArg, 0.43 +/- 0.05; Arg + MeArg, 0.65 +/- 0.07; C, 0.46 +/- 0.05). We conclude that the L-arginine/NO pathway is involved in toxic ARF of the rat.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Kidney Injury↗
Effects of beta-lactoglobulin and kappa-casein genetic variants and concentrations on syneresis of gels from renneted heated milk.
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Animals↗
Effect of subclinical mastitis on milk plasminogen and plasmin compared with that on sodium, antitrypsin and N-acetyl-beta-D-glucosaminidase.
The effect of subclinical mastitis on levels of plasminogen and plasmin in milk from cows in a high-yielding herd was investigated. Comparisons were made with levels of milk Na, antitrypsin and N-acetyl-beta-D-glucosaminidase (NAGase). In samples from mastitic quarters plasminogen activity, as measured after activation to plasmin, increased by only 21% and plasmin by 82%, while NAGase increased by 307%. Plasminogen was the only component that was normally distributed, all other components showed more or less skewed distributions. Plasmin and plasminogen were significantly related to the other components. However, plasminogen plateaued when the other components continued to increase. There was thus no further increase in plasminogen with the severity of inflammation as with the other components. Plasmin showed a similar although less pronounced tendency. Results of treatment of mastitic whey samples with acid suggested that the non-linear increase in plasmin activity was due to interaction with acid-labile proteinase inhibitors. Mastitis led to dissociation of plasminogen and plasmin from the casein micelles. The degree of activation of plasminogen was higher with casein-associated than with soluble plasminogen in both healthy and mastitic milks. Plasmin was very closely related to milk Na, which is a sensitive indicator of epithelial integrity. It is suggested that plasmin contributes to Na leakage into milk by degrading membrane proteins of the epithelial lining. Plasminogen and antitrypsin, which are both plasma proteins, were not identically affected by stage of lactation, indicating nonidentical modes of transport from plasma to milk.
Acetylglucosaminidase↗